Endodontics torabinejad

Principles and Practiceof

ENDODONTICS


ENDODONTICSTHIRD EDITION

RICHARD E. WALTON, DMD, MSProfessor

Department of EndodonticsThe University of IowaCollege of Dentistry

Iowa City, Iowa

MAHMOUD TORABINEJAD, DMD, M5D, PhDProfessor and Program Director

Department of EndodonticsSchool of Dentistry

Loma Linda UniversityLoma Linda, California

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Library of Congress Cataloging-in-Publication DataWalton, Richard E., 1939-

Principles and practice of endodontics / Richard E. Walton, Mahmoud Torabinejad.--3rd ed.

p. ; cm.I ncludes bibliographical references and index.I SBN 0-7216-9160-91. Endodontics. I. Torabinejad, Mahmoud. II. Title.

[ DNLM: 1. Root Canal Therapy. 2. Endodontics. WU 230 W241 p 2002]RK351 .W35 2002617.6'342--dc21 2001042814

Editor-in-Chief John SchreferEditor: Penny RudolphDevelopmental Editor: Jaime PendillProject Manager: Patricia TannianProduction Editor: John CaseyBook Designer: Renee Duenow

PRINCIPLES AND PRACTICE OF ENDODONTICS ISBN: 0-7216-9160-9

Copyright © 2002 by W.B. Saunders CompanyPrevious editions copyrighted 1989, 1996

All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic ormechanical, including photocopy, recording, or any information storage or retrieval system, without permission in writing fromthe publisher.

Printed in the United States of America

Last digit is the print number:

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6 5 4 3 2 1

Contributors

Frances M. Andreasen, DDSAssociate Professor of Dental TraumatologyPediatric Dentistry and Oral and Maxillofacial SurgeryDental School, Health Sciences FacultyCopenhagen UniversityCopenhagen, Denmark

Jens 0. Andreasen, DDS, Odont. Dr.Associate DirectorDepartment of Oral and Maxillofacial SurgeryUniversity HospitalCopenhagen, Denmark

Leif K. Bakland, DDSProfessor and Chair, Department of EndodonticsDean for Advanced EducationSchool of Dentistry, Loma Linda UniversityLoma Linda, California

J. Craig Baumgartner, DDS, MS, PhDProfessor and Chairman, Department of

EndodontologyDirector, Advanced Education Program-EndodonticsOregon Health Sciences UniversityPortland, Oregon

Stephen Cohen, MA, DDSAdjunct Professor, Department of EndodonticsUniversity of the PacificSchool of DentistrySan Francisco, California

Shimon Friedman, DMDProfessor, Department of EndodonticsFaculty of DentistryUniversity of TorontoToronto, Ontario, Canada

Gerald N. Glickman, DDS, MS, MBAProfessor and Chairman, Department of EndodonticsDirector, Graduate Program in EndodonticsUniversity of Washington School of DentistrySeattle, Washington

Kenneth M. Hargreaves, DDS, PhDProfessor and Chair, Department of EndodonticsProfessor, Department of PharmacologyUniversity of Texas Health Science Center at San

AntonioSan Antonio, Texas

Gerald W. Harrington, DDS, MSDProfessor Emeritus, Department of EndodonticsUniversity of WashingtonSeattle, Washington

Graham Rex Holland, BDS, PhDProfessor, Department of CariologyRestorative Sciences and EndodonticsSchool of Dentistry, University of MichiganAnn Arbor, Michigan

Jeffrey W. Hutter, DMD, MEdChair, Department of EndodonticsDirector, Postdoctoral Program in EndodonticsGoldman School of Dental MedicineBoston UniversityBoston, Massachusetts

William T. Johnson, DDS, MSProfessor, Department of Family DentistryThe University of Iowa College of DentistryIowa City, Iowa

v

vi Contributors

Keith V. Krell, DDS, MS, MAClinical Associate Professor, Department of

EndodonticsThe University of Iowa College of DentistryIowa City, Iowa

Ronald R. Lemon, DMDProfessor and Chairperson, Department of

EndodonticsSchool of Dentistry, Louisiana State UniversityNew Orleans, Louisiana

Neville J. McDonald, BDS, MSClinical Professor and Division Head, EndodonticsDepartment of Cariology, Restorative Sciences and

EndodonticsSchool of Dentistry, University of MichiganAnn Arbor, Michigan

Harold H. Messer, BDSc, MDSc, PhDProfessor of Restorative DentistrySchool of Dental MedicineUniversity of MelbourneMelbourne, Victoria, Australia

Thomas R. Pitt Ford, BDS, PhDProfessor of EndodontologyGKT Dental InstituteKing's CollegeLondon, England

Alfred W. Reader, DDS, MSProfessor and Program Director, Department of

Graduate EndodonticsOhio State UniversityColumbus, Ohio

Eric M. Rivera, DDS, MSAssociate Professor and Graduate Program Director

and HeadDepartment of EndodonticsThe University of Iowa College of DentistryIowa City, Iowa

Ilan Rotstein, CDAssociate ProfessorChair of Surgical, Therapeutic, and Bioengineering

SciencesUniversity of Southern California School of DentistryLos Angeles, California

Gerald L. Scott, DDSClinical Assistant Professor, Department of EndodonticsDirector, Emergency ClinicThe University of Iowa College of DentistryIowa City, Iowa

Shahrokh Shabahang, DMDAssistant Professor, Department of EndodonticsSchool of Dentistry, Loma Linda UniversityLoma Linda, California

Asgeir Sigurdsson, DDS, MSAssociate Professor and Graduate Program Director,

Department of EndodonticsUniversity of North Carolina School of DentistryChapel Hill, North Carolina

Denis E. Simon III, DDS, MSAssociate Professor of Clinical EndodonticsLouisiana State University Health Science CenterSchool of DentistryNew Orleans, Louisiana

David R. Steiner, DDS, MSDAffiliate Professor, Graduate Endodontic ProgramUniversity of Washington School of DentistrySeattle, Washington

Calvin D. Torneck, DDS, MS, FRCD(C)Professor, Department of EndodonticsFaculty of DentistryUniversity of TorontoToronto, Ontario, Canada

Henry 0. Trowbridge, DDS, PhDProfessor Emeritus, Department of PathologyUniversity of PennsylvaniaPhiladelphia, Pennsylvania

Frank J. Vertucci, DMDProfessor and Chairman, Department of EndodonticsCollege of Dentistry, University of FloridaGainesville, Florida

James A. Wallace, DDS, MDS, MSD, MSDirector, Department of EndodonticsUniversity of Pittsburgh School of Dental MedicinePittsburgh, Pennsylvania

Lisa R. Wilcox, DDS, MSAdjunct Associate Professor, Department of EndodonticsThe University of Iowa College of DentistryIowa City, Iowa

Peter R. Wilson, MDS, MS, PhDAssociate ProfessorUniversity of Melbourne School of Dental ScienceMelbourne, Victoria, Australia

Preface

Endodontics deals with the diagnosis and treat-ment of pulpal and periradicular diseases. It is adiscipline that includes different procedures andas such is based on two inseparable bodies-artand science. Many advances have been made inboth the scientific and technologic aspects ofendodontics since the publication of the secondedition of this book 6 years ago. Despite thesechanges, the basic principles and practice of rootcanal therapy-eradication of root canal irritants,obturation of the root canal system, and preserva-tion of the natural dentition-remain unchanged.

This edition contains important and signifi-cant new endodontics information that has beencollected within the last 6 years. The new and up-dated information in this completely revised edi-tion is essential for those who elect general prac-tice and intend to treat uncomplicated cases.Although many changes have been made in con-tent, the overall emphasis and organization ofthis edition are the same as the first two editionsand are designed for dental students and generalpractitioners. We combined the chapters on diag-nosis and treatment planning and added two newchapters on endodontic therapeutics and geri-atric endodontics to reflect changes in practice.To familiarize our readers with the biology ofpulp and periradicular tissues, which is an essen-tial part of endodontic practice, we have includeda few chapters that cover embryology, anatomy,histology, physiology, pharmacology, pathology,and microbiology.

The chapters remain relatively concise andcontain updated information and references. Sev-eral color figures have been added to provide bet-ter visualization for the reader. To integrate theprinciples of biology and the practice of endo-dontics, we invited well-recognized contributingauthors who have direct association with predoc-toral endodontic education. The contributorswere asked to be precise and up to date and toprovide information that could be presented in a1-hour lecture or seminar. The intent of our text-book is to teach predoctoral students and generalpractitioners how to diagnose and treat uncom-plicated endodontic cases. This text is designed tobe neither a cookbook nor a preclinical laboratorytechnique manual.

We thank the contributing authors for theirdedication to teaching and for improving thelives of patients by preserving their natural denti-tion. We also express appreciation of the staff atHarcourt, whose collaboration and hard workhelped us to complete this edition. In addition,we recognize the many colleagues and studentswho gave us helpful suggestions and contributedmaterial to improve the quality of this text, whichhas become one of the most popular in our field.Please keep these suggestions coming. We appre-ciate the suggestions; they will be incorporated inour future editions.

RICHARD E. WALTONMAHMOUD TORABINEJAD

VII

Contents

Scope of Undergraduate Teaching in Endodontic Education, 1

Richard E. Walton and Mahmoud Torabinejad

2 /

Biology of the Dental Pulp and Periradicular Tissues, 3Calvin D. Tomeck and Mahmoud Torabinejad

3 /

Pulp and Periradicular Pathosis, 27Mahmoud Torabinejad

4 /

Diagnosis and Treatment Planning, 49Richard E. Walton and Mahmoud Torabinejad

5 /

When and How To Refer, 71Mahmoud Torabinejad and Denis E. Simon 111

6 /

Patient Education, 87Stephen Cohen and Mahmoud Torabinejad

7 /

Local Anesthesia, 99Richard E. Walton and Alfred W. Reader

8 / Isolation, 118Gerald L. Scott

9 /

Endodontic Radiography, 130

Richard E. Walton

10/

Endodontic Instruments, 151

Keith V. Krell

11 /

Internal Anatomy, 166Richard E. Walton and Frank J. Vertucci

12

Access Preparation and Length Determination, 182Richard E. Walton

13 /

Cleaning and Shaping, 206Richard E. Walton and Eric M. Rivera

ix

x Contents

14 / Obturation, 239Richard E. Walton and William T. Johnson

15 / Preparation for Restoration and Temporization, 268Harold H. Messer and Peter R. Wilson

16 /

Endodontic Microbiology, 282J. Craig Baumgartner

17 /

Endodontic Emergencies, 295Richard E. Walton and Jeffrey W. Hutter

18 /

Procedural Accidents, 310Mahmoud Torabinejad and Ronald R. Lemon

79 /

Evaluation of Success and Failure, 331Asgeir Sigurdsson

20 / Orthograde Retreatment, 345Shimon Friedman

21 / Preventive Endodontics: Protecting the Pulp, 369Henry O. Trowbridge

22 /

Management of Incompletely Formed Roots, 388Thomas R. Pitt Ford and Shahrokh Shabahang

23 /

Bleaching Discolored Teeth: Internal and External, 405llan Rotstein and Richard E. Walton

24 /

Endodontic Surgery, 424Neville J. McDonald and Mahmoud Torabinejad

25 /

Management of Traumatized Teeth, 445Leif K. Bakland, Frances M. Andreasen, and Jens O. Andreasen

26 /

Periodontal-Endodontic Considerations, 466Gerald W. Harrington and David R. Steiner

27 /

Endodontic Adjuncts, 485Gerald N. Glickman and James A. Wallace

28 /

Longitudinal Tooth Fractures, 499Richard E. Walton

29 /

Differential Diagnosis of Orofacial Pain, 520Graham Rex Holland

30 /

Endodontic Therapeutics, 533Kenneth M. Hargreaves and J. Craig Baumgartner

31 /

Geriatric Endodontics, 545Richard E. Walton

Appendix: Pulpal Anatomy and Access Preparations, 561Lisa R. Wilcox


ENDODONTICS

Scope of Undergraduate Teaching in Endodontic Education

he accepted definition of endodonticsis "That branch of dentistry concernedwith the morphology, physiology, and

pathology of the human dental pulp and peri-radicular tissues. Its study and practice encom-pass the basic and clinical sciences includingbiology of the normal pulp, the etiology, diag-noses, prevention, and treatment of diseases andinjuries of the pulp and associated periradiculartissues."'

In addition to these knowledge areas, the grad-uating dentist must be able to critically evaluatehis or her level of competency as a diagnosticianand clinician. Based on this evaluation, the grad-uate must recognize the effect of his or her ownlimitations in managing patients with conditionsfor which he or she possesses less than a compe-tency level of skill; those patients are referred tothe appropriate specialist for consultation and/ortreatment.

The purpose of this textbook is to supply theundergraduate dental student with basic knowl-edge in endodontics. This information is nec-essary to successfully complete an endodonticcurriculum in preparation for graduation. Theknowledge and skills are needed by the generalpractitioner to prevent, diagnose, and treat pulpaland/or periradicular pathoses and to recognizeother related disorders.

Principles and Practice of Endodontics is based onthe Curriculum Guidelines for Endodontics for pre-doctoral students. These guidelines were devel-oped by The American Association of DentalSchools Section on Endodontics, in response to arequest from the American Dental Association'sCouncil on Dental Education.2,3

The Guidelines represent a matrix for develop-ing an undergraduate endodontic curriculum.They specify that endodontic teaching has a

basis in, and interrelates with, biomedical sci-ences. In addition, clinical treatment must in-tegrate closely with other disciplines. This ma-trix would be universal. A recent survey ofdental schools in North America and Europeshowed consensus of undergraduate teaching inendodontics.'

Undergraduate Curriculum

As a prerequisite to or in conjunction with endo-dontic training, the student should have knowledgeof (1) oral anatomy and histology; (2) infection,inflammation, healing, and repair; (3) microbi-ology and immunology; (4) pain; (5) radiology;(6) caries and other pulpal irritants; (7) therapeuticagents; (8) systemic diseases; (9) medical emergen-cies; and (10) management of medically compro-mised patients.

Upon completion of predoctoral instruction,the graduating dentist must be able to manageuncomplicated endodontic procedures as a gen-eral practitioner. In preparation for this, thecore curriculum for undergraduates must include(1) diagnosis and treatment planning, (2) man-agement of the vital pulp, (3) uncomplicated rootcanal treatment, (4) management of proceduralerrors, (5) determination of success or failure,(6) primary management of trauma, (7) internalbleaching of discolored teeth, (8) management ofemergencies, and (9) management of uncompli-cated retreatments.

The graduating dentist should also be famil-iar with other endodontic procedures, recogniz-ing their role in the treatment of patients. Mostof these should be referred to the endodontictfor management. These include (1) challengingdiagnoses, (2) complicated root canal treatment,

1

2

1 / Scope of Undergraduate Teaching in Endodontic Education

(3) complicated emergency management, (4) dif-ficult retreatment, (5) long-term managementof trauma, (6) endodontic-periodontic interre-lationships, (7) endodontic-orthodontic prob-lems, (8) open apex management, (9) compli-cated cracked tooth, (10) endodontic surgery,and (11) intentional replantation.

The graduate must be able to perform self-evaluation. This is a critical evaluation of his orher level of competency diagnostically and tech-nically. The end result is independent thinkingand action; the ultimate benefit is providingquality care to the patient.

REFERENCES

1. American Association of Endodontists: Appropriate-ness of Care and Quality Assurance Guidelines, ed 3,Chicago, The Association, 1998, p.3.

2. American Association of Dental Schools, Section onEndodontics: Curriculum Guidelines for Endodontics,

J Dent Educ 50:190, 1986.3. Curriculum Guidelines for Endodontics, J Dent Educ

57:251, 1993.4. Qualtrough A, Whitworth J, Dummer P: Preclinical en-

dodontology: an international comparison, IntEndodonJ32:406, 1999.

Biology of the Dental Pulpand Periradicular Tissues

LEARNING OBJECTIVES

After reading this chapter, the student should be able to:

1 / Describe the development of pulp from its embryologic stage to its fully developed state.

2 / Describe the process of root development and maturation of the apical foramen.

3 / Recognize the anatomic regions of pulp.

4 / List cell types in pulp and state their function.

5 / Describe the fibrous and nonfibrous components of the extracellular matrix of pulp.

6 / Describe the blood vessels and lymphatics of pulp.

7 / List the neural components of pulp and describe their distribution and function.

8 / Discuss theories of dentin sensitivity.

9 / Describe pathways of efferent nerves from pulp to the central nervous system.

10 / Describe changes in pulp morphology that occur with age.

11 / Describe the structure and function of periradicular tissues.

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4

2 / Biology of the Dental Pulp and Periradicular Tissues

Embryology of the Dental Pulp

Early Development of Pulp

Root Formation

Formation of Lateral Canals and Apical

Foramen

Formation of Periodontium

Anatomic Regions and Their Clinical

I mportance

Pulp Function

I nduction

Formation

Nutrition

Defense

Sensation

Histology

Cells of the Dental Pulp

Odontoblasts

Preodontoblasts

Fibroblasts

Undifferentiated (Reserve) Cells

Cells of the Immune System

Extracellular Components

Fibers

Ground Substance

Calcifications

Blood Vessels

Afferent Blood Vessels (Arterioles)

Efferent Blood Vessels (Venules)

Vascular Physiology

Lymphatics

I nnervation

Neuroanatomy

Developmental Aspects of Pulp Innervation

Theories of Dentin Hypersensitivity

Age Changes in the Dental Pulp

Morphologic Changes

Physiologic Changes

Periradicular Tissues

Cementum

Cementoenamel Junction

Periodontal Ligament

Alveolar Bone

ental pulp is the soft tissue located inthe center of the tooth. It forms, sup-ports, and is an integral part of the

dentin that surrounds it. The primary function ofthe pulp is formative; it gives rise to odontoblaststhat not only form dentin but interact with dentalepithelium, early in tooth development, to initiatethe formation of enamel. Subsequent to toothformation, pulp provides several secondary func-tions related to tooth sensitivity, hydration, anddefense. Injury to pulp may cause discomfort anddisease. Consequently the health of the pulp isimportant to the successful completion of re-storative and prosthetic dental procedures. Inrestorative dentistry, for example, the size andshape of the pulp must be considered to deter-mine cavity depth. The size and shape of the pulp,in turn, may be influenced by the stage of toothdevelopment (related to patient age). The stage oftooth development may also influence the type ofthe pulp treatment rendered when a pulp injuryoccurs. Procedures routinely undertaken on afully developed tooth are not always practical fora tooth that is only partially developed. In suchcases special procedures not often used for themature tooth are applied. Because the symptomsas well as the radiographic and clinical signs ofpulp disease are not always readily differentiatedfrom the signs and symptoms of other dental andnondental diseases, a knowledge of the biology ofthe pulp also is essential for the development of arational treatment plan. For example, the appear-ance of periodontal lesions of endodontic origincan be similar to that of lesions induced by pri-mary disease of periodontium and lesions of non-dental origin. An inability to recognize this sim-ilarity may lead to misdiagnosis and incorrecttreatment. Comprehensive descriptions of pulpembryology, histology, and physiology are avail-able in several dental texts. This chapter presentsan overview of the biology of the pulp and theperiodontium: development, anatomy, and func-tion that affect pulp disease as well as periradicu-lar disease and its related symptoms.

Embryology of the Dental Pulp

EARLY DEVELOPMENT OF PULP

Pulp originates from ectomesenchymal cells (de-rived from the neural crest) of the dental papilla.Dental pulp is identified when these cells matureand dentin has formed. Differentiation of odon-toblasts from undifferentiated ectomesenchymalcells is accomplished through an interaction ofcells and signaling molecules mediated throughthe basal lamina and the extracellular matrix.'


5

The expression of various growth factors from thecells of the inner enamel membrane initiates thedifferentiation process.2 Several cell replicationsare required before an odontoblast appears. Intooth development, only the cells next to basallamina replicate fully into odontoblasts. Not fullyreplicated daughter cells derived from odonto-blasts remain in the subodontoblastic region aspreodontoblasts. Under specific circumstances dic-tated by the environment, these cells can replicateand form odontoblasts when required.'

Formation of dentin by odontoblasts heraldsthe conversion of dental - papilla to dental pulp.This formation begins with formation of extensivejunctional complexes and gap junctions betweenodontoblasts and the deposition of unmineralizedmatrix at the cusp tip (Figure 2-1). Deposition pro-gresses in a cervical (apical) direction in a rhyth-mic, regular pattern and averages about 4.S um/day. 4 Crown shape is predetermined by the prolif-erative pattern of the cells of the inner enamel ep-ithelium. The first dentin formed is called mantledentin. The deposition and size of the collagenfibers in mantle dentin are different from those forfibers of the circumpulpal dentin, which formsafter the odontoblast layer is organized and whichrepresents most of the dentin that is formed. Min-eralization occurs shortly after matrix has formed.Normally, 10 to 47um of the dentin matrix imme-diately adjacent to the odontoblast layer remainsunmineralized and is referred to as predentin. Itsabsence may predispose the dentin to internal re-sorption by odontoblasts.

As crown formation occurs, vascular and sen-sory neural elements begin migrating into thepulp in a coronal direction. The ingrowth ofunmyelinated sensory nerves (c fibers) occurs atabout the same time as that of the myelinatedsensory nerves (A8 fibers). Eventually the my-elinated nerves lose their myelin sheath and ter-minate in the subodontoblastic region as anunmyelinated plexus (plexus of Raschkow). Thisusually occurs after the tooth has erupted, androot formation has been completed.' Formationand mineralization of enamel begins at the cusptip shortly after the dentin has formed, a furtherexpression of epithelial-ectomesenchymal inter-actions in tooth formation.

ROOT FORMATION

The cells of the inner and outer enamel unite at apoint known as the cervical loop. This delineatesthe end of the anatomical crown and the sitewhere root formation begins. It is initiated by theapical proliferation of the two epithelial struc-tures, which combine at the cervical loop to form

a double layer of cells known as Hertwig's epithe-lial root sheath. The function of the sheath is sim-ilar to that of the inner enamel epithelium duringcrown formation. It provides the stimulus for thedifferentiation of odontoblasts, which form thedentin and the template to which the dentin isformed (Figure 2-2). Cell proliferation in the rootsheath is genetically determined; its pattern regu-lates whether the root will be wide or narrow,straight or curved, long or short, or single or mul-tiple. Multiple roots result when opposing partsof the root sheath proliferate horizontally as wellas vertically. As horizontal segments join and con-tinue to proliferate apically, an additional root ormultiple roots are formed. The pattern of prolif-eration also determines whether the roots are sep-arate or joined as can be noted in mandibular mo-lars and maxillary premolars. Patterns of rootsheath proliferation and progressive differentia-tion and maturation of odontoblasts are readilydiscernible when the developing root end isviewed microscopically (Figure 2-3).

FIGURE 2-7Late bell stage of tooth formation with early dentin forma-tion. dl, Dental lamina; d, newly formed dentin; o, odonto-blasts, oe, outer enamel epithelium; ie, inner enamel epithe-li um; cl, cervical loop; dp, dental papilla.

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FIGURE 2-2Apical region of developing incisor. ers, Epithelium rootsheath; p, pulp; d, dentin; n, nerve; v, venule.

After the first dentin (mantle dentin) hasformed, the underlying basement membranebreaks up, and the innermost root sheath cellssecrete a hyaline-like material, presumed to beenameloid, over the newly formed dentin. Afterits mineralization this becomes the hyaline layerofHopewell-Smith. This helps bind the soon-to-be-formed cementum to dentin.6 Fragmentation ofHertwig's epithelial root sheath occurs shortlyafterwards. This allows cells of the surroundingfollicle to migrate and contact the newly formeddentin surface, where they differentiate intocementoblasts and initiate acellular cementumformation. This cementum ultimately serves asan anchor for the developing principal periodon-tal fibers (Figure 2-4). In many teeth, cell rem-nants of the root sheath persist in the periodon-tium in close proximity to the root after rootdevelopment has been completed. These are theepithelial cell rests of Malassez. Normally function-less, in the presence of inflammation they canproliferate and may under certain conditionsgive rise to a radicular cyst.'

FIGURE 2-sHigher-power photomicrograph of Hertwig's epithelial rootsheath (ers) shown in Figure 2-2. New odontoblasts (no) aredifferentiating along the pulpal side of the root sheath andeventually forming dentin (d). Functioning odontoblasts (o)continue to form dentin after the root sheath begins to breakup (large arrowhead). A venule (v) exits the pulp near theroot sheath.

FORMATION OF LATERAL CANALS

AND APICAL FORAMEN

Lateral Canals

Lateral canals (or, synonymously, accessorycanals) are channels of communication betweenpulp and periodontal ligament. They form when alocalized area of root sheath is fragmented beforedentin formation. The result is direct communi-cation between pulp and lateral periodontal liga-ment via a channel through the dentin. Lateralcanals also can form when blood vessels, whichnormally pass between dental papilla and invest-ing dental follicle, become entrapped in the pro-liferating epithelial root sheath. Lateral canalsmay be large or small or multiple or singular; theymay occur anywhere along the root but predomi-nate in the apical third. In molars they may extendfrom the pulp chamber to furcation. Lateral canals


7

FIGURE 2-4Higher-power photomicrograph of developing root shows ce-mentoblasts (c) differentiating and producing cementum ondentin (d) subsequent to breakup of the epithelium rootsheath. Odontoblasts (o) are forming dentin on the pulpalside of the dentin.

are clinically significant; like the apical foramen they rep-resent pathways along which disease in pulp may extendto periradiculr tissues and occasionally allow disease inperiodontium to extend to pulp.

Apical Foramen

As the epithelial root sheath proliferates, it en-closes more dental papilla until only a basal (api-cal) opening remains. This opening is the princi-pal entrance and exit for pulpal vessels and nerves.During root formation the apical foramen is usu-ally located at the end of the anatomic root. How-ever, by the time tooth development has beencompleted, the apical foramen is smaller andmore eccentric. This eccentricity becomes morepronounced when apical cementum is formedand changes again with the continued depositionof cementum associated with coronal wear andtooth drifting.

There may be one foramen or multiple foraminaat the apex. Multiple foramina occur more often inmultirooted teeth. When more than one foramen ispresent, the largest one is referred to as the apicalforamen and the smaller ones as accessory canals(in combination, the apical delta). The diameter ofthe apical foramen in a mature tooth usuallyranges between 0.3 and 0.6 mm. The largest diam-eters are found on the distal canal of mandibularmolars and the palatal root of maxillary molars.'Foramen size is unpredictable, however, and can-not be accurately determined clinically.

FORMATION OF PERIODONTIUM

Tissues of the periodontium, which include the ce-mentum, periodontal fibers, and the alveolar bone,arise from ectomesenchyme-derived fibrocellulartissue that surrounds the developing tooth (den-tal follicle). After the mantle dentin has formed,enamel-like proteins are secreted into the space be-tween the basement membrane and the newlyformed collagen by the root sheath cells. This areais not mineralized with the mantel dentin but doesmineralize later and to a greater degree to form thehyalin layer of Hopewell-Smith. After mineralizationhas occurred, the root sheath undergoes fragmen-tation. This fragmentation allows cells from thefollicle to proliferate through the root sheath, dif-ferentiate into cementoblasts, and produce cemen-tum over the hyalin layer. Bundles of collagen,produced by fibroblasts in the central region ofthe follicle (Sharpey's fibers), are embedded in theforming cementum and serve as an anchor for thesoon-to-be-formed principal periodontal fibers.

Concomitantly, cells in the outermost area ofthe follicle differentiate into osteoblasts to formthe bundle bone that also will serve as an anchorfor the periodontal fibers. Later periodontal fi-broblasts produce collagen that links the an-chored fragments together to form the arrange-ment of principle periodontal fibers that suspendthe tooth in its socket. Areas of the periodontiumbetween the principal fibers remain as loose fi-brous connective tissue through which nerves andvessels that supply the periodontium pass. Undif-ferentiated (or partly differentiated) cells are plen-tiful in the periodontium and possess the abilityto form new cementoblasts, osteoblasts, or fibro-blasts, in response to specific stimuli. Cementumformed after the formation of the principle peri-odontal fibers is of the cellular type and plays alesser role in tooth support.

The blood supply to the periodontium is de-rived from the surrounding bone, gingiva, andpulpal vessels. It is extensive and supports the

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FIGURE 2-5Anatomic regions of the root canal system highlighting thepulp horn(s), pulp chamber, root canal, lateral canal, andapical foramen. The pulp, which is present in the root canalsystem, communicates with the periodontal ligament pri-marily through the apical foramen and the lateral canal(s).(Courtesy Orban Collection.)

high level of cellular activity in the area. The pat-tern of innervation is similar to that of the vascu-lature. The neural supply consists of small un-myelinated sensory and autonomic nerves andlarger myelinated sensory nerves. Some of the lat-ter terminate as unmyelinated neural structures,which are thought to be nociceptors and mech-anoreceptors. No proprioceptive properties havebeen attributed to these nerves.' °

Anatomic Regions and TheirClinical Importance

The tooth has two principal anatomic divisions,root and crown, that join at the cervix (cervical re-gion). Pulp space is similarly divided into coronaland radicular regions. In general, the shape andthe size of the tooth surface determine the shapeand the size of the pulp space. Coronal pulp issubdivided into pulp horn and pulp chamber(Figure 2-5). Pulp horns extend from the chamberinto the cuspal region. In some teeth, they are ex-tensive and may be inadvertently exposed duringroutine cavity preparation.

FIGURE 2-6A and B, Radiographic changes noted in the shape of the pulp chamber over time. The posterior bitewing radio-graphs were taken 15 years apart. The shapes of the root canal systems have been altered as a result of secondarydentinogenesis and in instances where deep restorations are present, by the deposition of tertiary dentin.C, Human mandibular molar showing deposition of secondary dentin (so) on the roof and floor of the pulpchamber; this tends to "flatten" the chamber.


9

As will be discussed later in this chapter under"Age Changes in the Dental Pulp," the pulp spacebecomes asymmetrically smaller over time, due tothe continued, albeit slower, production of dentin.Principally there is a pronounced decrease in theheight of the pulp horn and a reduction in the over-all size of the pulp chamber. In molars the apical-occlusal dimension is reduced more than themesial-distal dimension. Excessive reduction of thesize of the pulp space is clinically significant andcan lead to difficulties in locating, cleaning, andshaping the root canal system (Figure 2-6, A to C.

Anatomy of the root canal can vary not onlybetween tooth types but also within tooth types.Although at least one canal must be present ineach root, some roots have multiple canals,some comparable in size and others different.Understanding and appreciating all aspects of rootcanal anatomy are essential prerequisites to root canaltreatment.

Variation in the size and location of the apicalforamen influences the degree to which bloodflow to the pulp may be compromised after a trau-matic event. In this situation, young, partially devel-oped teeth have a better prognosis for pulp survival thanteeth with mature roots (Figure 2-7).

Posteruptive deposition of cementum in theregion of the apical foramen creates a disparitybetween the radiographic apex and the apicalforamen. It also creates a funnel-shaped openingto the foramen that is often larger in diameterthan the intraradicular portion of the foramen.The narrowest portion of the canal has been re-ferred to as the "constriction." However, a constric-

tion is not clinically evident in all teeth." Cemen-tum contacts dentin inside the canal coronal tothe cementum surface. That point is the cemento-dentinal junction (CDJ). The CDJ level varies notonly from tooth to tooth but also within a singleroot canal. One study estimated the junction tobe located 0.5 to 0.75 mm coronal to the apicalopening.' Theoretically, that is the point wherethe pulp terminates and the periodontal ligamentbegins. However, histologically and clinically it isnot always possible to locate that point. Cleaning,shaping, and obturation of the root canal shouldterminate short of the apical foramen and remainconfined to the canal to avoid unnecessary injuryto the periapical tissues. The determination of rootlength and the establishment of a working length are es-sential prerequisites to root canal preparation, for thatreason. The radiograph and electronic apex locators arehelpful in establishing the root length.

Pulp Function

The pulp performs five functions, some formativeand others supportive.

I NDUCTION

Pulp participates in the initiation and develop-ment of dentin, which, when formed, leads tothe formation of enamel. These events are inter-dependent in that enamel epithelium inducesthe differentiation of odontoblasts, and odon-toblasts and dentin induce the formation of

FIGURE 2-7Changes in the anatomy of the toothroot and pulp space. A, A small crown-root ratio, thin dentin walls, and di-vergent shape in the apical third ofthe canal are seen. B, Four years later,a longer root, greater crown-rootratio, smaller pulp space, and thickerdentin walls with a convergent shapeare seen.

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enamel. Such epithelial-mesenchymal interactionsare the essence of tooth formation.

FORMATION

Odontoblasts form dentin. These highly special-ized cells participate in dentin formation in threeways: (1) by synthesizing and secreting inorganicmatrix; (2) by initially transporting inorganic com-ponents to newly formed matrix; and (3) by creat-ing an environment that permits mineralization ofmatrix. During early tooth development, primarydentinogenesis is generally a rapid process. Aftertooth maturation, dentin formation continues ata much slower rate and in a less symmetrical pat-tern (secondary dentinogenesis). Odontoblasts canalso form a dentin in response to injury, whichmay occur in association with caries, trauma, orrestorative procedures. Generally this dentin is lessorganized than primary and secondary dentin andmostly localized to the site of injury. This dentin isreferred to as tertiary dentin. Morphologically ter-tiary dentin has a variety of appearances. It is alsoreferred to as reactive, reparative, irritation, or ir-regular dentin (Figure 2-8).

NUTRITION

Pulp supplies nutrients that are essential fordentin formation (for example, peritubular den-tin) and hydration via dentinal tubules.

DEFENSE

As mentioned previously, odontoblasts form den-tin in response to injury, particularly when theoriginal dentin thickness has been reduced dueto caries, attrition, trauma, or restorative proce-dures. Dentin can also be formed at sites where itscontinuity has been lost, such as a site of pulpexposure. This occurs through the induction, dif-ferentiation, and migration of new odontoblastsor odontoblast-like cells to the exposure site.1 2,13However, the structure of dentin produced in re-sponse to injury such as this may not resemblethat of dentin produced physiologically andhence may not afford the same degree of protec-tion to the underlying pulp tissue (Figure 2-9).

Pulp also has the ability to process and identifyforeign substances and to elicit an immune re-sponse to their presence. This is typical of theresponse of the pulp to dentinal caries.

SENSATION

Pulp transmits neural sensations mediatedthrough enamel or dentin to the higher nervecenters. These stimuli are usually expressed clin-ically as pain, although physiologic and psycho-physiologic studies indicate that pulp can trans-mit sensations of temperature and touch. 14,15

Pulp also transmits sensations of deep pain,which may be initiated by disease, principally in-

FIGURE z-sA, Reactive dentin formation under caries (c). Pulp displays chronic in-flammation and tertiary dentinogenesis on the inner walls of the pulpspace in the region of the dentinal tubules associated with the base ofthe carious lesion. B, Higher-power photomicrograph of tertiary dentinshown in A. PD, primary dentin; RD1, first period of tertiary dentin for-mation; CL, calciotraumatic line; RD2, second period of tertiary dentinformation. Note the progressive irregularities in tubule formation andchanges in the morphology of the odontoblasts (P) in that region.


1 1

flammatory disease. Pulp sensation mediatedthrough dentin and enamel is usually fast, sharp,and severe and is transmitted by A5 fibers (my-elinated fibers). Sensation initiated within thepulp core and transmitted by the smaller c fibersis slower, duller, and more diffuse.

Histology

Dentin and pulp are really a tissue complex; there-fore a discussion of pulp (particularly odonto-blasts) should include a discussion of dentinformation and maturation. It should also be re-membered that their histologic appearance varieschronologically and in accordance with their ex-posure to external stimuli. .

Under light microscopy, a young, fully developedpermanent tooth shows certain recognizable as-pects of pulp architecture. In its outer (peripheral)regions subjacent to predentin there is the odonto-blast layer. Internal to this layer is a relatively cell-free area (the zone of Weil). Internal to the cell-freezone is a higher concentration of cells (cell-richzone). In the center is an area containing mostlypulp cells and major branches of nerves and bloodvessels referred to as the pulp core (Figure 2-10).

Cells of the Dental PulpODONTOBLASTS

Odonroblasts are the most distinctive cells ofpulp. They form a single layer at its periphery andthey synthesize the matrix, which is mineralizedand becomes dentin. In the coronal part of thepulp space the odontoblasts are numerous andrelatively large and columnar in shape. They num-ber between 45,000 and 65,000/mm' in that area.In the cervical portion and midportion of the roottheir numbers are fewer and they are flattened(squamous) in appearance. Significantly, the mor-phology of the cell generally reflects its functionalactivity, with larger cells having a capacity to syn-thesize more matrix." Odontoblasts are end cellsand as such do not undergo further cell division(see "Preodontoblasts"). During their life span,which could equal the period of pulp vitality, theygo through functional, transitional, and restingphases, all marked by differences in cell size andorganelle expression.

The odontoblast consists of two major struc-tural and functional components, the cell bodyand the cell process. The cell body lies subjacent tothe unmineralized dentin matrix (predentin). Thecell process extends outwardly through a tubule inthe predentin and dentin. The distance to which

it extends has been debated among anatomistsfor years. Some studies have shown that theprocess extends only part way through the den-tin, while others have shown that it extendsthrough the full thickness of the dentin and ter-minates at or close to the dentinoenamel junc-tion (DEJ) or CDJ.17,18 The extent to which the cellprocess has been found appears to be influencedby the method of investigation. Today the issueremains unresolved; it is likely that there is varia-tion in its extent.

The cell body is the synthesizing portion of thecell and contains a basally located nucleus andan organelle structure in the cytoplasm that is typ-ical of a secreting cell. During active dentinogene-sis, endoplasmic reticulum and the Golgi appara-tus are prominent with numerous mitochondriaand vesicles (Figure 2-11). Cell bodies are joined bya variety of complex junctions consisting of gapjunctions, tight junctions, and desmosomes whoselocations are variable and determined by function.

FIGURE z-sPhotomicrograph of a mandibular permanent molar thatwas mechanically exposed earlier and capped with a pasteof calcium hydroxide and saline. Tertiary (reparative) irregu-lar dentin (id) at the site of exposure displays irregularities(arrowheads) that can be traced from surface to pulp. Theclear area at the pulp surface below the irregular dentin isan artifact.

12


FIGURE 2-10

A, Mandibular premolar showing major features of dentin-pulp anatomy. From the periphery inward there is themineralized dentin, predentin, odontoblasts, and cell-free and cell-poor zones of the pulp. The central pulp or pulpcore is cellular and contains the major nerves and blood vessels of the pulp. B, Odontoblast-predentin interfaceat higher power. Odontoblast cell nuclei (n) are aligned along the predentin. The arrow indicates an odontoblastprocess in a tubule in predentin. C, High-power photomicrograph of fibroblasts in the pulp core. At this magnifi-cation only the nuclei are apparent interspersed between collagen fibers of the extracellular matrix.

The junctions isolate the site where dentin isformed and regulate the flow of substances intoand out of the area.19 Secretory products of theodontoblasts are released through the cell mem-brane at the peripheral end of the cell body and thebasal end of the cell process .2° Initially this in-cludes organic components of the dentin matrixand mineralization crystals but subsequent to theinitial mineralization of the dentin only matrixcomponents are secreted. Odontoblasts are mostactive during primary dentinogenesis and duringreparative dentin formation. Activity is substan-tially reduced during ongoing secondary dentino-genesis.

PREODONTOBLASTS

New odontoblasts can arise after an injury that re-sults in a loss of existing odontoblasts. The prob-

ability is that preodontoblasts (cells that havepartly differentiated along the odontoblast line)do exist and reside in the cell-rich zone. These pre-cursor cells migrate to, and continue their differ-entiation at, the site of injury. To date, the specificcircumstances leading to this type of replacementare unknown, although certain growth factorssuch as bone morphogenic protein (BMP) andtransforming growth factor beta in combinationwith other tissue components appear to initiatethe change . 21

FIBROBLASTS

Fibroblasts are the most common cell type andare seen in greatest numbers in the coronal pulp.They produce and maintain the collagen andground substance of the pulp and alter the struc-ture of the pulp in disease. 12 Like odontoblasts,


13

FIGURE 2-11A, Odontoblast cell body. The nucleus (N) is proximal, and the numerous organelles such as rough endoplasmic reticulum (RER)and Golgi apparatus (G), which are responsible for synthesis of matrix components, occupy the central-distal regions. B, Pre-dentin (P) shows the orientation of collagen (C) to the odontoblastic process, which is the secretory organ that extends throughthe predentin into the dentin (D). (Courtesy Dr. P. Glick and Dr. D. Rowe.)

the prominence of their cytoplasmic organelleschanges according to their activity. The more ac-tive the cell, the more prominent the organellesand other components necessary for synthesisand secretion. Unlike odontoblasts, however,these cells do undergo apoptotic cell death andare replaced when necessary by the maturation ofless differentiated cells.

UNDIFFERENTIATED(RESERVE) CELLS

These cells represent the cell pool from whichconnective tissue cells of the pulp are derived.These precursor cells are found in the cell-rich zone and in the pulp core in close asso-ciation with blood vessels. They appear to bethe first cells to divide after injury.23 They are

reduced in number and this in concert withan increase in pulp calcification and bloodflow reduces the regenerative capabilities of thepulp.

CELLS OF THE IMMUNE SYSTEM

Macrophages, T lymphocytes, and dendritic cellsare also normal cellular inhabitants of the pulp.24Dendritic cells and their processes are foundthroughout the odontoblast layer and have aclose association with vascular and neural ele-ments. These cells are part of the surveillance andi nitial response system of the pulp. They captureand present antigens to the resident T cells andmacrophages. Collectively this group of cellsmakes up approximately 8% of the cell populationof the pulp.

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Extracellular ComponentsFIBERS

Type I collagen is the predominant collagen indentin whereas both type I and type III collagenare found within pulp in a ratio of approximately55:45. 25 Type I collagen is synthesized exclusivelyby odontoblasts and incorporated into dentinmatrix, whereas fibroblasts produce both the typeI and type III collagen incorporated into pulp.Small amounts of type V collagen have also beenfound in pulp.26 Fine reticular fibers are alsofound, but elastic and oxytalan fibers are not nor-mally present.

The proportion of collagen types is constantin the pulp, but with age there is an increase inthe overall collagen content and an increase inthe organization of collagen fibers into collagenbundles. Normally, the apical portion of pulpcontains more collagen than coronal pulp, facili-tating pulpectomy with a barbed broach or en-dodontic file during endodontic treatment.

in the form of a sol-gel that supports the cellsand acts as a medium for transport of nutrientsand metabolites. Alterations in composition ofground substance caused by age or disease may in-terfere with normal cell activity and lead to irregu-larities in cell function and mineral deposition.

CALCIFICATIONS

Pulp stones or denticles were once classified astrue or false depending on the presence or absenceof a tubular structure. However, this classificationhas been challenged, and a new nomenclaturebased on the genesis of the calcification has beensuggested.27 Pulp stones have also been classifiedaccording to location. Three types of pulp stoneshave been described: free stones, which are sur-rounded by pulp tissue; attached stones, which arecontinuous with the dentin; and embedded stones,which are surrounded entirely by dentin, mostlyof the tertiary type.

GROUND SUBSTANCE

Pulp ground substance is similar to that of otherloose connective tissue. It is composed principallyof glycosaminoglycans, glycoproteins, and water

FIGURE 2-12Pulp stones in the coronal pulp and linear, or diffuse, calcifi-cations in the radicular portion. (Courtesy Dr. S. Bernick.)

FIGURE 2-13Multiple pulp stones (arrows) in the pulp chamber and rootcanals of the anterior (A) and posterior (B) teeth of a youngpatient.


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Pulp stones may be seen in young and old pa-tients and may occur in one or several teeth. Theyoccur in normal pulp as well as in chronically in-flamed pulp. Contrary to popular opinion, theyare not responsible for painful symptoms, regard-less of size.

Calcifications may also occur in the form ofdiffuse or linear deposits (Figure 2-12). These areassociated with neurovascular bundles in the pulpcore. This type of calcification is seen most oftenin the aged or chronically inflamed pulp. Depend-ing on shape, size, and location, pulp calcifica-tions may or may not be detected on a dental ra-diograph (Figure 2-13). Large pulp stones areclinically significant in that they may block access tocanals or the root apex during root canal treatment.

Blood Vessels

Mature pulp has an extensive and unique vascularpattern that reflects its unique environment. Thevessel network has been examined using a vari-ety of techniques including India ink perfusion,transmission electron microscopy, scanning elec-tron microscopy, and microradiography.28-31

AFFERENT BLOOD

VESSELS (ARTERIOLES)

One and sometimes two afferent vessels enter thecanal via each apical foramen. These vessels are ofarteriolar diameter and are branches of the infe-rior alveolar artery, the superior posterior alveolarartery, or the infraorbital artery, which branchfrom the internal maxillary artery.

After the arteriole passes into the canal, there isa decrease in its smooth muscle coating and a cor-responding increase in the size of the vessellumen. This reduces the rate of blood flow. As thearterioles course toward the coronal pulp, theygive off smaller branches (metarterioles and pre-capillaries) throughout the pulp (Figure 2-14).The most extensive branching occurs in the sub-odontoblastic layer of the coronal pulp where thevessels terminate in a capillary bed (Figure 2-15).The loops of some of these capillaries extend be-tween odontoblasts and continue as venules. Inaddition, 'there is an extensive shunting systemcomposed of arteriovenous and venovenous anas-tomoses; these shunts become active after pulpinjury and repair .32 All afferent vessels (except cap-illaries) and arteriovenous shunts have neuromus-cular mechanisms to control regional blood flow.The endothelial cells also respond to a variety ofendogenous and exogenous substances.

EFFERENT BLOOD

VESSELS (VENULES)

Venules constitute the efferent (exit) side of thepulpal circulation and are slightly larger than thecorresponding arterioles. Venules enlarge as theymerge and advance toward the apical foramen.After exiting from the foramen, venules coalesceand drain posteriorly into the maxillary veinthrough the pterygoid plexus or anteriorly intothe facial vein.

Efferent vessels are thin-walled and show onlyscanty smooth muscle. Because they are not in-nervated they are largely passive and nonconstric-tive (Figure 2-16).

FIGURE 2-74Schematic of the pulpal vasculature. Smoothmuscle cells that surround vessels andprecapillary sphincters selectively controlblood flow. Arteriovenous shunts bypasscapillary beds.

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2 I Biology of the Dental Pulp and Periradicular Tissues

FIGURE 2-7SThe dense capillary bed in the sub-odontoblastic region is shown by resincast preparation and scanning electronmicroscopy. (Courtesy Dr. C. Kockapan.)

VASCULAR PHYSIOLOGY

Normal

The dental pulp is a highly vascularized tissue.Capillary blood flow in the coronal region is al-most twice that of the radicular region. Bloodsupply is regulated by local factors as well as bysensory and sympathetic nerves. Smooth muscleson vessels have both a- and /3-adrenergic recep-tors; therefore they respond by constricting whensympathetic nerves are stimulated or when vaso-constrictors are injected intravascularly.33.34

The presence of cholinergic pulp nerves hasnot been confirmed although the presence of va-soactive intestinal peptide, a neurokinin identi-fied with cholinergic nerve activity, has been. Nor-mally the blood flow through the peripheralcapillary bed of a mature tooth is well below max-imum capacity. Thus the full extent of the sub-odontoblastic capillary bed is not apparent whenpulp is viewed by standard light microscopy. Cap-illaries become more apparent when the vascula-ture is experimentally perfused or when a hyper-emia occurs.

Pulp tissue pressure has been measured at6 mm Hg compared with a capillary pressure of35 mm Hg and a venular pressure of 19 mm Hg.However, the lack of a reliable and consis-tent method of recording pulp tissue pressuremakes the accuracy of these measurementsquestionable . 35

Pathologic

As with similar types of connective tissue, pulpali njury appears to evoke a biphasic vascular re-

sponse. This consists of an initial vasoconstric-tion followed by vasodilation and increased vas-cular permeability. This latter phase appears to bemediated by neuropeptides released from afferentpain fibers. Localized edema associated with leak-age from the primary venules then occurs andraises the local tissue pressure. This, in turn, initi-ates a regional reduction in blood flow and lymphdrainage that leads to an increase in tissue carbondioxide and acidity.36 To compensate, the vascularflow to the injured area is reduced by a redirectionof blood into arteriovenous shunts and the effer-ent pulp vessels. This allows for slow resolution oftissue edema and restoration of a normal flow.32 Ifthe injury is severe enough, compensation cannotoccur and local ischemia and a progressive exten-sion of tissue destruction may result.

Recent studies have shown a reciprocal rela-tionship between the vascular flow and nocicep-tive nerve activity. 3' An increased rate of flow mayoccur during certain stages of inflammation andcontribute to a decrease in the pain threshold ofthe larger pulp nerves (A8 fibers) and result in anincreased response to thermal stimuli (hot andcold). Conversely, the restriction of blood flow cansuppress the activity of the larger (A8) nerves andagain change the nature of the pain experience.

Painful stimuli cause a release of substance Pand calcitonin gene-related peptide from the noci-ceptive c fibers in the pulp core .38 These peptideshave vasoactive properties that can cause increasedvascular permeability and edema. Because someteeth share afferent nerve fibers, a painful experi-ence in one tooth can lead also to vascular changesin another. This pattern of inflammation is re-


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FIGURE 2-16A small, thin-walled venule (V) filledwith erythrocytes lies within the cell-free zone. The peripheral pulp is below,with odontoblasts (0) and fibroblasts(F). (Courtesy Dr. T. Cipriano.)

ferred to as neurogenic inflammation and highlightsthe interdependence of normal tooth physiology.

LYMPHATICS

The presence of an active lymphatic system in thedental pulp was once a subject of debate. However,investigations performed at different times andwith different techniques have confirmed its exis-tence .39-41 Lymphatic vessels arise as small, blind,thin-walled vessels in the coronal region. Theypass through its middle and apical regions to exitas one or two larger vessels through the apicalforamen (Figure 2-17). The lymphatic vessel wallsare composed of an endothelium rich in organellesand granules. There are discontinuities in thewalls of the vessels similar to those found in capil-laries. However, unlike the blood vessels, there arealso discontinuities in the subjacent basementmembrane. These openings in the basement mem-brane and vessel walls permit passage of intersti-tial tissue fluid and, when necessary, lymphocytesinto the negative-pressure lymph vessel.

The presence of lymphocytes and the absenceof red blood cells in the lumen are characteristicfindings (Figure 2-18). Lymphatics assist in the re-moval of inflammatory exudates and transudatesas well as irritants such as cellular debris. After ex-iting from the pulp, some vessels join vessels fromthe periodontal ligament; all drain into regionallymph glands (submental, submandibular, or cer-vical) before emptying into the subclavian and in-ternal jugular veins. An understanding of lymphaticdrainage assists in diagnosis of infection of endodonticorigin.

I nnervation

The second and third divisions (V2 and V3) of thetrigeminal nerve provide the principal sensory in-nervation to the pulp of maxillary and mandibu-lar teeth, respectively. Mandibular premolars alsocan receive sensory branches from the mylohyoidnerve of V 3 , which is principally a motor nerve.Branches from this nerve reach the teeth via smallforamina on the lingual aspect of the mandible.Mandibular molars occasionally receive sensoryinnervation from the second and third cervicalspinal nerves (C 2 and C3)." This can create diffi-culties in anesthetizing these teeth with an infe-rior dental block injection only.

Cell bodies of trigeminal nerves are located inthe trigeminal ganglion. Dendrites from thesenerves synapse with neurons in the trigeminal nu-cleus at the base of the brain and upper spinalchord and then pass on to the higher centers.

Pulp also receives sympathetic (motor) inner-vation from T1 and to some extent C $ and T2 viathe superior cervical ganglion. These nerves enterthe pulp space alongside the main pulp blood ves-sels. Other branches from the superior cervicalganglion supply the periodontium, oral mucosa,and skin . 43 Activation of these nerves causes vaso-constriction and reduction of pulpal blood flow.Without activation there is a passive vasodilation.

NEUROANATOMY

Pulpal and Dentinal Nerves

Sensory nerves supplying the dental pulp aremixed nerves containing both myelinated and

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FIGURE 2-77Lymph drainage (black vessels) is depicted in immature den-tal pulp. Note the confluence with periodontal lymphatics.(Courtesy Dr. A. Goerig.)

FIGURE 2-78Lymphatic vessel in pulp (1) associated with an arteriole (a)and a venule (v). (Courtesy Dr. S. Bernick.)

unmyelinated axons (Figure 2-19). Myelinatedaxons are classified according to diameter and con-duction velocity. Among these the A8 axons (diam-eter 1 to 6 um), which are slow-conducting myeli-nated nerves, are the most numerous. A smallpercentage of the myelinated axons (1% to 5%) arefaster-conducting A beta axons (diameter 6 to 12 um).The A beta group can be touch or pressure sensitive.Myelinated sensory nerves give off an increasingnumber of branches as they ascend coronally. Ulti-mately they lose their myelin sheath and terminateas small unmyelinated branches either below theodontoblasts, around the odontoblasts, or along-side the odontoblast process in the dentinal tubule(Figure 2-20). There they form a syncytium ofnerves called the subodontoblastic plexus ofRaschkow (Figure 2-21). Stimulation of these fibersresults in a fast, sharp pain that is relatively well lo-calized. This plexus is best visualized histologicallyby the use of special staining methods.44 The nervesthat enter the dentinal tubules do not synapse withthe process but remain in close proximity with it

for only part of its length. Approximately 27% ofthe tubules in the area of the pulp horn a of ayoung, mature tooth contain an intratubularnerve. These nerves occur less often in the middle(11%) and cervical portions (8%) of the crown andnot at all in the root. Their incidence is higher inpredentin than in mineralized dentin."

Nonmyelinated nociceptive axons, or c fibers(diameter < 1 um), are the most numerous andare found chiefly in the pulp core. Their conduc-tion velocity is slower than the A8 fibers, and stim-ulation of these fibers produces pain that is slowerin onset and dull and diffuse in nature.

DEVELOPMENTAL ASPECTS

OF PULP INNERVATION

The types and relative number of nerves dependon the state of tooth maturity.5.46 Myelinatednerves enter the pulp about the same time as un-

2 1 Biology of the Dental Pulp and Periradicular Tissues

19

FIGURE 2-19Pulp nerves in region of the pulp core. A group of unmy-elinated (UNA) and myelinated (MNA) nerve axons areshown in cross section. A Schwann cell (SC) associated withone of the myelinated axons is evident. Nerves are sur-rounded by collagen fibers (CO).

myelinated nerves but, in most instances, do notform the subodontoblastic plexus until sometime after tooth eruption has occurred. Becausenormal responses to various pulp-testing modali-ties depend on a fully developed and functionalsubodontoblastic plexus of nerves, significant var-iations in responses of partially developed teeth tosuch testing modalities can occur. This underminesthe value of stimulatory tests for determining pulp statusin young patients particularly after trauma."

Intratubular nerves as well as the overall num-ber of pulpal nerves diminish with chronologic(55+ years) and physiologic tooth aging. The sig-nificance of this reduction in terms of pulp response totesting is undetermined.

Pathways of Transmission from Pulpto Central Nervous System

Mechanical, thermal, and chemical stimuli initiatean impulse that travels along the pulpal axons inthe maxillary (V2) or mandibular (W) branches ofthe trigeminal nerve to the trigeminal (Gasserian)

FIGURE 2-20A, Silver-stained section of pulp in a young human molardemonstrates arborization of nerves in the subodontoblasticregion and a nerve (arrow) passing between odontoblastsi nto the predentin area. (Courtesy Dr. S. Bernick.) B, Trans-mission electron micrograph demonstrates an unmyelinatednerve axon (arrow) alongside the odontoblast process in thedentin tubule at the level of the predentin. (CourtesyDr. G. R. Holland.)

ganglion, which contains the cell body of the neu-ron. Dendrites from the ganglion then pass cen-trally and synapse with second-level neurons in thetrigeminal nuclear complex located at the base ofthe medulla and the upper end of the spinal cord.Most of the painful stimuli that originate in thedental pulp are conducted along axons thatsynapse with neurons in the spinal portion of thecomplex most notably, the subnucleus caudalis.Other stimuli travel along axons that synapse withneurons that are located in other spinal nuclei(oralis and interoralis) and in the main sensory nu-cleus located in the base of the brain.

Some neurons in the trigeminal nuclear com-plex receive only nociceptive impulses; these areknow as nociceptive specific neurons; others,known as wide dynamic range neurons, receiveboth nociceptive and tactile input. Several periph-eral axons may converge on a single secondary

20


FIGURE 2-21Silver-stained section of pulp in a young human molar. Largenerve bundles can be identified in the pulp core. These branch

and form the subodontoblastic plexus (plexus of Raschkow),i dentified by arrows in the cell-free zone. (Courtesy Dr. S.Bernick.)

histamine, acetylcholine, or potassium chloride tothe dentin surface fails to produce pain. Further-more, when pain exists, application of local anes-thetic to dentin gives no relief.

Because of variations in the response of dentinto normal sensory stimuli, the mechanism re-sponsible for its sensitivity is unknown. Severaltheories have been proposed. Each theory hasshortcomings, which supports the premise thatmore than one mechanism may be responsible.The three mechanisms that have been consideredare (1) direct innervation of dentin, (2) odontoblasts asreceptors, and (3) hydrodynamic theory (Figure 2-22).

Direct Innervation

Nerves are present in dentin. However, thesenerves are present only in the predentin and theinner third of the mineralized dentin. They arenot present in the outer third, at the DEJ or theDCJ, which appear to be highly sensitive areas.Furthermore, unlike other innervated sites, whenpain-producing and pain-relieving substances areapplied to dentin they fail to elicit an action po-tential (nerve response). The consensus, therefore,is that although nerves of trigeminal origin arefound in dentin, direct stimulation of thesenerves is unlikely to be the principal mechanisminvolved in dentin sensitivity.

Odontoblasts as Receptors

neuron, bringing input from several peripheralareas to one second-level site.48 Information intoand out of that neuron is determined by the in-teraction of stimuli conducted along larger andsmaller fibers and the modulating effect of de-scending input from higher centers of the brain.This can markedly influence the pain experiencein terms of intensity and localization.49 Informa-tion recorded at the second-level site then travelsto reflex centers and to the opposite side of thebrain where it is carried via the trigeminothalamictract to the thalamus and the cortex. Pain can bemodified by psychologic as well as neurologic factors; thecomplexity of all the combinations possible makes the ex-perience distinctive to each individual.

This theory was initially considered when it wasdiscovered that odontoblasts were of neural crestorigin and that staining of odontoblasts foracetylcholine was positive. However, later researchshowed that the odontoblast process extendedonly part way through dentin and that the mem-brane potential of the odontoblast was too low topermit transduction. The theory, however, did re-gain some credibility when it was discovered thatin some teeth the process did extend through thefull thickness of dentin and that gap junctions(which permit electronic coupling) did exist be-tween odontoblasts and possibly between odon-toblasts and nerves.'° Currently, there is little sup-port for the transduction theory.

THEORIES OF DENTIN

HYPERSENSITIVITY

Pain elicited by scraping or cutting of dentin or byapplication of cold or hypertonic solutions givesthe impression that there may be a nerve pathwayfrom the central nervous system to the DEJ.However, no direct pathway has been identified;application of pain-producing substances such as

Hydrodynamic Theory

The hydrodynamic theory, as originally proposedby Brannstrom and Astrom," satisfies most ofthe experimental and morphologic data associ-ated with dentin sensitivity. The theory postu-lates that rapid movement of fluid in the dentinaltubules (inward or outward) results in distortionof nerve endings in the subodontoblastic nerve


21

FIGURE z-22Schematic drawing of theoreticmechanisms of dentin sensitivity.A, Classic theory (direct stimulationof nerve fibers in the dentin). B,Odontoblasts as a mediator be-tween the stimuli and the nervefibers. C, Fluid movement as pro-posed in hydrodynamic theory.( Modified from Torneck CD: Dentin-pulp complex. In Ten Cate AR, edi-tor, Oral histology, ed 4, St Louis,1994, Mosby.)

plexus (plexus of Raschkow) that generates anneural impulse and a sensation of pain. Whendentin is cut, or when hypertonic solutions areplaced on a cut dentin surface, fluid moves out-ward and pain is initiated. Procedures that blocktubules (such as applying resin to the dentin sur-face or the buildup of crystals within the tubulelumen appear to interrupt fluid flow and reducesensitivity.52

In intact teeth the application of hot and coldto the tooth surface produces different contrac-tion rates in dentin and dentinal fluid; this resultsin fluid movement and initiation of pain. This re-sponse is exaggerated when dentin is exposed.

The hydrodynamic theory has been acceptedbut not without obvious criticism. It requiresthe presence of a subodontoblastic nerve plexus,yet dentin hypersensitivity occurs in teeth witha severely damaged pulp. The "fluid" in thetubules of intact dentin may be a relatively densehydrogel with little hydraulic conductivity ratherthan simple tissue fluid as first proposed byBrannstrom. Finally sensitivity produced by ap-plication of hot and cold can be explained by thepresence of pulp thermoreceptors and by the hy-drodynamic theory.

Age Changes in the Dental Pulp

Pulp, like other connective tissues, undergoeschanges with time. Some of these changes are nat-ural (chronologic), whereas others may be a resultof injury (pathophysiologic) such as caries, peri-odontal disease, trauma, or restorative dental pro-cedures. Regardless of the cause, changes in pulpappearance (morphologic changes) and in pulpfunction (physiologic changes) do occur.

MORPHOLOGIC CHANGES

The most obvious morphologic change seen inchronologic aging of the pulp is a progressive re-duction in the volume of cellular elements in thepulp space. This occurs as a result of continued de-position of dentin (secondary and tertiary dentino-genesis) and pulp stone formation. Secondarydentin formation is asymmetrical. In the pulpchamber of molars, for example, there is greater de-position on the roof and floor than on the proxi-mal, facial, and lingual (palatal walls). Root canalsalso become smaller and threadlike in size. Pulpstone formation reduces the space further and re-stricts access to the apical foramen. Contrary topopular belief, no correlation has been establishedbetween pulp stones and dental pain. Pulp volumemay also be disproportionately reduced by the de-position of irregular (reparative) dentin in re-sponse to odontoblast injury. While the radio-graphic image of teeth affected by injury may showabsence of a pulp space, histologic examination ofthese teeth often reveals one to be present.53

Aging also results in a reduction in number ofpulp cells. Between the ages of 20 and 70, cell den-sity decreases by approximately SO%. This reduc-tion affects all cells, from the highly differentiatedodontoblast to the undifferentiated reserve cell.In addition, reduced formative activity leads to areduction in the size and synthesizing capacity ofodontoblasts.

The number of nerves and blood vessels is alsodecreased. Furthermore blood vessels often dis-play arteriosclerotic changes, and an increased in-cidence of calcification in the collagen bundlesthat surround the larger vessels and nerves. Thedecrease in sensory innervation may be partially respon-sible for a deceased responsiveness to pulp testing inolder patients.

22


PHYSIOLOGIC CHANGES

Aging of the pulp-dentin complex results in a de-crease in dentin permeability through a progres-sive reduction in tubule diameter (dentin scle-rosis) and through a decrease in tubule patency(dead tract formation). This provides a more pro-tected environment for the pulp and may dimin-ish the injurious effect of conditions such ascaries, attrition, and periodontal disease.

junction protects the underlying periodontiumfrom potential irritants in the oral cavity.

The pulp and the periodontium form a contin-uum at sites along the root where blood vesselsenter and exit the pulp such as the apical foramenand lateral and accessory canals (Figure 2-24). Attimes it is difficult to determine where the pulpends and the periodontium begins.

CEMENTUM

Periradicular TissuesThe periodontium, the tissues surrounding andinvesting the root of the tooth consists of the ce-mentum, periodontal ligament, and alveolar bone(Figure 2-23). These tissues originate from thedental follicle that surrounds the enamel organ;their formation is initiated when root develop-ment begins. After the tooth has erupted, the cer-vical portion of the tooth is in contact with theepithelium of the gingiva, which in combinationwith reduced dental epithelium on the enamelforms the dentogingival junction. When intact, this

Cementum is a bone-like tissue that covers theroot and provides attachment for the principalperiodontal fibers. Several types of cementumhave been identified.

1. Primary acellular intrinsic fiber cementum. Thisis the first cementum formed, and it is pres-ent before principle periodontal fibers arefully formed. It extends from the cervicalmargin to the cervical third of the tooth insome teeth and around the entire root inothers (incisors and cuspids). It is more min-eralized on the surface than near the dentinand it contains collagen produced initially bycementoblasts and later by the fibroblasts.

FIGURE 2-23Maxillary root surrounded by periodontal ligament (pl) andalveolar bone proper (ab). Periodontal fibers are inserted intocementum (c) on the tooth and into alveolar bone.

FIGURE 2-24Apical region of maxillary incisor showing apical foramen.t, Transitional tissue between periodontal ligament and pulp;o, odontoblasts; bv, blood vessel.

2 1 Biology of the Dental Pulp and Periradicular Tissues

23

2. Primary acellular extrinsic fiber cementum. Thisis cementum that continues to be formedabout the primary periodontal fibers afterthey have been incorporated into primaryacellular intrinsic fiber cementum.

3. Secondary cellular intrinsic fiber cementum.This cementum is bone-like in appearanceand only plays a minor role in fiber attach-ment. It occurs most often in the apical partof the root of premolars and molars.

4. Secondary cellular mixed fiber cementum. Thisis an adaptive type of cellular cementumthat incorporates periodontal fibers as theycontinue to develop. It is variable in its dis-tribution and extent and can be recognizedby the inclusion of cementocytes, its lami-nated appearance, and the presence of ce-mentoid on its surface.

5. Acellular afibrillar cementum. This is the ce-mentum seen on enamel, which plays norole in fiber attachment.

Although sometimes cellular, cementum is notvascularized and appears to resist resorptionmore than bone. Cementum formation is a con-tinuing process and is influenced by changes intooth position and function.

As mentioned earlier in this chapter the junc-tion between the cementum and the dentin (ce-mentodentinal junction) is ill defined and not uni-form throughout its circumference. Despite thisthe CDJ is often cited as the point at which rootcanal procedures should terminate especiallywhen the status of the periodontium is normal.Although many practitioners debate the probabilities andpracticalities of achieving this goal, most agree that it isessential to measure canal length accurately and to re-strict all procedures to the determined canal length.

Despite the relative resistance of cementum, in-flammatory lesions in the periodontal ligament andsurrounding bone can cause cementum resorption.If inflammation is eliminated, however, resorptionsites generally undergo repair and the integrity ofthe periodontium is restored. Mechanical pressuresuch as orthodontic movement can cause cemen-tum resorption. This is a noninflammatory type ofresorption and also can undergo repair after pres-sures have returned to physiologic levels. Occasion-ally cementum undergoes resorption without anidentifiable cause. This is referred to as idiopathicresorption. This resorption can be self-limiting or itmay progress and lead to loss of dentin.

CEMENTOENAMEL JUNCTION

It was once thought that the junction betweenenamel and cementum occurred in one of threepatterns at the cervical part of the tooth: (1) butt

junction, (2) gap between the two, and (3) overlapof cementum on enamel. Recent studies however,have shown that all three appear to occur at dif-ferent sites along the CEJ when the circumferenceof the junction is examined.53 It is possible that a sig-nificant discrepancy between cementum and enamel atthe CEJ can lead to an increased risk ofdentin sensitivity.

PERIODONTAL LIGAMENT

Periodontal ligament (PDL), like dental pulp, is aspecialized connective tissue. Its function relates inpart to the presence of specially arranged bundles ofcollagen fibers that support the tooth in the socketand absorb the forces of occlusion from beingtransmitted to the surrounding bone. The PDLspace is small, varying from an average of 0.21 mmin young teeth to US mm in older teeth. 48 Its uni-formity (as visualized in a radiograph) is one of thecriteria used to determine its health.

Lining the periodontal space are cementoblastsand osteoblasts. Interwoven between the principalperiodontal fibers is a loose connective tissue thatcontains fibroblasts, reserve cells, macrophages,osteoblasts, blood vessels, nerves, and lymphatics.Epithelial cell rests of Malassez are also present(Figure 2-2S). As already noted, these cells are ofno known significance in the healthy periodon-tium but can, during inflammatory states, prolif-erate and give rise to cyst formation.

The vasculature of the periodontium is exten-sive and complex. Arterioles that supply the PDLarise from the superior and inferior alveolarbranches of the maxillary artery in the cancellousbone. These arterioles pass through small open-ings in the alveolar bone of the socket, at timesaccompanied by nerves, and extend upward anddownward throughout the periodontal space.They are more prevalent in posterior than ante-rior teeth. Other vessels arise from the gingiva orfrom dental vessels that supply the pulp; these lat-ter vessels branch and extend upward into theperiodontal space before the pulpal vessels passthrough the apical foramen. The degree of collat-eral blood supply to the PDL and the depth of itscell resources impart an excellent potential for itsrepair subsequent to injury, a potential that is re-tained for life in the absence of systemic or pro-longed local disease.

The periodontium receives autonomic andsensory innervation. Autonomic nerves are sym-pathetic nerves that arise from the superior cervi-cal ganglion and terminate in the smooth muscleof the periodontal arterioles. Activation of thesympathetic fibers induces constriction of the ves-sels. As in the pulp, there is no convincing evi-dence that a parasympathetic nerve supply exists.

24


FIGURE 2-25Epithelial cell rests of Malassez (arrows), in the periodontalspace at the level of mid root. pdl, Periodontal ligament,c, cementum.

Sensory nerves that supply the periodontiumarise from the second and third divisions (V2 andV3) of the trigeminal nerve. They are principallymixed nerves of large and small diameter. Largefibers are A beta fibers, whereas small fibers are A5fibers and unmyelinated C fibers. Small fibersterminate as free endings and mediate pain sensa-tion. Large fibers are mechanoreceptors and ter-minate in special endings throughout the liga-ment but are in greatest concentration in theapical third of the periodontal space.54 These arehighly sensitive and record pressures in the liga-ment associated with micro and macro toothmovements.55 The ability of patients to identifyinflammation in the periodontium is a learned ex-perience not a physiologic one.

FIGURE 2-26Mandibular anterior teeth with normal, uniform periodontal

ligament space and identifiable lamina dura (arrows). Thisusually, but not always, indicates the absence of periradicu-l ar inflammation.

accommodate vessels, nerves, and investing con-nective tissues that pass from the cancellous por-tion of the alveolar process to the periodontalspace. Despite these perforations alveolar boneproper is denser than the surrounding cancellousbone and has a distinct opaque appearance whenimaged in a dental radiograph. On the radio-graph, alveolar bone proper is referred to as lam-ina dura (Figure 2-26). Its presence is equatedwith periodontal health and its absence (attenua-tion) with disease. However, radiographic changesassociated with periradicular inflammatory dis-ease usually follow, rather than accompany thedisease. The lesion is usually present before it isvisible radiographically. Significant bone loss isnecessary before a radiographic image is seen.

Alveolar bone proper is principally lamellar bonethat continually adapts to the stress of tooth move-ments. Because pressures are not constant, bone isconstantly remodeling (bone resorption and appo-sition). Current concepts of host response to periodontalinfections identify an alteration in this bone remodelingas the principal cause of the associated bone loss. 56

ALVEOLAR BONE

The bone of the jaws is referred to as the alveolarprocess. Bone that lines the socket and into whichthe principle periodontal fibers are anchored isreferred to as alveolar bone proper (bundle bone,cribriform plate). Alveolar bone is perforated to

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6. Lindskog S: Formation of intermediate cementum. II.A scanning electron microscopic study of the epithe-lial root sheath of Hertwig in the monkey, J Craniofac

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8. Kuttler Y: Microscopic investigation of root apices,J Am Dent Assoc 50:544, 1955.

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10. Lambritchs I, Creemers J, van Steenberghe D: Mor-phology of neural endings in the periodontal liga-ment. An electron microscopic study, J Periodontol Res27:191, 1992.

11. Min-Kai Wu, Wesselink PR, Walton RE: Apical termi-nus location of root canal treatment procedures, OralSurg Oral Med Oral Pathol Oral Radiol Endod 89:99, 2000.

12. Schroeder U, Sundstrom B: Transmission election mi-croscopy of tissue changes following experimentalpulpotomy of intact human teeth and capping withcalcium hydroxide, Odontol Rev 25:1, 1974.

13. Rutherford RB, Wahle J, Tucker M, et al: Induction ofreparative dentine formation in monkeys by recom-binant human osteogenic protein. Arch Oral Biol38:571, 1993.

14. Narhi MVO: The characteristics of interdental sensoryunits and their responses to stimulation, J Dent Res

64:564, 1985.

15. Kollman W, Mijatovic E: Age dependent changes inthermoperception in human anterior teeth, Arch Oral

Biol 30:711, 1985.

16. Couve E: Ultrastructural changes during the life cycleof human odontoblasts, Arch Oral Biol 31:643, 1986.

17. Brannstrom M, Garberoglio R: The dentinal tubulesand the odontoblast process, a scanning electron mi-croscopic study, Acta Odontol Scand 30:291, 1972.

18. Sigal MJ, Aubin JE, Ten Cate AR: A combined scanningelectron microscopy and immunofluorescence studydemonstrating that the odontoblast process extendsto the dentinoenamel junction in human teeth, AnatRec 210:453, 1984.

19. Turner DF, Marfurt CF, Sattelburg C: Demonstrationof physiological barrier between pulpal odontoblastsand its perturbation following routine restorative pro-cedures, JDent Res 68:1262, 1989.

20. Koling A: Freeze fracture electron microscopy of si-multaneous odontoblast exocytosis and endocytosisin human permanent teeth, Arch Oral Biol 32:153, 1987.

21. Tziafas D, Alvanou A, Panagiotakopoulos N, et al: In-duction of odontoblast-like cell differentiation in dog

dental pulps after in vivo implantation of dentin ma-trix components, Arch Oral Biol 40:883, 1995.

22. Torneck CD: Intracellular destruction of collagen inthe human dental pulp, Arch Oral Biol 23:745, 1978.

23. Torneck CD, Wagner D: The effect of calcium hydrox-ide cavity liner on early cell division in the pulp subse-quent to cavity preparation and restoration, J Endod

6:719, 1980.24. Jontell M, Bergenholtz G: Accessory cells in the im-

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25. Linde A: Dentin matrix proteins: composition andpossible functions in calcification, Anat Rec 224:154,

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26. Tsuzaki M, Yamauchi M, Mechanic GL: Bovine dentalpulp collagens: characterization of types III and V col-lagen, Arch Oral Biol 35:195, 1990.

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29. Harris R, Griffin CJ: The ultrastructure of small bloodvessels of the normal dental pulp, Aust Dent J 16:220,

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30. Takahashi K, Kishi Y, Kim S: A scanning electron mi-croscope study of the blood vessels of dog pulp usingcorrosion resin casts,JEndod 8:132, 1982.

31. Saunders RL, de CH: X ray microscopy of the peri-odontal and dental pulp vessels in the monkey and inman, Oral Surg Oral Med Oral Pathol 22:503, 1966.

32. Kim S: Microcirculation of the dental pulp in healthand disease, JEndod 11:465, 1985.

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35. Tonder KJH, Kvinsland 1: Micropuncture measure-ments of interstitial fluid pressure in normal and in-flamed dental pulp in cats, JEndod 9:105, 1983.

36. Heyeraas KJ, Kvinsland 1: Tissue pressure and bloodflow in pulp inflammation, Proc Finn Dent Soc88(suppl):393, 1992.

37. Olgart L, Gazelius B: Effects of adrenalin and fely-pressin (octapressin) on blood flow and sensory nerveactivity in the tooth, Acta Odontol Scand 35:69, 1977.

38. Grutzner E, Garry M, Hargreaves KM. Effect of injuryon levels of immunoreactive substance P and CGRP, J

Endod 18:553, 1992.

39. Walton R, Langeland K: Migration of materials in den-tal pulp of monkeys, J Endod 4:167, 1978.

40. Bernick S: Morphological changes in lymphatic vesselsin pulpal inflammation, JDent Res 56:841, 1977.

41. Marchetti C, Poggi P, Calligaro A, Casasco A: Lym-phatic vessels in the healthy human dental pulp, Acta

Anat (Basel) 140:329, 1991.

42. Bolding SL, Hutchins B: Histological evidence for acervical plexus contribution to the cat mandibulardentition, Arch Oral Biol 38:619, 1993.

43. Mumford JM: Orofacial pain: etiology, diagnosis and treat-

ment, ed 3, New York, 1982, Churchill-Livings tone.

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44. Bernick S: Innervation of the human tooth, Anat Rec

101:81, 1948.

45. Lilja T: Innervation of different parts of predentin and

dentin in young human premolars, Acta Odont Scand

37:339, 1979.46. Peckham K, Torabinejad M, Peckham N: Presence of

nerve fibers in the coronal odontoblast layer of teeth at

various stages of root development, Int Endod J 24:303,

1991.

47. Klein H: Pulp responses to an electric pulp stimulator

in the developing permanent anterior dentition, JDent

Child 45:23, 1978.

48. Dostrovsky JO: An electrophysiological study of ca-

nine, premolar and molar tooth pulp afferents and

their convergence on medullary trigeminal neurons,

Pain 19:1, 1984.

49. Sessle BJ, Hu JW, Amano N, Zhong G: Convergence of

cutaneous, tooth pulp visceral, neck and muscle affer-

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horn) and its implications for referred pain, Pain

27:219, 1987.

50. Koling A, Rask-Andersen H: Membrane junctions in

the subodontoblastic region, Acta Odontol Scand 41:99,

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51. Brannstrum M, Astrom A: The hydrodynamics of thedentine: its possible relationship to dentinal pain, Int

DentJ22:219, 1972.52. Pashley D: Dentin permeability and dentin sensitivity,

Proc Finn Dent Soc 88:31, 1992.

53. Freeman E: Periodontium. In Ten Cate AR, editor: Oral

histology, development, structure, and function, ed 4, St Louis,

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54. Cash RM, Linden RW: The distribution of mechano-

receptors in the periodontal ligament of the mandibu-

lar canine tooth of the cat, J Pbysiol (Loud) 330:439,

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55. Cash RM, Linden RW: Effects of sympathetic nerve

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9:498, 1998.

Pulp and Periradicular Pathosis

LEARNING OBJECTIVES

After reading this chapter, the student should be able to.

1/ Identify etiologic factors causing pulp inflammation.2 / Explain the mechanism of spread of inflammation in the pulp.

3 / Explain why pulp has difficulty in recovering from severe injury.

4 / List specific and nonspecific mediators of pulpal inflammation.

5 / Classify pulpal diseases and their clinical and histologic features.

6 / Describe the mechanisms and explain the consequences of the spread of pulpal inflammation intoperiradicular tissues and the subsequent inflammatory and immunologic responses.

7 / Classify periradicular lesions of pulpal origin.

8 / Identify and distinguish between histologic features and clinical signs and symptoms of acute apicalperiodontitis, chronic apical periodontitis, acute and chronic apical abscesses (suppurative apicalperiodontitis), and condensing osteitis.

9 / Describe the steps involved in repair of periradicular pathosis after successful root canal treatment.

10 / Identify and describe, in general, nonendodontic pathologic lesions that may simulate endodonticperiradicular pathosis.

27

28

3 / Pulp and Periradicular Pathosis

I rritantsIrritation of pulpal or periradicular tissues resultsin inflammation. The major irritants of these tis-sues can be divided into living and nonliving irri-tants. The living irritants are various microorgan-isms and viruses. The nonliving irritants includemechanical, thermal, and chemical irritants.

MICROBIAL IRRITANTS

Microorganisms present in the dental caries are themain sources of irritation of the dental pulp andperiradicular tissues. Carious dentin and enamelcontain numerous species of bacteria such as Strep-tococcus mutans, lactobacilli, and Actinomyces.' Thepopulation of microorganisms decreases to few ornone in the deepest layers of carious dentin! How-ever, direct pulp exposure to microorganisms is nota prerequisite for pulpal response and inflamma-tion. Microorganisms in caries produce toxins thatpenetrate to the pulp through tubules. Studieshave shown that even small lesions in enamel arecapable of attracting inflammatory cells in thepulp.3,4 As a result of the presence of microorgan-isms and their by-products in dentin, pulp is infil-trated locally (at the base of tubules involved incaries) primarily by chronic inflammatory cellssuch as macrophages, lymphocytes, and plasmacells. As the decay progresses toward the pulp, theintensity and character of the infiltrate change.

When actual exposure occurs, the pulp tissue isinfiltrated locally by polymorphonuclear (PMN)leukocytes to form an area of liquefaction necro-sis at the site of exposure (Figure 3-1).s After pulpexposure, bacteria colonize and persist at the site

I rritantsMicrobial IrritantsMechanical IrritantsChemical Irritants

Pulpal PathosisI nflammatory ProcessI mmunologic ResponseLesion Progression

Classification of Pulpal DiseasesReversible PulpitisI rreversible PulpitisHard Tissue Changes Caused by Pulpal

I nflammationPulpal Necrosis

Periradicular PathosisNonspecific Mediators of Periradicular

Lesions

Specific Mediators of Periradicular Lesions

Classification of Periradicular LesionsAcute Apical PeriodontitisChronic Apical PeriodontitisCondensing OsteitisAcute Apical Abscess

Chronic Apical Abscess (Suppurative ApicalPeriodontitis)

Healing of Periradicular Lesions FollowingRoot Canal Treatment

Extent of HealingProcess of Healing

Nonendodontic Periradicular PathosisDifferential DiagnosisNormal and Pathologic Entities

FIGURE 3-1A localized inflammatory reaction containing mainly poly-morphonuclear leukocytes (arrow) at the site of a cariouspulpal exposure (CE). The remainder of the coronal pulp isalmost free of inflammatory cells. (Courtesy Dr. 1H Simon.)

of necrosis. Pulpal tissue may stay inflamed for along period of time and may undergo necrosiseventually or become necrotic quickly. This de-pends on several factors: (1) the virulence of bac-teria, (2) the ability to release inflammatory fluidsto avoid a marked increase in intrapulpal pres-sure, (3) host resistance, (4) amount of circula-tion, and (5) most important, lymph drainage.Yamasaki et al.6 created pulpal exposure in ratsand showed that necrosis extended gradually fromthe upper portion of pulp to the apex. A periapicallesion ensued after pulpal inflammation andnecrosis. The lesions extended first horizontallyand then vertically before their expansion ceased.

As a consequence of exposure to the oral cavityand to caries, pulp harbors bacteria and theirbyproducts. Pulp usually cannot eliminate thesedamaging irritants. At best, defenses temporarilyhalt or slow the spread of infection and tissue de-struction. Sooner or later the damage will becomeextensive and will spread throughout the pulp.Then, bacteria or their by-products and other irri-tants from necrotic pulp will diffuse from thecanal periapically, resulting in development of se-vere inflammatory lesions (Figure 3-2).

Bacteria play an important role in the patho-genesis of pulp and periradicular pathoses. A num-ber of investigations have established that pulpaland/or periradicular pathosis does not developwithout the presence of bacterial contamination.7-10Kakehashi et al.' created pulpal exposures in con-ventional and gnotobiotic (germ-free) rats. Thisprocedure in the germ-free rats caused only mini-mal inflammation throughout the 72-day investi-gation. Pulpal tissue in these animals was not com-pletely devitalized but rather showed calcific bridgeformation by day 14, with normal tissue apical tothe dentin bridge (Figure 3-3, A). In contrast, au-toinfection, pulpal necrosis, and abscess formation


29

occurred by the eighth day in conventional rats(Figure 3-3, B).

Other investigators have examined the impor-tance of bacteria in the development of periradicu-lar lesions by sealing noninfected and infected

FIGURE 3-2Egress of irritants (closed arrow) from the root canal intothe periapical tissue causes inflammation (open arrow)and replacement of normal periradicular structures with agranulomatous tissue.

FIGURE 3-3A, No inflammation is seen in an exposed pulp (P) of a germ-free rat. Food particles and other debris (D) arepacked into the chamber. B, Pedradicular lesion is apparent in a conventional rat after pulp exposure. (CourtesyDr. H. Stanley.)

30


pulps in canals of monkeys.8 After 6 to 7 months,clinical, radiographic, and histologic examinationof teeth sealed with noninfected pulps showed anabsence of pathosis in periradicular tissues, whereasteeth sealed with necrotic pulps containing certainbacteria showed periapical inflammation. The bac-teriological investigations by Bergenholtz 9 andSundgvist10 examining the flora of human necroticpulps support the findings of Kakehashi et al . 7 aswell as those of Moller and Fabricius.8 These stud-ies examined previously traumatized teeth withnecrotic pulps with and without periradicularpathosis. Canals in teeth without apical lesionswere aseptic, whereas those with periapical patho-sis had positive bacterial cultures.

Examination of the amount of microbial in-oculum had demonstrated that higher levels ofcontamination led to greater inflammatory re-sponses." In contrast, lower levels of contamina-tion led to milder responses and a tendency forhealing and repair of pulpal and/or periapical tis-sues. A further relationship between the presenceof bacteria and inflammatory reactions becameapparent when bacteria were placed in cavitiesprepared in the dentin." This experiment showedthat bacterial compounds can permeate throughthe dentin and cause pulpal inflammation with-out direct pulpal exposure.

MECHANICAL IRRITANTS

In addition to bacterial irritation, pulp or peri-radicular tissues can also be irritated mechani-cally. Deep cavity preparations, removal of toothstructure without proper cooling, impact trauma,occlusal trauma, deep periodontal curettage, andorthodontic movement of teeth are the main ther-

mal and physical irritants of the pulp tissue. Ifproper precautions are not taken, cavity or crownpreparations damage subjacent odontoblasts(Figure 3-4). The number of tubules per unit sur-face area and their diameter increase closer to thepulp. As a result, dentinal permeability is greatercloser to pulp than near the dentinoenamel junc-tion or cementodentinal junction.13,14 Thereforethe potential for pulp irritation increases as moredentin is removed (i.e., as cavity preparation deep-ens). Pulp damage is roughly proportional to theamount of tooth structure removed as well as tothe depth of removal.15 Also, operative procedureswithout water coolant cause more irritation thanthose performed under water spray." Reactionsand vascular changes occurring in experimentallyinduced acute and chronic pulpitis demonstratedincreased permeability and dilation of blood ves-sels in the early stages of pulpitis.17

Impact injury with or without crown or rootfractures may cause pulpal damage (see Chapter25). The severity of trauma and degree of apicalclosure are important factors in recovery of thepulp. Teeth undergoing mild to moderate traumaand those with immature apexes have a betterchance of pulpal survival than those suffering se-vere injury or those with closed apexes.

Application of forces beyond the physiologictolerance of the periodontal ligament during or-thodontics results in disturbance of the bloodand nerve supply of pulp tissue." ," The resultingchanges include atrophy of cells and alteration ofnerve axons. In addition, orthodontic movementmay initiate resorption of the apex, usually with-out a change in vitality. Deep scaling and curet-tage may injure apical vessels and nerves, result-ing in pulpal damage (see Chapter 26).

FIGURE 3-4Crown preparation through enamel and

i nto 1 mm of dentin resulted in aspira-tion of odontoblasts (arrows) into thetubules and infiltration of the pulp byPM N leukocytes and lymphocytes. Thespecimen was taken 48 hours aftercrown preparation.


31

The periradicular tissue can be mechanically ir-ritated and inflamed by impact trauma, hyperoc-clusion, endodontic procedures and accidents,pulp extirpation, overinstrumentation, perfora-tion of the root, and overextension of the fillingmaterials. Mechanical irritation by instrumentsmay occur during canal preparation. Inaccuratedetermination of canal length is usually the causeof overinstrumentation and inflammation. In ad-dition, lack of an apical stop after cleaning andshaping can cause overextension of filling materi-als into the periapex, resulting in physical andchemical damage (Figure 3-5).

CHEMICAL IRRITANTS

Chemical irritants of the pulp include variousdentin cleansing, sterilizing, and desensitizingsubstances as well as some of the substances pre-sent in temporary and permanent filling materialsand cavity liners. Antibacterial agents such as sil-ver nitrate, phenol with and without camphor,and eugenol were used in an attempt to "sterilize"the dentin after cavity preparations. However,their effectiveness as dentin sterilizers is question-able, and their cytotoxicity can cause inflamma-tory changes in underlying dental pulp.20 Otherirritating agents include cavity cleansers such asalcohol, chloroform, hydrogen peroxide, and vari-ous acids, chemicals present in desensitizers, cav-ity liners and bases, as well as temporary and per-manent filling materials.

FIGURE 3-5I mproper instrumentation and extrusion of filling materialsi nto the periapical tissues cause periradicular inflammation(arrows).

Antibacterial irrigants used during cleaning andshaping of root canals, intracanal medications, andsome compounds present in obturating materialsare examples of potential chemical irritants of peri-radicular tissues. Most irrigants and medicamentsare toxic and are not biocompatible.21,22

Pulpal PathosisApart from anatomic configuration and diversityof inflicted irritants, pulp reacts to these irritantsas do other connective tissues. Pulpal injury re-sults in cell death and inflammation. The degreeof inflammation is proportional to the intensityand severity of tissue damage. Slight injuries, suchas incipient caries or shallow cavity preparations,cause little or no inflammation in the pulp. Incontrast, deep caries, extensive operative proce-dures, or persistent irritation usually producemore severe inflammatory changes. Dependingon the severity and duration of the insult and thehost response, the pulpal response ranges fromtransient inflammation (reversible pulpitis) to ir-reversible pulpitis and then to total necrosis.These changes often occur without pain andwithout the knowledge of patient or dentist.

I NFLAMMATORY PROCESS

Irritation of the dental pulp results in activationof a variety of biologic systems such as nonspecificinflammatory reactions mediated by histamine,bradykinin, and arachidonic acid metabolites.23Also released are PMN lysosomal granule prod-ucts (elastase, cathepsin G, and lactoferrin)," pro-tease inhibitors such as antitrypsin," and neu-ropeptides such as calcitonin gene-related peptide( CGRP) and substance P (SP)."

Unlike connective tissues in other parts of thebody, normal and healthy dental pulps lack mastcells. However, these cells are found in inflamedpulp (Figure 3-6). 27 Mast cells contain histamine,leukotrienes, and platelet-activating factors.Physical injury to mast cells or bridging of twoIgE molecules by an antigen on their cell surfacesresults in the release of histamine and otherbioactive substances present in mast cell gran-ules. The presence of histamine in the bloodvessel walls and a marked increase in histaminelevels indicate the importance of histamine inpulpal inflammation.28

Kinins, which produce many signs and symp-toms of acute inflammation, are produced whenplasma or tissue kallikreins contact kininogens.Bradykinin, SP, and neurokinin A have been identi-fied in dental pulp tissue using high-performance

32


FIGURE 3-6Mast cells are readily visible as dark-stained cells in this in-flamed human dental pulp.

FIGURE 3-7Numerous plasma cells stain positively for IgG in inflamedhuman dental pulp, indicating immunologic activity.

liquid chromatography.29 A recent in vitro studyshowed that bradykinin evokes immunoreactiveCGRP released from bovine dental pulp, which isalso positively enhanced by prostaglandin E2.3° As aresult of cellular damage, phospholipase A Z causesrelease of arachidonic acid from cell membranes.Metabolism of arachidonic acid results in forma-tion of various Prostaglandins, thromboxanes, andleukotrienes. Various arachidonic acid metaboliteshave been found in experimentally induced pulpi-tis. 31 The presence of these metabolites in inflamedpulps32 ,33 indicates that arachidonic acid metabo-lites participate in inflammatory reactions of thedental pulp.

The dental pulp is densely innervated with sen-sory fibers containing immunomodulatory neu-ropeptides such as SP and CGRP. Denervation ofthe rat molar pulp, caused by axotomy of the infe-rior alveolar nerve, resulted in enhanced pulp tissuedamage and a decrease in infiltration of immuno-competent cells.34 These findings indicate that pul-pal nerves are protective in nature and that theymay be involved in the recruitment of inflamma-tory/immunocompetent cells to the injured pulp.34

Mild to moderate pulpal injuries result insprouting of sensory nerves with an increase in

immunoreactive (1) CGRP.26,35 However, severe in-juries have the opposite effect, resulting in eitherreduction or elimination of CCGRP and SP.` Theseinvestigations indicate that pulpal neuropeptidesundergo dynamic changes after injury. A numberof recent studies have shown that stimulation ofthe dental pulp by caries results in the formationof various interleukins and recruitment of inflam-matory cells to the site of injury.36-40

I MMUNOLOGIC RESPONSE

In addition to nonspecific inflammatory reactions,immune responses also may initiate and perpetuatepulpal diseases. 13 Potential antigens include bacte-ria and their by-products within dental caries,which directly (or via tubules) can initiate differenttypes of reactions. Studies have shown that normaland uninflamed dental pulps contain immuno-competent cells such as T and B (fewer) lympho-cytes, macrophages, and a substantial number ofclass II molecules expressing dendritic cells similarmorphologically to macrophages .34 Elevated levelsof various immunoglobulins in inflamed pulps(Figure 3-7) show that these factors participate indefense mechanisms involved in protection of this

tissue . 4' Arthus-type reactions have been shown tooccur in the dental pulp.42 In addition, the presenceof immunocompetent cells such as T lymphocytes,macrophages, and class II molecules expressingcells appearing as dendritic cells (Figure 3-8) in in-flamed pulps indicates that delayed hypersensitivityreactions can also occur in this tissue . 34 Despitetheir protective mechanisms, immune reactions inthe pulp can result in the formation of smallnecrotic foci and eventually total pulpal necrosis.

LESION PROGRESSION

Mild pulpal injuries may not result in significantchanges. However, moderate to severe insults re-sult in localized inflammation 13 and release of ahigh concentration of inflammatory mediators.An increase in protease inhibitors in moderately toseverely inflamed pulp indicates the presence ofnatural modifiers.25 As a consequence of release ofa large quantity of inflammatory mediators, in-creased vascular permeability, vascular stasis, andmigration of leukocytes to the site of injury occur.Available information shows that the sensory neu-ropeptide CGRP is responsible for the increase ofblood flow during pulpal inflammation . 44

Elevated capillary pressure and increased capil-lary permeability move fluid from blood vessels intothe surrounding tissue. If removal of fluid byvenules and lymphatics does not match filtration offluid from capillaries, an exudate forms. The pulp isencased in rigid walls and forms a low-compliancesystem; therefore a small increase in tissue pressurecauses passive compression and even complete col-lapse of the venules at the site of pulpal injury..'Pressure increases occur in small "compartmental-ized" regions and progress slowly (Figure 3-9). Thus

FIGURE 3-9I rritation of pulp resulting from cavity preparation has resultedi n destruction of tissue in pulp horn (PH); note the band of in-flammatory lines next to pulp necrosis. There is normal pulpsubjacent to the inflammatory zone. (Courtesy Dr. N. Perrini).

pulp does not die by extensive increases in pressurewith subsequent strangulation.45,46

Pain is often caused by different factors. Re-lease of mediators of inflammation causes pain di-rectly by lowering the sensory nerve threshold.These substances also cause pain indirectly by


33

FIGURE 3-sMany dendritic cells (arrows) are present in an in-flamed dental pulp. (Courtesy Dr. M. Jontell.)

34


increasing both vasodilation in arterioles and vas-cular permeability in venules, resulting in edemaand elevation of tissue pressure. This pressureacts directly on sensory nerve receptors.

Increased tissue pressure, the inability of pulpto expand, and the lack of collateral circulationmay result in pulpal necrosis and the develop-ment of a subsequent periradicular pathosis.

Classification of Pulpal DiseasesBecause there is little or no correlation betweenthe histologic findings of pulpal pathosis andsymptoms,"," the diagnosis and classification ofpulpal diseases are based on clinical signs andsymptoms rather than on histopathologic find-ings. Pulpal conditions can be classified as re-versible and irreversible pulpitis, hyperplastic pul-pitis, and necrosis. Hard tissue responses includecalcifications and resorption.

REVERSIBLE PULPITIS

By definition, reversible pulpitis is inflammationof the pulp that is not severe. If the cause is elimi-nated, inflammation will resolve and the pulp willreturn to normal. Mild or short-acting stimulisuch as incipient caries, cervical erosion, or oc-clusal attrition, most operative procedures, deepperiodontal curettage, and enamel fractures re-sulting in exposure of dentinal tubules can causereversible pulpitis.

Symptoms

Reversible pulpitis is usually asymptomatic. How-ever, when present, symptoms usually form a par-ticular pattern. Application of stimuli such ascold or hot liquids or even air, may produce sharptransient pain. Removal of these stimuli, whichdo not normally produce pain or discomfort, re-sults in immediate relief. Cold and hot stimuliproduce different pain responses in normalpulp.49 When heat is applied to teeth with unin-flamed pulp, there is a delayed initial response;the intensity of pain increases as the temperaturerises. In contrast, pain in response to cold in nor-mal pulp is immediate; the intensity tends to de-crease if the cold stimulus is maintained. Basedon these observations, responses of both healthyand diseased pulps apparently result largely fromchanges in intrapulpal pressures.49

Treatment

Removal of irritants and sealing as well as insulat-ing the exposed dentin or vital pulp usually result

in diminished symptoms (if present) and reversalof the inflammatory process in the pulp tissue (Fig-ure 3-10). However, if irritation of pulp continuesor increases in intensity for reasons stated earlier,moderate to severe inflammation develops with ir-reversible pulpitis and eventually pulpal necrosis.

IRREVERSIBLE PULPITIS

Irreversible pulpitis is often a sequel to and a pro-gression from reversible pulpitis. Severe pulpaldamage from extensive dentin removal during op-erative procedures or impairment of pulpal bloodflow caused by trauma or orthodontic movementof teeth may also cause irreversible pulpitis. Irre-versible pulpitis is a severe inflammation that willnot resolve even if the cause is removed. The pulpslowly or rapidly progresses to necrosis.

Symptoms

Irreversible pulpitis is usually asymptomatic, orthe patient reports only mild symptoms. How-ever, irreversible pulpitis may also be associatedwith intermittent or continuous episodes ofspontaneous pain (with no external stimuli). Painof irreversible pulpitis may be sharp, dull, local-ized, or diffuse and may last only for minutes orfor hours. Localization of pulpal pain is more dif-ficult than localization of periradicular pain andbecomes more difficult as the pain intensifies. Ap-plication of external stimuli such as cold or heatmay result in prolonged pain.

Accordingly, in the presence of severe pain, pul-pal responses differ from those of uninflamedteeth or teeth with reversible pulpitis." For exam-ple, application of heat to teeth with irreversiblepulpitis may produce an immediate response;also, sometimes with the application of cold, theresponse does not disappear and is prolonged.Occasionally, application of cold in patients withpainful irreversible pulpitis causes vasoconstric-tion, a drop in pulpal pressure, and subsequentpain relief. Although it has been claimed thatteeth with irreversible pulpitis have lower thresh-olds to electrical stimulation, Mumford" foundsimilar pain perception thresholds in inflamedand uninflamed pulp.

Tests and Treatment

If inflammation is confined and has not extendedperiapically, teeth respond within normal limits topalpation and percussion. Extension of inflamma-tion to the periodontal ligament causes percussionsensitivity and better localization of pain. Rootcanal treatment or extraction is indicated for teethwith signs and symptoms of irreversible pulpitis.


3 5

FIGURE 3-10A, Mechanically exposed pulp horns of a mandibular molar with signs of reversible pulpitis were capped withmineral trioxide aggregate. B, On recall, a follow-up radiograph shows no calcific metamorphosis in the pulpchamber and the presence of normal responses during clinical examination.

Hyperplastic Pulpitis

Hyperplastic pulpitis (pulp polyp) is a form of ir-reversible pulpitis, which results from growth ofchronically inflamed young pulp into occlusalsurfaces. It is usually found in carious crowns of

young patients (Figure 3-11, A). Ample vascularityof young pulp, adequate exposure for drainage,and tissue proliferation are associated with for-mation of hyperplastic pulpitis. Histologic exam-ination of hyperplastic pulpitis shows surface

FIGURE 3-11Pulp polyp, also known as hyper-plastic pulpitis. A, The involvedtooth is usually carious with exten-sive loss of tooth structure. B, Thepulp remains vital and proliferatiesfrom the exposure. (Courtesy Dr.Matthew Davis.)

36


epithelium and underlying inflamed connectivetissue (Figure 3-11, B). Cells of oral epithelium areimplanted and grow over the exposed surface toform an epithelial covering.

Hyperplastic pulpitis is usually asymptomatic.It appears as a reddish cauliflower-like outgrowthof connective tissue into caries that has resultedin a large occlusal exposure. It is occasionally as-sociated with clinical signs of irreversible pulpitissuch as spontaneous pain as well as lingering painto cold and heat stimuli. The threshold to electri-cal stimulation is similar to that found in normalpulps. The teeth respond within normal limitswhen palpated or percussed. Hyperplastic pulpitiscan be treated by pulpotomy, root canal treat-ment, or extraction.

HARD TISSUE CHANGES CAUSEDBY PULPAL INFLAMMATION

As a result of irritation, two distinct hard tissuechanges may be induced: calcification or resorption.

Pulp Calcification

Extensive calcification (usually in the form ofpulp stones or diffuse calcification) occurs as a re-

FIGURE 3-12Calcific metamorphosis. This does not represent pathosis perse and may occur with aging or low-grade irritation.

sponse to trauma, caries, periodontal disease, orother irritants. Thrombi in blood vessels and col-lagen sheaths around vessel walls are possible nidifor these calcifications.

Another type of calcification is the extensiveformation of hard tissue on dentin walls, often inresponse to irritation or death and replacement ofodontoblasts. This process is calcific metamorphosis(Figure 3-12). As irritation increases, the amountof calcification may also increase, leading to par-tial or complete radiographic (but not histologic)obliteration of the pulp chamber and root canals'A yellowish discoloration of the crown is often amanifestation of calcific metamorphosis. The painthreshold to thermal and electrical stimuli usuallyincreases, or often the teeth are unresponsive.

Responses to palpation and percussion areusually within normal limits. In contrast to softtissue diseases of the pulp, which have no radi-ographic signs and symptoms, calcification ofpulp tissue is associated with various degrees ofpulp space obliteration. A reduction in coronalpulp space followed by a gradual narrowing of theroot canal is the first sign of calcific metamorpho-sis. This condition in and of itself is not a patho-sis and does not require treatment.

Internal (Intracanal) Resorption

Inflammation in the pulp may initiate resorption ofadjacent hard tissues. The pulp is transformed intovascularized inflammatory tissue with dentinoclasticactivity; this resorbs the dentinal walls, advancingfrom the center to the periphery (Figure 3-13)." Mostcases of intracanal resorption are asymptomatic. Ad-vanced internal resorption involving the pulp cham-ber is often associated with pink spots in the crown.

Teeth with intracanal resorptive lesions usuallyrespond within normal limits to pulpal and peri-apical tests. Radiographs reveal a radiolucencywith irregular enlargement of the root canal com-partment (Figure 3-14). Immediate removal of in-flamed tissue and institution of root canal treat-ment is recommended; these lesions tend to beprogressive and eventually perforate to the lateralperiodontrum. When this occurs, pulpal necrosisensues, creating major problems in treatment op-tions. Teeth with perforated resorption are diffi-cult to treat nonsurgically.

PULPAL NECROSIS

As stated before, pulp is encased in rigid walls, ithas no collateral blood circulation, and its venulesand lymphatics collapse under increased tissuepressure; therefore irreversible pulpitis leads toliquefaction necrosis. If exudate produced during

COLOR FIGURE 3-1A, After coronal exposure in a monkey molar, amalgam was placed to induce pulp necrosis. Seven months later,the radiographic appearance of periapical lesions was evident. This molar and surrounding tissues were removedin block section and prepared for histologic examination. B, The first molar shown in A. The direction of spreadof inflammation is toward the bifurcation. Space occupied by amalgam (A). C, Inflammation is replacing peri-odontal and bony structures. Root and bone resorption (R) is adjacent to the lesion, which is consistent withchronic apical periodontitis. D, Region near arrows in C. Note the distinction between the inflammatory lesionbelow and the intact periodontium above.

continued

COLOR FIGURE 3-1, CONT'DE, Apical foramen as shown in C. There is funneling resorption of the foramen as well as active root resorption(R) . Neutrophils (N) are concentrated at the foramen, where irritants are escaping the canal. F, Modified bacter-i al Gram stain shows that bacteria (arrow) are confined to the canal space. There are not colonies of bacteria inthe periradicular lesion, a common finding. G, Periradicular granulomatous inflammation. There is a mix ofi nflammatory cells: polymorphonuclear leukocytes (N), plasma cells (P), lymphocytes (L), and macrophages (M).H, Periradicular cyst. The cyst cavity (C) is lined by epithelium (arrows) and contains an amorphous material. Theempty space is an artifact; fluids within the cavity washed out during histologic processing.

continued

COLOR FIGURE 3- 1, CONT'D1, Lymphocytes (small arrows). Plasma cells (large arrows) have an eccentric nucleus with adjacent "clear zone"and a basophilic outer rim of cytoplasm. J, Eosinophil (arrow) with distinct eosinophilic granules and bilobed nu-cleus. Plasma cells and lymphocytes are also visible. K, Polymorphonuclear leukocytes are concentrated in this field.These have multilobed nuclei; many of these are degenerating and have disrupted cell walls. L, Giant cells (arrows)with multiple nuclei. Macrophages (M) with lighter-stained nuclei and diffuse cytoplasm. M, Macrophages (arrows)are larger and often have ingested material, as indicated by a "foamy" cytoplasm in these cells. N, Lymphocytes,with their densely basophilic nuclei, dominate this field. (I to N courtesy Dr. C. Kleinegger.)

COLOR FIGURE 3-2A, An acute apical abscess has created severe and diffuse facial swelling. B, The vestibular swelling is a result ofthe necrotic pulp in the right lateral incisor. C, An access cavity was made earlier in the lingual surface of thistooth in an attempt to obtain drainage. D, Histologic examination of acute apical abscess shows edematoustissue heavily infiltrated by degenerating PMN leukocytes.

COLOR FIGURE 3-3A, A sinus tract stoma associated with a necrotic pulp in the left central incisor. B, Histologic examination of the peri-radicular tissue associated with this tooth shows numerous lymphocytes, plasma cells, and macrophages (foam cells).


37

irreversible pulpitis is absorbed or drains throughcaries or through a pulp exposure into the oralcavity, necrosis is delayed; the radicular pulp mayremain vital for long periods. In contrast, closureor sealing of an inflamed pulp induces rapid andtotal pulpal necrosis and periradicular pathosis."In addition to liquefaction necrosis, ischemicnecrosis of pulp occurs as a result of traumatic in-jury that causes disruption of the blood supply.

Symptoms

Pulpal necrosis is usually asymptomatic but maybe associated with episodes of spontaneous painand discomfort or pain (from the periapex) onpressure. Unlike in teeth with vital pulps, in teethwith necrotic pulps, pain provoked with applica-tion of heat is not due to an increase in intrapul-pal pressure. This pressure registers zero afterheat application to teeth with necrotic pulps. 49 Itis commonly believed (but is unlikely) that apply-

ing heat to teeth with liquefaction necrosis causesthermal expansion of gas present in the rootcanal, which provokes pains' In fact, cold, heat, orelectrical stimuli applied to teeth with necroticpulps usually produces no response.

Tests and Treatment

The presence of various degrees of inflammatoryresponses ranging from reversible pulpitis tonecrosis in teeth with multiple canals is possibleand may occasionally cause confusion duringtesting for responsiveness. Furthermore, effects ofnecrosis are seldom confined within canals. So,because of the spread of inflammatory reactionsto periradicular tissues, teeth with necrotic pulpsare often sensitive to percussion. Sensitivity topalpation is an additional indication of periradic-ular involvement. Root canal treatment or extrac-tion is indicated for these teeth.

FIGURE 3-73I nternal resorption in canal. Clast cells (arrow) actively resorbdentin. This process may be progressive, finally perforatingthe root.

FIGURE 3-74Hard tissue resorption that causes disappearance of normalradiographic evidence of the root canal usually indicates ani nternal resorption defect.

Periradicular PathosisAs a consequence of pulpal necrosis pathologicchanges can occur in the periradicular tissues. In

38


contrast to pulp, periradicular tissues have an al-most unlimited source of undifferentiated cellsthat participate in inflammation as well as repair.In addition, these tissues have a rich collateralblood supply and lymph drainage. The interac-tion between the irritants emanating from thecanal space and the host defense results in activa-tion of an extensive array of reactions to protectthe host. Despite these benefits, some of these re-actions are associated with destructive conse-quences such as periradicular bone resorption.Depending on severity of irritation, duration, andhost response, periradicular pathoses may rangefrom slight inflammation to extensive tissue de-struction. The reactions involved are highly com-plex and are usually mediated by nonspecific me-diators of inflammation as well as by specificimmune reactions (Figure 3-IS)."

NONSPECIFIC MEDIATORSOF PERIRADICULAR LESIONS

Nonspecific mediators of inflammatory reactionsinclude neuropeptides, fibrinolytic peptides, kinins,complement fragments, vasoactive amines, lysoso-

mal enzymes, arachidonic acid metabolites, and cy-tokines.23 Neuropeptides have been demonstratedin inflamed periapical tissues of experimental ani-mals; apparently these substances play a role in thepathogenesis of periradicular pathoses."

Severance of blood vessels in periodontal liga-ment or bone during canal instrumentation canactivate intrinsic as well as extrinsic coagulationpathways. Contact of the Hageman factor withcollagen of basement membranes enzymes suchas kallikrein or plasmin, or endotoxins from in-flamed root canals activates the clotting cascadeand the fibrinolytic system. Fibrinopeptides re-leased from fibrinogen molecules and fibrindegradation products released during the proteol-ysis of fibrin by plasmin contribute to inflamma-tion. Trauma to the periapex during root canaltreatment can also activate the kinin system and,in turn, the complement system. C3 complementfragments have been found in periradicular le-sions.55 Products released from the activated sys-tems contribute to the inflammatory process andcause swelling, pain, and tissue destruction.

Mast cells are normal components of connec-tive tissues and are present in normal periodontal

FIGURE 3-75Pathways of inflammation and bone resorption by nonspecific inflammatory mediators and specific immunereactions.


39

ligament and in periradicular lestons. 56,57 Physi-cal or chemical injury causes release of vasoac-tive amines such as histamine, which are chemo-tactic for leukocytes and macrophages. Inaddition, lysosomal enzymes cause cleavage ofCS and generation of CSa, a potent chemotacticcomponent, and liberation of active bradykininfrom plasma kininogen." Periradicular lesionsshow increased levels of lysosomal hydrolyticarylsulfatase A and B compared with normal tis-sues.58 Significant levels of PGEZ and leuko-triene B 4 have also been found in these lesions.23Other studies have confirmed these findings,demonstrating lower levels of PGE Z associatedwith either larger periapical lesions59 or cessa-tion of symptoms subsequent to emergencycleaning and shaping.60 With immunohisto-chemical staining PGE Z , - PGF2 alfa , and 6-keto-

PGF1 alfa (a stable metabolite of PGI2) have beenobserved in inflamed pulp tissue and periapicallesions . 61,62 Regions staining positively forprostaglandins gradually extended apically intoareas not yet inflamed within the pulp tissue.Periapical lesions demonstrated macrophageand fibroblast cell types staining most heavilyfor the prostaglandins evaluated. Use of in-domethacin, a prostaglandin inhibitor, experi-mentally reduces bone resorption, indicatingthat prostaglandins are also involved in thepathogenesis of periradicular lesions . 23.63 , 64

Various cytokines such as interleukins, tumornecrosis factors, and growth factors are involved inthe development and perpetuation of periradicu-lar lesions. 38,65-69 Kawashima and Stashenko68 ex-amined the kinetics of expression of 10 cytokinesin experimentally induced murine periapical le-

sions. Their results showed that a cytokine net-work is activated in the periapex in response tocanal infection and that T helper cell-modulatedproinflammatory pathways may predominate dur-ing periapical bone resorption.

SPECIFIC MEDIATORSOF PERIRADICULAR LESIONS

In addition to the nonspecific mediators of in-flammatory reactions, immunologic reactionsalso participate in the formation and perpetua-tion of periradicular pathosis (see Figure 3-1S).Numerous potential antigens may accumulate innecrotic pulp, including several species of mi-croorganisms, their toxins, and altered pulp tis-sue. Root canals are a pathway for sensitization . 23The presence of potential antigens in the rootcanals and IgE immunoglobulin, and mast cells inpathologically involved pulp and periradicular le-sions indicates that a type I immunologic reactionmay occur.19

Various classes of immunoglobulins have beenfound in these lesions .23,70 These include specificantibodies against a number of bacterial speciesin infected root canals . 71,72 In addition, differenttypes of immunocompetent cells such as antigen-presenting cells (Ia antigen-expressing nonlym-phoid cells), macrophages, 73 PMN leukocytes, andB as well as T cells have been found in humanperiradicular lesions .74,75 The presence of immunecomplexes (Figure 3-16) and immunocompetentcells such as T cells (Figure 3-17) indicates thatvarious types of immunologic reactions (types IIthrough IV) can initiate, amplify, or perpetuatethese inflammatory lesions . 23

FIGURE 3-16Using the anticomplement immunofluo-rescence technique, immune complexesare identified (arrows) in human peri-apical lesions.

40


FIGURE 3-77

T lymphocytes (arrows) are identifiedi n a human periapical lesion by an im-munohistochemical technique.

Classification ofPeriradicular Lesions

Periradicular lesions have been classified on thebasis of their clinical and histologic findings. Aswith pulpal disease, little correlation exists be-tween the clinical signs and symptoms and dura-tion of lesions compared with the histopathologicfindings.' Because of these discrepancies and forconvenience, these lesions are classified into fivemain groups: acute apical periodontitis, chronicapical periodontitis, condensing osteitis, acuteapical abscess, and chronic apical abscess. Lesionsassociated with significant symptoms such aspain or swelling are referred to as acute (sympto-matic), whereas those with mild or no symptomsare identified as chronic (asymptomatic).

ACUTE APICAL PERIODONTITISEtiology

Acute apical periodontitis would be better de-scribed as symptomatic apical periodontitis. Thefirst extension of pulpal inflammation into theperiradicular tissues is called acute apical peri-odontitis (AAP). Eliciting irritants include inflam-matory mediators from an irreversibly inflamedpulp or egress of bacteria toxins from necroticpulps, chemicals (such as irrigants or disinfectingagents), restorations in hyperocclusion, overin-strumentation, and extrusion of obturating mate-rials. The pulp may be irreversibly inflamed ornecrotic.

cation or occlusal contact. If AAP is an extensionof pulpitis, signs and symptoms will include re-sponsiveness to cold, heat, and electricity. If AAPis caused by necrosis, teeth do not respond to vi-tality tests. Application of pressure by fingertip ortapping with the butt end of a mirror handle cancause marked to excruciating pain. "Thickening"of periodontal ligament (PDL) space may be a ra-diographic feature of AAP (Figure 3-18). However,usually there is a normal PDL space and an intactlamina dura.

Histologic Features

In AAP, PMN leukocytes and macrophages are vis-ible within a localized area at the apex. At timesthere may be a small area of liquefaction necrosis(abscess). Bone and root resorption may be pre-sent histologically; however, resorption is usuallynot visible radiographically.

Treatment

Adjustment of occlusion (when there is evidenceof hyperocclusion), removal of irritants or apathologic pulp, or release of periradicular exu-date usually results in relief.

CHRONIC APICAL PERIODONTITISEtiology

Chronic apical periodontitis (CAP) results frompulpal necrosis and usually is a sequel to AAP.

Signs and Symptoms

By definition, CAP is without symptoms or is as-sociated with slight discomfort and would be bet-

Signs and Symptoms

Clinical features of AAP are moderate to severespontaneous discomfort as well as pain on masti-


41

FIGURE 3-18After cementing a three-unit bridge, thepremolar developed clinical signs andsymptoms of acute apical periodontitis,and the radiograph shows a thickenedperiodontal ligament space (arrow).

ter classified as asymptomatic apical periodontitis.Because the pulp is necrotic, teeth with CAP donot respond to electrical or thermal stimuli. Per-cussion produces little or no pain. There may beslight sensitivity to palpation, indicating an al-teration of the cortical plate of bone and exten-sion of CAP into the soft tissues. Radiographicfeatures range from interruption of the laminadura to extensive destruction of periradicularand interradicular tissues (Figure 3-19).

Histolo9ic Features

Histologically, CAP lesions are classified as eithergranulomas or cysts. A periradicular granuloma con-sists of granulomatous tissue infiltrated by mastcells, macrophages, lymphocytes, plasma cells, andoccasional PMN leukocytes (see Color Figure 3-1immediately following page 36) Multinucleatedgiant cells, foam cells, cholesterol clefts, and epi-thelium are often found.

The apical (radicular) cyst has a central cavityfilled with an eosinophilic fluid or semisolid ma-terial and is lined by stratified squamous epithe-lium (Figure 3-20). The epithelium is surroundedby connective tissue that contains all cellular ele-ments found in the periradicular granuloma.Therefore an apical cyst is a granuloma that con-tains a cavity or cavities lined with epithelium (seeColor Figure 3-l, H). The origin of the epitheliumis the remnants of Hertwig's epithelial sheath, thecell rests of Malassez. These cell rests proliferateunder an inflammatory stimulus. The actual gen-esis of the cyst is unclear.

The reported incidence of endodontic lesionsis inconsistent. Variations may be due to samplingmethods and the histologic criteria used for diag-nosis. Nobuhara and del Rio" examined peri-

FIGURE 3-19Chronic apical periodontitis. Extensive tissue destruction inthe periapical regions of a mandibular first molar as a resultof pulpal necrosis. A lack of symptoms and radiographiclesions is diagnostic.

radicular biopsy specimens of lesions that were re-fractory to root canal treatment and showed most(59%) to be granulomas, with some (22%) cysts, afew (12%) scars, and a scattering (7%) of othertypes of lesions." Percentages such as these aremisleading. Many lesions are combinations oftypes and contain granulomatous inflammation,cysts, and areas of scarring; also, the samples usu-ally do not include abscesses, which would not berecovered intact during surgery. Also, the entirelesion is usually not recovered for biopsy; onlyfragments are obtained during curettage.

42


Treatment

Removal of inciting irritants (necrotic pulp) andcomplete obturation usually result in resolutionof CAP (Figure 3-21). There is no evidence thatapical cysts do not resolve after adequate rootcanal treatment or extraction.

CONDENSING OSTEITISEtiology

Condensing osteitis (focal sclerosing osteomyelitis),a variant of chronic (asymptomatic) apical peri-odontitis, represents an increase in trabecular bonein response to persistent irritation. The irritant dif-fusing from the root canal into periradicular tissues

FIGURE 3-20This region of human apical cyst con-sists of a central cavity filled witheosinophilic material (EM) and a wallli ned with epithelium (arrows). (Cour-tesy Dr. N. Perrini.)

FIGURE 3-21A, Preoperative radiograph of a first molar shows pulpal necrosis and chronic apical periodontitis. B, A postop-erative radiograph 1 year after root canal therapy showing complete resolution of the periradicular pathosis.

is the main cause of condensing osteitis. This lesionis usually found around the apexes of mandibularposterior teeth, which show a probable cause ofpulp inflammation or necrosis. However, condens-ing osteitis can occur around the apex of any tooth.

Signs and Symptoms

Depending on the cause (pulpitis or pulpal necro-sis), condensing osteitis may be either asympto-matic or associated with pain. Pulp tissue of teethwith condensing osteitis may or may not respondto electrical or thermal stimuli. Furthermore,these teeth may or may not be sensitive to palpa-tion or percussion. Radiographically, the presence


43

of a diffuse concentric arrangement of radiopac-i ty around the root of a tooth is pathognomonic(Figure 3-22). Histologically, there is an increasein irregularly arranged trabecular bone and in-flammation."

Root canal treatment, when indicated, may re-sult in complete resolution of condensing osteitis.79Condensing osteitis is often confused with thenonpathologic entity, enostosis (sclerotic bone).

ACUTE APICAL ABSCESS

Etiology

Acute (symptomatic) apical abscess (AAA) is a lo-calized or diffuse (see Color Figure 3-2 followingpage 36) liquefaction lesion that destroys peri-radicular tissues. It is a severe inflammatory re-sponse to microbial and nonbacterial irritantsfrom necrotic pulp.

Signs and Symptoms

Depending on the severity of the reaction, pa-tients with AAA usually have moderate to severediscomfort or swelling. In addition, they occa-sionally have systemic manifestations of an infec-tive process such as a high temperature, malaise,and leukocytosis. Because this occurs only withpulp necrosis, electrical or thermal stimulationproduces no response. However, these teeth areusually painful to percussion and palpation. De-pending on the degree of hard tissue destructioncaused by irritants, the radiographic features ofAAA range from thickening of the PDL space (in-frequent) to a frank resorptive lesion (usual).

Histologic Features

Histologic examination in AAA usually shows alocalized destructive lesion of liquefaction necro-sis containing numerous disintegrating PMNleukocytes, debris, and cell remnants and an accu-mulation of purulent exudate (Figure 3-23). Sur-rounding the abscess is granulomatous tissue;therefore the lesion is best categorized as an ab-scess within a granuloma. Significantly, the ab-scess often does not communicate directly withthe apical foramen; thus an abscess often will notdrain through an accessed tooth.

Removal of the underlying cause (necroticpulp), release of pressure (drainage where possi-ble), and routine root canal treatment lead to res-olution of most AAAs.

CHRONIC APICAL ABSCESS(SUPPURATIVE APICALPERIODONTITIS)

Also classified as suppurative apical periodontitis(SAP), chronic (asymptomatic) apical abscess (CAA)results from a long-standing lesion that has causedan abscess which is draining to a surface.

Etiology

CAA (SAP) has a pathogenesis similar to that ofAAA. It also results from pulpal necrosis and isusually associated with CAP that has formed anabscess. The abscess has "burrowed" through boneand soft tissue to form a sinus tract stoma on theoral mucosa (see Color Figure 3-3 following page

FIGURE 3-22Condensing osteitis. Inflammation followed by necrosis in the pulp of the first molar has resulted in the diffuseradiopacity of periradicular tissue.

44


FIGURE 3-z3Histologic examination of acute apicalabscess shows edematous tissue heav-il y infiltrated by many degeneratingPMN leukocytes.

36) or sometimes onto the skin of the face. Thehistologic findings in these lesions are similarto those found in CAP. CAAs may also drainthrough periodontium into the sulcus andmay mimic a periodontal abscess or pocket (seeChapter 26).

shifting toward healing after the early responseshave subsided. However, for convenience and tosimplify the complex inflammatory-resorptiveprocess, they are studied as two separate entities.

Signs and Symptoms

Because drainage exists, CAA is usually asympto-matic except when there is occasional closure ofthe sinus pathway, which can cause pain. Clinical,radiographic, and histopathologic features ofCAA are similar to those described for CAP. Anadditional feature is the sinus tract, which may befined partially or totally by epithelium sur-rounded by inflamed connective tissue.80

EXTENT OF HEALING

The extent of healing is proportional to the de-gree and extent of tissue injury and the nature oftissue destruction. When injury to periradiculartissues is slight, little repair or regeneration is re-quired. However, extensive damage requires sub-stantial healing (see Figure 3-21). In other words,periradicular repair ranges from a relatively sim-ple resolution of an inflammatory infiltrate in thePDL to considerable reorganization and repair ofa variety of tissues.

Healing of Periradicular LesionsFollowing Root Canal TreatmentRegeneration is a process by which altered peri-radicular tissues are completely replaced by nativetissues to their original architecture and function.Repair is a process by which altered tissues are notcompletely restored to their original structures.Histologic examination of most tissue sections inexperimental animals and humans shows thathealing of periradicular lesions after root canaltherapy is repair rather than regeneration of theperiradicular tissues. Inflammation and healingare not two separate entities and in fact constitutepart of one process in response to tissue injury.On the molecular and cellular levels it is impossi-ble to separate the two phenomena. Inflammationdominates the early events after tissue injury,

PROCESS OF HEALING

The sequence of events leading to resolution ofperiradicular lesions has not been studied exten-sively. Based on the processes involved in repair ofextraction sites (which may not be totally synony-mous), after the cause is removed, inflammatoryresponses decrease and tissue-forming cells (fi-broblasts and endothelial cells) increase; tissue or-ganization and maturation ensue.81 Bone that hasresorbed is replaced by new bone; resorbed ce-menrum and dentin are repaired by cellular ce-mentum. The PDL, which is the first tissue af-fected, is the last to be restored to normalarchitecture. Histologic examination of periradic-ular lesions that were healing showed evidence inthe form of cementum deposition, increased vas-cularity, and increased fibroblastic and osteoblas-tic activity.82 Recent studies showed that some cy-


45

tokines play an important role during healing ofperiradicular lesions. 83 8'

With some lesions it is apparent that not alloriginal structures are restored. Variations areseen in different fiber or bone patterns. These maybe seen radiographically with a widened laminadura or altered bony configuration.

Nonendodontic PeriradicularPathosisDIFFERENTIAL DIAGNOSIS

A number of radiolucent and radiopaque lesionsof nonendodontic origin simulate the radi-ographic appearance of endodontic lesions. Be-cause of their similarities, dentists must use theirknowledge and perform clinical tests in an orderlymanner to arrive at a diagnosis and avoid criticalmistakes. Pulp vitality tests are the most impor-tant aids in differentiating between endodonticand nonendodontic lesions. Teeth associated withradiolucent periradicular lesions have necroticpulps and therefore generally do not respond to vi-tality tests. In contrast, lesions of nonpulpal originusually do not affect the blood or nerve supply toadjacent tooth pulp; therefore the vitality (respon-siveness) of these teeth remains unaffected.

Unfortunately, many clinicians use only radi-ographs for diagnosis and treatment without tak-ing a complete history of the signs and symptomsand performing clinical tests. Many nonendodon-tic radiolucent lesions (including those caused bypathoses and those with normal morphology)mimic endodontic pathoses and vice versa. There-fore to avoid grievous mistakes, all relevant vital-ity tests, radiographic examinations, clinical signsand symptoms, and details of the patient historyshould be used.

NORMAL ANDPATHOLOGIC ENTITIES

Most radiographic changes are, in fact, endodon-tic and arise from pathologic changes in the pulp.However, other radiographic variations, such asanatomic variations as well as benign and malig-nant lesions, may simulate the appearance of peri-radicular lesions.85

Normal Structures

Such anatomic variations include large marrowspaces adjacent to the apexes of teeth, sub-mandibular fossae, maxillary sinus, apical dentalpapillae of developing teeth, nasopalatine fora-

FIGURE 3-24A mental foramen (arrow) simulating a periapical lesion ofpulpal origin. Pulp tests are within normal limits, indicatingthat this radiolucency could not be endodontic pathosis.

men, mental foramen (Figure 3-24), and lingualdepressions in the mandible. Associated teeth re-spond to vitality tests and show no clinical signsand symptoms of any disease process. In addition,by changing the cone angulation, the location ofthese radiolucent lesions can be moved relative totheir original positions and to the root apexes.

Nonendodontic Pathoses

Benign lesions with radiographic appearancessimilar to those of periradicular lesions include(but are not limited to) the initial stages of peri-radicular cemental dysplasia (Figure 3-25), earlystages of monostotic fibrous dysplasia, ossifyingfibroma, primordial cyst, lateral periodontalcyst, dentigerous cyst, nasopalatine duct cyst,solitary bone cyst, central giant cell granuloma,central hemangioma, hyperparathyroidism, myx-oma, and ameloblastoma. Usually (but not al-ways) the radiographic lamina dura around theapexes is intact, and responses to pulp tests are

46


normal. The final diagnosis of these lesions is of-ten based on surgical biopsy and histopathologicexamination .86

Malignant lesions that may simulate endodon-tic periradicular lesions and are often metastatic

FIGURE 3-25A periapical radiolucency in the early stages of cementomacan simulate a periapical lesion of pulpal origin. However, thepulps are responding within normal limits.

include lymphoma (Figure 3-26), squamous cellcarcinoma, osteogenic sarcoma, chondrosarcoma,and multiple myeloma. Unlike endodontic le-sions, these lesions are usually associated withrapid and extensive hard tissue (bone and tooth)destruction. Ordinarily the teeth in the affectedregion remain responsive to vitality tests, al-though occasionally the pulps or sensory nervesare disrupted and are nonresponsive. For a morecomplete list and description of lesions that maymimic the radiographic appearance of endodon-tic lesions of pulpal origin an oral pathology textshould be consulted.87

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Diagnosis and Treatment Planning

LEARNING OBJECTIVES


1 / Define and differentiate subjective symptoms and objective findings.2 / Interpret the significance of the subjective symptoms and objective findings in the identification of diseases

of pulp and periradicular tissues.3 / State the reasons and procedures used for reviewing the chief complaint, medical and dental histories, and

present illness.4 / Identify findings that affect diagnosis or treatment planning.5 / Identify the aspects of pain most important in diagnosis.6 / State the importance of and procedures used for extraoral and intraoral examination of soft and hard

tissues.7 / Discuss the purpose of and procedures used for clinical examinations including visual (mirror and explorer)

examination, periodontal evaluation, and mobility.8 / Describe the importance of and steps involved in performing clinical pulp and periapical tests such as direct

dentin stimulation, electrical and thermal pulp tests, percussion, and palpation.9 / Describe radiographic findings that may indicate pulpal or periapical pathosis.10 / Describe when caries removal is a diagnostic test, when caries removal is required, and probable pulpal

diagnosis according to findings.11 / Describe the indications and procedures used for test cavity, selective anesthesia, and transillumination

tests.12 / Identify the significant subjective findings and objective tests that are most indicated in differential

diagnosis.13 / State the pulpal and periapical diagnosis, using appropriate terminology, according to the diagnostic

findings.14 / Describe conditions for which root canal treatment is indicated and contraindicated.15 / Design an appropriate general treatment plan according to the pulpal and periapical diagnosis.16 / Determine the number of appointments appropriate for different situations.17 / Recognize and diagnose when it is appropriate to plan adjunctive endodontic treatments such as vital pulp

therapy, bleaching, root amputation, endodontic surgery, intentional replantation, autotransplantation,hemisection, apexification, endodontic endosseous implants, orthodontic extrusion, and retreatments.

18 / Identify problems (operative complications, cracked tooth, periodontal problems, isolation difficulties,restorability, strategic value, patient management, medical complications, abnormal root or pulp anatomy,i mpact trauma, and restricted opening) that require treatment modifications.

49

50

4 / Diagnosis and Treatment Planning

OUTLINE

DiagnosisChief ComplaintHealth HistorySubjective ExaminationObjective ExaminationRadiographic ExaminationSpecial TestsSelective AnesthesiaLongitudinal Crown FracturesDifficult DiagnosesDiagnostic Findings and Terminology

Treatment PlanningTo Treat or Not to TreatTreatment Related to DiagnosisNumber of AppointmentsDiagnosis and Treatment PlansTreatment ChoicesTreatment Modifiers

Prognosis

iagnosis and treatment planningare activities that separate and distin-guish the dentist from auxiliary person

nel. Expanded-duty personnel may be trained toperform routine endodontic technical proce-dures. However, only the dentist has training inbasic and clinical sciences; this entitles the dentistalone to (1) perform all diagnostic tests, (2) inter-

pret the test results differentially, (3) psychologically

manage the patient during testing procedures, and(4) formulate an appropriate diagnosis and treat-ment plan.

Differential diagnosis of orofacial disorders isdemanding and may confuse both patient andclinician because there is a tendency to equate acomplaint of pain with an endodontic problem.In addition to teeth, other structures and organssuch as the periodontium, jaws, sinuses, ears, rem-poromandibular joints, masticatory musculature,nose, eyes, and blood vessels can induce pain thatmay mimic dental pain.1,2 Other pathologic con-ditions such as neuralgia, multiple sclerosis, my-ocardial ischemia, or psychiatric disorders mayproduce the same symptoms. To avoid misdiag-nosis (Figure 4-1) and to rule out orofacial pain ofnonpulpal or periradicular origin, a step-by-stepsystematic approach to diagnosis and treatmentplanning must be followed:

1. Ascertain the chief complaint.2. Take pertinent information related to the

patient's medical and dental history.3. Conduct thorough subjective, objective,

and radiographic examinations.4. Analyze the data obtained.5. Formulate an appropriate diagnosis and

treatment plan.Endodontics has a wide scope and includes vi-

tal pulp therapy, nonsurgical root canal treat-ment, endodontic surgery, retreatment, hemisec-tion or root amputation, bleaching, intentionalreplantation, endodontic endosseous implants,apexification or apexogenesis, transplantation,treatment of trauma, periodontal-endodonticpathosis, and orthodontics-endodontics. Obvi-ously, the area most commonly dealt with andthe one that receives the most attention is rootcanal treatment. In addition, the student andgeneral practitioner should have sufficient exper-tise to perform some other endodontic treatmentmodalities in clinical practice, but other aspectsare complex and should be considered for refer-ral. These aspects are discussed further in thischapter.

This does not mean that the graduating den-tist should be knowledgeable about diagnosis andtreatment planning in only a limited area of en-dodontics, that is, root canal treatment. In fact,


5 1

the practicing general dentist should be very skilled in di-agnosis and treatment planning over a broad base. Thegeneral dentist has initial and repeated contactwith the patient. He or she must be able to recog-nize the pathosis or disorder, diagnose the entity,and suggest the appropriate treatment plan. Afurther decision then is whether the general den-tist has enough experience to treat the conditionor whether the patient should be considered forreferral.

The dentist with this knowledge is aware of in-dications and contraindications for treatment andcan predict success or failure based on his or herown findings. The choice of who shall perform thetreatment is then decided by consultation with thepatient and is based on the mode of delivery de-signed for the best care for that patient. To sum-marize: The graduating dentist should be profi-cient in diagnosis and treatment planning andshould be treating patients with uncomplicatedproblems but referring those with complications.

This chapter suggests a systematic approach todiagnosis and treatment planning primarily as re-lated to root canal treatment. Diagnosis, treat-ment planning, and therapeutic aspects of otherentities are found in their respective chapters.

DiagnosisCHIEF COMPLAINT

The chief complaint is generally the first informa-tion obtained. This is the problem expressed in thepatient's own words about the condition thatprompted him or her to seek treatment. The chiefcomplaint should be recorded as reported in non-technical language; for example, "I have an infectedtooth and a gum boil," or "I have a toothache thatmay be causing my sinus problem."

To avoid obtaining misleading information,patients should be allowed to verbalize problemsin a way that allows them to voice their desire forrelief "Take care of the problem and stop mypain." When the patient is unaware of any prob-lem or has been referred for diagnosis or treat-ment, these facts should also be recorded (as "nochief complaint") for future reference.

FIGURE 4-7

A reliance on "clinical experience" rather than on adequatetests resulted in the wrong treatment. The dentist relied on aradiograph only (no tests) and concluded that the lateral in-cisor was the painful problem tooth. After treatment, with nochange in the level of pain, the patient was referred for root-end surgery. Examination of preoperative and postoperativeradiographs as well as clinical tests showed that treatmenthad been performed on a tooth with normal pulp. The centrali ncisor was found to have pulp necrosis and an acute apicalabscess. Immediate pain relief followed root canal treatmenton the correct tooth.

Demographic Data

Demographic data identify the patient's charac-teristics.

HEALTH HISTORY

Taking a comprehensive health history for newpatients and reviewing and updating the data ofprior patients constitute the first step in diagno-sis. A complete health history for a new patientconsists of routine demographic data, medicalhistory, current medications, dental history, chiefcomplaint, and present illness.

Medical History

Advances in medicine and public awareness ofdental maintenance have led to treatment beingrendered for patients of all ages, not only theyoung or those without medical problems. Thepatient population is, on average, of increasingage and has a higher incidence of pulpal or peri-radicular pathoses.3 Older individuals tend tohave more medical problems also.

5 2


The end result is that there are more older pa-tients who are seen with special problems'; theseconsiderations are discussed in more detail inChapter 31. Consequently, many patients (particu-larly the elderly) have had systemic diseases, in-juries, or surgery or are taking medications that in-terfere with treatment procedures. In addition, theroot canal serves as a conduit between the externalenvironment (oral cavity) and the general system.There is increasing concern (and emerging data)that oral conditions may cause systemic manifes-

tations.5,6 There is also the possibility and some ev-idence' that intracanal bacteria may be introducedinto the general circulation; the significance is atyet unknown but of concern nevertheless.

A thorough medical history not only aids diag-nosis but also provides information about a pa-tient's susceptibility and reactions to infectionand about bleeding, prescribed medications, andemotional status. Because a medical history is notintended to be a complete clinical examination,extensive medical questionnaires are unnecessary.An abbreviated screening form contains ques-tions about present and past serious illnesses, in-juries, and surgery. If there is medical evidence ofsevere or obscure physical or psychologic disease

FIGURE 4-2The presence of short roots, an absence of pathosis in the pe-riapical tissues of the incisors, and a history of orthodonticsi ndicate that resorption is due to tooth movement.

that might interfere with diagnosis or treatment,further investigation and consultation with otherhealth professionals are indicated.

There are no specific medical conditions thatcontraindicate root canal treatment other thanthose that affect any dental procedure. These con-ditions include irradiation of local tissues or dis-eases that compromise the immune system, such asacquired immunodeficiency syndrome (AIDS)"and severe heart disease.'" ' Other areas of concernthat may require special measures are the increasingincidence of latex allergies,12,13 glucocorticosteroidreplacement therapy, hepatitis, delayed hemostasis,certain cardiac conditions, and joint replacement.

Dental History

The dental history is a summary of present andpast dental experiences. It provides valuable infor-mation about the patient's attitudes toward oralhealth, care, and treatment. Such information notonly has diagnostic importance, but it also affectstreatment planning. The questionnaire shouldask for information about past and present signsand symptoms. This history is a very importanti nitial step in making a specific diagnosis.

In addition to some obvious findings that aredirectly related to endodontic problems, the his-tory reveals past dental experience and clues tothe patient's psychologic makeup as well as ex-plaining subtle clinical findings. For example,asymptomatic short roots or root resorption maybe attributed to orthodontics (Figure 4-2). Painmay develop in a recently restored tooth or afterextensive periodontal therapy. This informationnot only identifies the source of a patient's com-plaint but also aids in selecting a specific test ortreatment modality.

SUBJECTIVE EXAMINATION

Present Illness

Some routine information related to personaldata, medical history, and dental history as well asthe chief complaint may be obtained by staff.However, the dentist should review and be famil-iar with the data before proceeding further. Of-ten, the first contact between patient and dentisttakes place during collection of data about thepresent illness.

Most patients with endodontic pathoses areasymptomatic or have mild symptoms. If pulp orperiradicular pathosis is suspected because ofother findings, the dentist notes the absence ofsignificant symptoms and moves on to objectivetests. However, patients may have notable levels ofpain and distress. These patients require a careful,


5 3

systematic subjective examination with pointed,probing questions. An interesting and often con-fusing entity is tooth-related pain experiencedwith changes in ambient pressure. This phenome-non is known as barodontalgia and affects pa-tients who experience a pressure increase or de-crease. It has been described in high-altitudeflying14 and scuba diving.'

Pain and discomfort associated with pulpaland periradicular diseases do not usually affect apatient's physical state and have little or no effecton vital signs, skin color, or muscle tone. How-ever, severe pulpal or periradicular pain may affectvital signs. Regardless of degree, such pain signif-icantly alters emotional status. Because of appre-hension and emotional as well as occasional phys-ical instability, endodontic patients are handledwith extra care. Professional appearance, attitude,and a proper atmosphere are the main factorsneeded to establish good rapport (see Chapter 6).In a friendly and compassionate environment, pa-tients express problems openly. With such a thor-ough approach, patients often volunteer many de-tails about the location, onset, character, andseverity of the pain. After listening with keen in-terest, the dentist, in a sympathetic and unhurriedmanner, should ask further questions about theseverity, spontaneity, and duration of the painand the stimuli that induce or relieve it. Medica-tions taken for pain relief and their effectivenessare also important.

Significant Aspects of Pain

Pain of high intensity is usually intermittent,whereas low-intensity pain is often continuous andprotracted.'-' In contrast to protracted pain, whichis steady and dull, paroxysmal pain consists of avolley of bright jabs. Pain may also be described aspricking, stinging, burning, aching, or throbbing.Often, severe pulpal or periapical pain is synchro-nized with cardiac systole. Myofascial pain is usu-ally dull, whereas the pain of neuralgia is brightand paroxysmal." Identification of the nature ofthe pain helps to differentiate dental pain frompain in other tissues. These important considera-tions are discussed in detail in Chapter 29.

Pain is a complex entity. Many aspects of painare not particularly diagnostic and do not differen-tiate dental from nondental problems or indicatethe severity. However, some aspects of pain arestrongly indicative of pulpal and/or periradicularpathosis and thus of the treatment required. Theseare the (1) intensity, (2) spontaneity, and (3) persistence.

I ntensity. The more intense the pain (i.e., dis-ruptive to a patient's lifestyle), the more likely it isthat irreversible pathosis is present. Intense pain

is likely to be of recent onset, is unrelieved by anal-gesics, and has prompted the patient to seek treat-ment. Long-standing pain is usually not intense.Pain of a mild or moderate nature of long dura-tion is not, by itself, particularly diagnostic en-dodontically. Intense pain may arise from irre-versible pulpitis or from symptomatic (acute)apical periodontitis or abscess.

Spontaneous Pain. Spontaneous pain occurswithout an eliciting stimulus. If pain awakens thepatient or begins without stimulus, it is sponta-neous. As described previously, spontaneous com-bined with intense pain usually indicates severepulpal and/or periradicular pathosis.

An interesting and very diagnostic occurrenceis intense, continuous pain relieved only by cold.Patients with this kind of pain often appear fortreatment clutching a glass of ice water that theysip to retain cold on the aching tooth. This pain ispathognomonic of irreversible pulpitis.

Continuous Pain. This lingering type of paincontinues and may even increase in intensity afterthe stimulus is removed. For example, the patientreports prolonged pain after drinking cold liq-uids. Another describes intense continuous painafter chewing. Continuous pain with thermalstimulus usually indicates irreversible pulpitis.Continuous pain after application of pressure toa tooth indicates periradicular pathosis.

After taking the medical and dental historiesand identifying the main subjective signs andsymptoms of the patient's present illness (as de-scribed previously), the dentist often arrives at atentative diagnosis.

Tentative Diagnosis

By expanding on the present illness and askingcareful subjective questions about the patient'sproblem, the dentist can often determine thepresence or absence of pathologic changes in pulpor periapical tissues. The quality and quantity ofpresent and past pain as well as other importantsubjective findings often rule out confusingnonendodontic entities. The urgency of treat-ment is also determined. Careful questioning andinterpretation of the patient's responses often of-fer strong clues to a tentative diagnosis of pulpalor periradicular pathosis. The tentative diagnosisis then confirmed or denied by hands-on oral ex-amination and clinical tests.

OBJECTIVE EXAMINATION

During this stage, extraoral and intraoral tissuesare examined, tested, and compared bilaterally forthe presence or absence of pathosis.

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Extraoral Examination

General appearance, skin tone, facial asymmetry,swelling, discoloration, redness, extraoral scars orsinus tracts, and tender or enlarged facial or cervi-cal lymph nodes are indicators of physical status.A careful extraoral examination helps to identifythe cause of the patient's complaint as well as the

presence and extent of an inflammatory reactionin the oral cavity (Figure 4-3).

Intraoral Examination

Soft Tissue. This examination includes a thor-ough visual and digital test of the oral soft tissues.The lips, oral mucosa, cheeks, tongue, palate, and

FIGURE 4-3Extraoral sinus tract. A, This surface lesion (arrow) was misdiagnosed and treated unsuccessfully by a dermatol-ogist for several months. Fortunately, the patient's dentist then recognized it to be a draining sinus tract with itssource being a mandibular anterior tooth. B, The pulp was necrotic owing to severe attrition with pulp exposure.C, After proper root canal treatment only. D, the sinus tract and surface lesion resolved completely (arrow).


55

muscles are evaluated and abnormalities arenoted. Alveolar mucosa and attached gingiva areexamined for the presence of discoloration, in-flammation, ulceration, and sinus tract forma-tion. A sinus tract stoma parulis usually indicatespresence of a necrotic pulp or suppurative apicalperiodontitis and sometimes a periodontal ab-scess (Figure 4-4). Gutta-percha placed in the si-nus tract occasionally allows localization of thesource of these lesions.

Dentition. Teeth are examined for discol-orations, fractures, abrasions, erosions, caries,large restorations, or other abnormalities. A dis-colored crown is often pathognomonic of pulpalpathosis (Figure 4-5) or is the sequela of earlierroot canal treatment. Although in some cases thediagnosis is very likely at this stage of examina-tion, a prudent diagnostician should never pro-ceed with treatment before performing appropri-ate confirmatory clinical and radiographicexaminations.

Clinical Tests

Clinical tests include use of a mirror and an ex-plorer and periodontal probing as well as indi-cated pulpal and periapical tests. There are limita-tions inherent in most of these tests; some cannotbe used on each tooth, and the test results them-selves may be inconclusive. Therefore, it is risky torely on a single test; other supplemental confir-matory tests should be performed. These tests arenot absolute and tend to be somewhat crude.They require care in performance and caution in

interpretation. Importantly, these are not tests ofteeth; they are tests of a patient's response to a vari-ety of perceived stimuli. The testing responseprocess is very complex and involves both the pe-ripheral and central nervous systems as well as oc-casional complications related to the emotionalstatus of the patient, thus often giving rise tofalse-negative and false-positive test results. Thepatient may not understand or may wrongly per-ceive or misinterpret a stimulus. For these rea-sons, the series of subjective and objective testsand findings often are inconsistent and results are

FIGURE 4-4I ntraoral sinus tract. Purulence is expressed from this asymp-tomatic lesion associated with pulp necrosis of the first molar.

FIGURE 4-5The discolored incisor (A) was associated with a necrotic pulp andchronic apical periodontitis (B).

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confusing for strict interpretation. There is noeasy resolution; patience and insight are required,and experience is helpful.

Mirror and Explorer. A mirror and an explorer re-veal gross or recurrent caries, pulp exposures,crown fractures, defective restorations, and coro-nal leakage in teeth with previous root canal ther-apy. In some instances (i.e., gross coronal decay),the mirror and explorer may provide sufficient in-formation to arrive at a final diagnosis. However,because pathologic changes usually cannot be de-termined by this method alone, other clinical testsare required.

Control Teeth. An important adjunct to pulpand periapical tests is the use of controls (com-parisons). These are healthy teeth that should re-spond normally. Control teeth have three func-tions: (1) the patient learns what to expect fromthe stimulus; (2) the dentist can observe the na-ture of the patient's response to a certain level ofstimulus, and (3) the dentist can determine thatthe stimulus is capable of invoking a response.For example, posterior teeth in adults, particu-larly molars, may be unresponsive to thermaltests. This would make cold invalid as a testingmodality if ice is placed on a healthy molar andthe patient experiences no sensation.

Periapical Tests

Percussion. Percussion may determine the pres-ence of periradicular inflammation. A marked pos-

itive response indicates inflammation in the peri-odontium. Because inflammatory changes in peri-odontal ligament are not always of pulpal originand may be induced by periodontal disease, the re-sults should be confirmed by other tests. However,in some cases other tests cannot be performed, andpercussion might be the best indicator of signifi-cant periradicular pathosis. One difference is thatpercussion pain related to periodontal inflammationis more likely to be in the mild to moderate range.Periapical inflammation is probable if the pain is verysharp, causing a withdrawal response.

Percussion is performed by tapping on the in-cisal or occlusal surface with the end of a mirrorhandle held parallel or perpendicular to the crown.With severe subjective pain, tapping the teeth isavoided; gentle apical pressure is applied with digi-tal manipulation of the tooth. To establish a basisfor comparison, the percussion test should also beperformed on control teeth. Another very good testis to have the patient bite hard on an object, suchas a cotton swab, with the suspected and a controltooth. This test is confirmatory if the patient re-ports pain upon mastication (Figure 4-6).

Palpation. Like percussion, palpation determineshow far the inflammatory process has extended pe-riapically. A positive response to palpation indicatesperiradicular inflammation. Palpation is firm pres-sure on the mucosa overlying the apex (Figure 4-7).Pressure is applied by a fingertip and, like the per-cussion test, at least one control tooth should beincluded.

FIGURE 4-6Biting test. Having the patient bite and grind firmly on a cot-ton swab is effective in confirming pain on mastication.

FIGURE 4-7Palpation. Applying firm pressure with the little finger overthe apex of the suspect tooth helps confirm periradiculari nflammation.


5 7

Pulp Vitality Tests

Direct dentin stimulation, cold, heat, and electric-ity determine the response to stimuli and occa-sionally can identify the offending tooth by an ab-normal response. Response does not guarantee apulp's viability or health but at best indicates thepresence of some nerve fibers carrying sensory impulses.There is wide variation in the pulpal response ofboth normal and pathologically involved teeth.Because of inherent limitations, these testsshould always have adequate controls, and resultsshould be interpreted carefully.

Selecting the Appropriate Pulp Test. The selectiondepends on the situation. Additional meaningfulinformation is collected when stimuli similar tothose that the patient reports will provoke painare used during clinical tests. When cold (or hot)food or drink initiates a painful response, a cold(or hot) test is conducted in place of other viabil-ity tests. Replication of the same symptoms in atooth often indicates the offender. Overall, elec-trical stimulation is similar to cold (refrigerant) inidentifying pulp necrosis; heat is the least reliablestimulus.

Direct Dentin Stimulation. This is probably themost accurate and, in many cases, the best pulp vi-tality test. Exposed dentin may be scratched withan explorer; however, the absence of a response isnot as indicative as the presence of a response.Caries are probed deeply with an explorer to non-carious dentin, sudden, sharp sensation indicatesthat the pulp contains vital tissue.

When other tests are inconclusive or cannot beused and a necrotic pulp is suspected, a test cavityis helpful. For example, a tooth with a porcelain-fused-to-metal crown often cannot be tested accu-rately by standard thermal or electrical tests. After

careful subjective examination and an explana-tion of the nature of the test to the patient, prepa-ration without anesthesia is done with a smalland sharp bur. With a vital pulp, the surface of therestoration or the enamel can be penetrated with-out too much discomfort. If the pulp is vital,there will be a sudden sensation of pain whendentin is reached. In contrast, if discomfort orpain is absent, the pulp is probably necrotic; anaccess preparation has already been started andthe procedure may be continued.

Cold Tests. Three methods are generally usedfor cold testing: regular ice, carbon dioxide (dryice), and refrigerant. Carbon dioxide requires spe-cial equipment (Figure 4-8), whereas refrigerant ina spray can is more convenient (Figure 4-9). As toeffectiveness, regular ice delivers less cold and isnot as effective as refrigerant or CO2 ice. Onestudy found that refrigerant sprayed on a largecotton pellet markedly reduced temperaturewithin the chamber.16 Overall, refrigerant sprayand CO2 are equivalent for pulp testing.

After the tooth is isolated with cotton rolls anddried, an ice stick or large cotton pellet saturatedwith refrigerant is applied. This stimulus appliedover a vital pulp usually results in sharp, briefpain. This short, sharp response may occur re-gardless of pulp status (normal or reversible or ir-reversible pulpitis). However, an intense and pro-longed response usually indicates irreversiblepulpitis. In contrast, necrotic pulps do not re-spond. A false-negative response is often obtainedwhen cold is applied to teeth with constrictedcanals (calcific metamorphosis), whereas a false-positive response may result if cold water contactsgingiva or is transferred to adjacent teeth with vi-tal pulps.

FIGURE 4-8Carbon dioxide ice testing. A, A carbon dioxide tank and special "ice maker" are required. B, A carbon dioxide

i ce stick is formed (arrow). The stick is held in gauze and touched to the facial surfaces of suspect and controlteeth. This technique can be used in teeth with various types of restorations. (Courtesy Dr. W. Johnson.)

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Cold is more effective on anterior teeth thanon more insulated posterior teeth. Therefore, lackof a response to cold on control posterior teeth in-dicates another vitality test. Electric pulp testingis reliable after cold testing; the pulp's responsive-ness is unaffected by cold."

Heat Tests. Teeth may be isolated by a rubberdam to prevent false-positive responses. Varioustechniques and materials are used. Gutta-perchais heated in a flame and applied to the facial sur-face. The best, safest, and easiest technique is torotate a dry rubber prophy cup to create frictionalheat (Figure 4-10) or to apply hot water. A flame-heated instrument is difficult to control andshould be handled with care.

A mechanical, battery-powered device, such asthe Touch-n-Heat, is better controlled and will de-liver heat safely and effectively. Heat is not usedroutinely but is helpful when the major symptomis heat sensitivity, and the patient cannot identifythe offending tooth. After applying heat, the tem-perature is gradually increased until pain iselicited. As with cold, a sharp and nonlingeringpain response indicates a vital (not necessarilynormal) pulp.

Significance of Thermal Tests. An exaggerated andlingering response is a good indication of irre-versible pulpitis. Absence of response in conjunc-tion with other tests compared with results oncontrol teeth usually indicates pulpal necrosis. Aswith cold, calcific metamorphosis may cause afalse-negative response. As mentioned earlier, onetest is seldom conclusive for the presence or absence ofpulpal or periapical disease.

Electrical Pulp Testing. Many devices are avail-able commercially for electrical pulp tests. All arepowered by batteries and deliver a direct currentof high-frequency electricity that is varied. Thestimulus is usually applied to the facial surface todetermine the presence or absence of sensorynerves and supposedly of a vital pulp.

Electrical pulp testers with digital readouts arepopular. These are not inherently superior toother electrical testers but are more user-friendly.All are used in a similar manner. It is very impor-tant to clean, dry, and isolate the teeth. Scrub thesurface with a cotton roll and isolate it with thesame roll, then dry thoroughly with the air sy-ringe. A small amount of toothpaste or other con-ducting medium (the most effective conductingmedium has not been identified) is placed on theelectrode. An electrical circuit is established by us-ing a lip clip or having the patient touch the metalhandle. 18 The electrode is placed on the facial orlingual surface (Figure 4-11), and the level of cur-rent is gradually increased until it surpasses theperception threshold. Sensation may be tingling,stinging, "full," or hot. The presence of a response

FIGURE 4-9Refrigerant sprayed on a cotton roll, swab, or pellet (best) isconvenient and effective for determining pulp responsiveness.

FIGURE 4-70A prophy cup run at high speed without lubricant generatescontrolled heat for pulp testing.


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usually indicates vital tissue, whereas the absenceof such a response usually indicates pulpal necro-sis. The electrical pulp tester is not infallible andmay produce false-positive or false-negative re-sponses 10% to 20% of the time." Calcific meta-morphosis may cause a false-negative response.Warning: Contrary to popular opinion and persistentnotions, different response levels with different teeth asshown by the number on the device do not indicate stagesof pulp degeneration. Electrical testers do not mea-sure the degree of health or disease of a pulp. Be-cause false-positive and false-negative responsesare common, reactions to these tests should be in-terpreted (with some skepticism) only as yes or noresponses. Further careful interpretation, com-parison, and correlation with other findings andtests must be done; then a tentative determina-tion of vitality or necrosis is appropriate.

Blood Flow Determination. Instruments that de-tect pulp circulation are part of a developing tech-nology that is likely to produce new approachesfor determining the presence of vital pulp tissuein an otherwise nonresponsive tooth. An exampleis the previously traumatized tooth that has an in-tact blood supply, but no intact sensory nervesand therefore is unresponsive to stimuli. Thesevery sensitive devices will detect pulp blood com-ponents or blood flow in these situations. Sensorsare applied to the enamel surface, usually on boththe facial and lingual nerves. Blood flow is shownby beams of light (dual wavelength spectropho-tometry),20 pulse oximetry,21 or laser Dopplerflowmetry.22,23 Blood components are demon-

strated by detecting oxyhemoglobin '24 low con-centrations of blood,25 or pulsations in the pulp.These approaches are still more experimentalthan clinically practical, and the devices are ex-pensive. As the technology improves and becomesless costly, and more experience is gained, theiruse as sensitive pulp testers in the future is likely.

Periodontal Examination

Periapical and periodontal lesions may mimiceach other and therefore require differentiation(see Chapter 26). It is also important to establishthe periodontal health of the tooth or teeth aspart of overall treatment planning.

Probing. Probing is an important clinical testthat is often overlooked and underused for di-agnosing periapical lesions. Bone and periodon-tal soft tissue destruction are induced by bothperiodontal disease and periradicular lesionsand may not be easily detected or differentiatedradiographically.

A periodontal probe determines the level ofconnective tissue attachment. Also, the probepenetrates into an inflammatory periapical lesionthat extends cervically. Probing is a diagnostic aidthat has prognostic value. The prognosis for atooth with a necrotic pulp that induces cervicallyextending periapical inflammation is good afteradequate root canal treatment. However, the out-come of root canal treatment on a tooth with se-vere periodontal disease usually depends on thesuccess of periodontal treatment. Teeth withmarked periodontal disease involvement are poorcandidates for endodontic procedures. Probingdepths should be recorded for future comparison.

Mobility. The mobility test partially determinesthe status of both the periodontal ligament andprognosis. Teeth with extreme mobility usuallyhave little periodontal support. Occasionally anextensive periradicular lesion may alter the peri-odontal support markedly; mobility usually de-creases dramatically after successful root canaltreatment.

Mobility is determined by placing the indexfinger on the lingual aspect and applying pressurewith the mirror handle on the opposite facial sur-face. Movement of more than 2 to 3 mm or de-pression indicates that the tooth is a poor candi-date for root canal treatment if the mobility is dueprimarily to periodontal disease and not to peri-radicular pathosis.

FIGURE 4-77Electric pulp tester. A special minitip (electrode) with a smallspot of conductive medium is useful for electrical pulp test-i ng where tooth structure availability is limited.

RADIOGRAPHIC EXAMINATION

Perhaps radiographs should be termed "the greatpretenders." Dentists tend to rely excessively on

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FIGURE 4-12Horizontal as well as vertical bone loss is ev-ident in this quadrant. All teeth are respon-sive to vitality tests; therefore, the resorptivedefects represent a severe periodontal con-dition and not pulp or periradicular pathosis.Root canal treatment is not indicated.

FIGURE 4-13Characteristic appearance of an endodontic lesion. This radi-ograph shows loss of lamina dura and a hanging-drop ap-pearance. There was a history of trauma in this patient. A filmmade at a different angle would show the lesion remainingat the apex. (Courtesy Dr. L. Wilcox.)

radiographs to supply conclusive diagnostic in-formation. Certainly they are useful and necessaryas diagnostic and treatment aids. But the use ofradiographs to diagnose pulpal or periradicularpathosis has been exaggerated, and many limita-tions are overlooked. Pathologic changes in thepulp are not visible; likewise, periradicular lesionsproduce no radiographic changes in the earlystages. Evidence of pathosis often appears only

when the inflammatory process spreads tomedullary bone, particularly to the corticalplates .26,27 Radiographs are only two-dimensional;various projections may allow several views of thesame structures, permitting three-dimensional in-terpretation. With these and other limitations, itis evident that good-quality films are only one ofthe tools used for diagnosis.

Radiographs allow evaluation of tooth-relatedproblems (e.g., carious lesions, defective restora-tions, and root canal treatments), abnormal pul-pal and periradicular appearances, malpositionedteeth, relationship of the neurovascular bundle tothe apexes, the general bony pattern, and peri-odontal disease (Figure 4-12).

Periapical Lesions

Radiolucent and radiopaque entities in the jaws(both normal structures and nonendodonticpathosis) may be confused with endodonticpathosis. Obviously, such confusion may lead tomisdiagnosis and incorrect treatment. Periradicu-lar lesions of pulpal origin usually have four char-acteristics: (1) the lamina dura is lost apically; (2)the lucency remains at the apex regardless of thecone angle; (3) the lucency tends to resemble ahanging drop; and (4) usually a cause of the pulpnecrosis is evident (Figure 4-13).

The dentist should remember the most impor-tant diagnostic radiographic relationship be-tween the pulp and the periapical tissues: A well-developed radiolucent periapical lesion is invariablyassociated with and results from a necrotic pulp! A siz-able radiolucency in the periapical region of atooth with a vital pulp is not of endodontic originand is either a normal structure or a nonen-dodontic pathosis.


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FIGURE 4-14Condensing osteitis. A, Surrounding the distal root apex is diffuse trabeculation. B, This contrasts with the con-tralateral molar, which demonstrates a normal, sparse trabecular pattern.

Radiopaque changes also occur. Condensing os-teitis is a reaction to pulp or periradicular inflam-mation and results in an increase in medullarybone.28 It has a diffuse circumferential medullarypattern with indistinct borders (Figure 4-14). Thewell-circumscribed, more homogeneous normalstructure that occurs commonly in the mandibularposterior region is enostosis (or sclerotic bone);this is a nonpathologic condition.

New radiographic technology permits early de-tection of bony changes, allowing new approachesto differential diagnosis. Digital subtraction radi-ography "reads" subtle early changes with periapi-cal bone resorption." Digital radiometric analysisand computed tomography may distinguish bonypathoses such as granulomas and cysts.30 Radiovi-siography and magnetic resonance imagingdemonstrate changes of resorptive lesions overtime.31 However, all these technologies are stillneither perfected nor cost effective nor offer sig-nificant diagnostic benefits for routine clinical ap-plication"; undoubtedly these or similar deviceswill prove useful in the future.

Pulpal Lesions

Few specific pathologic entities that relate to irre-versible pulpitis are visible radiographically. Aninflamed pulp with dentinoclastic activity mayshow abnormally altered pulp space enlargementand is pathognomonic of internal resorption (Fig-ure 4-15). Extensive diffuse calcification in thechamber may indicate long-term, low-grade irrita-tion (not necessarily of irreversible pulpitis).

Dentin formation that radiographically "obliter-ates" the canals (usually in patients with a historyof trauma) does not in itself indicate pathosis(Figure 4-16). These teeth ordinarily require notreatment, but when treatment is necessary (seeFigure 4-15, B), they can be managed with reason-able success . 33

SPECIAL TESTS

After subjective and objective examinations andclinical tests have been completed, it is usuallypossible to make an accurate diagnosis and cre-ate a reasonable treatment plan. However, if spe-cial circumstances prevent making a definitivediagnosis, additional tests such as caries re-moval, selective anesthesia, and transillumina-tion are options.

Caries Removal

Determining the depth of caries penetration isnecessary in some situations for definitive pulpdiagnosis. A common clinical situation is thepresence of deep caries on radiographs, no signif-icant history or presenting symptoms, and a pulpthat responds to clinical tests. All other findingsare normal. The final definitive test is completecaries removal to establish pulp status.

Penetration of caries into a symptomatic pulpindicates irreversible pulpitis, requiring root canaltreatment. Nonpenetration usually indicates re-versible pulpitis (although a percentage of pulpsare irreversibly inflamed without exposure); the

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FIGURE 4-75Differing pulp responses to injury. A, Central incisor shows extensive, perforating internal resorption; the lateralincisor has calcific metamorphosis. B, Special techniques manage these problems with both surgical and nonsur-gical treatment.

FIGURE 4-16Calcific metamorphosis. A, This lesion has resulted from repeated insults from caries and restorations. B, Thisdentin formation ("obliteration") resulted from trauma and irritation to the pulp. Neither A nor B is pathosis. Oc-casionally apical pathosis does develop; this is a treatment challenge. (B courtesy Dr. L. Wilcox.)


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tooth is then restored atraumaticalty. The patientis informed of possible future treatments.

Selective Anesthesia

This test is in contrast to the test cavity, which isperformed in symptomatic as well as pain-freeteeth. The selective anesthesia test is useful inpainful teeth, particularly when the patient can-not isolate the offending tooth even to a specificarch. If a mandibular tooth is suspected, amandibular block will confirm at least the regionif the pain disappears after the injection.

Individual tooth anesthesia is most effective inthe maxilla. Anesthetic should be administered inan anterior to posterior direction because of thedistribution of the sensory nerves. Because an in-ferior alveolar nerve block anesthetizes all teeth inthe quadrant, selective anesthesia is not useful forthe mandible. The periodontal ligament injectionwill often anesthetize multiple teeth3' and shouldnot be used to identify a suspect tooth. Selectiveanesthesia is most useful to identify which archhas the tooth that is the source of pain.

Transillumination

This test helps to identify longitudinal crownfractures because a fracture will not transmit thelight. Transillumination produces contrastingdark and light at the fracture site.

LONGITUDINAL CROWN FRACTURES

These fractures seem to be increasing in numberand are a challenge for both diagnosis and treat-ment. There are some classic signs occurring of-ten that indicate a cracked tooth. This is a fairlycommon cause of endodontic pathosis and there-fore requires consideration during diagnosis.More detail about diagnosis and management ofthese fractures is in Chapter 28.

DIFFICULT DIAGNOSES

Some perplexing conditions defy diagnosis evenafter thorough subjective, objective, and radi-ographic examinations.35 Usually these situationsdo not require immediate treatment and the pa-tient may be scheduled for a return visit for fur-ther evaluation or possibly dental and medicalconsultations. Collection and careful analysis ofdata by consultation with others are prudent toprevent misdiagnosis and mistreatment of thesepatients. It is a mistake to feel compelled to treatall patients who express symptoms immediately.Often time or a different approach wilt permit the

correct diagnosis and logical treatment. Also,symptoms that have significant pathosis as theirsource tend to be isolated to the offending toothwith time. Symptoms unrelated to significantpathosis will generally subside. Patients usuallyaccept this explanation and are willing to wait fora definitive diagnosis.

DIAGNOSTIC FINDINGSAND TERMINOLOGY

Use of a data form to accumulate diagnostic find-ings serves three purposes: first, it ensures that allpertinent information has been assessed and in-cluded; second, it ensures that findings have beenrecorded and may be analyzed; and third, it al-lows future reference to findings noted at the ini-tial appointment. Figure 4-17 is an example ofsuch a form.

The findings are arranged in a rational order toarrive at a pulpal or periradicular diagnosis. Thisprocess is summarized in Table 4-1. Consistencyof all findings does not always exist because of thevariations and unpredictability of diagnoses andof patient responses. In addition to diagnosingpathoses and determining what treatment is indi-cated, the approach used must fit into the pa-tient's overall needs and treatment plan. To ac-complish this, the practitioner should know theindications and contraindications for root canaltherapy and recognize conditions that make treat-ment difficult. This knowledge, combined withthe diagnosis, determines the treatment plan.

Treatment PlanningOnce the nature of the pathosis has been deter-mined, treatment decisions must be made. Themajor decision is whether root canal treatment isnecessary or some other approaches are preferred.Some teeth may require extraction or a temporarymeasure (i.e., an emergency situation) with defin-itive root canal treatment at a future appoint-ment. At times the decision as to the treatmentapproach becomes complicated. For example,with failed root canal treatment, whether to re-treat or to manage surgically involves a number ofconsiderations.36 Many patients with these prob-l ems are best referred to an endodontist.

TO TREAT OR NOT TO TREAT

After diagnosis and treatment plan have been for-mulated, the next step is to discuss these with thepatient so he or she will understand the problemand its management. A common question is, "But

64


FIGURE 4-17A sample form used in diagnosis and treatment planning. (Adapted from Krell K, Walton R: Odontalgia: diagnos-i ng pulpal, periapical, and periodontal pain. In Clark J, editor: Clinical dentistry, Philadelphia, 1987, Harper & Row.)

doctor, it doesn't hurt. Is it necessary to do this atall, or can't we just wait and see if it does botherme?" One explanation of the necessity for imme-diate treatment is that progressive disease (pulpand/or periapical) is present, and early manage-ment enhances the chances for successful treat-ment. A good explanation to the asymptomaticpatient is that this problem is a time bomb tickingaway. The problem is that we cannot know when itwill go off, but it probably will do so at an inop-portune time. Management is better, easier, andmore predictable before such symptoms occur.

TREATMENT RELATEDTO DIAGNOSIS

The pulpal diagnosis in general dictates the ap-proach. If the various states of pulp pathosis arelisted, that is, normal pulp, reversible pulpitis,irreversible pulpitis, and necrosis, a line isdrawn between reversible and irreversible pulpi-

tis. Those entities on the reversible side may ormay not require noninvasive treatment; those onthe irreversible side require extraction or rootcanal treatment or at least removal of the in-flamed portion of the pulp with pulpotomy orpartial pulpectomy.

The periapical diagnosis indicates the specificnature of the procedure to be followed, usually inconjunction with root canal treatment. In otherwords, a periradicular lesion has developed onlybecause significant, severe pulp pathosis exists.This requires root canal therapy (if appropriate)and sometimes other surgical procedures such asextraction, or incision and drainage.

NUMBER OF APPOINTMENTS

Although traditionally a point of debate, mostinvestigations indicate that, in general, single-appointment root canal treatment is acceptable.37-39However, the general dentist should approach

4 1 Diagnosis and Treatment Planning

6 5

Diagnostic Terminology

this type of treatment with caution and carefulpatient selection.

Multiple Appointments

There are situations that require more than a sin-gle appointment. One is the condition that iscomplex or time consuming. Related to this andmost important is patient management and thetolerance level of patient and operator. If fatigueor frustration on the part of either occurs, the ap-pointment is terminated, a temporary filling isplaced, and another appointment is scheduled.

Another situation is the patient with severe peri-radicular symptoms or persistent canal exudation.These are often emergencies, and the tolerance levelof the patient is low. Also, flare-ups between ap-pointments occur more often in these situations."Posttreatment flare-up is considerably more diffi-cult to manage if the canals are obturated.

A third indication may be a diagnosis of pulpnecrosis and asymptotic apical pathosis. There issome preliminary evidence (not conclusive) thathealing may be better if there are two visits andcalcium hydroxide is placed as an intracanalmedicament.41

Effects on Prognosis and Pain

The long-term prognosis and patient symptomsafter treatment are two major concerns related tothe number of appointments. As yet, most stud-ies indicate that in the asymptomatic patient,posttreatment pain 37,42,43 i s unrelated to whethertreatment is completed in single or multiple ap-pointments. Effects on prognosis are uncertainto date. Again, single-appointment root canaltreatment should always be approached withsome caution and with consideration of each in-dividual case.

66


When to Conclude the Appointment

The questions to be answered are as follows: Whatshould be completed to minimize interappoint-ment problems? At what point may a temporaryfilling be placed? Studies have not indicated all fac-tors that dictate what must be accomplished; how-ever, there is no increase in posttreatment symp-toms from incomplete cleaning and shaping.40,44But, when there is pulpal necrosis, there may beimproved healing if debridement is completed andintracanal calcium hydroxide is placed . 45

DIAGNOSIS ANDTREATMENT PLANS

Specific treatment approaches are indicated, de-pending on the diagnosis and the individual situ-ation. The following general recommendationsare made accordingly. Variations or alterations in spe-cific treatment options are dictated by circumstances.

Pulpal Diagnosis

Normal or Reversible Pulpitis. Root canal treat-ment is not indicated (unless elective). In patientswith reversible pulpitis, the cause is usually re-moved and restoration follows (if necessary).

Irreversible Pulpitis. Root canal treatment,pulpotomy, partial pulpectomy, or extraction isrequired. Ultimately total pulp removal is pre-ferred; attempting to maintain a damaged pulp,for example, by capping a carious exposure, islikely to result in long-term failure.46 Partial pulpremoval is a temporary measure in certain cir-cumstances (emergency or apexogenesis). Totalpulpectomy is not always accomplished with theuse of broaches alone, which leave shreds of pulptissue. The pulp is totally removed only whencleaning and shaping are essentially complete. Atthe initial appointment, if circumstances do notpermit complete pulpectomy, pulpotomy or par-tial pulpectomy is acceptable .4'

Necrosis. Root canal treatment or extraction isindicated. Necrotic debris may be removed com-pletely on the first visit. Again, this situation in-cludes establishing working lengths and complet-ing cleaning and shaping. Careful instrumentationand copious irrigation are important. If a situationdoes not permit total debridement, partial debride-ment is acceptable.

Caustic pungent chemical medicaments arecontraindicated; these are of no benefit. If morethan minimal preparation has been done (morethan 25 file), calcium hydroxide paste may beplaced in the canal.

Rarely should these teeth be left open to theoral cavity. 48,49 Occasionally the tooth might be

left open if a continuous, copious flow of exudateexists during canal preparation. Adjunctive treat-ment with pulp necrosis may be necessary, de-pending on the periradicular diagnosis.

Periradicular Diagnosis

There are more treatment variations related toperiradicular status. With significant periradicu-lar pathosis, associated pulp necrosis exists. Itshould be remembered that the most importantfactors in the resolution of periradicular pathosis,whether acute or chronic, are debridement and re-moval of irritants from the pulp space! These arealways prerequisites. Of course, ultimate successdepends on coronal and radicular obturation aswell as debridement .so

Normal. No special treatment approach isrequired.

Acute Apical Periodontitis. Because this is a small(but painful) inflammatory lesion, there is no spe-cial treatment required. It is critical to remove theinflamed pulp or necrotic debris and other irri-tants. Pain comes primarily from fluid pressure;some exudate or transudate may be released intothe canal space when it is opened or during instru-mentation. This may be a small amount and maynot be visible clinically, but will aid in pain relief.

Intracanal medicaments do not reduce symp-toms. However, to inhibit bacteria with pulpnecrosis, calcium hydroxide is placed in thecanal(s), and the access is closed with a cotton pel-let and a temporary filling. Occlusal reduction inpatients with severe percussion sensitivity mayease symptoms.''

Chronic Apical Periodontitis. This lesion is associ-ated with pulp necrosis. The size of the lesion gen-erally is not a factor in choosing the treatment ap-proach (Figure 4-18). Calcium hydroxide is placedas an intracanal medicament, and the accessopening is sealed with dry cotton and a temporaryfilling.

Acute Apical Abscess

Debridement. Because this lesion is accompa-nied by pain and/or swelling, different ap-proaches are necessary. Most critical is debridement ofirritants from the canal space; therefore, complete ornearly complete cleaning and shaping with copi-ous, careful irrigation are desired.

Drainage. Next in importance is drainagethrough the tooth or soft tissue. Treatment (inci-sion and drainage, extraction) varies, dependingon the presence or absence of swelling, extent ofinvolvement, and other factors. Specific details onmanaging acute apical abscess are discussed inChapter 17.


6 7

Suppurative Apical Periodontitis(Chronic Apical Abscess)

Because this lesion is asymptomatic owing to in-traoral or extraoral drainage of an abscess," nospecial treatment measures are necessary. Again,the key is debridement; the tract or parulis shouldresolve spontaneously once irritants from thepulp space are removed (see Figure 4-3). A persis-tent draining sinus tract indicates a misdiagnosis(is it a periodontal abscess?), a missed canal, or in-adequate debridement or obturation. Generally,the sinus tract resolves a few days to a month af-ter debridement and obturation. Calcium hydrox-ide should be placed in the canal(s) and in the ac-cess cavity, which is always closed temporarilybetween appointments.

Condensing Osteitis. This entity requires no spe-cial treatment. Because it occurs with differentpulp conditions, treatment will vary. Condens-ing osteitis resolves in approximately 50% ofteeth after successful root canal treatment.'' Thereis no apparent problem if the condensing os-teitis does not resolve; no further treatment is re-quired unless there are other findings that indi-cate failure.

TREATMENT CHOICES

Routine Cases

There are some procedures that the graduatingdentist (and general dentist) should be able toperform. According to the Curriculum Guidelinesfor Endodontics (see Chapter 1), sufficient educa-tional experience in specific procedures must beprovided to the student. Obviously, there is varia-tion between and even within individual institu-tions; however, the practicing dentist often ac-quires additional skills by advanced formaltraining, experience, or continuing education.

Most uncomplicated root canal treatment pro-cedures can and should be done by the generalpractitioner. The most important point is to iden-tify the routine nature of each case and plan ac-cordingly. So, what is within the capabilities ofthe general practitioner, and which patientsshould be considered for referral? This informa-tion is covered in detail in Chapter 5.

Difficult Procedures

Difficult procedures include a wide spectrum ofproblems. Managing difficulties depends on theknowledge and skills of the general practitioner.Equally important is access to the appropriate in-struments and materials. With all these consider-ations, the practitioner (in collaboration with thepatient) decides what to treat. The decision to treat

FIGURE 4-18Because of its size, this lesion is likely to be an apical radicu-l ar cyst. The lesion is related to pulp necrosis in the left cen-tral incisor. Although superimposed over the apex of the ad-jacent incisor, the pulp is not affected and therefore does notrequire treatment. Proper root canal treatment of the left in-cisor would lead to resolution without surgery.

or refer is based on the individual patient case and not ona predetermined set of criteria.

TREATMENT MODIFIERS

Complications

While progressing through the diagnostic process,the practitioner makes observations that modifythe treatment approach. A decision may be madeto extract a tooth that is nonrestorable, has severeperiodontal involvement, or is noncritical to theoverall treatment plan or if the patient is disinter-ested in comprehensive care. Other conditionsthat may require modifications include severecaries, failed root canal treatment, operative prob-lems, isolation difficulties (Figure 4-19), abnormalroot or pulp anatomy (Figure 4-20), medical com-plications, and calcifications (Figure 4-21). Anyone or a combination of these may designate a pa-tient with a complex problem that should be con-sidered for consultation or referral (see Chapter 5).

68

4 I Diagnosis and Treatment Planning

FIGURE 4-79I solation problem. Deep subgingival caries require an adjunctive surgicalprocedure for adequate isolation and restoration.

FIGURE 4-20Anatomic difficulties. A, Dens invaginatus has resulted in communication and resultant necrosis of the pulp. In-complete dentin formation and an irregular internal form make these teeth anatomically difficult to clean, shape,and obturate. The size of the periradicular lesion does not itself contraindicate nonsurgical treatment. B, A se-verely curved root and the position make treatment for this third molar difficult.

Adjunctive Procedures

Many procedures often are beyond the trainingand experience of the general practitioner.These include but are not limited to surgery,complex bleaching, replantation, retreatment,

transplantation, apexification, root resection,and management of cracked teeth. The general-ist should understand these techniques and howthey mesh with the overall treatment plan andexplain them to the patient. These adjunctive


69

FIGURE 4-21Anatomic difficulties. A, Numerous insults from caries, restorations, and restorative procedures have resulted incalcific metamorphosis in the molar. A very small canal contains necrotic tissue sufficient to cause apical patho-sis. Note that cervical caries are also altering the pulpal anatomy on the adjacent premolar (arrows). B, Removalof the crown and an extensive search failed to locate the canals. Periradicular surgery with a root end filling willbe necessary.

procedures are described in more detail in otherchapters.

PrognosisPatients are entitled to the best dental care. Un-fortunately, this is not always available or is notpresented during discussion of the treatmentplan. The practitioner should calculate a progno-sis for each situation, including a contingency prog-

nosis if problems are encountered after treatmenthas begun.

It has been reported (as a summarization ofrelative success and failure rates) that successrates for treatment by general practitioners arelower than those of specialists or specialty clin-ics.'° Although there may be a number of reasonsfor this, certainly a major one is the tendency ofgeneral practitioners to attempt treatments thatare inappropriate or beyond their abilities." Thus,to provide the best treatment, the generalist andspecialist must communicate, share treatmentproblems, and exchange ideas for providing thebest treatment for their patients."

REFERENCES

1. Drinnan AJ: Differential diagnosis of orofacial pain,Dent Clin North Am 22:73, 1978.

2. Moore R, Miller ML, Weinstein P, et al: Cultural per-ceptions of pain and coping among patients and den-tists, Commun Dent Oral Epidemiol 14:327, 1986.

3. Eriksen H: Endodontology epidemiologic considera-tions, Endod Dent Traumatol 7:189, 1991.

4. Walton R: Endodontic considerations in the geriatricpatient, Dent Clin North Am 41:795, 1997.

5. Slavkin H: Does the mouth put the heart at risk? J Am

Dent Assoc 130:109, 1999.6. Murray C, Saunders W: Root canal treatment and gen-

eral health: a review of the literature, Int EndodJ 33:1,

2000.7. Debelian G, Olsen 1, Tronstad L: Anaerobic bacteremia

and fungemia in patients undergoing endodontictherapy: an overview, Ann Periodontol 3:281, 1998.

8. Gerner N, Hurlen B, Dobloug J, Brandtzaeg P:Endodontic treatment and immunopathology of peri-apical granuloma in an AIDS patients, Endod DentTraumatol4:127, 1988.

9. Cooper H: Root canal treatment on patients with HIVinfection, Int Endod J 26:369, 1993.

10. Findler M, Galili D, Meidan Z, et al: Dental treatmentin very high risk patients with active ischemic heartdisease, Oral Surg Oral Med Oral Pathol 76:298, 1993.

11. Niwa H, Sato Y, Matsuura H: Safety of dental treat-ment in patients with previously diagnosed acute my-ocardial infarction or unstable angina pectoris, Oral

Surg Oral Med Oral Pathol Oral Radiol Endod 89:35, 2000.12. Kleier D, Shibilski K: Management of the latex hyper-

sensitive patient in the endodontic office, J Endod

25:825, 1999.13. Dias de Andrade E, Ranali J, Volpato M, et al: Allergic

reaction after rubber dam placement, J Endod 26:182,

2000.

70


14. Kollmann W: Incidence and possible causes of dentalpain during simulated high altitude flights, J Endod19:154, 1993.

15. Bell WE: Orofacial pains, ed 2, Chicago, 1979, Year Book.16. Jones D: Effect of the type carrier used on the results

of dichlorodifluoromethane application to teeth,JEndod 25:692, 1999.

17. Pantera E, Anderson R, Pantera C: Reliability of elec-tric pulp testing after pulpal testing with dichlorodi-fluoromethane, JEndod 19:312, 1993.

18. Pantera E, Anderson R, Pantera C: Use of dental in-struments for bridging during electric pulp testing,JEndod 18:37, 1992.

19. Peterson K, Soderstrom C, Kiani-Anaraki M, Levy G:Evaluation of the ability of thermal and electrical tests toregister pulp vitality, Endod Dent Traumatol 15:127, 1999.

20. Nissan R, Trope M, Zhang C, Chance B: Dual wave-length spectrophotometry as a diagnostic test of thepulp chamber contents, Oral Surg Oral Med Oral Patbol74:508, 1992.

21. Schnettler J, Wallace J: Pulse oximetry as a diagnostictool of pulpal vitality, JEndod 17:488, 1991.

22. Evans D, Reid J, Strang R, Stirrups D: A comparison oflaser Doppler flowmetry with other methods of assess-i ng the vitality of traumatised anterior teeth, EndodDent Traumatol 15:284, 1999.

23. Emshoff R, Kranewitter R, Norer B: Effect of LeFort Iosteotomy on maxillary tooth type related blood flowcharacteristics, Oral Surg Oral Med Oral Pathol OralRadiol Endod 89: 88, 2000.

24. Noblett C, Wilcox L, Johnson W, et al: Detection ofpulpal circulation in vitro by pulse oximetry, J Endod2:1, 1996.

25. Diaz-Arnold A, Arnold M, Wilcox L: Optical detectionof hemoglobin in pulpal blood, JEndod 22:19, 1996.

26. Bender IB: Factors influencing the radiographic ap-pearance of bony lesions, J Endod 8:161, 1982.

27. Lee S, Messer H: Radiographic appearance of artifi-cially prepared periapical lesions confined to cancel-lous bone, Int Endod j 19:64, 1986.

28. Maixner D, Green TL, Walton R, Leider A: Histologicalexamination of condensing osteitis (abstract), J Endod18:196, 1992.

29. Tyndall D, Kapa S, Bagnell C: Digital subtraction radi-ography for detecting cortical and cancellous bonechanges in the periapical region, JEndod 16:173, 1990.

30. Shrout M, Hall M, Hildebolt C: Differentiation of pe-riapical granulomas and radicular cysts by digital ra-diometric analysis, Oral Surg Oral Med Oral Pathol OralRadiol Endod 76:356, 1993.

31. Lockhart P, Kim S, Lund N: Magnetic resonance imag-ing of human teeth, J Endod 6:237, 1992.

32. Holtzmann D, Johnson WT, Southard T, et al: Stor-age-phosphor computed radiography versus film radi-ography in the detection of pathologic periradicularbone loss in cadavers, Oral Surg Oral Med Oral PatholOral Radiol Endod 86:90, 1998.

33. Akerblom A, Hasselgren G: The prognosis for en-dodontic treatment of obliterated root canals, JEndod14:565, 1988.

34. D'Souza JE, Walton RE, Peterson LC: Periodontal liga-ment injection: an evaluation of the extent of anesthe-sia and postinjection discomfort, J Am Dent Assoc114:341, 1987.

35. Krell K, Walton R: Odontalgia: diagnosing pulpal, pe-riapical, and periodontal pain. In Clark J, editor, Clini-cal dentistry, Philadelphia, 1986, Harper & Row.

36. Kvist T, Reit C: Results of endodontic retreatment: Arandomized clinical study comparing surgical andnonsurgical procedures, JEndod 25:814, 1999.

37. Roane JB, Dryden JA, Grimes EW: Incidence of post-operative pain after single- and multiple-visit en-dodontic procedures, Oral Surg Oral Med Oral Patbol55:68, 1983.

38. Pekruhn RB: The incidence of failure following single-visit endodontic therapy, JEndod 12:68, 1986.

39. Jurcak J, Bellizzi R, Loushine R: Successful single-visitendodontcs during Operation Desert Shield, J Endod19:412, 1993.

40. Walton R, Fouad A: Endodontic interappointmentflare-ups: prospective study of incidence and related fac-

tors,J Endod 18:172, 1992.41. Katebzadeh N, Sigurdsson A, Trope M: Radiographic

evaluation of periapical healing after obturation of in-fected root canals: an in vivo study, Int Endod J 33:60,2000.

42. Mulhern JM, Patterson SS, Newton CW, Ringel AM: In-cidence of postoperative pain after one-appointmentendodontic treatment of asymptomatic pulpal necrosisin single-rooted teeth,J Endod 8:370, 1982.

43. Fava L: A comparison of one- versus two-appointmentendodontic therapy in teeth with non-vital pulps, IntEndod J 22:179, 1989.

44. Maddox D, Walton R, Davis C: Effects of medicamentsand other factors on the incidence of post-treatmentendodontic pain, J Endod 3:447, 1977.

45. Trope M, Delano O, Orstavik D: Endodontic treat-ment of teeth with apical periodontitis: single vs. mul-tivisit treatment, JEndod 25:345, 1999.

46. Banthel C, Rosenkranz B, Leuenberg A, Roulet J-F:Pulp capping of carious exposures: Treatment out-come after 5 and 10 years, JEndod 26: 525, 2000.

47. Oguntebi B, DeSchepper E, Taylor T, et al: Postopera-tive pain incidence related to the type of emergencytreatment of symptomatic pulpitis, Oral Surg Oral MedOral Patbol 73:479, 1992.

48. Weine FS, Healy HJ, Theiss EP: Endodontic emergencydilemma: leave tooth open or keep it closed? Oral SurgOral Med Oral Patbol 40:531, 1975.

49. August DS: Managing the abscessed open tooth: in-strument or close? Part II. JEndod 8:364, 1982.

50. Bystrom A, Happonen RP, Sjogren U, Sundqvist G:Healing of periapical lesions of pulpless teeth after en-dodontic treatment with controlled asepsis, EndodDent Traumatol 3:58, 1987.

51. Rosenberg P, Babick P, Schertzer L, Leung A: The effectof occlusal reduction on pain after endodontic instru-mentation, JEndod 24:492, 1998.

52. Calman HI, Eisenberg M, Grodjesk JE, Szerlip L: Theexternal fistula, its diagnosis and importance, DentRadiog Photog 53:26, 1980.

53. Hedin M, Polhagen L: Follow-up study of periradicu-lar bone condensation, Scand J Dent Res 79:436, 1971.

54. Molven O: The frequency, technical standard and re-sults of endodontic therapy, Nor Tannlasg Tidsskr86:142, 1976.

55. Scharwatt B: The general practitioner and the en-dodontist, Dent Clin North Am 23:747, 1979.

When and How to Refer

LEARNING OBJECTIVES


1 / Understand the importance of referral.

2 / Classify complications of endodontic procedures.

3 / Identify factors complicating diagnosis.

4 / Discuss factors that make root canal treatment difficult.

5 / Describe factors that make determination of prognosis difficult.

6 / Identify situations that might require consultation with a physician or a dental specialist.

7 / Identify which procedures should be within the capabilities of the generalist.

8 / Identify which procedures are ordinarily not within the graduating dentist's realm of training or experience

and which patients should be considered for referral.

9 / Recognize reasons for referral after treatment is initiated.

10 / Describe the relationship, responsibilities, and communication modes among the general dentist, patient,

and endodontist.

71

72

5 / When and How to Refer

I dentification and Classification of Cases

Case Selection System

Patient Considerations

Health and Medical History

Local Anesthesia

Physical Limitations

Objective Clinical Findings

Diagnosis

Radiographs

Anatomic Complications

Additional Factors

Restorability and Isolation

Existing Restorations

Cracked Tooth

Root Resorption

Endodontic-Periodontic Lesion

Traumatic Injuries

Previous Endodontic Treatment

Procedural Accidents

Separated Instrument or Canal Blockages

Ledging

Perforations

Emergencies

Persistent Signs and/or Symptoms

Persistent Radiographic Pathosis

Persistent Probing Defect or Sinus Tract

Referral During Treatment

Flare-ups


I nability to Locate Root Canals

Financial Considerations

Referral to a Specialist

What Is Expected of a General Practitioner

I nstructions to Endodontist

Explanation to Patient

What Is Expected of an Endodontist

Treatment Performed

Feedback to Dentist

Feedback to Patient

I dentification and Classificationof Cases

The decision about what to treat and what to referdepends on different risk factors, including theskills of the dentist and the case difficulty.6 Thereare three general categories of cases based on theircomplexity:

1. Average risk. An experienced practitionershould expect to achieve a favorable out-come based on the pretreatment evalua-tion of the risk factors.

patient deserves the best quality ofcare possible. Depending on the treat-ment, the general dentist may be best

suited to deliver that care. In some situations, ei-ther a general dentist or a specialist may effica-ciously perform the procedure. However, in morecomplex cases, the specialist will provide the bestcare.'

Referrals are part of comprehensive health caremanagement and are appropriate when the pa-tient's needs are beyond the generalist's capabili-ties.2 By definition, standard of care means that thequality of endodontic care provided to patients by thegeneral dentist should be similar to that provided by anendodontist.3 Because of the subjectivity of criteriaused to evaluate degrees of complexity, it is diffi-cult to determine when to proceed versus when torefer. Epidemiologic data show that success ratesfor root canal treatment are lower for generaliststhan for specialists. 4 A possible contributing fac-tor for this finding is that general dentists oftenattempt treatment that is beyond their abilities.An objective measure of when and which patientsto refer is very important.

This chapter presents guidelines for determin-ing case complexity using specific risk factors andthen rating them systematically. Application ofthis system allows a general dentist to recognizepatients with problems within their scope andtreat them accordingly.' It should also help gen-eral practitioners to avoid mishaps and misunder-standings and ultimately to provide the besttreatment for their patients.

Obviously, there are referral considerationsother than case complexity. For example, a generaldentist may have the training and experience tomanage a particular situation but may choose notto do so, preferring to concentrate on other as-pects of treatment. Or a dentist may have learnedthat he or she cannot complete certain proceduresquickly enough for cost effectiveness. This chap-ter does not discuss these considerations.


73

2. High risk. An experienced practitioner withadvanced training may be able to managethese situations, but caution should be ob-served. These patients may be consideredfor referral if one or more of the risk fac-tors fall in this range.

3. Extreme risk. The preoperative conditionsshow exceptionally difficult situations;even the most skilled practitioner will bechallenged. These patients should be con-sidered for referral.

Complexity may be related to diagnostic, pro-cedural, or prognostic difficulties.

Diagnostic difficulties include confusing test re-sults, nonspecific or unusual patterns of painfrom periradicular lesions of nonpulpal origin,endodontic or periodontal lesions, and resorp-tion. Radiographic problems may be either tech-nical or interpretive.

Procedural difficulties may relate to the patient'sphysical limitations, medical history, or manage-ment problems, inadequate anesthesia, isolationdifficulties, tooth restorability, or complex toothanatomy. Additional complications include thepresence (or absence) of restorations, the presenceof previous obturating materials or posts, trau-matic injuries and fractures, endodontic emergen-cies, and procedural accidents.

Prognostic difficulties are associated with persis-tent symptoms and or/lesions and failure to healafter prior treatment.

Case Selection System

This system involves the recognition and rating ofrisks associated with endodontic therapy. Everycase has certain unique difficulties that deserveobservation and rating before the dentist makesthe ultimate decision to treat or refer a patient.This program presents a means of evaluating eachcase based on degree of difficulty by consideringrisk factors related to the patient and the toothand parameters affecting treatment and progno-sis. Determining the various factors yields a sys-tematic, measurable rating.

Each factor is given a numerical value. Thesevalues are average risk (rate 1), high risk (rate 2), andextreme risk (rate 3). If all ratings fall in the averagecategory, a general practitioner usually can treatthe patient. If one or more factors fall in the high-risk category, the patient may be treated by an ex-perienced generalist or referred. Patients with oneor more factors in the extreme range should be con-sidered for referral to an endodontist. For example,a relatively straightforward root canal treatment

for a central incisor may be best managed by re-ferral if the patient has a very limited oral openingand film placement would be difficult, or if thecanal space is calcified as a result of trauma orother complicating factors.

Figure 5-1 is a working model reproduction of theEndodontic Case Difficulty Assessment Form selectionsystem. Consideration involves a checklist thatrates all factors systematically. At first, the processseems cumbersome; however, repeated usage andfamiliarity will reduce risk for both patient anddentist. This should allow the dentist to provideoptimum quality care.

Patient ConsiderationsHEALTH AND MEDICAL HISTORY

General practitioners may treat medical complica-tions that affect diagnosis and/or treatment andpatients who require premedication. However,severity must be evaluated. In patients with moreserious disorders, an endodontist may best pro-vide treatment. Specialist care is generally moreexpedient and offers better prevention and man-agement of complications during treatment. Dia-betes and anticoagulant therapy are examples of asystemic condition and a medication that may af-fect the decision of whether to refer. Consultationwith the patient's physician before decidingwhether to refer is advisable when the medical his-tory indicates a potential problem.

LOCAL ANESTHESIA

Some patients report an "allergy" to local anesthet-ics. However, a true allergic reaction to commonlyused local anesthetics, particularly the amides, is al-most nonexistent.' Tachycardia is often confusedwith an allergy. A patient may report adverse reac-tions to an anesthetic with epinephrine. This isprobably apprehension and not truly an "allergy."

A major dilemma is highly inflamed pulp, par-ticularly in mandibular molars.8 Difficulty withanesthesia may transform a cooperative patientinto a budding dental phobic. When difficulty isencountered in obtaining profound anesthesia,referral should be considered. Endodontists areaccustomed to dealing with these situations.

PHYSICAL LIMITATIONS

Physical limitations may present problems forproviding proper treatment. If the patient cannotbe suitably reclined or if the mouth opening issuch that access is compromised, referral shouldbe considered. Even endodontists are challenged,

FIGURE 5-1Endodontic case difficulty assessment form. (Reprinted with permission from the American Association of Endodontists.)


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and oral anatomy (e.g., shallow palatal vault orlarge and narrow dental arches) may hinder thistask. Also, some apprehensive patients are proneto gag or cannot maintain film position. Whencase rating is considered, possible difficulties inobtaining diagnostic or treatment films must bekept in mind.

ANATOMIC COMPLICATIONS

A number of anatomic factors are related to de-velopmental and acquired tooth morphology.

Pulp Chamber

As the tooth ages, pulp chamber space decreases.Chamber size and pulp stones, as well as the ex-tent of calcifications in the canal system, must beconsidered (Figure 5-3).

Calcific Metamorphosis

In addition to chamber calcification, the canalsmay show calcific metamorphosis from dentin de-position (Figure 5-4).s Considered are the visibil-ity of the canals, the canal orifices, and the general

but they may have encountered the problem anddevised a solution. A second molar in one patientmay be easier to manipulate than a premolar inanother patient. The area should be inspectedcarefully; if problems are detected before the rub-ber dam is placed, the patient should be referred.

Objective Clinical FindingsDIAGNOSIS

Appropriate treatment follows accurate diagno-sis. Many procedures are done inappropriately (ornot done) because of diagnostic errors. The end-odontist is experienced, and the generalist maybe unfamiliar with that particular problem. Re-ferred pain is a prime example of a condition that oftenpresents the practitioner with a significant diagnosticchallenge. Unless a definitive diagnosis is obtained,no treatment should be rendered, and the patientreferred.

RADIOGRAPHS

Diagnostic and treatment films of good qualityare critical (Figure 5-2). Patient characteristics

FIGURE 5-2A, Periapical radiolucency (A) and mesial radiolucency in the apical third (8). The canals are calcified, the root isnarrow, and there is a hint of a significant mesial concavity in the coronal third (C). The tooth is also crowned,thereby increasing access complexity. This case is considered as high risk. B, Postoperatively, the mesial radiolu-cency resulted from the buccal root exiting several millimeters shorter than the palatal root with a significant dis-tal curvature. The practitioner must manage the unexpected should problems arise during treatment.

FIGURE 5-4Apical pathosis-the canal is not visible (calcific metamor-

phosis); this situation is rated as extreme risk.

decrease in canal size as evident on radiographs'(Figure 5-5).

Number of Canals

A good rule is to always expect "extra" canals orroots unless the preoperative film clearly shows adistinct number of canals; the reality is that moremay exist (Figures 5-6 and 5-7). There are difficul-ties with multiple canals. For example, manymandibular incisors have two root canals andmandibular premolars may have multiplecanals." ,' ' A significant percentage of mandibularfirst molars have two canals in the distal root, andmesiobuccal roots of maxillary molars often havetwo canal systems.'z

Root Curvature

Canals are rarely straight, although roots may ap-pear so on a facial radiograph. Curvature factorsi nclude the direction, severity, and number ofcurves (Figure 5-8). Especially common are "re-curvatures" of the mesial roots of mandibularmolars, in which the apices bend toward eachother. Another treatment challenge is the bayonetcurve (Figure 5-9). This should be considered ex-tremely difficult (rate 3).

Root Length

Long root canal systems are a challenge to treat.Very short roots also pose unique problems.

FIGURE 5-3Pulp chamber and root canals show calcific metamorphosis; this situation is rated as extreme risk.

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5 I When and How to Refer

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FIGURE 5-5A, Calcific metamorphosis in the mesial root plus chamber narrowing and orifice angulation, which compromisethe access into the mesial canals. B, The postoperative radiograph reveals four canals, gradual curvature of mesialcanals, and apical delta with accessory canals in the distal root. Slight sealer overextensions should not adverselyaffect healing. This tooth should be treated by an experienced practitioner, but with caution.

FIGURE 5-6Mandibular molars with an "extra" distolingual root; this situation is rated as high risk.

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FIGURE 5-7

A, Unusual anatomy. Note the abrupt curvature in the middle and apical third, suggesting a third canal. B, Post-operative image. The difficulty of this situation should be a consideration for referral to a specialist.

FIGURE 5-8

A, Extreme curvature of the mesiobuccal root of tooth 14. This nearly 90° curve (A) would place this situation inthe extreme risk category and the patient should be considered for referral. B, Note the curvature of the disto-buccal root in the postoperative radiograph.


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FIGURE 5-9

A, Dilaceration in the apical third. The degree and location of curvature strongly suggest caution and a consider-ation for referral. B, Note in the postoperative radiograph that the apical third curvature has been maintained.

Degree of Apical Closure

The size of the apical opening correlates with thedifficulty of the situation. Recently erupted teethwith immature apices are complicated to treat andoften require special procedures. Outcome andduration of treatment are unpredictable; theseteeth are difficult to manage (see Chapter 22).Problems with teeth in which the initial apicalforamen is between file sizes 50 and 70 are catego-rized as high risk.

Tooth Location and Malpositioning

Generally, second and third molars, especiallymaxillary molars, are difficult to reach, particu-larly in a patient with a limited opening. Buccallypositioned maxillary second molars are associ-ated with a variety of treatment problems. Ro-tated, tipped, or crowded teeth may also compli-cate isolation and access as well as inhibitadequate cleaning and shaping or obturation(Figure 5-10).

Additional Factors

RESTORABILITY AND ISOLATION

Severe caries or other damage may render thetooth too difficult to isolate or to restore; extrac-tion may be the best alternative. In some instancescrown lengthening may be necessary to create bi-ologic width. Referral to a periodontist for suchtreatment should be considered. Also, an en-dodontist may combine crown lengthening withroot canal treatment in the same appointment(Figure 5-11).

EXISTING RESTORATIONS

Many teeth requiring root canal treatment havecastings." Access through gold is easier than thatthrough nonprecious metals. Porcelain is some-what fragile, creating difficulties in access andpreparation. If the tooth is a bridge abutment, theangulation and length of span must be considered.Often, restoration anatomy does not duplicate the

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FIGURE 5-10Rotated lateral incisor may create isolation and access problems; this situation is rated as high risk.

FIGURE 5-11Mesial abutment requires crown lengthening for root canal treatment as well as for the creation of biologic widthfor restoration.

original crown anatomy, and the pulp chamber isdifficult to locate. When the chamber and orificesare not visible in the preoperative film or theanatomy of the underlying tooth is questionable,the rating is high risk (see Figure 5-2).

Other considerations include the size of thecrown and the presence of precision attachmentsas well as parallelism between the long axis of thecrown and the long axis of the root. These consid-

erations are particularly important in premolars,maxillary lateral incisors, and mandibular in-cisors. These teeth are narrow and there is littleroom for error.

CRACKED TOOTH

Cracked or fractured teeth are often difficult to di-agnose and treat. Symptoms can vary from vague


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FIGURE 5-12A, Complexity caused by trauma. Previous treatment of 23 and 24. Tooth 25 is symptomatic, with percussion sen-sitivity and non responsiveness to pulp testing. Tooth 26 shows internal resorption that is asymptomatic. Care mustbe taken to completely clean and shape the canal system, as is demonstrated in the postoperative image. B, Thissituation exhibits a high degree of difficulty.

pain while chewing to extreme pulpalgia. Defini-tive diagnosis must be achieved before treatment;then the prognosis must be determined based onthe degree of fracture (see Chapter 28).

ROOT RESORPTION

Resorption can be either internal (intracanal) orexternal (extracanal).

All instances of perforating (pulp-periodontalcommunication) resorption are complex. Externalresorption may take one of the following forms:

1. Inflammatory resorption is related to pulpnecrosis. A periradicular lesion may causeapical resorption. Lateral resorption usuallyresults from impact trauma.

2. Replacement resorption occurs after impactinjuries (luxation or avulsion). This resorp-tion is associated with fusion, then replace-ment, of tooth structure with bone.

3. Idiopathic (unknown) or known etiology is unre-lated to pulpal or periradicular pathosis (e.g.,resorption due to orthodontic treatment).

Patients with tooth resorption, whether inter-nal or external, are high risk, and should be re-ferred for evaluation and treatment (Figure S-12).

Limited internal (intracanal) resorption maynot present treatment complications, but externalapical resorption may drastically alter the geome-try of the root canal. A structure that was onceround may now be irregular and difficult to cleanand seal. Extensive apical resorption may be bestmanaged by referral.

Endodontic-Periodontic Lesion

Another diagnostic dilemma arises with patientswith periodontal problems who also have pulpalproblems. If there is doubt about whether theproblem is endodontic or periodontal (or has an-other cause), the patient should be referred. Differ-ential diagnosis of periodontal and endodonticlesions is discussed in Chapter 26. Marginal peri-odontitis is best evaluated by a periodontist. Anendodontist or a periodontist or both canbest differentiate endodontic from periodontal

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FIGURE 5-13

Combined endodontic-periodontal problem. A, This tooth may have been considered hopeless from a periodontalperspective. B, However, correct diagnosis and root canal treatment resolved most of the periradicular pathosis,although the periodontal component persists.

pathosis (Figure 5-13). Referral is best for patientsneeding surgical procedures such as hemisectionor root resection.

Traumatic Injuries

Trauma to the dentition has two treatment com-ponents: primary and secondary management.Primary management is the first contact the in-jured patient has with a dentist; secondary man-agement is the follow-up care. Primary care is re-quired for patients with severe trauma such asluxations, displaced root fractures, and avulsions;the general dentist may render treatment immedi-ately after the injury. Primary care includes pa-tient management, repositioning, replantation,splinting, and suturing of soft tissue lacerations.

For secondary follow-up care the patient shouldbe referred to an endodontist, who can determinean appropriate schedule for long-term manage-ment, recall, or treatment as necessary. Somechanges may have a delayed onset. Examples of

complications range from reversible pulpal inflam-mation to pulpal necrosis. These phenomena mayor may not be obvious owing to variability in pulpresponse to testing, lack of symptoms, and so on.More subtle changes may include resorption (bothexternal and internal), calcific metamorphosis,tooth discoloration, and obscure root fractures. Be-cause many changes occur gradually, these patientsmust be followed over a prolonged period of time,preferably by an endodontist.

Previous Endodontic Treatment

Teeth are more difficult to retreat than to treatoriginally. Thus, rating of these cases is limitedto rate 2 or rate 3 (Figure 5-14). These situationsrequire a variety of approaches, including con-ventional retreatment, surgery, or combinedtreatment. Endodontists are more skilled thangeneral practitioners in diagnosing and manag-ing the myriad of problems presented and aremore experienced in crown and post removal. Be-


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FIGURE 5-14A, Previously attempted root canal treatment with very shortobturation. The mesial root appears ledged. The tooth is per-cussion sensitive; also note the apical radiolucency of the dis-tal root. Such retreatment cases should be considered as highor extreme risk. B, Only an experienced practitioner shouldmanage this patient; referral is recommended.

be referred. If pain or swelling continues afteremergency treatment and the general practitionercannot assist the patient, an endodontist shouldbe consulted or the patient should be referred.

PERSISTENT SIGNS

AND/OR SYMPTOMS

If pain and/or swelling persist or develop aftertreatment, the patient should be referred or anendodontist should be consulted. The symptoms

Emergencies

Emergencies are not addressed on the ratingform, but are a significant part of decision mak-ing in the daily practice of general dentistry. Gen-eral practitioners should be able to diagnose andtreat most uncomplicated preoperative, interap-pointment, and postobturation emergencies.However, more severe problems are difficult tomanage. For example, if the generalist cannotcontrol the patient psychologically or is unable toobtain profound anesthesia, the patient should

Perforations

Cases involving root or crown perforations canonly be rated as rate 3. Patients with these condi-tions should be referred to an endodontist. De-pending on the size, location, and strategic im-portance of the tooth, several options areavailable. These treatment approaches, as well aslong-term assessment, are generally beyond theexpertise of a general practitioner.

LEDGING

If a canal is ledged far from the working length,prognosis is compromised. The generalist shouldrefer the patient to an endodontist. Canals thathave not been ledged too far from the workinglength can be obturated, and the patient can befollowed by the general practitioner. If retreat-ment or surgery is subsequently needed, the pa-tient should be referred.

Procedural AccidentsSEPARATED INSTRUMENT

OR CANAL BLOCKAGES

A separated instrument or other blockage mayhave a significant effect on prognosis. Consulta-tion with an endodontist may be advisable. Dif-ferent approaches are possible, and probably re-quire an endodontist's expertise.

cause of the complexity of retreatment, most pa-tients should be referred. Generally, because end-odontists commonly retreat teeth that have hadpreviously unsuccessful root canal treatment,they have not only the experience but also an ar-mamentarium useful for both nonsurgical andsurgical approaches. Retreatments are becomingmore commonplace as a result of procedural ac-cidents of various types, described herein.

Referral to a SpecialistCommunicating to the patient the need for refer-ral for consultation and diagnosis or treatmentmust be done skillfully to avoid misunderstand-ing. The patient must realize that the most impor-tant consideration is optimal care. The reasonsand timing of referral vary. Factors to be consid-ered are the expertise of the dentist, treatmentcomplexity, specialist availability, and other man-agement factors. The patient is reminded that thespecialist is generally able to handle problemsmore skillfully. Most patients understand and ac-cept referral.

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may have several causes: lack of debridement,lack of obturation, missed canals, root fractures,and so on. Extraction, retreatment, or surgical in-tervention may be required.

PERSISTENT RADIOGRAPHICPATHOSIS

If periradicular lesions persist or develop afterroot canal treatment, consultation may be indi-cated. The endodontist may retreat, performsurgery, or advise the generalist on appropriatemeasures to resolve the problem.

PERSISTENT PROBING DEFECTOR SINUS TRACT

If a probing defect of pulpal origin or a sinus tractdoes not resolve after treatment, the patientshould be referred. In addition, a new defect orsinus tract indicates treatment failure; referralshould be considered.

Referral During TreatmentTiming of referral is important. A poor practice is toinitiate treatment with the idea that if problems arise, areferral can be made at the time. Patients prefer tohave a procedure started and completed by thesame dentist. This saves appointment time forboth patient and dentist. In addition, an initialreferral prevents potential procedural errors bythe general practitioner. The most importantconsideration is the effect on prognosis of amidtreatment referral. Preferably, the endodon-tist performs the entire procedure without hav-ing to correct iatrogenic problems. Also, withmidtreatment referral, the patient may lose confi-dence in the original dentist. Another majorproblem is economics; monetarily, someoneloses. The endodontist certainly is entitled to afull fee (or often more than a full fee; a treatmentis generally more difficult if started by someoneelse). If the patient is responsible for two fees forthe same tooth, ill will is created. It is far betterfor the general dentist to study the case and rec-ommend referral than to "bail out" in the middleof treatment.

However, during treatment unanticipatedproblems may arise that require referral; a call tothe endodontist and an explanation to the patientare in order. Reasons for possible midtreatmentreferral include flare-up (pain and/or swelling),procedural accidents, inability to achieve ade-quate anesthesia, and other factors that hindercompletion of root canal therapy.

FINANCIAL CONSIDERATIONS

Monetary considerations are important. Compli-cated problems, particularly those that involveprolonged treatment periods of months or yearstend to be financial losses for the general dentist.

INABILITY TO LOCATE ROOTCANALS

Enhanced lighting and magnification improvethe chances of locating canals. However, the great-est aid is experience. Rather than gouging or per-forating while attempting to find a canal, referralshould be considered. The endodontist may alsohave difficulty in locating canals. Locating canals iseasier if the chamber has not already been altered.

PROCEDURAL ACCIDENTS

Procedural accidents occur during treatment.Again, the specialist's experience allows a betterassessment of the probable outcome as well as themeans of addressing the problem.

FLARE-UPS

Usually most pain or swelling occur before initialtreatment. After emergency measures, pain usu-ally substantially decreases in 24 to 48 hours.Flare-ups are not common. 14 Occasionally, how-ever (particularly with an acute apical abscess),symptoms do not subside or arise de novo. Thegeneralist may elect to treat such flare-ups withappropriate local procedures and therapy (anal-gesics and occasionally antibiotics for severe cel-lulitis). These flare-ups, however, are considera-tions for referral. There are rare situations inwhich severe endodontic infection results in a po-tentially life-threatening crisis. When the problemis out of control or is not responding to treat-ment, there must be a call for help!


85

After briefly explaining the treatment neededand the options, a simple explanation is in order:"Mrs. Jones, because of the type of treatment, youneed to obtain the best possible results. I wouldlike you to see Dr. Smith, who routinely treatsroot canal problems. Dr. Smith is an expert in thisfield, and it would be to your advantage to go to aspecialist. When Dr. Smith has completed treat-ment, you will return to me so that I can restoreyour tooth permanently."

Patients occasionally are reluctant to ventureinto another new office experience; empathy andwords of encouragement help this transition. Ex-plaining the treatment complexity (if such is thecase) is helpful in supporting the reason for referral.

Sometimes a generalist and endodontist maymeet, each bringing all records and diagnosticaids, for a "team planning session." Patients ap-preciate that their health care providers collabo-rate for optimum diagnosis and treatment plan-ning. Overall, clear and prompt communicationenhances comprehensive patient care and reducespatient misunderstandings and dissatisfaction.15Both referring dentist and endodontist have spe-cific responsibilities in a referral case.

What is Expected of a GeneralPractitioner

I NSTRUCTIONS TO ENDODONTIST

Explicit written instructions and appropriate ra-diographs (original or duplicate) should be sentto the endodontist. Preferably this is done by mailbecause there is less opportunity for error. A callfrom one office to the other is acceptable, butthere is more chance for misunderstanding whencommunication is verbal. It is undesirable to givethe information verbally only to the patient andexpect the patient to relay the information accu-rately to the endodontist. Also it is inadvisable tomake patients deliver radiographs and instruc-tions in writing to the specialist. Of course, attimes this may be necessary, for example, in anemergency situation.

Generally, the patient is instructed to make hisor her own appointment. As an alternative, the re-ceptionist contacts the endodontist's office toarrange an appointment before the patient leaves.This ensures better patient compliance in seekingfurther care. The receptionist should explain theneed for an appointment and should supplyenough information for proper scheduling.

When appropriate, particularly if a key tooth isinvolved, the endodontist should be informed (inwriting) how the tooth is to be restored and

briefed on the overall treatment plan. If there arecomplications, this information gives the end-odontist ideas about alternative approaches.

EXPLANATION TO PATIENT

After patient and generalist discuss the treatmentplanning, there is an explanation of "what isgoing to happen." The patient should understandthat often the first appointment is for examina-tion and consultation; procedures are performedwhen the endodontist and patient agree on atreatment plan.

Information is supplied about what to expectat the endodontic office. This information neednot be detailed; that is the responsibility of the en-dodontist. Patients are concerned and need reas-surance that the procedure will not be unpleasantand that no significant problems are likely tooccur. However, there should be no overstating oroverselling of the procedure. Guaranteeing a suc-cessful outcome by the endodontist is unfair andgives the patient false expectations.

What is Expectedof an Endodontist

Specialists serve both the patient and referringdentist. Their responsibilities are to both; theyshould deliver appropriate treatment and commu-nicate with the practitioner as well as the patient.

TREATMENT PERFORMED

Usually the procedure is limited to that requestedby the referring dentist. Occasionally, differentdeterminations are made, such as diagnostic ortreatment difficulties or periodontal problems.The endodontist should first contact the referringdentist before proceeding and should inform thepatient about the new treatment plan.

FEEDBACK TO DENTIST

When treatment is complete, the referring dentistshould receive written confirmation from the end-odontist that includes a radiograph of the obtu-ration. A note is included about how the toothwas treated, anticipated recalls, prognosis (bothshort-term and long-term), unusual findings orcircumstances, and, at times, suggestions aboutthe permanent restoration and when it should beplaced. Other findings related to adjacent struc-tures or to the treated tooth are also included (forexample, recurrent caries on other teeth, peri-odontal problems, or defective restorations).

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FEEDBACK TO PATIENT

Before and during treatment, the endodontist ex-plains all of the important aspects of the proce-dure and the anticipated outcome. After comple-tion of treatment, the patient is informed aboutprognosis, appropriate follow-up care, and theneed to return to the referring dentist for contin-ued care and any possible additional future pro-cedures. At this final appointment, the reception-ist may call the generalist's office to arrange thenext visit.

REFERENCES

l. Molven O: The frequency, technical standard and re-sults of endodontic therapy, Nor Tannlasg Tidsskr86:142, 1976.

2. Scharwatt BR: The general practitioner and endodon-tist, Dent Clin North Am 23:747, 1974.

3. Cohen S, Schwartz S: Endodontic complications andthe law, J Endod 13:191, 1987.

4. Ericksen H: Endodontology-epidemiologic considera-tion, Endod Dent Trauma 7:189, 1991.

5. Rosenberg RJ, Goodis HE: Endodontic case selection-to treat or to refer, JAm DentAssoc 123:57, 1992.

6. Caplan D, Reams G, Weintraub J: Recommendationsfor endodontic referral among practitioners in a den-tal HMO,J Endod 25:369, 1999.

7. DiPrio JT, Talbert RL, Yee GC, Posey LM, editors: Phar-macotherapy, a patbophysiologic approach. New York, 1989,Elsevier, p. 642.

8. Seltzer S, Bender IB: The dental pulp: biologic considera-tions in dental practice, ed 3, St Louis, 1990, IshiyakuEuro-America, p. 127.

9. Kuyk J, Walton R: Comparison of radiographic ap-pearance of root canal size to its actual diameter, JEndod 16:528, 1990.

10. Benjamin KA, Dowson J: Incidence of two root canalsin human mandibular incisor teeth, Oral Surg Oral MedOral Pathol Oral Radiol Endod 58:589, 1984.

11. Vertucci FJ: Root canal morphology of mandibularpremolars, JAm DentAssoc 97:47,1978.

12. Vertucci FJ: Root canal anatomy of human permanentteeth, Oral Surg Oral Med Oral Pathol Oral Radiol Endod58:589, 1984.

13. Burns R, Herbranson E: Tooth morphology and cavitypreparation. In Cohen S, Burns RC, editors, Patbways ofthe pulp, ed 8, St Louis, 2001, Mosby.

14. Walton R, Fouad A: Endodontic inter-appointmentflare-ups: a prospective study of incidence and related

factors,J Endod 18:172, 1992.15. Kramer S: Communications regarding referrals, Risk

Manage Rep I(IV):4, 1989.

Patient Education

LEARNING OBJECTIVES


1 / Describe endodontic procedures in terms understandable to a layperson.

2/ Explain to the patient in understandable terms why and when root canal treatment is or is not indicated.

3 / Make clear to the patient that there are alternatives to endodontic treatment.

4 / Describe briefly the steps involved in root canal treatment.

5/ Explain to the patient the number of appointments needed, potential postoperative discomfort, potential

complications, and cost of treatment.

6 / Discuss the importance of a timely restoration after treatment, the need for recall examinations, and signs

or symptoms of endodontic treatment failure.

7 / Explain to the patient the reasons for retreatment.

8 / Explain what is involved in retreatment and the alternatives to retreatment.

9 / Explain why referral to an endodontist is necessary in certain cases.

10 / Provide the information needed for clear informed consent for endodontic procedures.

11 / Describe and discuss the verbal and nonverbal signals that support a patient's willingness to listen to the

doctor.

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Nonverbal Messages

Professional Appearance and Manner

Sense of Sincere Caring

Listening

How Patients Process Information

Doctor-Patient Interaction

I nformed Consent

Dentist-Patient Dialogue

Art of Communication

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6 1 Patient Education

he word doctor is derived from theLatin "to teach." Complete treatment ofany patient involves educating the pa

tient about the treatment to be rendered and theoptions available. An open exchange is part of theeducation of the patient; it establishes communi-cation between doctor and patient and creates anopen clinician-patient relationship. Such a rela-tionship fosters trust and relieves anxiety.

Not every patient is interested in learning abouttreatment; occasionally patients may tell the dentistthat they do not care to know. However, becausethere is always at least one treatment alternative, theclinician must attempt to communicate informationabout treatment options. No single approach can beused to communicate this necessary information topatients. To do this appropriately, the doctor mustbe sensitive not only to what the patient says but alsoto facial expressions and body language of each pa-tient. The words "root canal treatment" cause dreadin many patients. This sometimes unarticulated fearinterferes with patients' understanding about thetreatment to be provided. The doctor's reassurancebecomes the foundation for the patient's receptivityto information about root canal treatment.

Nonverbal Messages

The expression "We do not get a second chance tomake a first impression" holds especially true forthe doctor-patient relationship. When a doctorgreets a new patient, the patient forms an impres-sion from several nonverbal messages, includingthe following:

PROFESSIONAL APPEARANCEAND MANNER

The patient observes whether the doctor and thestaff are dressed appropriately and whether the den-tal environment (i.e., the reception area and thetreatment room) are clean, modern, and tasteful.

SENSE OF SINCERE CARING

If the staff and the doctor make the patient feel asif he or she is the most important person at thatmoment, it helps to establish a sense of trust andrapport that provides the foundation for effectivecommunication.

Listening

Commonly, patients are fearful of the prospect ofhaving root canal treatment; often they are anx-ious to discuss their anxieties. If staff and doctor

Yoshida

Sticky Note

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6 / Patient Education

89

make it evident that they are truly listening with-out distraction to everything the patient is saying,the patient feels as if he or she is really beingheard. This, too, provides further support for ef-fective communication. The doctor and staffmust immediately create an environment inwhich the patient experiences them as caring pro-fessionals. This will lessen the fear and anxietythat are often impediments to effective communi-cation in the treatment room. Commonly, pa-tients have had prior personal experience or haveheard of an experience from others that fosters astereotypical image of root canal treatment aspainful. A sense of dread can significantly impaira patient's ability to listen well and to hear whatthe doctor is trying to communicate.

The doctor should confront this unspoken anx-iety immediately by asking the patient, "Do youhave any concerns about root canal treatment?"This gives the patient an opportunity to expressany concerns and fears about anticipated pain. Be-cause of what is known about pain control today,the doctor can, even before the dental examinationand diagnostic testing, provide the patient an al-most ironclad assurance that root canal treatmentwill be relatively painless. The doctor should statethis fact calmly and confidently and allow the pa-tient to respond with any questions.

A typical inquiry may be, "But will it hurt after

the root canal treatment?" A truthful and reassur-ing response is that some mild to moderate tran-sient discomfort is common after anesthesia sub-sides, but this can be managed with analgesics,such as nonnarcotic pain control medications(e.g., nonsteroidal antiinflammatory drugs). Fur-thermore, the postoperative experience should notinterfere with normal business and social activi-ties. If any pain occurs that is stronger than ex-pected, the patient should be assured and reas-sured that he or she can reach the doctor forprompt relief at any time any day. This verbal reas-surance should be reinforced by written instruc-tions that are easily understood by a layperson.1Because of the increasing diversity of our society,reflected in part by the prevalence of English as asecond language for many people, printed instruc-tions in other languages (e.g., Spanish, Chinese,etc.) is a helpful adjunct. When the issue of painhas been fully discussed and the patient's fears al-layed, the foundation for imparting informationabout root canal treatment has been established.

HOW PATIENTS PROCESSINFORMATION

Each patient processes information in his or herown way. Some respond to information they read.For this kind of information, brochures are pub-

lished by the American Association of Endodon-tists, and a slide series is available through theAmerican Dental Association. These materialscover virtually the full range of endodontic proce-dures. Other patients respond to informationthey hear. The doctor (not the staff) must pa-tiently explain the significant facts about rootcanal treatment. Because individuals retain infor-mation differently, it is prudent to explain theprocedures in detail and to encourage all patientsto read the appropriate brochures as well. Thisprovides a higher level of assurance that the pa-tient understands the doctor's examination andrecommended treatment. However, it is impor-tant for the clinician to use more subtle, nonver-bal signals to support continued communication.These more subtle nonverbal signals include thefollowing.

DOCTOR-PATIENT INTERACTIONBody Positions

The position of a doctor standing above a seatedpatient (or a patient lying back in a chair) tends toinfantilize the patient. Rather, the patient shouldbe seated at the same level as the doctor. This es-tablishes the patient as an equal and supports re-sponsible communication.

Eye Contact

The doctor must maintain frequent eye contactwith the patient. Eye contact during transmissionof information connects doctor and patient andengenders confidence.

Body Language

The doctor should be attentive to the patient'sbody language as well as to his or her own. The de-fensive position of crossed arms or legs indicatesthat the patient is not open to receiving informa-tion. In contrast, the more relaxed position ofholding the hands in the lap with uncrossed legssuggests that the patient is listening well and un-derstands what is being said.

I nformed Consent

Not all patients really want to know the details ofroot canal treatment. Many doctors have heardpatients say, "As long as it doesn't hurt, I don'tcare what you do." In an earlier time these pa-tients would have been treated without furtherdiscussion. However, today the doctor is requiredto inform a patient fully before proceeding withtreatment. For patients who do not want to know

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about root canal treatment, the following proce-dure is recommended:

The patient is asked to sign and date a writ-ten informed consent form (Figure 6-1 andBox 6-1). The dental assistant should notein the treatment record that the patient de-clined to receive information about en-dodontic therapy.The patient is reminded that if he (or she)changes his (or her) mind, he (or she) is freeto ask questions at any time.Fees for service are clearly explained (andmust be understood by the patient) beforetreatment is initiated!

Dentist-Patient DialogueMost patients are curious about and interested intheir treatment. For these patients, the followinginformation should be discussed, not in a rote

FIGURE 6-1Informed consent form.


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manner, but in anticipation of the questions com-monly asked. Here are examples of typical ques-tions, with the answers the dentist might give.

• What is endodontics? Teeth are composed of ahard structure surrounding a soft, living tis-sue (Figure 6-2). This is called the pulp(sometimes called "the nerve"), which con-tains blood vessels, fibers, and nerves. En-dodontics (root canal treatment) is the diag-nosis and treatment of inflamed or diseasedpulps.

• Why does the pulp ("nerve") become inflamed ordiseased? Some of the main causes of pulpproblems include tooth decay, the treat-ment of tooth decay (fillings, crowns, and soon), trauma, and advanced gum disease(Figures 6-3 and 6-4).

• How can you tell if the pulp is inflamed or dis-eased? Some of the symptoms of an inflamedpulp include prolonged toothache whenyou have hot or cold liquids in your mouth,spontaneous (unprovoked) toothache, painwith chewing or biting, and pain when youlie down. Some of the signs of diseased pulpinclude evidence of decay or evidence of ashadow (abscess) at the end of the root,drainage, or swelling (Figure 6-5).

FIGURE 6-3The crown may be damaged by decay, which has reached thepulp (nerve), causing severe damage.

FIGURE 6-2This and the following diagrams (Figures 6-3 through 6-16)provide a format and description suitable for patient educa-tion. This diagram schematically demonstrates normal,healthy structures.

FIGURE 6-aA blow may fracture the crown, exposing and damaging thepulp (nerve).

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FIGURE 6-5After severe injury, the pulp may die. Bacteria then enter thespace. Irritants from the pulp go into bone and cause an areaof disease, with resorption (erosion) of bone and ligament atthe end of the root. This may form an abscess (arrows).

FIGURE 6-6After local anesthesia (novocaine), the first step is to apply arubber dam with a metal clamp.

FIGURE 6-7An opening is made into the crown with a bur (drill).

FIGURE 6-8Small metal instruments (files) plane (rasp) the insides of thecanal. This process cleans and enlarges the canal. Differentnumbers indicate different sizes of files.


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FIGURE 6-9An inert rubber-like material called gutta-percha is packedtightly into the canal; this seals the end of the root and fillsand seals the length of the canal.

FIGURE 6-10Different types of restorations (fillings) are required. Some re-quire placement of a post into the canal to hold the restora-tion in place.

FIGURE 6-77A crown (cap) is cemented over the post and tooth.

FIGURE 6-12I f the patient will need more than one treatment or whenroot canal treatment is completed, a temporary filling is usu-ally placed.

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How do you do root canal treatment? After thetooth is numb, I apply a rubber sheet to iso-late the tooth and make an opening into thecenter of the tooth to reach the pulp (nerve).With very small instruments I remove thepulp and sculpt the space it occupied. I ster-ilize, fill, and seal the root canal inner spacewith a rubber-like material that will preventbacteria from entering this space (Figures 6-6to 6-9). To restore the missing parts or brokenpiece of the tooth, a post may be placed insidethe tooth (Figure 6-10). The tooth may alsorequire a crown (Figure 6-11).

III

How many visits will it take to complete this treat-ment? Today, treatment for most teeth oftencan be completed in one visit, which willtake 1 to 1'/z hours. Treatment for otherteeth may require two visits, and a fewmight even require more. If more than onevisit is needed, I will place a temporary fill-ing in the tooth (Figure 6-12).IfI have root canal treatment, how likely is it that I'llkeep my tooth? When root canal treatment isdone thoroughly, there is a very good chanceof success (Figure 6-13); however, some treat-ment may fail no matter how well the treat-ment is done (Figure 6-14). In these instances,retreatment or endodontic surgery may rem-

FIGURE 6-13I f the canals are cleaned, filled, and sealed, the bone lost at

the root tip will heal with new bone and ligaments.

edy the lingering problem. These treatmentsare usually best done by a specialist.What is endodontic surgery? Endodontic surgerycorrects the problem from the end of the root(Figure 6-15). Under local anesthesia thegum tissue is gently lifted so that the dentistcan find the end of the root (Figure 6-15, Aand B). Then the inflamed tissue is removedaround the end of the root and a filling isplaced there to prevent the problem from re-curring. To secure the gum tissue, severalstitches are placed (Figure 6-15, C). A fewdays later, the stitches are removed. This pro-cedure usually leads to complete healing(Figure 6-15, D).Will this tooth in the front of my mouth turn darkafter root canal treatment? Years ago someteeth like this eventually darkened overtime. Based on what we do today, it is un-likely that you will see any change in color.However, if this should occur, we can oftenbleach the tooth back to a normal shade.Bonding veneers and crowns are additionalchoices for the few teeth that might darken.Will the root canal treatment be painful? Almostnever. Years ago it really was not always pos-sible to control pain (Box 6-2). Today, with abetter understanding of local anesthesia,

FIGURE 6-14I f there are defects or problems with the treatment, the area

of disease will spread and an abscess may form. This usually

reauires retreatment of the root canal.


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profound anesthesia is more predictable.After the anesthetic dissipates, there willprobably be transient soreness for a fewdays, which can be controlled with nonnar-cotic pain pills. However, if there should be

unexpected strong pain, you can call andtalk with me directly any time, any day.If I don't have root canal treatment, what are myother choices? It depends on the nature of theproblem. Generally speaking, other choices

FIGURE 6-15Some treatment failures or other situations may require surgery. A, After anesthesia, the gum tissue is raised toexpose the root end. B, The root end is cut off, and a filling is placed to seal the end. C, Several sutures (stitches)are placed to hold down the gum to allow healing. D, If the problem is resolved, the bone will heal around theroot tip.

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are doing nothing at present (postpone-ment) or extracting the tooth (probably re-quiring a bridge or implant to fill the space).( NOTE: If the patient is suffering, a delay intreatment is not reasonable, so the choice isbetween endodontiss and extraction.) Somesituations present additional choices, suchas apical surgery or replantation.Can you explain the steps involved in bridge con-struction? Yes. After extraction of the in-volved tooth and healing of the wound, theadjacent teeth are prepared (ground down),which can result in pulpal (nerve) inflam-mation. Finally, a bridge is constructed con-sisting of two crowns and a fake tooth (Fig-ure 6-16).After root canal treatment, will 1 bane a deadtooth? No. Years ago this is what it wascalled. Today we know that the tooth is stillquite alive after root canal treatment be-cause it has a blood supply to the ligamentthat keeps the tooth firmly in its socket. Be-cause there is a blood supply, the tooth con-tinues to receive nutrition and remainsquite healthy.

-Will I need to get my tooth filled after the rootcanal treatment? Yes. If your care requires aspecialist who treats complicated situations(an endodontist), I will refer you. If the pro-cedure is straightforward and uncompli-cated, I can do this quite well myself. In ei-ther case, the treatment should be promptlycompleted by final restoration.After the root canal treatment and the finalrestoration ("filling'), will I have to do anything

more? Yes, I will want to examine the tooth 6months to 1 year later to assess long-termhealing. When you return for follow-up, Iwill take an x-ray, check your gum tissue,and reexamine the final restoration. Thetooth should feel comfortable to you. Thetooth must also be firm, functional, and ap-pear normal on the x-ray film. Even thoughthe tooth feels comfortable to you, if I donot see complete repair on the film, I mayrefer you to an endodontist for further con-sultation and possibly additional treatment.Why does my tooth have to be retreated? Dr. Doejust did the root canal treatment 2 years ago. I'llhave to call Dr. Doe to find out what prob-lems he encountered when he did the rootcanal treatment. ( NOTE: If the root canaltreatment is incomplete [i.e., the canal fill-ing is several millimeters too short from theapex, or if a root canal is completelyunfilled], the patient must be given thisinformation in an informative-but notalarming-manner. The purpose of this por-tion of patient education is to inform andnot alarm the patient. It is an egregiouserror to use harsh and judgmental terms be-fore knowing all the facts.) This informa-tion will help me decide what should bedone to try to correct this failure.How much will root canal treatment cost? The feefor this treatment is $-. Alternative: Iwill ask my financial secretary to explain thefees for complete treatment. Customarilythere is a set fee, whether it takes one, two,or more appointments to complete it.

Art of Communication

In the treatment room there is an extended dia-logue of informing (giving information) and listen-ing (receiving information). Both patient and doc-tor are informing. The doctor informs the patientabout treatment, prognosis, alternatives, follow-up, and so on. Patients inform the doctor aboutwho they are, what they want, what they fear, and

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FIGURE 6-16Replacing a missing tooth. A, If a tooth is lost, a space re-mains; this space is unsightly and can cause problems. B, Theteeth on each side are cut down. C, The bridge is made andcemented. A replacement tooth is attached to the crowns oneach side.

so on. Both are also listening. The doctor listens forthe subtext that will lead to better care. The patientlistens for information and reassurance.

A doctor both heals and cures; the healing be-gins with the first opportunity for an extended di-alogue that we call patient education. Patient ed-ucation must be preceded by doctor education,not just the technical information learned in

dental school but also the process of self-discov-ery that leads to an open heart and compassion.When patients make a true connection with thedentist, they are able and willing to learn; onlythen does the dentist truly earn the title "Doctor."

REFERENCES

1. Alexander RE: Patient understanding of postsurgicalinstruction forms, Oral Surg Oral Med Oral Pathol OralRadiol87:153, 1999.

2. Christensen G: Educating patients, J Am Dent Assoc130:731, 1999.

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Local Anesthesia

LEARNING OBJECTIVES

Atter reading this chapter, the student should be able to:

1/ Explain why apprehension and anxiety, fatigue, and tissue inflammation create difficulties in obtaining

profound anesthesia.

2/ Define pain threshold and the factors affecting pain threshold.

3/ Describe patient management techniques that will facilitate obtaining adequate anesthesia.

4/ List techniques that are helpful in giving "painless" injections.

5/Describe the "routine" approach to conventional local anesthesia: when and how to anesthetize.

6/ Describe circumstances that create difficulties in obtaining profound anesthesia using conventional

techniques.

7/ Describe when to use supplemental methods of obtaining pulpal anesthesia if standard block or infiltration

methods fail.

8/ Review techniques of intraosseous, periodontal ligament, and intrapulpal injections.

9 / Discuss how to obtain anesthesia for specific pulpal and periradicular pathoses: irreversible pulpitis,

symptomatic teeth with pulpal necrosis, asymptomatic teeth with pulpal necrosis, and surgical procedures.

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100

7 I Local Anesthesia

Factors Affecting Endodontic Anesthesia

Apprehension and Anxiety

Fatigue

Tissue Inflammation

Previous Unsuccessful Anesthesia

I nitial Management

Psychologic Approach

"Painless" Injections

When to Anesthetize

Adjunctive Pharmacologic Therapy

Conventional Anesthesia

Mandibular Anesthesia

Anesthetic Agents

Related Factors

Alternative Techniques

Maxillary Anesthesia

Anesthetic Agents

Related Factors


Anesthesia Difficulties

Supplemental Anesthesia

I ndications

Anesthetic Agents

I ntraosseous Anesthesia

Periodontal Ligament Injection

I ntrapulpal Injection

Alternative Primary Techniques

Anesthetic Management of Pulpal or

Periradicular Pathoses

I rreversible Pulpitis

Symptomatic Pulp Necrosis

Asymptomatic Pulp Necrosis

Anesthesia for Surgical Procedures

I ncision for Drainage

Periradicular Surgery

When a tooth which is loose or painful is to beextracted, the nose of the patient should berubbed with brown sugar, ivy and green oil; he isadvised to hold his breath, a stone is then placedbetween his teeth, and he is made to close hismouth. The fluid which causes the pain is thenseen to flow from the mouth in such quantity as

frequently tofill three pots; after having cleansedthe nose with pure oil, rinsed the mouth withwine, the tooth is no longer painful, and may

easily be extracted.SCRIBONIUS, 47 AD

his historical anecdote illustratesScribonius' description of a method ofobtaining "anesthesia." He was con

vinced that he could perform painless extractionsusing what was apparently a rather crude tech-nique of pressure anesthesia. Our concern for thepatient continues: How are adequate levels ofanesthesia attained to keep our patients relativelycomfortable during endodontic procedures? Ob-taining profound anesthesia for the endodonticpatient is difficult and challenging. Many patientsrecount vivid (and often valid) accounts ofpainful experiences. Although routine anesthetictechniques are usually effective for restorativedentistry, endodontic procedures present specialsituations that require additional techniques andspecial approaches.

Factors AffectingEndodontic Anesthesia

Emotional considerations as well as tissuechanges impair the effectiveness of local anesthe-sia.' A patient who is psychologically distraughtwith an inflamed pulp will have a decreased painthreshold; that is, less stimulus is required to pro-duce pain.'

In addition, the trigeminal nerve, which sup-plies primary sensory innervation to oral struc-tures, is a complex entity. Knowledge of its morecommon anatomical features will aid in success-ful anesthesia.

APPREHENSION AND ANXIETY

Many endodontic patients have heard horror sto-ries about root canal treatment. The cause maynot be the treatment but the experience of apainful or "infected" tooth. They vividly recall the

7 / Local Anesthesia

101

pain, swelling, and sleepless nights associatedwith the tooth before treatment. The procedureitself is generally less threatening-a survey of en-dodontic patients completing therapy indicatedthat 96 percent would agree to have future rootcanal treatment. 3 Therefore because they fear theunknown and have heard unfavorable stories, pa-tients will be apprehensive or anxious. This emo-tion plays a role in their perceptions and also af-fects how they react to pain.4,5 Many patientseffectively mask this apprehension!

ties in obtaining anesthesia in such patients. Often,psychologic management and supplemental tech-niques are required.

I nitial ManagementThe early phase of treatment is most important. Ifthe patient is managed properly and anesthetictechniques are done smoothly, the pain thresholdelevates. The result is more predictable anesthesiaand a less apprehensive, more cooperative patient.

FATIGUE

Over a course of days many patients with atoothache have not slept well, not eaten properly,or otherwise not functioned normally. In addi-tion, many are apprehensive or anxious about theappointment. The end result is a patient with adecreased ability to manage stress and with lesstolerance for pain.

TISSUE INFLAMMATION

Inflamed tissues have a decreased threshold ofpain perception.6 This is the "hyperalgesia" phe-nomenon. In other words, a tissue that is in-flamed is much more sensitive and reactive to alower stimulus.' Therefore an inflamed tissue re-sponds painfully to a stimulus that otherwisewould be unnoticed or perceived only mildly. Be-cause root canal treatment procedures generallyinvolve inflamed pulpal or periradicular tissues,this phenomenon has obvious importance. A re-lated complication is that inflamed tissues aremore difficult to anesthetize.8

A good example of the phenomenon of in-creased sensitivity (a form of hyperalgesia) is sun-burn. Exposed tissues that have been burned areirritated and inflamed. The skin has now becomequite sensitive (decreased pain threshold) to con-tact and is painful. This same principle also ap-plies to inflamed pulpal and periradicular tissues.9

PREVIOUS UNSUCCESSFULANESTHESIA

Unfortunately, profound pulpal anesthesia is notalways obtained with conventional techniques. Pre-vious difficulty with teeth becoming anesthetizedis associated with a likelihood of subsequent un-successful anesthesia.'° These patients are likely tobe apprehensive (decreased pain threshold) andgenerally identify themselves by comments such as"Novocaine never seems to work very well on me"or "A lot of shots are always necessary to deaden myteeth." The practitioner should anticipate difficul-

PSYCHOLOGIC APPROACH

The psychologic approach involves the four Cs:control, communication, concern, and confi-dence. Control is important and is achieved by ob-taining and maintaining the upper hand. Commu-nication is accomplished by listening andexplaining what is to be done and what the pa-tient should expect. Concern is shown by verbaliz-ing awareness of the patient's apprehensions. Con-fidence is expressed in body language and inprofessionalism, giving the patient confidence inthe management, diagnostic, and treatment skillsof the dentist. Management of the four Cs effec-tively calms and reassures the patient, therebyraising the pain threshold.

"PAINLESS" INJECTIONS

Patients generally have a fear of dental injec-tions .3,11 A good practice-builder and a method ofwinning confidence and cooperation is to masterinjection techniques that are nearly painless.12 As-suredly, patients will inform their friends andfamily that their dentist does not "hurt whenhe/she gives me a shot." Although most injectionscannot be totally pain-free, there can be a mini-mum of discomfort. This also relaxes the patientand effectively raises the pain threshold and thetolerance level.

Obtaining Patient Confidence: Patient confi-dence is critical. Before any injection is given, es-tablishing communication, exhibiting empathy,and informing patients of an awareness of theirapprehension as well as their dental problem willmarkedly increase confidence levels." Most im-portant, having the patient's confidence will givecontrol of the situation to the dentist; this is arequisite!

Topical Anesthetic: Use of a topical anesthet-ics is popular as an adjunct to painless injec-tions.14 Some investigators have shown topicalanesthetics to be effective, whereas others havenot.15,16 The most important aspect of using topi-

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cal anesthesia is not primarily the actual decreasein mucosal sensitivity but rather the demon-strated concern that everything possible is beingdone to prevent pain. Also operating is the powerof suggestion that the topical anesthetic will re-duce the pain of injection." When a topical anes-thetic gel is used, a small amount on a cotton-tipped applicator is placed on the dried mucosafor 1 to 2 minutes before the injection."

A relatively new device is an intraoral adhesive,20% lidocaine patch. When in place for S minutes,it was shown to reduce the pain of needlestick."

Solution Warming: A common belief is thatan anesthetic solution warmed to or above bodytemperature is better tolerated and results in lesspain during injection. However, in a clinical trial,investigators found that patients could not differ-entiate between prewarmed and room tempera-ture anesthetic solutions .2° Therefore warminganesthetic cartridges is not necessary.

Needle Insertion: Initially, the needle is in-serted gently into the mucosal tissue. This will bealmost unnoticed by the patient, regardless of theneedle gauge.

Small-Gauge Needles: A common concept isthat smaller needles cause less pain, but this is nottrue for dental needles. Patients cannot differenti-ate between 2S-, 27-, or 30-gauge needles duringinjections.21 These sizes also have similar deflec-tion patterns and resistance to breakage.22,23 As arecommendation, a 27-gauge needle is suitablefor most conventional dental injections.

Slow Injection: Slow injection is a very effec-tive means of decreasing pressure and patient dis-comfort during injection. Slow deposition of solu-tion permits its gradual distribution into thetissues. This is particularly important in the max-illary anterior region (a very sensitive area) and inregions where tissue is tightly bound (posteriorpalate and nasopalatine area). As a general rule,solution deposition should take approximately1 minute per cartridge.

Two-Stage Injection: A two-stage injectionconsists of initial very slow administration of ap-proximately a quarter-cartridge of anestheticunder the mucosal surface; this will be nearlypainless. After regional numbness occurs, addi-tional anesthetic is given to the full depth at thetarget site, usually with minimal pain. The two-stage injection is indicated for apprehensive andanxious patients or pediatric patients but may beused for anyone. It is also useful in any region in-cluding the inferior alveolar nerve block.

WHEN TO ANESTHETIZE

Preferably, anesthesia should be given at each ap-pointment. There is a common belief that instru-

ments may be used in canals with necrotic pulpsand periradicular lesions painlessly without anes-thesia. Occasionally, there may be vital tissue in theapical few millimeters of the canal. This inflamedtissue contains nerves and is sensitive.24 Not only isthis vital tissue contacted during instrumentation,but also pressure is created. These may cause dis-comfort if the patient is not anesthetized.

There is an antiquated notion that canallength can be determined in a nonanesthetizedpatient by passing an instrument into a necroticcanal until the patient shows an "eye blink re-sponse." Unfortunately, patient perceptions andresponses are too variable for accuracy. Pain maybe felt when the instrument is far short of theapex, or some patients may have no sensationeven when the instrument is several millimetersbeyond the apex. Use of nonanesthesia for lengthdetermination cannot replace radiographs or anapex locator for accuracy. Another misconceptionis that after the canals have been cleaned andshaped, it is not necessary to anesthetize the pa-tient at the obturation appointment. However,during obturation pressure is created and smallamounts of sealer may be extruded beyond theapex. This may be quite uncomfortable. Many pa-tients (as well as the dentist) are more at ease if re-gional hard and soft tissue anesthesia is present.

ADJUNCTIVE PHARMACOLOGICTHERAPY

Sedation (intravenous, oral, or inhalation) mayenhance local anesthesia, particularly in patientswho want to cooperate but are extremely appre-hensive. A discussion on agents that control anxi-ety is included in Chapter 30.

Conventional AnesthesiaSuccess of local anesthesia is variable. Two surveysof patients and dentists indicated that some pa-tients were not adequately anesthetized duringrestorative treatment." , " Overall, of 10 patientstreated, 3 may feel pain during the procedure. Thisis a significant number! A number of factors affectanesthesia, such as the type of procedure (en-dodontic, extraction, restorative, periodontal, andso on), arch location (maxillary or mandibular),anxiety level, and the presence of inflamed tissue.

Many clinical studies have subjectively evalu-ated local anesthetic agents and techniques. Ameasurement of pulpal anesthesia before begin-ning a procedure is obtained with an electric pulptester or with application of carbon dioxide (dryice) or spray refrigerant. No pulpal response afteradministration of anesthetic means probable pro-


103

found anesthesia in asymptomatic teeth with vitalpulps.26,27 Experimental studies have investigatedthe use of local anesthesia; these are discussed inthe following sections. Conventional injectiontechniques are detailed in other textbooks.

Mandibular AnesthesiaANESTHETIC AGENTS

The most commonly used agent is 2% lidocainewith 1:100,000 epinephrine. This agent is indi-cated for procedures in this chapter unless speci-fied otherwise.

Lidocaine is a safe and effective drug. 2829 Vaso-constrictors are generally safe. In a few circum-stances (patients taking tricyclic antidepressantsor nonselective -adrenergic blocking agents, or pa-tients with moderate to severe cardiovascular dis-ease), there is the potential for problems . 3o

RELATED FACTORS

Although the most common method ofmandibular anesthesia is the inferior alveolarnerve block, this injection also has the greatestnumber of failures. 25,31 What are the expectedsigns of successful or unsuccessful anesthesiaafter administering one cartridge?

Lip Numbness: Numbness usually occurs in 5to 7 minutes.32-37 What does lip numbness mean?It indicates only that the injection blocked thenerves to the soft tissues of the lip, not necessarilythat pulpal anesthesia has been obtained .3"-37 If lipnumbness is not obtained, the block has been"missed." If this occurs frequently, the techniqueshould be reviewed.

Onset of Pulpal Anesthesia: Pulpal anesthe-sia usually occurs in 10 to 15 minutes .32-37 In somepatients onset occurs sooner and in others it isdelayed. 32-37

Duration: Duration of pulpal anesthesia inthe mandible is very good.32-37 Therefore if suc-cessful, anesthesia usually (but not always) per-sists for approximately 21/2 hours.

Success: The incidence of successful mandibu-lar pulpal anesthesia tends to be more frequent inmolars and premolars and least frequent in ante-rior teeth . 27,33-37 Not all patients achieve pulpalanesthesia after what appears to be a clinicallysuccessful (lip and chin numb) inferior alveolarnerve block; other approaches are required inthese patients.

ALTERNATIVE TECHNIQUES

Increasing the Volume: Increasing the vol-ume of anesthetic from one to two cartridges does

not increase the success rate of pulpal anesthesiawith the inferior alveolar nerve block . 33

Alternative Solutions: Mepivacaine 2% with1:20,000 levonordefrin, 4% prilocaine with1:200,000 epinephrine, or solutions without vaso-constrictors (3% mepivacaine plain and 4% prilo-caine plain) are alternatives to 2% lidocaine with1:100,000 epinephrine for pulpal anesthesia witheffects that last at least 1 hour .

34,37,38

Alternative Injection Locations: Neither theGow-Gates nor the Akinosi technique is superiorto the standard inferior alveolar injection . 39-42

These techniques are not replacements but areuseful when standard approaches cannot be used(for example, trismus).

Infiltration Injections: Labial or lingual infil-tration injections used alone are not effective forpulpal anesthesia in anterior or posterior teeth . 41-15

Long-Acting Anesthetics: Clinical trials ofbupivacaine and etidocaine have been con-ducted in oral surgery, endodontics, and peri-odontics." - " These agents provide a prolongedanalgesic period and are indicated when postop-erative pain is anticipated. However, not all pa-tients want prolonged lip numbness . 4 7 For thosepatients, analgesics may be prescribed. Com-pared with lidocaine, bupivacaine has a some-what slower onset but almost double the dura-tion of pulpal anesthesia in the mandible(approximately 4 hours).52

Accuracy of Needle Placement: Accurateanatomic positioning is no guarantee of a suc-cessful block .53,54 Interestingly, even locating theinferior alveolar nerve with ultrasound before theinjection did not improve success.55 The anes-thetic solution may not completely diffuse intothe nerve trunk to reach and block all nerves evenif deposited at the correct site.56

Accessory Innervation: Anatomic evidencesuggests that accessory innervation exists frombranches of the mylohyoid nerve .57,58 An experi-mental study using a mylohyoid injection lingualand inferior to the retromolar fossa in addition toan inferior alveolar nerve block showed no en-hancement of pulpal anesthesia.59 The contribu-tion of the mylohyoid nerve to pulpal sensitivity isprobably insignificant.

Cross-Innervation: Cross-innervation fromthe contralateral inferior alveolar nerve has beenimplicated in failure to achieve anesthesia in ante-rior teeth after an inferior alveolar injection.Cross-innervation does occur in incisors but isnot the primary cause of anesthetic failure .43

Pain and Inflammation: Most studies haveevaluated anesthesia in the absence of symp-toms and inflammation; results differ if theseconditions are present.8,60 Patients who havesymptomatic pulpal or periapical pathosis (or

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who are anxious) present additional anesthesiaproblems.'"' ,"

Maxillary AnesthesiaANESTHETIC AGENTS

Unless otherwise specified, the conventional solu-tion is used, that is, 2% lidocaine with 1:100,000epinephrine.

RELATED FACTORS

Anesthesia is more successful in the maxilla thanin the mandible. The most common injection forthe maxillary teeth is infiltration. Several eventscan be expected with this technique when one car-tridge is used.

Lip Numbness: Lip numbness usually occurswithin a few minutes. Lip or cheek numbnessdoes not correspond entirely to the duration ofpulpal anesthesia because the pulp does not re-main anesthetized as long as these soft tissues......

Success and Failure: Infiltration results in ahigh incidence of successful pulpal anesthesia.Therefore it is more successful than the inferioralveolar nerve block .62-65

Onset of Pulpal Anesthesia: Pulpal anesthe-sia usually occurs in 3 to 5 minutes. Occasionally,onset is slower in first molars .62-6s

Duration: A problem with maxillary infiltra-tion is duration .62-65 In about a third of patients,pulpal anesthesia of the anterior teeth declinesafter about 30 minutes, with most losing anesthe-sia by 60 minutes .64-65 In premolars and firstmolars, about a third of patients have no pulpalanesthesia at 45 minutes, with half losing anes-thesia by 60 minutes .62-65 Frequently, additionallocal anesthetic must be administered dependingon the duration of the procedure and the toothgroup affected.

ALTERNATIVE TECHNIQUESVolumes of Solution

For infiltrations, increasing the volume (two car-tridges instead of one) increases the duration ofpulpal anesthesia .6s A suggestion for anteriorteeth and premolars is to give two cartridges ini-tially, or to give one initially and inject anotherapproximately 30 minutes later. In first molars,administration of two cartridges initially willspeed onset and prolong duration .63

Alternative Solutions

In maxillary infiltrations, prilocaine, mepivacaine,and lidocaine (all with vasoconstrictors) act simi-

larly.64 65 Solutions without vasoconstrictors (3%mepivacaine plain and 4% prilocaine plain) pro-vide a short duration of pulpal anesthesia, averag-ing 15 to 20 minutes .61,65

Long-acting anesthetics do not provide pro-longed pulpal anesthesia in a maxillary infiltra-tion (as they do in a mandibular block) .6'. 6 2

Other Techniques

The posterior superior alveolar (PSA) block anes-thetizes the second and third molars and usuallythe first molar.66 On occasion, an additionalmesial infiltration injection is necessary to anes-thetize the first molar. Generally, the PSA injec-tion is indicated when all molar teeth requireanesthesia. When one tooth is treated, infiltra-tions are preferred.

The infraorbital block results in lip numbnessbut does not predictably anesthetize incisorpulps.67,68 It usually anesthetizes the premolars,but duration is less than one hour .67,68 Essentially,the infraorbital injection is similar to infiltrationover the premolars.

The second division block usually anesthetizespulps of molars and some second premolars butdoes not predictably anesthetize anterior toothpulps.69 The high tuberosity technique is pre-ferred to the greater palatine approach because itis easier and less painful .69

Pain and Inflammation

Again, results will differ from the normal whenanesthesia is given to patients with either or bothof these conditions.

Anesthesia DifficultiesWhat follows is a classic scenario. The diagnosis isirreversible pulpitis. The dentist administers thestandard block or infiltration. The patient reportsclassic signs of anesthesia (lip numbness and adull feeling of the tooth or quadrant). After isola-tion, access preparation is begun. When the bur isin enamel, the patient feels nothing. Once the burenters dentin or possibly not until the pulp is ex-posed, the patient feels sharp pain. Obviously,pulpal anesthesia is not profound; additionalanesthetic is required. Why does the problemoccur? There are three main reasons and theories.

1. The anesthetic solution may not penetrateto the sensory nerves that innervate thepulp, especially in the mandible. A localanesthetic, articaine, was synthesized toprovide good lipid solubility and protein


105

binding, with presumably more predictableanesthesia. However, articaine's action hasproved to be similar to that of other localanesthetics.'°

2. Local tissue or nerve changes occur becauseof inflammation. One popular theory isthat the lowered pH of inflamed tissue re-duces the amount of the base form of theanesthetic available to penetrate the nervemembrane." Consequently, there is less ofthe ionized form within the nerve to achieveanesthesia. This theory has no experimentalsupport and is an unlikely cause of anesthe-sia difficulties. It does not explain the majorproblem, which is the mandibular molarwith pulpitis that is not anesthetized by aninferior alveolar injection. The injection siteis distant from the area of inflammation;changes in tissue pH would be unrelated tothe anesthesia problem. A more plausibleexplanation is the hyperalgesia theory:nerves arising in inflamed tissue have al-tered resting potentials and decreased ex-citability thresholds; these changes are notrestricted to the inflamed pulp itself but af-fect the entire neuronal membrane, extend-ing to the central nervous system.8,9 Localanesthetic agents are not sufficient to pre-vent impulse transmission, owing to theselowered excitability thresholds."

3. Patients in pain often are apprehensive,which lowers their pain threshold. A viciouscycle may be established: Initial apprehen-sion leads to decreased pain threshold,which leads to anesthesia difficulties, whichleads to increased apprehension, which re-sults in loss of control and confidence, andso on. Therefore if this cycle becomes evi-dent, the practitioner should stop treat-ment immediately and regain control orschedule another appointment or considerreferral to an endodontist. Most patientswill endure some pain during the initialstages of root canal treatment if they haveconfidence in the dentist. However, they willnot tolerate being hurt repeatedly!

Supplemental AnesthesiaINDICATIONS

A supplemental injection is used if the standardinjection is not effective. It is useful to repeat aninjection only if the patient is not exhibiting the"classic" signs of soft tissue anesthesia. Generally,if the classic signs are present, reinjection is inef-fective. For example, after the inferior alveolar (IA)injection, the patient develops lip, chin, and

tongue numbness and quadrant "deadness" ofthe teeth. However, he or she cannot tolerate pulpor dentin invasion with a bur. To think that rein-jjection using the IA approach will be successful iswishful thinking; failure the first time is usuallyfollowed by failure on the second attempt. Thedentist should go directly to a supplemental tech-nique. Three such injections are (1) the in-traosseous (10), (2) the periodontal ligament(PDL), and (3) the intrapulpal (IP). The PDL and10 injections are the preferred approaches withthe IP injection being reserved for special situa-tions.

ANESTHETIC AGENTS

With any of the three supplemental techniques, aconventional anesthetic agent is indicated. There-fore 2% lidocaine with 1:100,000 epinephrine isused unless an alternative is suggested.

INTRAOSSEOUS ANESTHESIA

The IO injection is a supplemental technique thathas been shown to be effective through substan-tial research and clinical usage. It is particularlyuseful in conjunction with a conventional injec-tion when it is likely that supplemental anesthesiawill be necessary, e.g., pulpitis in mandibular pos-terior teeth." -73 The IO injection allows placementof a local anesthetic directly into the cancellousbone adjacent to the tooth. There is an intra-osseous system of two components (Figure 7-1).One part is a slow-speed handpiece-driven perfo-rator, which drills a small hole through the corti-cal plate. The anesthetic solution is delivered intocancellous bone through a matching 27-gauge ul-trashort injector needle (Figure 7-2).

FIGURE 7-7Components for intraosseous injection. The perforator (top) isa small, sharp, latch-type drill to make an opening throughsoft tissue and bone. The needle (bottom) is a short and smallgauge to insert and inject directly through the opening.

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FIGURE 7-2I ntraosseous injection technique. A, Location and angulation of the perforator. B, Perforator "breaks through"cortical bone into medullary space. C, Needle is inserted directly into opening. D, Anesthetic is injected intomedullary bone, where it diffuses widely to block dental nerves.

Technique

The area of perforation and injection is on a hori-zontal line of the buccal gingival margins of theadjacent teeth and a vertical line that passesthrough the interdental papilla distal to the toothto be injected. A point approximately 2 mm belowthe intersection of these lines is selected as theperforation site. The soft tissue is first anes-thetized by infiltration. The perforator is placedthrough the gingiva perpendicular to the corticalplate. With the point gently resting against bone,the handpiece is activated in a series of short

bursts, using light pressure, until there is a "breakthrough" into cancellous bone (taking approxi-mately 2 to 5 seconds).74-77

Holding the standard syringe in a "pen-gripping" fashion, the needle is aligned with andinserted into the perforation. Approximately halfa cartridge of anesthetic solution is SLOWLY de-livered over a 1- to 2-minute time period withlight pressure! If back-pressure is encountered,the needle is rotated approximately a quarter turnand deposition is reattempted. If this attempt isunsuccessful, the needle should be removed and

7 1 Local Anesthesia

107

checked for blockage. If the needle is not blocked,it is reinserted or the site is opened with a newperforator and the injection is repeated.

A recent, useful innovation is an interosseousinjection system using a plastic sleeve that re-mains in the perforation. This serves as a guidefor the needle and may remain in place through-out the procedure if reinjection is necessary.

Perforator "Breakage": Rarely, the metal per-forator "separates" from the plastic shank. Theperforator is easily removed with a hemostat;there are no reports of a perforator breaking intoparts. 73,75-80

Injection Discomfort: When the IO injectionis used as a primary injection, neither perforation,needle insertion, nor solution deposition ispainful for most patients . 15,77 However, when theIO injection is used as a supplemental injection ina patient with irreversible pulpitis, moderate painmay occur. 7L72

Selection of Perforation Site: Distal perfora-tion and injection to the tooth will result in thebest anesthesia . 75`2 An exception would be in sec-ond molars where a mesial site is preferred. 15-77

When necessary, a lingual approach may also besuccessful.

Onset of Anesthesia: The onset of anesthesiais rapid ...... There is no "waiting period" for anes-thesia.

Success: For use as a primary injection, successrates are good; lower success rates are seen with3% mepivacaine.75,77

For use as a supplemental injection after the IAblock, excellent success has been reported for 2%lidocaine with 1:100,000 epinephrine, 2% mepiva-caine with 1:20,000 levonordefrin, and 1.5% etido-caine with 1:200,000 epinephrine .76,79,82 However,because of adverse cardiovascular reactions withthe long-acting anesthetics (etidocaine and 0.5%bupivacaine with 1:200,000 epinephrine), theseagents should not be used." Mepivacalne 3% issuccessful, but the duration of pulpal anesthesiais shorter.81

For use as a supplemental injection with irre-versible pulpitis, high success rates (around 90%)have been reported .72,73 Mepivacaine has a 80%success rate, which increases to 98% with a second10 injection."

Failure: If the anesthetic solution squirts outof the perforation, there will be failure (a rare oc-currence)." Reperforation or choosing anotherperforation site would then be necessary.

Duration: With a primary IO injection, dura-tion of pulpal anesthesia declines steadily over anhour . 75 ,77 There is an even shorter duration with3% mepivacaine or 1.5% etidocaine with 1:200,000epinephrine compared with 2% lidocaine with

1:200,000 epinephrine .,77,"4 With a supplemental 10injection after the IA block, duration of pulpalanesthesia is very good .76,79,82 A solution of 3% me-pivacaine will result in a shorter duration.81 Forirreversible pulpitis, the 10 injection shouldprovide anesthesia for the entire debridementappointment.71-73

Postoperative Problems: With primary andsupplemental techniques, patients report no painor mild pain. Less than 5% will develop exudateand/or localized swellings at the perforation site,possibly from overheating of the bone during per-foration."-"°

Systemic Effects: With both primary and sup-plemental techniques using 1.8 ml of 2% lidocainewith 1:100,000 epinephrine, most patients per-ceive an increased heart rate . 751-78,85 With 0.9 ml of2% lidocaine with 1:100,000 epinephrine, 1.8 mlof etidocaine with 1:200,000 epinephrine, or1.8 ml of 2% mepivacaine with 1:20,000 lev-onordefrin, there is a similar increased heartrate . 78,79,82 When these agents are used, the patientshould be informed of this tachycardia to lessenhis or her anxiety. No significant heart rate in-crease occurs with 3% mepivacame plain . 81,85

Medical Contraindications: Patients with car-diovascular disease or those taking tricyclic anti-depressants or nonselective /3-adrenergic blockingagents should not receive 10 injections of epi-nephrine- or levonordefrin-containing solutions.85Mepivacaine 3% plain is preferred.

PERIODONTAL LIGAMENTI NJECTION

The PDL injection is also a useful technique if aconventional injection is unsuccessful. The PDL(or intraligamental) injection technique has gen-erated considerable research and has spawned themarketing of a variety of special syringes. Thetechnique (regardless of the device used) is clini-cally effective and is a valuable adjunct. .38,86,87 It isparticularly useful if a rubber dam is in place; theneedle may be inserted between the tooth andrubber dam margin.

Technique: The procedure (Figure 7-3) is notdifficult but does require practice and familiarity.A standard syringe or pressure syringe is equippedwith a 30-gauge ultrashort needle or a 27-or a25-gauge short needle. The needle is inserted intothe mesial gingival sulcus at a 30-degree angle tothe long axis of the tooth. The needle is supportedby the fingers or hemostat and is positioned withmaximum penetration (wedged between root andcrestal bone). Heavy pressure is SLOWLY appliedon the syringe handle for approximately 10 to20 seconds (conventional syringe), or the trigger is

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SLOWLY squeezed once or twice with resistance(pressure syringe). Back pressure is important. Ifthere is no back-pressure (resistance) -that is, ifthe anesthetic readily flows out of the sulcus-theneedle is repositioned, and the technique repeateduntil back-pressure is attained. The injection isthen repeated on the distal surface. Only a smallvolume (approximately 0.2 ml) ofanesthetic is de-posited on each surface.

Mechanism of Action: The PDL injection forcesanesthetic solution through the cribriform plate(Figure 7-4) into the marrow spaces and into the

FIGURE 7-3Periodontal ligament injection. A, Needle insertion usingthe fingers to prevent needle buckling. B, A hemostat maybe substituted for fingers to support and direct the nee-dle. The injection may be given with or without the rubberdam in place. C, Note the direction and position of theneedle (arrows). The tip of the needle will be wedged be-tween the crestal bone and the root surface. D, Angle ofthe needle relative to the long axis of the tooth (left). Withapproximately a 30-degree orientation, the needle tip willbe positioned close to the midline of the root.

vasculature in and around the tooth (Figures 7-5and 7-6).88-90 The primary route is not the periodon-tal ligament; the mechanism ofaction is not relatedto direct pressure on the nerves 91,92

Injection Discomfort: When the PDL injec-tion is used as a primary injection, needle inser-tion and injection are usually only mildly uncom-fortable in posterior teeth; in anterior teeth, thePDL injection may be quite painful.93,95 Patientsmust be informed of this possibility.

Onset of Anesthesia: Onset of anesthesia israpid; there is no waiting period to begin the clin-


109

FIGURE 7-4An extraction socket of a secondmolar. The bone of the cribriformplate is very porous, particularly inthe cervical region (arrow). Duringthe periodontal ligament injection,this is the region of passage ofmost anesthetic solution into themedullary space.

FIGURE 7-5A single periodontal ligament injection of carbon dye adja-cent to a dog's tooth demonstrates the distribution of dyeparticles. Particles are concentrated at the i njection site (/) aswell as in the medullary bone (MB), the apical foramen (AF),and the pulp (P) of the injected tooth. Dye particles havebeen spread through the periodontal ligament (PDL) of boththe injected and the adjacent teeth.

FIGURE 7-6A single injection of dye was made in the distal periodontall i gament. This frontal section, including the tooth apex andsurrounding structures, shows that dye distributes to the pulp(P), periodontal ligament space (PDL), medullary bone space(MB), and mandibular canal (MC). The widespread distribu-tion of solutions from the periodontal ligament injection mayanesthetize the adjacent teeth.

11 0


ical procedure." 8793-96 If anesthesia is still not ad-equate, reinjection is indicated.

Success: For use as a primary injection, goodsuccess rates have been reported for restorativeprocedures and extractions. More difficulty inachieving adequate pain control occurs in en-dodontic treatment. One study showed highersuccess rates in posterior teeth than in anteriorteeth.94

For use as a supplemental injection (standardtechniques have failed to provide adequate anes-thesia), good success rates (83 to 92%) areachieved .38,86,87,96 Reinjection increases the successrate . 86,87

Duration: The duration of profound pulpalanesthesia (either primary or supplemental) is ap-proximately 10 to 20 minutes . 9 Z -9 4 The operatormust work quickly and be prepared to reinject.

Postoperative Discomfort: When PDL in-jection is used as a primary technique, postoper-ative discomfort (mostly mild pain) usually oc-curs. 93-95 The duration of discomfort rangesfrom 14 hours to 3 days .93-95 The discomfort isrelated to damage from needle insertion ratherthan to the pressure of depositing the solu-tion. 95 Many patients report that their toothfeels "high in occlusion. "93,94

Selective Anesthesia: It has been suggestedthat the PDL injection may be used in the differ-ential diagnosis of poorly localized, painful irre-versible pulpitis. 9 7 However, adjacent teeth areoften anesthetized with PDL injection of a singletooth.92-95 Therefore this injection is not useful fordifferential diagnosis.

Systemic Effects: PDL injection of epineph-rine-containing solutions may cause systemicchanges (a transient decrease in blood pressureand increase in heart rate). 98 Generally, in mostdental patients effects are minimal, but tachycar-dia may be noticed, requiring explanation.

FIGURE 7-7Example of a special syringe used for the peri-odontal ligament injection. Although these de-vices are capable of injecting with more pressure,they have not been shown to be superior to thestandard syringe.

Other Factors: Different needle gauges (25-, 27-,or 30-gauge) are effective .86 Special pressure sy-ringes have been marketed (Figure 7-7); these havenot proved to be more effective than a standardsyringe .86,87,95 Anesthetic solutions without vaso-constrictors (3% mepivacaine plain) or with re-duced vasoconstrictor concentrations (bupiva-caine or etidocaine with 1:200,000 epinephrine)are not very effective, producing a limited dura-tion of anesthesia. 93,99,100

Safety to the Periodontium: Clinical and an-imal studies have demonstrated the relativesafety of the PDL injection.9 2-94,101,104 Minor localdamage is limited to the site of needle penetra-tion (Figure 7-8); this subsequently undergoes re-pair. In rare instances, periodontal infectionshave occurred. 94 Histologic areas of root resorp-tion after PDL injections have also been reported,which also heal with time. 105,106 There are no stud-ies on the effects of injecting into an area of peri-odontal disease, but an adverse effect is unlikely.

Safety to the Pulp: Clinical and animal stud-ies have shown no adverse effects on the pulp afterPDL injections . 92-94,105,107,108 However, physiologicchanges in the pulp do occur, including a rapidand prolonged marked decrease in blood flowcaused by epinephrine.109 This vascular impair-ment has no demonstrated damaging effect, evenin conjunction with restorative procedures." 0 ThePDL injection probably would not result in severepulpal injury, although this has not been studiedwith extensive (crown) preparations or in teethwith caries.

Safety to Primary Teeth: Minor enamel hy-poplasia of succedaneous teeth has been seenafter PDL injections in primary teeth."' However,this effect was caused by the cytotoxicity of thelocal anesthetic rather than by the actual injec-tion. Therefore the PDL injection may be used foranesthetizing primary teeth.9 1

7 1 Local Anesthesia

111

INTRAPULPAL INJECTION

Indications: On occasion, the IO and PDL injec-tions, even when repeated, do not produce pro-found anesthesia; pain persists when the pulp isentered. This is an indication for an IP injection.However, the IP injection should not be usedwithout first administering an IO or PDL injec-tion. The IP injection is very painful without someother supplemental anesthesia.

Advantages and Disadvantages: Althoughthe IP injection is popular, it has disadvantages aswell as advantages, making it the third supple-mental injection of choice. The major drawback isthat the needle is inserted directly into a vital andvery sensitive pulp; the injection may be exquis-itely painful. Also, the effects of the injection areunpredictable if it is not given under pressure.Duration of anesthesia, once attained, is short(1S to 20 minutes). Therefore the bulk of the pulpmust be removed quickly and at the correct work-ing length to prevent recurrence of pain duringinstrumentation. Another disadvantage is thatobviously the pulp must be exposed to permit di-rect injection; often problems with anesthesiaoccur before exposure.

The advantage is the predictability of pro-found anesthesia if the IP injection is given under

back-pressure. Onset will be immediate, and nospecial syringes or needles are required, althoughdifferent approaches may be necessary to attainthe desired pressure.

Mechanism of Action: Strong back-pressurehas been shown to be the major factor in produc-ing anesthesia. 112,113 Depositing anesthetic pas-sively into the chamber is not adequate; the solu-tion will not diffuse throughout the pulp.Therefore the anesthetic agent is not solely re-sponsible for intrapulpal anesthesia, being depen-dent on pressure.

Technique: Again, the patient must be in-formed that a "little extra" anesthetic will ensurecomfort; there will be "a sharp sensation."

One technique creates back-pressure by stop-pering the access with a cotton pellet to preventbackflow (Figure 7-9).113,114 Other stoppers, suchas gutta-percha, waxes, or pieces of rubber, havebeen used. If possible, the roof of the pulp cham-ber should be penetrated by a half-round bur; theneedle will then fit snugly in the bur hole.

Another approach is an injection into eachcanal after the chamber is unroofed. A standard sy-ringe is usually equipped with a bent short needle.With fingers supporting the needle shaft to preventbuckling, the needle is positioned in the access

FIGURE 7-8Photomicrographs of the injection site at the time of injection. A, Areas visible are the enamel space (E) and thecementoenamel junction region (CEJ). The needle tract (T), which ends in a gouge in cementum (arrow), is ap-parent in the connective tissue. No tissue changes are evident outside the penetration site, including the moreapical tissues. B, Region T in part A. Needle tract and adjacent tissues contain small chips of cementum (C), ery-throcytes (E), and debris (D), which presumably have been carried in by the needle.

112


opening and then moved down the canal, whileslowly expressing the anesthetic, to the point ofwedging. Maximum pressure is then applied slowlyon the syringe handle for S to 10 seconds. If thereis no back-pressure, anesthetic flows out of the ac-cess opening. The needle is wedged deeper or with-drawn and replaced with a larger gauge needle (orstoppered with a cotton pellet), and the injection isrepeated. This may be necessary in each canal.

ALTERNATIVE PRIMARYTECHNIQUES

Electronic dental anesthesia and transcutaneouselectronic nerve stimulation are two fairly recenttechniques that have been promoted as means ofattaining anesthesia without injection. Both in-volve electronic devices. These devices use electri-cal stimulation (of low or high frequency) appliedto tissues surrounding the teeth. Although some

FIGURE 7-9I ntrapulpal injection technique. A, A 45-degree bend is placed on the needle using the needle cap. B, For stop-pering the injection site, a cotton pellet is pulled over the needle. C, The needle is placed in the opening in theroof of the chamber (forewarn the patient of discomfort!). D, The cotton pellet is packed tightly into the accessopening, and the syringe handle is pushed slowly. The patient often feels sharp pain with resistance on the sy-ringe handle; this resistance usually indicates successful anesthesia.

studies have shown good results, others haveshown little effect on pain suppression whenthese techniques are used as the sole means ofanesthesia.115-118 Additional investigations areneeded to clarify the mechanisms of action as wellas clinical effectiveness for endodontic proce-dures before they can be recommended.

Anesthetic Management ofPulpal or Periradicular PathosesI RREVERSIBLE PULPITIS

With irreversible pulpitis, the teeth most difficultto anesthetize are the mandibular molars fol-lowed by (in order) mandibular and maxillarypremolars, maxillary molars, mandibular ante-rior teeth, and maxillary anterior teeth. The vitalinflamed pulp must be invaded and removed.

Also, pulpal tissue has a very concentrated sen-sory nerve supply, particularly in the chamber.These factors, combined with others related toinflammatory effects on sensory nerves and fail-ures occurring with conventional techniques,make anesthetizing patients with painful irre-versible pulpitis a challenge.

Different clinical situations present surprises.In some cases, inflamed vital tissue exists only inthe apical canals; the tissue in the chamber isnecrotic and does not respond to pulp testing.Obviously, in this situation the chamber is en-tered with no problem, but when the operator at-tempts to place a file to length, severe pain results.IO or PDL injections are helpful and an IP injec-tion may be used. However, irreversible pulpitismust be differentiated from a symptomatic apicalpathosis because, in the latter condition, IO, PDL,and IP injections are contraindicated.

General Considerations: Conventional anes-thesia, using primary techniques, is administered.After signs of soft tissue anesthesia occur, thepain abates and the patient relaxes. Frequently,however, upon access opening or when the pulp isentered, pain results because not all sensorynerves have been blocked. A useful procedure is topulp test the tooth with cold or an electric pulptester before the access is begun.38,70,71 If the pa-tient responds, an IO or PDL injection is given.However, no response does not ensure completeanesthesia . 26,3 ', 70 ,71 The patient is always informedthat the procedure will be immediately discontin-ued if pain is experienced or if there is a "premo-nition" of impending pain. Appropriate supple-mentary injections are then used. Occasionally, allattempts fail; in this case, it is best to place a tem-porary restoration and schedule another appoint-ment or refer the patient to an endodontist.

Mandibular Posterior Teeth: A conventionalinferior alveolar injection is administered, usuallyin conjunction with a long buccal injection. Be-cause of the high failure rate of anesthesia forthese teeth, an IO or PDL injection is routinely ad-ministered before access is begun . 31,11, 71 If pain isfelt, the IO or PDL injection may be repeated oran IP injection is given if the pulp is exposed. Usu-ally, once the pulp is removed, further pain is min-imal owing to the longer duration of mandibularanesthesia . 33-37,52

Mandibular Anterior Teeth: An inferior alve-olar injection is given. If pain is felt, an IO injec-tion is administered. If this is unsuccessful, an IPinjection is added.

Maxillary Posterior Teeth: Approaches arethe same as those outlined under "General Con-siderations" except that the initial dose is doubled(3.G ml) for buccal infiltration. The injection site


11 3

may be a PSA block for molars. Infiltration of0.5 ml of anesthetic over the palatal apex en-hances pulpal anesthesia.119 If pain is felt duringthe access, an IO or PDL injection is administered.Seldom is an IP injection needed.

The duration of anesthesia in the maxilla is lessthan that in the mandible . 6z-6s Therefore if pain isexperienced during instrumentation, additionalprimary or supplemental injections are necessary.

Maxillary Anterior Teeth: Anesthetic is ad-ministered initially as a labial infiltration and, oc-casionally, as a palatal infiltration for the retainer.Rarely is an IO injection needed; the PDL injec-tion also is not very effective.94 The duration ofanesthesia may be less than 1 hour, requiring ad-ditional infiltration. 62-65

SYMPTOMATIC PULP NECROSIS

This diagnosis indicates pain and/or swellingand therefore periradicular inflammation. Be-cause the pulp is necrotic and apical tissues areinflamed, anesthesia problems are different.These teeth may be painful when manipulatedduring treatment.

For the mandible, an inferior alveolar nerveblock and long buccal injection are administered.For maxillary teeth, if no swelling is present, anes-thesia is given with a conventional infiltration orblock. If soft tissue swelling is present (cellulitis orabscess), a regional block plus infiltration on ei-ther side of the swelling is administered. Access isbegun slowly. Usually the pulp chamber is enteredwithout discomfort if the tooth is not torqued ex-cessively. File placement and debridement alsocan be performed without much pain if instru-ments are used gently.

Occasionally, conventional injections do notprovide adequate anesthesia. IO, PDL, or IP injec-tions are contraindicated. Although effective forvital pulps, these injections are painful and inef-fective with apical pathosis. Rather, the patientshould be informed that profound anesthesia isnot present owing to inflammation in the bone.As an alternative with maxillary molars, a PSA in-jection or second division nerve block (hightuberosity injection) may be given. In anteriorteeth and premolars, an infraorbital injection isadministered to provide some degree of bone andsoft tissue anesthesia.

In patients with severe preoperative pain with-out drainage from the tooth (or when no swellingcan be incised), a long-acting anesthetic (such asbupivacaine or etidocaine) may help control post-operative pain in mandibular teeth. However, theduration of analgesia is usually not so long topreclude use of oral analgesics.

11 4


ASYMPTOMATIC PULP NECROSIS PERIRADICULAR SURGERY

Asymptomatic teeth are the easiest to anesthetize.Although it may be tempting to proceed withoutanesthesia, vital sensitive tissue may be encoun-tered in the apical portion of canals.

The conventional injections are usually ad-ministered: inferior alveolar nerve block and longbuccal injection for mandibular teeth and infil-tration (or PSA block) in the maxilla. Usually thepatient remains comfortable. Rarely, there maybe some sensitivity during canal preparation thatrequires an 10 or PDL injection. IP injection isnot indicated because bacteria and debris may beforced periradicularly. In the maxilla an addi-tional infiltration may be necessary during longerprocedures.

Anesthesia forSurgical ProceduresINCISION FOR DRAINAGE

Patients tolerate the procedure better when someanesthesia is present before incision and drainplacement are begun. However, profound anes-thesia is difficult, which should be explained tothe patient. In the mandible, inferior alveolarplus long buccal injections (for posterior teeth)or labial infiltration (for anterior teeth) are ad-ministered. In the maxilla, infiltration is given atseveral sites peripheral to the swelling. As an al-ternative, a PSA or second-division block maysuffice for molars and an infraorbital injectionfor anterior teeth and premolars. For palatalswellings, a small volume of anesthetic is infil-trated over the greater palatine foramen (for pos-terior teeth) or over the nasopalatine foramen(for anterior teeth). With swelling over eitherforamen, lateral infiltration is indicated. An ad-junctive measure is to spray ethyl chloride on thearea just before incision.

Injection directly into a swelling is contraindi-cated. These inflamed tissues are hyperalgesic anddifficult to anesthetize. Traditional beliefs arethat the anesthetic solution may be affected bythe lower pH and is rendered less effective andthat direct injection will "spread the infection";neither belief is proved. Nevertheless, althoughthese ideas may have some merit, reasons foravoiding injection into a swelling are the painfrom the pressure and ineffectiveness. Theoreti-cally, the area of swelling (cellulitis) has an in-creased blood supply; thus anesthetic is trans-ported quickly into the systemic circulation,diminishing the anesthetic effect. Also, edemaand purulence may dilute the solution.

Additional considerations in periradicularsurgery involve anesthesia of both soft tissue andbone. Also, inflammation is usually present. Inthe mandible the inferior alveolar injection is rea-sonably effective. Additional infiltration injec-tions in the vestibule are useful to achieve vaso-constriction, particularly in the mandibularanterior region. In the maxilla, infiltration injec-tions are generally effective; usually larger vol-umes are necessary to provide anesthesia over thesurgical field.

If the area of operation is inflamed or the pa-tient is apprehensive, anesthesia may not be to-tally successful. After the flap is reflected, if anes-thesia is inadequate, attempts to enhance orregain anesthesia (through additional infiltra-tions or injecting the sensitive area) are not par-ticularly effective.

As a prophylactic measure, an 10 or PDL injec-tion is administered at the site, after the above in-jections and before the surgery. This seems to en-hance depth of anesthesia and may provide betterhemostasis.

Use of a long-acting anesthetic has been advo-cated.46,47 In the mandible, this is reasonably effec-tive. In the maxilla, long-acting agents have ashorter duration of anesthesia and decreased epi-nephrine concentrations, which result in morebleeding during surgery." ,"' After periradicularsurgery, administration of a long-acting anes-thetic has been suggested." However, postsurgicalpain is usually not severe and can be managed byanalgesics. 120

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11 6


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lary infiltrations, JEndod 14:193, 1988 (abstract).

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ficacy of volumes of lidocaine in human maxillary in-

filtration, JEndod 13:128, 1987 (abstract).64. Mason R, Reader A, Beck M, Meyers W: Comparison

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Assoc 117:337, 1988.

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anesthesia, J Endod 16:192, 1990 (abstract).

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131:635, 2000.

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73. Parente, SA, Anderson RW, Herman WW, et al: Anes-

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74. Stabident Instruction Manual, Miami, 2000, FairfaxDental Inc.

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of the intraosseous injection after an inferior alveolarnerve block, JEndod 22:481, 1996.

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mandibular first molars, Oral Surg Oral Med Oral PatholOral Radiol Endod 83:30, 1997.

78. Reitz J, Reader A, Nist R, et al: Anesthetic efficacy of

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79. Guglielmo A, Reader A, Nist R, et al: Anesthetic effi-

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82. Stabile P, Reader A, Gallatin E, et al: Anesthetic effi-cacy and heart rate effects of the intraosseous injec-tion of 1.5% etidocaine (1:200,000 epinephrine) afteran inferior alveolar nerve block, Oral Surg Oral Med

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11 7

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1/ Describe the reasons for rubber dam isolation during endodontic procedures.

2/ List a rubber dam clamp selection for anterior, premolar, and molar teeth.

3/ Identify those clamps that have several applications. (Which two are "universal?")

4/ Describe techniques for application of clamp/rubber dam in single-tooth isolation.

5 / Describe techniques to stop salivary or hemorrhage "seepage" into the operative field.

6 / Recognize situations in which special isolation approaches are necessary.

7 / Describe the technique to use in those special situations.

8 / Describe surgical techniques to use as adjuncts to attain required isolation.

9/ Identify patients with difficult isolation situations who should be considered for referral.

Isolation

LEARNING OBJECTIVES

118

81 Isolation

119

Reasons for Use of the Rubber Dam

Protection

Facilitate and Increase Efficiency

Minimize Cross-Infection

Legal Considerations

Additional Considerations

Preparation for Placement

Areas of Potential Leakage

Coronal Considerations

Gingival Preparation

Replacement of Missing Crown Structure

Equipment

Rubber Dam Material

Frames

Combinations

Clamps (Retainers)

Additional Instruments

Clamp Substitutes

Application of the Rubber Dam

Hole Placement

Clamp Selection

Placement Techniques

Rubber Dam Positioning

Disinfection of Operating Field

Aids for a Leaking Dam

Prevention

Corrective Methods

Modifications for Difficult Isolation

Situations

Unusual Crown to Root Alignment

Little Remaining Tooth Structure

Root Caries

Unusual Tooth Position

Unusual Tooth Shape

Bridges or Orthodontic Appliances

Porcelain Restoration

Multiple Tooth Isolation

Emergency Situations

When and What to Refer

Problems with inadequate Isolation

Other Situations

solation requires proper placement ofthe rubber dam. This device will isolatethe pulp space from saliva and hemor

rhage and protect tissues from irrigating solu-tions, other chemicals, and instruments.

The rubber dam was first introduced in 1863 bySanford Barnum, a New York dentist. His inventionwas a way to achieve isolation for the placing of goldfoil. Shortly thereafter his colleague, C. E. Francis,pleaded, "Gentlemen of the profession-learn to useBarnum's rubber dam, and when you thoroughlyunderstand its true value, you will bless the name ofthe worthy dentist whose ingenuity gave us so valu-able a boon."' Surveys indicate that rubber damusage is inconsistent, with many dentists seldom ornever using the rubber dam for endodontic proce-dures.2 Some use it occasionally, and about half usea rubber dam for isolation almost always.' This in-dicates a need for better understanding of the ratio-nale for its use . 4

Reasons for Useof the Rubber DamPROTECTION

The rubber dam prevents aspiration or accidentalswallowing of endodontic instruments and irrig-ants. It also affords protection from injury causedby rotary and hand instruments.5 The patientshould not be exposed to these avoidable risks.

The dentist and assistant are also protected.Aerosol spray from the haridpiece and air-watersyringe are potentially harmful. Use of the rubberdam minimizes this risk; the aerosol will deflectoff the clean rubber dam rather than mixing withsaliva and oral debris.6,7 Contamination of the en-vironment is also reduced because the dentalteam has less direct contact with the patient's oraltissues and fluids.

FACILITATE ANDI NCREASE EFFICIENCY

The rubber dam (1) improves visibility; (2) preventssalivary leakage, thus providing a dry field; (3) pre-vents fogging of the mirror; (4) relaxes the patient,who need not fear swallowing instruments nor suf-fer the unpleasant taste of chemicals or irrigants;and (5) minimizes conversation and the need (per-ceived or actual) for frequent rinsing.

MINIMIZE CROSS-INFECTION

There is increasing concern about transmissionof infectious diseases [especially acquired im-

120

8 / Isolation

munodeficiency syndrome (AIDS), tuberculosis,and hepatitis); use of the rubber dam may reducethe risk of spreading these diseases.' The rubberdam, although helpful, must not be consideredtotal protection; other preventive measures areessential as well.

LEGAL CONSIDERATIONS

All dental schools in the United States require useof the rubber dam during endodontic procedures.Its routine usage during root canal treatment is a stan-dard of care. In fact, expert testimony is not re-quired to justify claims of negligence when an in-strument is swallowed or aspirated. Liability is soevident that a jury is deemed competent enoughto determine negligence. Although the reasons forrubber dam application are primarily facilitativeand biologic, legal ramifications make its usemandatory.

ADDITIONAL CONSIDERATIONS

The necessity for rubber dam isolation is appar-ent. It is important to recognize early those situa-tions in which isolation will be difficult or time-consuming; this is part of treatment planning.Before treatment is initiated, isolation must becarefully considered. Occasionally, it is best forpatients with difficult isolation situations to bereferred to an endodontist because special tech-niques may be required.

Preparation for PlacementRoot canal treatment begins with considerationof several factors before actual rubber damplacement.

AREAS OF POTENTIAL LEAKAGE

Areas having a potential for leakage include sub-gingival caries and defects such as fractures, de-fective restorations, and open margins.

CORONAL CONSIDERATIONS

Margins of existing restorations are evaluatedboth radiographically and clinically. Defectiverestorations may allow leakage between the oralcavity and pulp space. The entire restoration, or atleast the defective portion, must be removed earlyand before the access preparation is completed.

The extent and presence of caries should alsobe an early determination. Caries may communi-cate with the oral cavity and pulp chamber. Gen-

erally all caries are removed to prevent leakageduring and after treatment.

GINGIVAL PREPARATION

When restorations or carious lesions extend sub-gingivally or when crown destruction is excessive,sound tooth structure may require exposure bygingivectomy or crown lengthening.

Gingivectomy: Gingival tissue is removed toexpose an intact surface to allow clamp place-ment. When gingivectomy is necessary to restorenormal gingival architecture for restoration, it isbest done before root canal treatment is initiated.This simplifies isolation and aids in determiningrestorability.

Crown Lengthening: Crown lengthening is amore involved procedure that requires flap reflec-tion and contouring of bone and gingival° Heal-ing requires approximately 6 weeks; the toothshould not be clamped during that time. Rootcanal treatment and crown lengthening are oftenbest accomplished at the same appointment. Be-cause of the treatment complexity, these patientsmay benefit by being referred.

REPLACEMENT OF MISSINGCROWN STRUCTURE

The perfect access preparation for maximal visi-bility and ease of straight-line access is through acrown sectioned in the cervical third, thus open-ing the chamber wide. Therefore adding restora-tive materials or placing bands or temporarycrowns only hinders treatment. However, pre-treatment occasionally requires a provisionalrestoration before rubber dam placement.

Temporary Restoration: A reinforced ce-ment, such as IRM (Cavit is not acceptable), issuitable. This is indicated in regions that are diffi-cult to isolate (such as subgingival interproximalcaries) but where crown lengthening or gingivec-tomy is not required. The cement should main-tain proximal contact or, if little tooth structureremains, be contoured to help prevent interproxi-mal food impaction.

Buildups: These procedures are usually notnecessary. However, when gingival procedures ortemporary restorations to facilitate isolation arenot feasible, amalgam, glass ionomer, or compos-ite buildups may suffice.11-13 Special retentive ap-proaches are required.14

Disadvantages to buildup procedures are thatthey are time-consuming, may hinder visibilityand access to the canal space, and usually must beredone before the permanent restoration is placed.Generally, there is no need for such procedures.

Bands: Copper and orthodontic bands havebeen advocated as an isolation aid and as a meansof protecting weakened cusps.'' Bands are time-consuming to adapt properly, generally leak,often come loose, and usually cause gingival irri-tation. Therefore they are rarely indicated. Ifcusps have been undermined or are otherwiseweakened, it is preferable to reduce their height byseveral millimeters and then, if necessary, onlaywith the temporary material.

Temporary Crowns: Temporary crowns arealso of dubious value in aiding isolation. Thereare suggestions that temporary crowns be ce-mented and then access made through the oc-clusal surface. Temporary crowns have the samedisadvantages as bands (described above). Twoadditional disadvantages outweigh any transientbenefits provided by temporary crowns. First, theyare often displaced by the force of the clamp ortension of the rubber dam. Second, there is loss oforientation and impaired visibility. Therefore ac-curate access preparation, canal locating, andoverall treatment through a temporary crown aremore difficult.

Temporary crowns may be used between ap-pointments after the canal space or chamber hasbeen sealed off with another temporary materialand after the rubber dam has been removed. Thetemporary crown is then adjusted and cementedtemporarily and removed at the next appoint-ment. Before the root canal treatment begins, it isusually preferable to remove a temporary crownthat has been placed earlier.

Equipment

RUBBER DAM MATERIAL

Rubber dams are available in several colors andfour thicknesses or weights. There is also a nonla-tex dam (nonallergenic) material. Although colorchoice is largely personal preference, the light-colored (yellow) dam has advantages. It allows bet-ter illumination and is transparent enough to fa-cilitate film placement when making radiographs.Of the four thicknesses (light, medium, heavy, andextra heavy),the light and medium are preferred.The light is easier to slide between the teeth andputs the least amount of tension on the clamp.However, it is difficult to tuck and does not seal aswell. Medium weight is slightly more difficult toapply but fits better at the gingival margin andprovides better soft tissue retraction. Thicknessdoes not have a consistent effect on tear resistanceproperties.16 Experience, different isolation condi-tions, and personal preference will dictate rubberdam selection for each situation.

FRAMES

Four frames are commonly used for endodonticprocedures. The Young's frame is metal (ra-diopaque) and must be removed while taking ra-diographs. The Nygaard-Ostby and the Star Visi-frames are radiolucent and need not (should not)be removed while radiographs are being made.The Nygaard-Ostby frame attaches the rubberdam on all four sides and requires more care inhole placement, because it is more difficult to ad-just the height of the superior border of the dam.The Plast--Frame is autoclavable plastic and can befolded to one side for radiographs. All four framescomfortably hold the dam away from the pa-tient's face and require no napkin under the dam.

COMBINATIONS

Recently frame and rubber dam combinationshave been introduced (Figure 8-1). One has a pli-able oval plastic frame around the perimeter ofthe rubber dam and is available in three sizes. An-other has a plastic tube inserted in prepared holesin the rubber dam material and comes in one size.A third is autoclavable. All appear to provide ade-quate protection, are easy to apply, do not inter-

FIGURE 8-1Two rubber dam and frame combinations: Quickdam andHandiDam. These are easily applied and disposable, but aremore costly.

8 / Isolation

121

122

8 / Isolation

fere with making radiographs, and eliminatebulky and cumbersome frames.

CLAMPS (RETAINERS)

Styles and Shapes

Figure 8-2. Winged clamps are preferred for effi-cient dam application. Recently, a series of clampswith a dull finish has been introduced to reducelight reflection. Plastic, disposable clamps are alsoavailable.

Many different styles and shapes designed for dif-ferent situations are available. One manufacturerlists an assortment of more than 50 clamps. Alarge number of clamps is neither necessary nordesirable for isolation. A complete selection in-cludes (1) anterior teeth: Ivory 9 or Ash 9; (2) pre-molars: SSW 20, 27, Ivory 0, 2, 9, 1, and IA; and(3) molars: SSW 18, Ivory 14, 14A, and 56, andAsh 8. Five clamps that will manage most rootcanal treatment isolation situations are shown in

Universal Clamp Designs

Two designs (Figure 8-2), the "butterfly" Ivory 9and the Ivory 56, are suitable for most isolations.The butterfly design (no. 9) has small beaks and isdeep reaching and is useful for most anterior andpremolar teeth. The no. 56 is used for molars.Both usually provide isolation, particularly in dif-ficult situations.

Small radius beaks can be positioned fartherapically on the root; this will stretch the dam cervi-cally in the interproximal space. With teeth that aresmaller or abnormally shaped, a clamp (no. 14, 9,or 2) with smaller radius beaks is necessary.

Additional Designs: Clamps that may be nec-essary when little coronal tooth structure remainshave beaks that are inclined apically. These aretermed deep-reaching clamps (Figure 8-3).

For stability, four-point contact between thetooth and beaks of the clamp is necessary and dic-

FIGURE 8-2Top, Butterfly design clamp Ivory 9 for anterior teeth and pre-molars. Middle left Hu-Friedy 56 for molars. Middle right Ivory2 for molars when a smaller beaked, deeper-reaching clamp isnecessary. Lower left Hu-Friedy 14. Lower right, Hu-Friedy14 A for molars of different sizes. Nos. 56 and 9 can be used inmost situations. Note the nonglare finish on Hu-Friedy clamps.

FIGURE s-aTwo styles of deep-reaching clamps: A and B, Ivory 14; C andD, 14A. These are often more stable when coronal toothstructure is missing.

rates the size selected. Fatigued anterior and pre-molar clamps may be used for unusual molar ap-plications (Figure 8-4). Clamps may also be mod-ified by grinding to adapt to unusual situations."Plastic clamps are more easily modified.

ADDITIONAL INSTRUMENTS

Punch: Any punch is acceptable. The punchshould be sharp to make a clean hole and not tearor nick the dam.

Forceps: Any forceps are acceptable. One typehas projections extending from the beaks to allowbetter control in clamp placement. Also, the pro-jections allow greater pressure gingivally and pro-vide more maneuverability for seating the front orrear of the clamp.

Tucking Instruments: A plastic instrument orspoon excavator slides the dam off the wings ofthe clamp and then inverts the edge of the dam. Astream of air will dry the area and helps to invertthe dam.

Dental Floss: Dental floss is used to pass thedam between both contacts. With single toothisolation, at least the mesial and often the distalsurface should be flossed through the contact.Checking contacts for tightness before dam place-ment is advisable. Floss may be used to ligate thenecks of the teeth to hold the dam if a clampcannot be used.

Saliva Ejector: A saliva ejector enhances pa-tient comfort. The tip may be positioned underthe dam, or the patient may maneuver it underthe dam as needed.

FIGURE 8-4A butterfly design clamp (Ivory 9) may be used on a posteriortooth. This unusual clamp selection allows isolation gingivalto the caries.

CLAMP SUBSTITUTES

In some circumstances, floss holds the dam inplace by ligating the tooth. In these cases, multi-ple isolation is usually needed (Figure 8-5). Flosscan also be used with a bead from a necklace, arubber polishing disc, or a rubber anestheticplunger.' Floss is threaded through the hole inthe bead or rubber disc or around the plunger,leaving enough to ligate when the bead is placedon the lingual surface (Figure 8-6). Wedjets (Hy-genic Corp.) are also a means of holding the rub-ber dam in position.' Ortho separators may also

FIGURE 8-5Multiple isolation secured with floss, useful when a clampcannot be placed.

FIGURE 8-6Rubber dam secured with bead (anesthetic cartridge stopper)and floss ligation.

8 / Isolation

123

124

8 / Isolation

FIGURE 8-7Rubber dam and clamp properly at-tached to a frame before placementas a unit. Note that the dam isstretched tightly across the top andbottom with slack in the middle forease of placement.

A simple method of hole placement is as fol-lows: (1) engage the dam on the frame, (2) centerthe dam over the patient's mouth, (3) push thedam over the tooth to be isolated, (4) mark thedam, and (5) remove and punch the dam.

CLAMP SELECTION

The appropriate clamp with four-point contact isselected. To prevent swallowing or aspiration ifdisplacement occurs, floss is attached to theclamp bow. A floss tie is unnecessary if the clampand dam are placed together.

FIGURE s-sRubber dam, clamp, and frame being placed as a unit; this isusually faster and more effective than other techniques.

be placed around the neck of the tooth to holdthe dam in position.

Application of the Rubber DamHOLE PLACEMENT

The hole is located so that the dam covers the en-tire mouth and extends up to the nose. The damshould cover the nose to reduce inhalation ofaerosol particles and to control objectionableodors. Some patients are uncomfortable with thedam over their nose. Placing the hole 1 inch offthe center of the dam toward the quadrant beingisolated will usually suffice.

PLACEMENT TECHNIQUES

After the necessary preparation procedures de-tailed earlier have been completed, the dam isplaced using one of the following three methods.

Method 1: Placement as a unit. Placement ofrubber dam, clamp, and frame as a unit is pre-ferred. This is most efficient and is applicable inmost cases.

1. Place the dam on the frame so that it isstretched tightly across the top and bottombut has slack in the middle (Figure 8-7).

2. Punch the hole in the dam and attachclamp wings to the dam.

3. Place the dam, frame, and clamp as a unitto engage the tooth near the gingival mar-gin (Figure 8-8). Finger pressure is usuallynecessary on the forceps or the clamp be-cause of resistance from the rubber as it isstretched.

8l Isolation

125

FIGURE 8-9Placement of clamp and rubber dam for better visibility of theneck of the tooth. The rubber dam is attached to the clampbow and is held out of the way for unobstructed vision whilethe clamp is positioned. Then the rubber dam is stretchedaround the clamp and the neck of the tooth.

4. Slide the dam off the clamp wings to allowthe dam to constrict around the toothneck. Draw the dam through the contactswith floss.

5. Adjust the dam on the frame for patientcomfort.

Method 2: Placement of clamp and dam andthen the frame (Figure 8-9). This method is seldomused but may be necessary when an unobstructedview is required while the clamp is positioned.

Method 3: Placement of the rubber dam andframe and then the clamp. This is the preferredmethod for applying a butterfly clamp. Better vi-sualization is possible when the hole is stretchedover the tooth and gingiva first (Figure 8-10) andthen the clamp is placed (Figure 8-11).

RUBBER DAM POSITIONING

FIGURE 8-10The rubber dam is stretched over the tooth before clampplacement.

FIGURE 8-11The clamp is placed to hold the prepositioned and pre-stretched rubber dam (see Figure 8-10).

After placement, the rubber dam is adjusted onthe frame so that the mouth is completely cov-ered. Tension is adjusted to minimize bunchingand to retract soft tissue without dislodging theclamp (Figure 8-12).

DISINFECTION OF THE

OPERATING FIELD

Various chemicals and techniques have beentried to remove and destroy bacterial contami-nants from the tooth surface, clamp, and sur-

rounding rubber dam. These include alcohol,quaternary ammonium compounds, sodiumhypochlorite, organic iodine, mercuric salts, andhydrogen peroxide. An effective technique is asfollows: (1) plaque is removed by rubber cup andpumice; (2) the rubber dam is placed; (3) thetooth surface, clamp, and surrounding rubberdam are scrubbed with 30% hydrogen peroxide;and (4) the surfaces are swabbed with 5% tinc-ture of iodine or with sodium hypochlorite. 2 °

12 6

8 / Isolation

FIGURE 8-72Final position of the adjusted rubber dam, clamp, and frame.Floss should be drawn through the contacts. The tooth, clampand surrounding dam may now be cleaned and disinfected.The dam edge may be folded away from the nose.

FIGURE 8-13Silicone sealant (OraSeal) is injected in an area of leakage.The material is then pressed and adapted into place with awet cotton pellet.

Aids for a Leaking DamPREVENTION

Proper tooth and site preparation, clamp selection,hole positioning, placement on the tooth, and finalsealing with floss all reduce leakage problems.'-'

CORRECTIVE METHODS

If seepage occurs, one of the following techniqueswill usually correct the problem:

Cavit: Cavit is somewhat useful. Cavit is placedat the site and compacted with a large wet cottonpellet. A major disadvantage is that, with longerprocedures, Cavit usually will crack and leak, re-quiring replacement.

Sealants: Special sealants are applied topically(Figure 8-13), or, if leakage is anticipated, theymay be applied to the undersurface of the dam be-fore placement.zz

Rubber base adhesive: This is easily paintedon the dam in an area of minor seepage."

Floss ligation: Floss around the cervical re-gion helps to keep the dam inverted. Ligation isuseful during isolation of multiple teeth but istime consuming.

Additional corrective methods: Use of cyano-acrylate, a prosthetic block-out putty, Stomadhe-sive, or a denture adhesive-zinc oxide mixture hasalso been proposed for correction of seepage. 19,24,25

Modifications for DifficultI solation SituationsUNUSUAL CROWNTO ROOT ALIGNMENT

Sometimes the crown is misaligned with the rootor has been modified by large restorations. To en-hance proper angulation or orientation to thechamber, access preparation in those situationsshould be done before rubber dam placement.First, the location and long axis of the tooth aredetermined by visualizing and palpating the rootprominence. Second, as a guide for the bur, a pen-cil line is drawn on the crown aligned with thelong axis of the root.'° The rubber dam is placedwhen the chamber (or canal) is located.

LITTLE REMAININGTOOTH STRUCTURE

Teeth with severe loss (particularly subgingival) ofcoronal tooth structure compromise rubber damplacement. One of the following can be used toensure adequate isolation.

1. Use of a deep-reaching ("A" style or smallbeak) clamp often solves the problem andis the first method attempted (Figure 8-14).

2. Adjacent teeth are clamped, giving multi-ple isolation. This is slightly less effective

8 / Isolation

12 7

FIGURE 8-14A deep-reaching clamp secures the rubber dam on a toothwith little clinical crown.

FIGURE 8-15Clamp beaks may be placed on anesthetized gingiva if thecoronal tooth structure is not sufficient to secure the clamp.This does no permanent damage to the gingiva.

than single-tooth isolation and usually re-quires the use of other aids such as flossligation and/or sealants.

3. The clamp beaks may be placed on anes-thetized gingiva (Figure 8-15). Theremust be sufficient gingival purchase toprevent the clamp from cutting throughthe gingival sulcus and, in essence, per-forming a crude, unplanned gingivec-tomy. Plastic clamps create less gingivaltrauma. Patients experience minimal dis-comfort after clamp placement on thegingiva.

4. Gingivectomy or flap reflection or crownlengthening can be performed beforeisolation.

5. Build-up procedures are generally notrecommended.

ROOT CARIES

Subgingival caries are a challenge. 26 Placement ofthe clamp and dam cervical to the caries (see Fig-ure 8-4) should be attempted, but may be unsuc-cessful. Caries removal is necessary and often re-quires a temporary restoration. The challenge isto avoid introducing restorative material into thecanal space. One technique is to remove cariesfirst followed by access. Then a tight-fitting file isplaced into the canal apical to the defect. A tem-porary or permanent restoration is placed. When

set, the blocking instrument is removed, leavingthe canal patent.

UNUSUAL TOOTH POSITION

Teeth that are inclined because of crowding orthat have tipped owing to tooth loss present iso-lation problems. Isolation can usually be accom-plished by careful clamp selection. Other methodsinclude clamping the adjacent tooth (multipleisolation) or ligation with floss, floss and bead, orWedjets.

UNUSUAL TOOTH SHAPE

Occasionally coronal configuration makes toothclamping difficult. Beak placement below theheight of contour may not be possible if teeth arenot fully erupted. Crown reduction for full cover-age usually removes the gripping area. Remedies,in order of preference are the following:

1. Deep-reaching clamp2. Gingival clamping3. Acid etch composite on buccal and/or lin-

gual surface to retain clamp or dam"4. Grooves on buccal and lingual surfaces for

clamp retention5. Orthodontic separators over the necks of

the teeth6. Gingivectomy or crown lengthening

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8 / Isolation

BRIDGES OR ORTHODONTIC

APPLIANCES

These are usually approached in the same manner assingle-tooth isolation. Because of openings, it maybe necessary to punch two holes, cut a slit betweenthe holes, and then use a sealant; this is the easiesttechnique (Figure 8-16). More elaborate methodshave been designed-for example, cutting a slit and

FIGURE 8-16I solation with an orthodontic appliance. A slit is made be-tween the two end punch holes. Seepage is then preventedby silicone sealant placement. This could also be treated byremoving the arch wire and using single-tooth isolation.(Courtesy Dr. M. Davis.)

then suturing the dam closed under the pontics orby ligating interproximally." However, such proce-dures are complicated and rarely necessary.

PORCELAIN RESTORATION

Placing a clamp on porcelain may cause crazing,although not consistently... 3 ° It is best to avoidclamping such restorations if the quality of porce-lain condensation is uncertain. Damage isavoided by clamping the adjacent tooth or byusing floss or floss and bead ligation. An alterna-tive is to stretch an unpunched dam over thetooth and secure the dam with the appropriateclamp. Then with a hot instrument a hole ismelted over the access preparation. The accessmust be done before rubber dam placement.

MULTIPLE TOOTH ISOLATION

When more than one tooth requires treatment,isolation is accomplished with multiple clamps(Figure 8-17) or with clamps and floss ligation orother combinations (Figure 8-18). For anteriorteeth (or tooth), all teeth would have to be iso-lated and the rubber dam would be stretched andclamped over the first premolars.

EMERGENCY SITUATIONS

Occasionally a patient has such intense pain that heor she cannot tolerate the clamp. Multiple isolationis usually preferred by clamping another tooth. Analternative is floss, floss and bead, or Wedjets liga-tion with either single or multiple isolation.

FIGURE 8-17Example of multiple isolation when several teeth are under-going treatment. This may also need to be used when aclamp cannot be conveniently placed, such as on a crown-prepared tooth.

FIGURE 8-18To isolate this double-abutted bridge, a combination of tech-niques is used. One large rubber dam opening is necessary.OraSeal is packed around the clamp. A cotton roll on the lin-gual aspect reduces seepage. (Courtesy Dr. C. Koloffon.)

8 / Isolation

129


If isolation is not obtainable, patients should beconsidered for referral.

PROBLEMS WITHINADEQUATE ISOLATION

Patients with the following conditions should beconsidered for referral: (1) gross and persistentbacterial contamination of the pulp space andpossibly the periapex; (2) excessive time requiredfor treatment; (3) frustration and delays whenleakage occurs or with dam displacement; and (4)anxiety or discomfort for the patient when isola-tion fails or when solutions violate the oral cavity.

OTHER SITUATIONS

Patients with the following should be consideredfor referral: (1) badly broken-down teeth withminimal coronal tooth structure remaining.These are a challenge-attempting multiple-toothisolation leads to seepage; (2) bridge abutmentswith problem seepage; (3) full crown preparationsthat are difficult to clamp, when multiple isola-tion is difficult, (4) malpositioned teeth withunique isolation problems; and (5) the most distaltooth in the arch if it cannot be clamped.

Individual capabilities (experience, training,and interest) determine which patients the practi-tioner might treat and which should be referred.In assessing these capabilities from a legal per-spective, courts have set the standard of care asthat provided by the specialist, not the generaldentist. Consideration of the patient's time andcomfort are also important factors. Finally, noth-ing is more upsetting to a full schedule or morefrustrating to both practitioner and patient thandifficulties encountered during treatment. Lower-ing the practitioner's stress levels is an additionalincentive for considering referral.

REFERENCES

1. Francis C: The rubber dam, Dental Cosmos 7:185, 1866.2. Joynt R, Davis E, Schreier P: Rubber dam usage among

practicing dentists, Oper Dent 14:176, 1989.3. Marshall K: The use of rubber dam in the UK, Br Dent

J 168:286, 1990.4. Marshall K: Isolation and tissue control: the role of

rubber dam, Endod Pract 1:40, 1998.5. Huggins D: The rubber dam: insurance policy against

litigation, JIndiana Dent Assoc 65:23, 1986.6. Miller R, Micik R: Air pollution and its control in the

dental office, Dent Clin North Am 22:453, 1978.

7. Wong R: The rubber dam as a means of infection con-trol in an era of AIDS and hepatitis, J Indiana DentAssoc67:41, 1988.

8. Cochran M, Miller C, Sheldrake M: The efficacy of therubber dam as a barrier to the spread of micro-organismsduring dental treatment, JAm DentAssoc 119:141, 1989.

9. Cohen S, Schwartz S: Endodontic complications andthe law, JEndod 13:191, 1987.

10. Gutmann J, Dumsha T, Lovdahl P, Hovland EJ: Prob-lem solving in endodontics, ed 2, St Louis, 1992, Mosby.

11. Morgan L: Solving endodontic isolation problemswith interim buildups of reinforced glass ionomer ce-ment,JEndod 16:450, 1990.

12. Kahn H: Coronal build-up of the degraded tooth be-fore endodontic therapy, JEndod 8:83, 1982.

13. Estafan DJ, Harris R, Estafan A: A simplified approachto isolating a single tooth before endodontic therapy,JAmDent Assoc 130:846, 1999.

14. Greene R, Sikora F, House J: Rubber dam applicationto crownless and cone-shaped teeth, J Endod 10:82,1984.

15. Linden R: Using a copper band to isolate severely bro-ken teeth before endodontic procedures, J Am DentAssoc 130:1095, 1999.

16. Svec T, Powers J, Ladd G, Meyer T: Tensile and tearproperties of dental dam, j Endod 22:253, 1996.

17. Weisman M: A modification of the no. 3 rubber damclamp, JEndod 9:30, 1983.

18. Ireland 1: The rubber dam: its advantages and applica-tion, Tex Dentj 24:6, 1962.

19. Aesaert, G: The use of rubber dam in difficult clinicalsituations, Endod Pract 3:6, 2000.

20. Hermsen K, Ludlow M: Disinfection of rubber damand tooth surfaces before endodontic therapy, GenDent 35:355, 1997.

21. Fors V, Berg J, Sandberg H: Microbiological investiga-tion of saliva leakage between the rubber dam and toothduring endodontic treatment, J Endod 12:396, 1986.

22. Glick D: Use of a protective emollient as an endodon-tic aid, Oral Surg Oral Med Oral Patbol 24:250, 1967.

23. Bramwell D, Hicks M: Solving isolation problems withrubber dam adhesive, JEndod 12:363, 1986.

24. Roahen J, Lento C: Using cyanoacrylate to facilitaterubber dam isolation of teeth, JEndod 18:517, 1992.

25. Weisman M: Remedy for dental dam leakage prob-lems, JEndod 17:88, 1991.

26. Iglesias A, Urrutia C: Solution for the isolation of theworking field in a difficult case of root canal therapy,JEndod 21:394, 1995.

27. Wakabayashi H, Ochi K, Tachibana H, et al: A clinicaltechnique for the retention of a rubber dam clamp,JEndod 12:422, 1986.

28. Liebenberg W: Manipulation of rubber dam septa: anaid to the meticulous isolation of splinted prostheses,JEndod 21:208, 1995.

29. Madison S, Jordon R, Krell K: The effects of rubberdam retainer on porcelain fused-to-metal restorations,JEndod 12:183, 1986.

30. Zerr, M, Johnson W, Walton R: Effect of rubber dam re-tainers on porcelain-fused-to-metal, Gen Dent 44:132,1996.

Endodontic Radiography

LEARNING OBJECTIVES


1/ Describe the importance of radiographs in endodontic diagnosis and treatment.

2/ Discuss special applications of radiography to endodontics.

3/ Discuss reasons for limiting the number of exposures.

4/ Identify normal anatomic features in the maxilla and mandible on radiographs.

5/ Describe radiographic characteristics to differentiate between endodontic and nonendodontic (normal and

pathologic) radiolucencies and radiopacities.

6/ Describe the reasons for varying horizontal and vertical cone angulations on working radiographs to create

i mage shift.

7 / Describe how to determine the third dimension on angled radiographs (i.e., facial-lingual structures

[SLOB] rule).

8 / Describe structural elements of the tooth as visualized on both facial and angled projections.

9/ Discuss how to detect the presence and to locate undiscovered canals or roots on angled working

radiographs.

10/ Describe techniques for making "working" radiographs (i.e., film placement and cone alignment with

rubber dam in place).

11/ Describe specific details of film placement and cone alignment for each tooth on working radiographs.

12/ Describe the limitations of rapid processing of working films.

13/ Describe the radiographic technique for locating a "calcified" canal.

14/ Discuss the limitations of radiographic interpretation.

15/ Describe some new technologies and their application to endodontic radiography now and in the future.

130

I mportance of Radiography in Endodontics

Diagnosis

Treatment

Recall

Special Applications

Radiographic Sequence

Diagnostic Radiographs

Working Films

Obturation

Recall

Exposure Considerations

Cone-Image Shift

Principles

I ndications and Advantages

Disadvantages

Endodontic Radiographic Anatomy

I nterpretation

Limitations

Differential Diagnosis

Endodontic Pathosis

Nonendodontic Pathosis

Anatomic Structures

Special Techniques

Bitewing Projections

Fil m-Cone Placement

Rapid Processing

Viewers

New Technology

9 / Endodontic Radiography

131

We are sick of the roentgen ray ... you can seeother people's bones with the naked eye, and alsosee through eight inches ofsolid wood. On therevolting indecency of this there is no need todwell. But what we seriously put before theattention of the Government... that it will callfor legislative restriction of the severest kind.Perhaps the best thing would be for all civilizednations to combine to burn all works on theroentgen rays, to execute all the discoverers, andto corner all the tungstate in the world andwhelm it in the middle of the ocean.

EDITORIAL IN PALL MALL GAZETTELONDON, 1896

bviously (and fortunately), theconcern expressed by the editorial inthis London publication did not be

come the popular view of radiography. Radio-graphs are essential; they are a second set of "eyes"for the dentist. This is particularly true in en-dodontics, in which so many diagnostic and treat-ment decisions are based on radiographic find-ings. Because most structures of concern are notvisible to the naked eye, there is considerable de-pendence on radiographs, which are an obviousnecessity and a blessing. But they also may besomewhat of a liability from the standpoint ofboth safety and time, and unfortunately they areoften overinterpreted.

A radiographic exposure is an irreversible pro-cedure, and therefore only necessary exposures aremade. With the increasing emphasis and justifi-able concern for radiation safety, overall radiationexposure must be minimized.' However, theamount of radiation dosage to oral and other tis-sues has been calculated to be very low and causeminimal (but some) risk. 2,3

Another concern is the time required to makeand process individual radiographs-time ismoney. Therefore, in the interests of both safetyand time, only the radiographs necessitated by theprocedure should be made.

This chapter will discuss radiography as ap-plied to endodontic procedures. Radiography as adiscipline in dentistry has increased in impor-tance with advances in technology and has re-cently been granted specialty status, thereby re-placing endodontics as the youngest dentalspecialty.' Technology has exploded in recentyears, with new devices and approaches that re-quire special training and experience. How thesenew devices and approaches apply to diagnosis

Yoshida

Sticky Note

X-Ray

13 2


and treatment in endodontics will be discussedlater in this chapter.

Importance of Radiographyi n Endodontics

Radiographs perform essential functions in threeareas. However, they have limitations that requirespecial approaches. A single radiograph is but atwo-dimensional shadow of a three-dimensionalobject. For maximum information, the third di-mension must be visualized and interpreted.' Thethree general areas of application are diagnosis,treatment, and recall; each requires its own specialapproach.

DIAGNOSIS

Diagnostic radiology involves not only identifyingthe presence and nature of pathosis but also deter-mining root and pulp anatomy and characterizingand differentiating other normal structures.

Identifying Pathosis: Radiographs must bestudied carefully by someone with a workingknowledge of the changes that indicate pulpal,periapical, periodontal, or other bony lesions.Many changes are obvious, but some are subtle.

FIGURE 9-9A, The facial projection of this premolar gives some limitedi nformation about pulp/root morphology." Fast break" (smallarrow) usually indicates canal bifurcation. A double rootprominence on the mesial surface (large arrow) indicates twobulges and a concavity; its absence on the distal surface in-dicates a flat or convex root surface. B, The same premolarfrom the proximal view. The presence of two definitivecanals, each in its own "root bulge," is confirmed.

Determining Root and Pulpal Anatomy: De-termining the anatomy involves not only identify-ing and counting the roots and canals but also de-termining curvatures, canal relationships, andcanal location .6-8 Identification also involves char-acterizing the cross-sectional anatomy of individ-ual roots and canals (Figure 9-1).

Characterizing Normal Structures: Numer-ous radiolucent and radiopaque structures oftenlie in close proximity. Frequently, these structuresare superimposed over and obscure crowns androots. These must be distinguished and differen-tiated from pathosis and from dental anatomy.

TREATMENT

"Working" radiographs are made while the rubberdam is in place, creating problems in film place-ment and cone positioning. These radiographsare exposed during the treatment phase and havespecial applications.

Determining Working Lengths

Distance from a reference point to the radio-graphic apex is determined precisely. This estab-lishes the distance from the apex at which thecanal is to be prepared and obturated."

Moving Superimposed Structures: Radi-opaque anatomic structures often overlie and ob-scure roots and apexes. By using special cone an-gulations, these radiopaque structures can be"moved" to give a clear image of the apex.

Locating Canals: Canal location is obviouslyessential to success. Standard and special tech-niques allow the practitioner to determine the po-sition of canals not located during access.

Differentiating Canals and Periodontal Lig-ament Spaces: Canals end in the chamber and atthe apex. A periodontal ligament space ends on asurface and in a furcation (molars) and demon-strates an adjacent lamina dura (Figure 9-2).

Evaluating Obturation: Length, density, con-figuration, and the general quality of obturationin each canal are determined.

RECALL

Ultimate success is verified at specified intervals ofmonths or years after treatment. Because failuresoften occur without signs or symptoms, radio-graphs are essential to evaluate periapical status."

Identifying New Pathosis: The presence andnature of lesions that have arisen after treatmentare best detected on radiographs. These lesionsmay be periapical, periodontal, or nonendodon-tic. Importantly, such lesions frequently present


13 3

with no overt signs or symptoms and are de-tectable only on radiographs (Figure 9-3).

Evaluating Healing: Pretreatment lesionsshould be resolving or should have resolved. In asuccessful (healed) treatment, restitution of gen-erally normal structures should be evident on re-call radiographs (Figure 9-4).

SPECIAL APPLICATIONS

Radiographs should be used to their maximumadvantage. There are alternative techniques thatgreatly enhance the ability to make an accurateand definitive diagnosis and to control treatmentprocedures. Although the techniques may be ap-plied to disciplines other than endodontics, thefollowing apply and are essential to diagnosis andtreatment.

Cone-Image Shift: Varying either the verticalor, particularly, the horizontal cone angulationfrom parallel alters images and enhances interpre-tation.'" These shifts reveal the third dimensionand superimposed structures. Shifts also permitidentification and positioning of objects that liein the facial-lingual plane.

FIGURE 9-3Failed root canal treatment because of missed root or canal.This mesial angled radiograph clearly shows the untreated

li ngual root (arrow). (Courtesy Dr. L. Wilcox.)Working Films

Essential for aid in treatment, working films areexposed when necessary but with discretion.

FIGURE 9-2This distal angulation shows the root surface outline (largearrow) and a periodontal ligament space (small arrow) withan adjacent lamina dura. The file is in the mesiobuccal canal(same lingual, opposite buccal [SLOB] rule).

FIGURE 9-4Same tooth as shown in Figure 9-3. Recall radiograph after9 months shows almost complete regeneration of bone, indi-

cating a healing lesion. A permanent restoration must beplaced as soon as possible. (Courtesy Dr. L. Wilcox.)

134


Radiographic Sequence

Radiographs are made in a recommended orderand number for each procedure. The minimumnumber are described here; special situations re-quire extra exposures.

DIAGNOSTIC RADIOGRAPHS

Number

The number of exposures depends on the situa-tion. For diagnosis in most cases, only a single ex-posure is necessary. A properly positioned film andcone (usually a parallel projection is best) permitsvisualization at least 3 to 4 mm beyond the apex.The initial diagnostic film is used primarily to de-tect pathosis and to provide general informationon root and pulp anatomy. Usually it is not neces-sary at this time to make additional films for iden-tification of extra canals; this will be accomplishedlater with shifted working length radiographs.

Frequently, several films are available for study,for example, if a full mouth survey has been taken.If other films are at hand, each will give a slightlydifferent view of the same tooth (Figure 9-5). Ex-amine that tooth on each film in which it appears.

indicate healing or nonhealing. Paralleling de-vices enhance reproducibility.

There may be special situations in which theparalleling technique is not feasible, such as a lowpalatal vault, maxillary tori, exceptionally longroots, or an uncooperative or gagging patient;these may necessitate an alternative techniques. Asecond choice is the modified paralleling tech-nique, and least accurate is the bisecting angle.

Angulation

Unquestionably, the most accurate radiographsare made using a paralleling technique. 13 The ad-vantages are, first, less distortion and more clarityand, second, reproducibility of film and coneplacement with preliminary and subsequent ra-diographs. Reproducibility is important when as-sessing whether changes occurring in the periapex

WORKING FILMS

Special situations require special considerations.Although the basic principles of doing everythingpossible to obtain the best quality radiograph arefollowed, there are definite limitations in makingworking films. These require cooperation by thepatient if they hold the film in position.

These radiographs are usually neither parallelnor bisecting angle. The technique used is calledmodified paralleling.14 Essentially, the film is notparallel to the tooth, but the central beam is ori-ented at right angles to the film surface. In en-dodontic working films, a further modification ismade by varying the horizontal cone angle. Spe-cific details of film and cone placement and filminterpretation are discussed later in this chapter.

Working Length: Generally, establishment ofworking length should require only a single expo-sure. If a root contains or may contain two super-imposed canals, either a mesial or distal angleprojection is absolutely necessary; the straight fa-cial view is not particularly helpful.'-' Additionalworking length films may be required later forconfirmation of working lengths to detect thepresence or lengths of newly discovered canals

FIGURE 9-5A, Facial projection of incisorssuggests a single canal and asingle root. B, Distal (canine)projection gives a different per-spective. The canals of the lat-eral and central incisors areseen to bifurcate in the middlethird of the root (arrow) and re-unite in the apical third.

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(Figure 9-6), or for reexposure if an apex has beencut off in the first radiograph.

Master Cone: The same principles used withworking length films apply. With proper tech-nique, only one radiograph is necessary to evalu-ate the length of the master gutta-percha cone.

Exposure and Film: As with diagnosticfilms, adequate clarity (and decreased exposure)is achieved by using an E film at intermediatekilovoltage." Clarity is particularly importantwhen trying to visualize the tips of files or smallapexes to determine working lengths. The F film,very recently introduced, requires 20% to 2S% lessexposure than E film. There are no studies yet asto quality and usefulness of this new film type.

Other Considerations: Additional workingfilms are often required. For example, they areuseful as aids in locating a canal or in determiningthe occurrence of procedural accidents (perfora-tions, separated instruments, or ledges). Varia-

tions in cone positioning and angulation aremade as required.

OBTURATION

The same basic principles used for diagnostic ra-diographs apply. At least a parallel projectionshould be made. It may be desirable to supple-ment this with an angled film to visualize separatesuperimposed canals for separate evaluation ofeach. The exposure factors used for diagnostic ra-diographs are duplicated for obturation. How-ever, the radiograph gives only a rough indicationof obturation length and quality.17,18

RECALL

The same principles used for diagnostic and ob-turation radiographs (parallel projection and ex-posure factors) apply to recall radiographs. There

FIGURE 9-6I dentifying and locating a canal. This incisor was rotated, requiring mesially angled working radiographs. A, The filei s off-center as indicated by the mesial root surface (arrows). Therefore, the file is in the facial canal. B, A search tothe lingual locates the lingual canal. There is a common canal apically.

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FIGURE 9-7A, The film is positioned parallel to the plane of the arch. The cone has the central ray (arrow) directed towardthe film at right angles. This is the basic cone-film relationship used for horizontal or vertical angulations. B, Therei s a clear outline of the first molar but limited information about superimposed structures (canals that lie in thebuccolingual plane). The arrow points to a periodontal ligament space adjacent to a superimposed root bulge, notto a second canal. (From Walton R: Dent Radiogr Photogr 46:51, 1 973.)

is one exception. If treatment is deemed to bequestionable or a failure, additional angled radio-graphs are often required to search for a previ-ously undetected canal or other abnormality.

Exposure Considerations

Proper x-ray machine settings and careful film pro-cessing are important for maximal quality and in-terpretative diagnostic and working radiographs.Both D (Ultraspeed) and E (Ektaspeed) films havebeen used and compared. Although D film hasbeen shown to have slightly better contrast, overallsuitability is equivalent between the two filmtypes.19 The newer Ektaspeed Plus film produces animage similar in quality to Ultraspeed film, but re-quires only half the radiation of Ultraspeed .z°

The optimal setting for maximal contrast be-tween radiopaque and radiolucent structures is70 kV. Exposure time and milliamperage should beset individually on each machine. Therefore, the pre-ferred film types are E and Ektaspeed Plus to mini-mize x-irradiation, at 70 kV to maximize clarity.

Cone-Image Shift

The cone-image shift reveals the third dimension.

PRINCIPLES

Image Shift

Superimposed Structures. The cone-image shifttechnique separates and identifies the facial andlingual structures.-' An example is the mesiobuc-cal root of a maxillary molar that contains two su-perimposed canals. The cone shift separates andpermits visualization of both canals.

Facial-Lingual Determination. Principles of rela-tive movement of structures and film orientationare applied to the differentiation of object posi-tion (Figures 9-7 and 9-8).

SLOB Rule

As the cone position moves from parallel, whethertoward the horizontal or toward the vertical, theobjects on the film shift away from the directionof the cone (or in the direction of the centralbeam). In other words, when two objects and thefilm are in a fixed position and the radiationsource (cone) is moved, images of both objectsmove in the opposite direction (Figure 9-9). Thefacial (buccal) object shifts farthest away; the lin-gual object shifts less. The resulting radiographshows a lingual object that moved relatively in thesame direction as the cone and a buccal objectthat moved in the opposite direction.21 This prin-


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FIGURE 9-8A, The horizontal angulation of the cone is 20 degrees mesial from the parallel, right angle position (mesial pro-

j ection). B, The resultant radiograph demonstrates the morphologic features of the root or canal in the third di-mension. For example, two canals are now visible in the distal root of the first molar. (From Walton R: Dent

Radiogr Photogr 46:51, 1973.)

FIGURE 9-9Central (x-ray) beam passing directly through a root containing two canals will superimpose the canals on the

fil m. When the cone is shifted to the mesial or distal aspect, the lingual object will move in the same direction asthe cone; the buccal object will move in the opposite direction (SLOB rule). (Courtesy Dr. A. Goerig.)

ciple is the origin of the acronym SLOB (same lin-gual, opposite buccal) (Figure 9-10).

One way to visualize this is to close one eye andhold two fingers directly in front of the open eye sothat one finger is superimposed on the other. Bymoving the head one way and then the other, theposition of the fingers relative to each other shifts.

The same effect is produced with two superim-posed roots (the fingers) and the way in which theymove relative to the radiation source (the eye) andthe central beam (the line of sight). When thecone-shift technique is used, it is critical to deter-mine what is facial and what is lingual. Otherwise,serious errors may occur.

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I NDICATIONS AND ADVANTAGES

Separation and Identification of Superim-posed Canals: This is necessary in all teeth thatmay contain two canals lying in a faciolingualplane.

Movement and Identification of Superim-posed Structures: Occasionally, a radiopaque ob-ject may overlie a root. An example is the zygo-matic process, which often obscures the apexes ofmaxillary molars.' Because this dense structurelies facial to the roots, a mesial shift of the cone"pushes" the zygoma distally (Figure 9-11). In ad-dition, a decrease in vertical angulation of thecone "pushes" the zygoma superiorly.

Determination of Working Length: Individ-ual superimposed canals may be traced from ori-fice to apex (Figure 9-12).

Determination of Curvatures: The SLOB ruleapplies. Depending on the direction of movementof the curvature relative to the cone, it can be deter-mine whether this curvature is facial or lingual. Theseverity of the curvature can also be determined.

Determination of Facial-Lingual Locations:The SLOB principle is applied to locating some-thing on a root surface or within a canal. One ex-ample might be the site of a perforation: to whichsurface does it extend, facial or lingual? Two ra-diographs at different horizontal angles readilydisclose this (Figure 9-13).

FIGURE 9-10The SLOB rule.

Identification of Undiscovered Canals

The SLOB procedure applies during access. Ananatomic axiom is that ifa root contains only a single

FIGURE 9-11A, Malar process of maxillary zygoma (arrow) obscures the apex and blocks the view of the obturation. B, Slightmesial shift of the cone "pulls" the lingually positioned root apex (arrow) to the mesial for visibility.


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FIGURE 9-12A, Mesial projection gives limited information about morphologic features and relationship of four canals. B, Cor-

rect distal projection for mandibular molars "opens up" roots. Mesial canals are easily visualized for their entire

l ength. The distal canal is a single wide canal because instruments are close and parallel.

FIGURE 9-13A, A perforation of the post preparation is indicated by the mesial lesion, although the perforation is not visibleon this facial projection. The perforation will be visible toward the buccal or lingual aspect; this will be revealedon an additional angled radiograph. B, The tip of the post has moved slightly distal on this mesial projection; theperforation is therefore located toward the buccal aspect (SLOB rule).

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FIGURE 9-14Technique for locating a canal missed during access preparation and searching of the chamber. A, Distal radio-graph with a single file in the mesial root shows the file skewed buccally. Therefore, another canal would be lo-

cated toward the lingual aspect. The vertical radiolucent lines (arrows) are periodontal ligament spaces of themesial root. B, A careful search toward the lingual aspect reveals the canal.

canal, that canal will be positioned close to the center of theroot. Ifa single canal is discovered initially on accesspreparation, an instrument is placed in the canal.Then a radiograph must be made either mesial ordistal because another canal may be present. If theinstrument is skewed considerably off center, an-other canal must be present (Figure 9-14). The lo-cation of the missed canal is determined by apply-ing the SLOB rule.

Location of "Calcified" Canals: This proce-dure also applies during access preparation. An-other endodontic anatomic axiom is that a root al-ways contains a canal. The canal may be very tiny, orit may be difficult or impossible to find or negoti-ate, but it is present. Also, canals are frequentlynot visible on radiographs. A single canal will liein the center of the root. Therefore, when search-ing for an elusive canal by penetrating progres-sively deeper with a bur, occasionally two workingradiographs must be made. One is made from thestraight facial view and the other from either themesial or distal view. The straight facial radio-graph gives the mesial-distal location of the burpenetration; the mesial or distal angled radio-graph indicates the facial-lingual angulation ofthe bur. The direction is adjusted accordingly to-ward the center of the root where the canal surelylies (Figure 9-15).

DISADVANTAGES

The cone-image shift has inherent problems andtherefore on occasion should not be used, or theangulation of the cone should be minimized.

Decreased Clarity: The clearest radiographwith the most definition is a parallel or modifiedparallel projection . 22 When the central beamchanges direction relative to object and film (pass-ing through the object and striking the film at anangle), the object becomes blurred. Distinctionsbetween radiolucent and radiopaque objects showless contrast. This blurred or fuzzy appearance in-creases as the cone angle increases; other struc-tures are more likely to be superimposed. There-fore, for maximum clarity, the cone angle shoulddeviate only to the extent necessary to obtain suf-ficient shift for interpretive purposes.

Superimposition of Structures: Objects thatordinarily have a natural separation on parallel ra-diographs may, with cone shift, move relative toeach other and become superimposed. One exam-ple is the roots of a maxillary molar. A parallel ra-diograph generally shows three separate roots andseparate apexes. A mesial or distal angled radio-graph moves the palatal root over the distobuccalor mesiobuccal root, decreasing the ability to dis-tinguish the apexes clearly (Figure 9-16). Anotherexample is an increase in the vertical angulation


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FIGURE 9-15Location of a canal that has undergone severe calcific metamorphosis. Initial searching is done without a rubberdam. A, A small, receded canal and missing crown make orientation and canal search difficult. B, Facial radio-graph taken during access shows that preparation is mesial to the canal. (Remember, the canal occupies the cen-ter of the root.) C, Mesial radiograph shows that access is also misdirected to the buccal aspect; the canal willbe centered (arrow). Therefore, the subsequent search must be to the distal and lingual aspects. D, On redirect-i ng the bur, the single canal is discovered in the center of the root. Now the rubber dam is placed.

of the cone in the maxillary incisor region; thismay "pull" the apexes "into" the radiodense ante-rior nasal spine.

Endodontic RadiographicAnatomyINTERPRETATION

Radiographs can be termed "the great pre-tenders"-they often are as misleading as they are

helpful.23,24 There is a definite tendency to try to

extract more information from a radiograph thanis present. The practitioner must remember thatonly hard tissues, not soft tissues, are visible.

LIMITATIONS

Studies of interpretation of bony lesions haveshown that considerable bone must be resorbedbefore the lesion is clearly visible.25 ,26 This, ofcourse, varies with root location and thickness ofthe overlying cortical bone. In most regions, aperiradicular lesion tends to be most evident ra-diographically if cortical bone has resorbed.

FIGURE 9-16A, Facial parallel projection shows maximum clarity on the first molar. B, Mesial shift of 30 degrees reduces con-trast and the distinction between radiopaque and radiolucent objects. Also, roots are now superimposed, makinginterpretation more difficult.

However, resorption of only medullary bone maybe sufficient for visualization. 27,28 In either case, aperiradicular inflammatory lesion must be welldeveloped and fairly extensive before an obviousradiolucency can be seen.

Differential DiagnosisENDODONTIC PATHOSIS

Radiolucent Lesions

These have four distinguishing characteristicsthat aid in differentiating them from nonen-dodontic pathoses (Figure 9-17):

1. Apical lamina dura is absent, having beenresorbed.

2. A "hanging drop of oil" shape is characteris-tic of the radiolucency. This is a generaliza-tion because these lesions may have a varietyof appearances.

3. The radiolucency "stays" at the apex regard-less of cone angulation.

4. A cause of pulpal necrosis is usually (butnot always) evident.

The ultimate differentiation is not the radio-graph but the pulp test. If a developed, sizable radi-olucency is an endodontic lesion, it must result froma necrotic (and therefore nonresponsive) pulp.

Radiopaque Lesions

These lesions are better known as condensing os-teitis or, synonymously, focal sclerosing osteomy-

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FIGURE 9-17Characteristics of apical radiolucency strongly suggest en-dodontic pathosis. Lamina dura is not present, and the lesionhas a "hanging drop of oil" appearance. The cause of pulpalnecrosis is also evident.


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FIGURE 9- 18Condensing osteitis. There is diffusenessand a concentric arrangement of in-creased trabeculation around the apex.Close inspection shows a radiolucent le-sion at the apexes also.

elitis. Such lesions have an opaque diffuse appear-ance; histologically they represent an increase intrabecular bone. 29 The radiographic pattern is oneof diffuse borders and a roughly concentricarrangement around the apex (Figure 9-18). Pulpalnecrosis and a radiolucent inflammatory lesionmay or may not be present. Frequently, condensingosteitis and apical periodonritis are present to-gether. The pulp is often vital and inflamed.

NONENDODONTIC PATHOSIS

Radiolucent Lesions: These are varied but infre-quent. Bhaskar, in his oral pathology handbook,30lists 38 radiolucent lesions of the jaws, 35 ofwhich are nonendodontic and have a variety ofconfigurations and locations. Importantly, manyare positioned at or close to the apexes and radi-ographically mimic endodontic pathosis. Again,the pulp test provides the cardinal differentiation-nonendodontic lesions are associated with a re-sponsive tooth.

Radiopaque Lesions: Frequently interpretiveerrors are made in identifying radiopaque struc-tures located in the apical region of the mandibularposterior teeth. Unlike condensing osteitis, theseare not pathologic and have a more well-definedborder and a homogeneous structure. They are notassociated with pulpal pathosis (Figure 9-19).

ANATOMIC STRUCTURES

Several anatomic entities are superimposed on ormay be confused with endodontic pathosis. Al-though most radiology courses cover identificationof these structures, it is not uncommon for a prac-titioner to fail to identify these normal structureswhen there is an existing or suspected endodonticproblem. Common sources of confusion are the

FIGURE 9-19Enostosis (or sclerotic bone) is represented by the dense, ho-mogeneous, defined radiopacity. This is not a pathosis and iscommon in the posterior mandible near the apexes, althoughit may occur in any region. This radiodense area would haveappeared on earlier radiographs.

areas created by sparse trabecular patterns, particu-larly in the mandible. Another problem area is theapical region of the maxillary anterior teeth. Onemust remember to look through these radiolucenciesfor an apical lamina dura.

Mandible: The classic example of a radiolu-cency that may overlie an apex is the mental fora-men over a mandibular premolar.31 This is easilyidentified by noting movement on angled radio-graphs and by identifying the lamina dura (Fig-ure 9-20). 32

Maxilla: This region contains several struc-tures (both radiolucent and radiopaque) that maybe confused with endodontic pathosis. Examplesare the maxillary sinus, incisive canals, nasal fossa,

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FIGURE 9- 20A, Radiolucent area over the apex could be mistaken for pathosis. B, Pulp testing (vital response) and a more dis-tal angulation show the radiolucency to be a buccally placed (SLOB rule) mental foramen.

FIGURE 9-21Bitewing radiograph shows importantfeatures clearly: relationship of bone togingival extent of caries (arrow) aswell as depth of caries and restora-tions relative to the pulp (arrows).(Courtesy Dr. C. Koloffon.)

zygomatic process, and anterior nasal spine.Again, characteristics of the structure as well aspulp responsiveness to tests are important in dif-ferentiation.

Special TechniquesBITEWING PROJECTIONS

Although not truly a "special technique," bite-wing projections are often helpful in diagnosisand treatment planning. The relationships of

film, cone, and tooth give a more consistent par-allel orientation (Figure 9-21).

FILM-CONE PLACEMENTFilm Selection

Posterior packet film should be used for every pro-jection in all patients except children. The anterior(narrow) films are unnecessary and in fact are fre-quently not wide enough to pick up an apex on anangled radiograph. Use of wider packet film obvi-ously requires special placement for anterior pro-


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FIGURE 9-22Narrow palate requires placement of posterior packet filmdistally. Note that the superior edge of the film is distal to thetuberosities.

FIGURE 9-23A hemostat is used for grasping the film and as a cone posi-tioning and orientation device.

jections (Figure 9-22). The film type recommendedfor diagnostic radiographs is E (Ektaspeed) film.16

Film Holders

There are devices or special adaptations of paral-leling devices that can be used for endodonticworking films. 33 However, with some practice,nothing is more effective than a hemostat forease and adaptability. The hemostat also is con-veniently placed and sterilized in a kit with otherinstruments. The hemostat handle aligns thecone in both the vertical and horizontal planes(Figure 9-23). Having the patient hold the filmwith direct finger pressure is discouraged. This isawkward and frequently results in a bent filmwith a distorted radiographic image (Figure 9-24).The film surface must remain flat!

The hemostat-held film is placed by the opera-tor. Then the patient holds the hemostat in thesame position. The cone is aligned parallel to thehemostat in the frontal plane (vertical angula-tion) (Figure 9-25) and at 90 degrees to the handle(horizontal plane) (Figure 9-2G). Because the han-dle is at an angle of 90 degrees to the film surface,the central beam strikes the film at the same90-degree angle. This is the modified parallel tech-nique because the film is often not parallel to thetooth. However, with the modified parallel tech-nique, distortion is minimal and is not significantin working radiographs. 14

FIGURE 9-24Pressure on film often causes bending, producing a distortedi mage. This bent film "stretches" the apical half of the root, mak-i ng accurate interpretation and length determination impossible.

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FIGURE 9- 25Vertical angulation of the cone is set byaligning the long axis of the cone (arrow)with the end of the hemostat handle.

FIGURE 9-26Horizontal angulation is determined bylooking down from the top of the pa-tient's head. The position is set by align-i ng the long axis of the cone (centralbeam) 90 degrees (arrow) to the longaxis of the hemostat handle (line). Mesialand distal horizontal angulations arethen varied accordingly.

Film Placement

Usually films are positioned in the standard peri-apical projection. However, there are exceptions.Because of the film width and the relative narrow-ness of the arches, maxillary and mandibular an-terior projections require film placement fartherposteriorly.

In the maxillary posterior region, particularlywhen imaging molars, the film is placed on theside of the median raphe opposite the teeth to beradiographed. This has the effect of positioningthe top of the film in a more superior position rel-ative to the apexes (Figure 9-27).

In the mandibular posterior region, the filmis positioned toward the midline (under thetongue). Also, if the mouth is closed slightly, themylohyoid muscle relaxes and permits the filmto drop inferiorly.

The rubber dam frame is not removed duringfilm placement. A lower corner or edge of the rub-ber dam is released to allow insertion and posi-tioning of hemostat and film (see Figure 9-25).

Cone Alignment

Indicated cone positions (Figures 9-28 and 9-29)(facial, mesial, or distal) are as follows.

Facial. Maxillary anterior teeth rarely havemore than a single root and a single canal; onlya facial (straight-on) projection is required. Thisis also true for maxillary molars unless a secondmesiobuccal (mesiolingual) canal is detectedand negotiated during access. The straight facialprojection provides maximum resolution andclarity (which is difficult at best with maxillarymolars).


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FIGURE 9-27Positioning the film on the opposite side ofthe median raphe has the effect of "pulling"the upper edge of the film more superior rel-ative to the apexes.

FIGURE 9-28Correct film-cone placement on themandible.

FIGURE 9-29Correct film-cone placement on the maxilla.

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Mesial. The mesial projection is indicated formaxillary and mandibular premolars and formandibular canine teeth. A mesial projection isused for maxillary molars with a mesiolingualcanal.

Distal. The distal projection is used formandibular incisors and mandibular molars. Thedistal is preferred to the mesial projection formandibular molars because of the relative posi-tion of the canals. Generally, the distal angle moreeffectively "opens up" the mesial root.

To summarize, angled working radiographsare made for maxillary premolar and molars witha mesiolingual canal and for all mandibularteeth. The maxillary projections are mesial andthe mandibular projections are: incisor-distal;canine-mesial; premolar-mesial; and molar-distal. An acronym for the cone angles on themandible is DMMD.

RAPID PROCESSING

Different techniques and special solutions areavailable for fast processing (less than 1 minute)of working films and may be of benefit for speedviewing. If these rapid processing techniques areused, films may not retain their quality with timeunless they are thoroughly fixed and washed.34Therefore, if a film is to be processed rapidly, adouble-packet film should be used, with the du-plicate processed in the routine manner.

ers magnify the image and block out peripherallight (Figure 9-30). This enhances the readabilityand interpretation of the film. 35 Other techniquesor adaptations are also useful, such as a standardmagnifying glass and small slide viewers.

New TechnologyNew approaches to radiography have been and arebeing developed. These are unique; some will im-prove existing techniques in addition to decreas-ing the radiation dose to patients. This new tech-nology includes digital radiography, digitalsubtraction radiology, and tomography.36-38

These systems are of considerable interest, of-fering the advantages of reduced radiation to thepatient, increased speed of obtaining the image,ability to be transmitted, computer storage andenhancement, and a system that does not requirea darkroom or x-ray processor.39 However, thesesystems generally show no superiority to conven-tional radiographs for diagnosis or for workingfilms.40-43 Furthermore, computer-image enhance-ment does not seem to improve diagnostic inter-pretation significantly. 44,45

Ease of use and cost are factors that currentlypreclude routine use of these systems in the gen-eral dental office. Endodontists, however, require

VIEWERS

There are several types of radiographic viewers,both commercial and adapted. Commercial view-

FIGURE 9-30Magnifier-viewer blocks out peripheral light for better con-trast. Contained within is a lens that magnifies the imagefour times.

FIGURE 9-31A digital imaging workstation for the dental operatory. Thesystem integrates filmless digital images with an intraoralcamera into a standard PC. (Courtesy Trophy USA.)

9 I Endodontic Radiography

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many working films and are finding the speed andversatility of digital radiography to be useful. Ascosts decrease and technology improves, there isno doubt that these or similar devices will comeinto more common usage by all groups of practi-tioners. This includes some very elaborate equip-ment that combines digital radiography and in-traoral photography (Figure 9-31).

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38. Kullendorf B, Grondahl K, Rohlin M, Nilsson M: Sub-traction radiology of interradicular bone lesions, ActaOdontol Scand 50:259, 1992.

39. Baker W, Loushine R, West L, et al: Interpretation ofartificial and in vivo periapical bone lesions comparingconventional viewing versus a video conferencing sys-tem, J Endod 26: 39, 2000.

40. Borg E, Kallqvist A, Grondahl K, et al: Film and digitalradiography for detection of simulated root resorp-tion cavities, Oral Surg Oral Med Oral Pathol 86:110,1998.

41. Holtzmann D, Johnson W, Southard T, et al: Storage-phosphor computed radiography versus film radiogra-phy in the detection of pathologic periradicular boneloss in cadavers, Oral Surg Oral Med Oral Patbol 86:90,1998.

42. Sullivan J, Di Fiore P, Koerber A: RadioVisiography inthe detection of periapical lesions, JEndod 26:32, 2000.

43. Burger C, Mork T, Hutter J, Micoll B: Direct digital ra-diography versus conventional radiography for esti-mation of canal length in curved canals, J Endod25:260, 1999.

44. Kullendorff B, Petersson K, Rohlin M: Direct digitalradiography for the detection of periapical bone le-sions: a clinical study, Endod Dent Traumatol 13:183,1997.

45. Scarfe W, Czerniejewski W, Farman A, et al: In vivo ac-curacy and reliability of color-coded image enhance-ments for the assessment of periradicular lesion di-mensions,. Oral Surg Oral Med Oral Patbol Oral Radiol

Endod 88:603, 1999.

Endodontic Instruments

LEARNING OBJECTIVES


1 / Define a basic set of instruments appropriate for these procedures: diagnosis, emergency treatment, canal

preparation, obturation, and bleaching.

2 / Describe the general physical properties of endodontic instruments and show how these characteristics

are related to their use.

3 / Describe the design (longitudinal, cross-sectional, and tip configuration) of the more common canal

preparation instruments and their mode of use.

a / Explain the basis for sizing and taper (standardization) of hand-operated instruments.

s / Describe proper use of instruments to prevent breakage within the canal.

6 / Recognize visible changes in instruments that will predispose to breakage.

7 / Describe techniques used for sterilization and disinfection of instruments.

s / Select appropriate sterilization methods for each instrument type.

9 / Identify procedures and chemicals that might cause deterioration of files and how to recognize that

deterioration.

10 / Describe and differentiate between conventional files and files of alternative designs.

11 / Define the differences between stainless steel and nickel titanium intracanal instruments including both

physical properties and usage characteristics.

12 / Describe the action and use of rotary instruments for both cleaning and shaping canals.

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15 2

10 / Endodontic Instruments

Physical Characteristics

I nstrument Fabrication

Hand-Operated Instruments

Physical Properties

Standardization

Variations

Engine-Driven Instruments

I ntracanal Usage

Hand Instruments

Rotary Instruments

Obturation

Lateral Condensation

Vertical Condensation

Adjunctive Instruments

Diagnostic Instruments

I nstruments Unique to Root Canal Treatment

Sterilization and Disinfection

Sterilization

Disinfection

I nstruments for Different Procedures

Examination

Cleaning and Shaping

Obturation

Emergency

Bleaching

n considering endodontic instru-ments, those that are hand-operated(such as files and reamers) are the most

important. However, other specialized instruments,such as explorers and excavators, have been de-signed to adapt to root canal treatment require-ments. Originally, instruments for root canal treat-ment were few in number and crude in design.` Theearliest hand-operated devices had long handlesthat were best suited for preparation of anteriorteeth. As root canal treatment diversified, smaller"finger" instruments were developed for posteriorteeth. In addition to being more adaptable, theseprovided improved tactile sense for the operator.'New designs in endodontic instruments have beenintroduced, and will continue to evolve.

This chapter reviews the types of metals usedas well as important aspects of the physical prop-erties and usage characteristics of endodontic in-struments. A basic armamentarium will be de-scribed for each procedure as well as systems foreffective sterilization. Detailed information aboutall aspects of manufacturing and testing of intra-canal instruments is beyond the scope and intentof this chapter. However, certain essential facts, asidentified in the learning objectives, will be pre-sented to enable effective use (and not abuse) ofthese instruments.

The nomenclature follows the recommenda-tions of the international Organization for Stan-dardization (ISO):

1. Hand-operated include K-type reamers andfiles, broaches, Hedstrom-type files, andso on.

2. Engine-driven are hand types that have alatch that inserts into a slow-speed hand-piece. These include rotary (Gates-Gliddenand Peeso) engine-driven reamers and filesand reciprocating files or reamers.

3. Ultrasonic and sonic are diverse in design.Some resemble barbed broaches, some re-semble files, and others are diamond-coated wires. All insert into a dedicated vi-bratory handpiece that energizes theinstrument. These are further described inChapter 13.

4. Nickel titanium has been adapted both for bandinstruments and rotary applications. Severaldesigns have developed. Both hand- andengine-driven instruments have variousconfigurations. The cross section of the in-struments takes many shapes.

In addition to canal preparation, other hand-operated instruments are adapted for other as-pects of root canal treatment, for example, canalidentification and obturation.


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FIGURE 10-1Longitudinal and cross-sectionalshapes of various hand-operatedi nstruments. (Those marked withan asterisk are brand names.)Note that small sizes of K-reamers,K-files, and K-Flex* have a differentshape than the larger sizes.

Physical Characteristics

To debride a region of the canal space completely,the instrument must contact and plane all walls.'Despite continual improvements in design andphysical properties, there are still no instrumentsthat totally clean and shape all root canal spaces.Irregular canal spaces do not correspond to andcannot always be well prepared by an instrumentwith a regular (round) shape. In addition, stain-less steel instruments are relatively inflexible,which renders them not particularly adaptable tocanal curvatures. Nickel-titanium instrumentsare more flexible and adapt more readily to fine,curved canals' but have no advantage over stain-less steel files in irregular canal spaces .s' These in-congruencies between reality and ideal shape re-quire judicious and skillful use of canalpreparation instruments to maximize debride-ment and to avoid procedural errors.

INSTRUMENT FABRICATION

A hand-operated reamer or file begins as a roundwire that is modified to form a tapered instru-ment with cutting edges. The instrument is usedwith a twisting (reaming) or pulling (filing) mo-tion in an attempt to produce clean, smooth, sym-metrical canal walls. However, the prepared canalis rarely round when viewed in cross section.

Several factors inherent in the stainless steelwire that hand-operated instruments are madefrom have to be considered. How is adequate flexi-bility maintained without instrument fatigue?How much abuse can these files endure before fa-tigue and failure ensue? How does the operatorknow when the file has been fatigued to a criticalpoint? And finally, how does an operator maintainan efficient cutting edge while at the same timeavoid cutting new, nonanatomic canal spaces?

With nickel-titanium files, these same ques-tions must be addressed. These instruments havedifferent physical properties and different usagecharacteristics. Importantly, they can also fatigueand separate when used incorrectly or overused.

HAND-OPERATED INSTRUMENTS

Several cross-sectional shapes of files are commer-cially available (Figure 10-1). Two techniques formanufacturing these instruments have beendeveloped.

Machined

This technique involves machining (grinding)the instrument directly on a lathe; an example isthe Hedstrom-type file (Figure 10-2). All nickel-titanium instruments are machined.

Some manufacturers produce K-type filesusing the machined (lathe-grinding) process (Fig-ure 10-3). This change from the grinding andtwisting manufacturing process results in differ-ent physical and working properties from theoriginal K-type file.$ ,9 For instance, the machinedfile has less rotational resistance to breakage thana ground-twisted file of the same size. 9

Ground-Twisted

Another technique consists of first grinding, thentwisting. Raw wire is ground into tapered geomet-ric blanks; (square, triangular, and rhomboid)(Figure 10-4). The blanks are then twisted coun-terclockwise to produce helical cutting edges.These are K-type files and reamers. K-type fileshave more twists per millimeter of length than thecorresponding size of K-type reamer. Both have apyramidal tip (7S ± IS degrees) that is producedby grinding after twisting.

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1 0 / Endodontic Instruments

FIGURE 10-2Hedstrom file, machined by rotating a wire on a lathe. Notethe spiral shape. These are efficient cutters (on the pullstroke) but are more susceptible to separation when lockedand twisted.

FIGURE 10-3A and B, A machined K-type file. Note that the transitionangle at the leading cutting edge of the tip is rounded, ren-dering it noncutting.

Clinical Use

Besides their configuration, the difference betweenfiles and reamers is their intended use. Files aremanipulated with a rasping, or push-pull planing,motion. This motion is more efficient when thereare many flutes or spirals on the instrument shaftmaking contact with the canal walls; the flutes areat right angles to the long axis. Reamers aretwisted and withdrawn; therefore, cutting takesplace during rotation. This motion is most effi-cient with a cutting edge that more closely paral-lels the instrument shaft. Reamer configuration iscreated by imparting fewer twists, resulting in in-creased flute spacing; this tends to prevent clog-ging of the cutting edge.'° Files can be both filedand reamed; reamers can only be reamed. Becausethey are less versatile, reamers are seldom used.

FIGURE 10-4Ground-twisted instruments. A, A square file blank groundfrom wire. After twisting counterclockwise, the appearance ofa file (more flutes) (B) and reamer (fewer flutes) (C).

PHYSICAL PROPERTIES

Materials researchers and manufacturers have cer-tain theories or hypotheses about file properties,such as "Flexibility is increased by increasing thelength or decreasing the cross-sectional diameter"


155

and "The more acute the cutting angle, the moreefficient a blade is in removing a substance."" ,"These theories are more applicable to the labora-tory than to the clinical situation. Because ofbench-top research, certain important limits tospecific physical properties have been identifiedand incorporated into a series of standards for themanufacture of hand-operated instruments.However, clinical behavior may not directly relateto such in vitro testing.

Standards for K-type files and reamers were firstpublished in 1976 as American Dental Association(ADA) specification No. 28. 13 These standards weredeveloped specifically for hand-operated instru-ments used in the canal. Therefore, standards wereestablished for fracture resistance by twisting, stiffnessof the files and reamers, and corrosion resistance. Inaddition to physical characteristics, these stan-dards established dimensions as well as acceptabletolerances in manufacturing.

Flexibility, sharpness, and corrosion resistanceare properties related to metal and design. Tradi-tional metals have included stainless or carbonsteel. Compared to stainless steel, many carbonsteel instruments have been shown to cut some-what more efficiently"; they are similar in otherrespects. However, carbon steel is little used be-cause it is more susceptible to corrosion by auto-claving and irrigating solutions."

By changing the cross-sectional design fromsquare to triangular or rhomboid and decreasing thenumber of flutes per millimeter, greater flexibility isgained. Blank nickel-titanium wire is even moreflexible. Nickel-titanium alloy possesses a modulusof elasticity that is one-fourth to one-fifth that ofstainless steel, allowing a wide range of elastic defor-mation. 16 An advantage of this increased flexibilityis that a file follows the canal curvature with less de-formation (transportation) during enlargement. Adisadvantage of the increased flexibility is the inabil-ity to precurve the file for introduction into canalsof posterior teeth when there is a decreased interoc-clusal opening. Another disadvantage is that cuttingefficiency of nickel-titanium files may be reducedwith clinical usage compared with stainless steel be-cause of the greater elasticity. Therefore to best uti-lize the properties offered with nickel-titanium files,engine-driven configurations have been developed.All of the present nickel-titanium instruments in-corporate a U shaped groove with a flat land area.When the instrument is rotated, the flutes will planethe canal wall while the land area keeps the instru-ment centered, primarily in fine, curved canals.

among different brands as to taper or tip configu-ration. ADA specification No. 28 established stan-dards for instrument taper, tip geometry, and sizecriteria for 19 different sizes of instruments as wellas acceptable tolerance of manufacturing error."Also implemented was a color code for instrumenthandles for identification and an additional filesize (No. 06). 1 ' In 1982, ADA specification No. 58standardized and established the minimal physi-cal criteria for Hedstrom files. 18 The most recentrevisions of ADA specifications No. 28 and No. 58were published in 1989. These further clarifiedminimal physical criteria and added newer criteriafor plastic handle retention on files.l 9 To date, nostandards have been developed for nickel-titaniumor the lathe-cut K-type instruments.

Despite specific size and shape requirements,hand-operated instruments do not demonstrate re-liable and consistent dimensional standardization."

Lengths

Files and reamers are available in three shaftlengths: 21, 25, and 31 mm. Shorter instrumentsafford improved operator control and easier ac-cess to posterior teeth, to which limited openingimpairs access. The 25- and 31-mm instrumentsare used for longer roots.

Sizing

Dimensions of K-type files and reamers are desig-nated according to the diameters of the instru-ment at specified positions along its length (asstated in ADA specification No. 289) (Figure 10-5).File tip diameters increase in 0.05-mm incrementsup to the size 60 file (0.60 mm at the tip), and thenby 0.10-mm increments up to size 140. The diam-eter at the tip of the point is known as Do . The spi-ral cutting edge of the instrument must be at least16 mm long, and the diameter at this point is Dl ,.The file diameter increases at a rate of 0.02 mm perrunning millimeter of length.

Another "standard" introduced by one of thenickel-titanium rotary series (Profile)is a 29% con-stant increase in tip diameters between sizes; eachfile tip increases by a constant percentage ratherthan the random increases seen in ISO sizing.

The nickel titanium rotary instruments haveother variable tapers of 0.04 and 0.06. For everymillimeter of length, the diameter increases by 0.04or 0.06 mm. These greater tapers make these moreaggressive in creating marked flaring preparation.

STANDARDIZATION Tip Design

Original (conventional style) K-type files wereavailable in only six sizes with no uniformity

Originally the tip angle of K-type files and ream-ers was approximately 75 degrees plus or minus

156


FIGURE 10-5The specifications for standardiza-tion of files and reamers.

15 degrees (see Figure 10-1). This design was in-tended to provide cutting efficiency without an ex-cessively sharp transition angle. Newer designshave different tip angles and designs in an attemptto minimize canal alterations. Some machinedK-files incorporate a so-called nonaggressive tip ornoncutting tip (see Figure 10-3) to provide lessdentin cutting by reducing the sharp tip transitionangle. The flexible file type (Flex-R) has a conicalnoncutting file tip with a tip angle of 70 degreesand a guiding collar angle of 35 degrees. The in-tent is to guide the file through the curve ratherthan cutting only the outer canal wall. 21,22

Another modification in file design is theLightspeed. Unlike other instruments that haveseveral millimeters of cutting or planing area, thisnickel-titanium instrument has a cutting area ofabout 3 mm. The tip is noncutting and looks sim-ilar to a small Gates-Glidden drill. (A further de-scription of the Lightspeed instrument is foundunder "Unique Designs").

Torsional Limits

less plastic deformation before failure occurs.'Therefore, this tendency toward less visible defor-mation before separation requires more cautionwith the use of machined files to avoid instru-ment failure. 9

Under test conditions, the nickel-titanium files(all are machined) have increased resistance to frac-ture compared with stainless steel files . 23 OnlyLightspeed instruments have incorporated a desig-nated separation point at 18 mm to allow for re-trieval of broken instruments. The ADA and ISOare presently working on new torsionalz4 standardsfor all nickel-titanium and stainless steel rotary in-struments." Nickel titanium metal may have ad-vantages over stainless steel, although these advan-tages have not been conclusively demonstrated inclinical usage or in clinical trials . 6,16

Color Coding

Color coding of file handles designates size. Colorcoding of the newer nontraditional instrumentsvaries according to the manufacturer.

Torsional limit is the amount of rotational torquethat can be applied to a "locked" instrument to thepoint of breakage (separation). Obviously, an in-strument should have sufficient strength to be ro-tated and worked vigorously without separating inthe canal. Standards for steel hand-preparation in-struments were established for rotational limits(point of breakage) at various forces. Smaller in-struments (less than size 20) can withstand morerotations without breaking than larger (greaterthan size 40) instruments.

Machined K-type files have different physicaland working properties than ground-twisted files.There is no difference in torsional strength be-tween ground-twisted and machined files. How-ever, machined files are weaker, demonstrating

VARIATIONS

Broaches: Barbed broaches are stainless steel in-struments with plastic handles. The tapered wirebroach is barbed by scoring and prying a tag ofmetal away from the long axis of the wire (Fig-ure 10-6). Barbs entangle and remove canal con-tents. This instrument should be neither bound inthe canal nor aggressively forced around a canal cur-vature. Either action may cause the barbs to engagethe canal wall, preventing the broach from being re-moved intact or fracturing. Barbed broaches shouldnot be reused. Single barbed broaches are availablein presterilized bubble packaging.

Unique Designs: An innovative nickel-titaniuminstrument, the Lightspeed (Figure 10-7), has been

FIGURE 10-6Barbed broach showing the barbs pulled away from the in-strument shaft.

recently introduced that incorporates three distinctfeatures: a noncutting pilot tip, a small fluted area,and a small flexible shaft. Both hand-operated andengine-driven instruments are available. These in-struments tend to stay centered in curved canals ifused properly.ZS Although interesting, these havenot been shown to be superior to conventionalhand instruments and are prone to separation ifoverused. 26,27

ENGINE-DRIVEN INSTRUMENTS

Rotary Instruments: Some preparation tech-niques require slow-speed rotary instruments tofacilitate preparation, primarily in establishingstraight-line access (Figure 10-8), although engine-driven reamers and files for cleaning and shapingare also marketed. Most common are Gates-Glidden drills and Peeso reamers. Table 10-1shows the comparative ISO sizes of both Gates-Glidden drills and Peeso reamers.

Gates-Glidden drills and Peeso reamers aremade from either carbon or stainless steel. Carbon

FIGURE 10-7I nnovative file design of the rotary nickel-titanium Lightspeedi nstrument. The end of the instrument does the work; thenoncutting tip and the small flexible shaft tend to stay cen-tered during preparation of the canal.


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FIGURE 10-8A, Gates-Glidden drill. Note the noncutting tip and the ellip-tical shape. B, Peeso reamer. Note the noncutting "safe" tipand parallel sides. These are stiffer and more aggressive thanthe Gates-Glidden drill. Both can be used for straight-line ac-cess preparation.

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FIGURE 10-9Nickel-titanium rotary files of varying design. A, 0.04 andgreater tape (GT) titanium files (Profile). B, Quantec files byAnalytic; note the aggressive taper of the file on the bottom.

steel has inferior properties, particularly lessstrength, and therefore should not be used. Corro-sion is not a problem with stainless steel, butdulling occurs with sterilization procedures andrepeated usage.

Gates-Glidden Drills: These drills are ellipti-cally (flame) shaped burs with a latch attachment.Gates-Glidden drills are used to open the orifice.They also achieve straight-line access by removingthe dentin shelf and rapidly flaring the coronaland middle third of the canal.

Gates-Glidden drills are designed to break highin the shank region. This allows easier removal ofthe broken instrument from a tooth; fracture nearthe cutting head may block a canal. No ADA spec-ification exists for torsional failure of rotary in-tracanal instruments, but Gates-Glidden devicesusually do fracture where intended . 28,29 Impor-tantly, these drills must be continuously rotated.If they stop, the head may lock in the canal, withtorsional failure and fracture. Gates-Gliddendrills are available in 15-and 19-mm lengths. Theshorter instruments are helpful in posterior teeth,where access to the canal orifice is limited.

Peeso Reamers: These reamers are also used asadjunctive devices in canal preparation. They arebasically similar to Gates-Glidden drills but haveparallel cutting sides rather than an ellipticalshape. These instruments are available with orwithout safe tips. Peeso reamers have been sug-gested as a means of improving straight-line ac-cess, although they are less well controlled thanGates-Glidden drills . 3° Both types are aggressiveand can rapidly overenlarge the canal.

Rotary Flaring Instruments

Engine-Driven Reamers: These instrumentsare used for cleaning and shaping. The traditionaltypes are of stainless steel. Because of theirrelative stiffness, they are difficult to control andgenerally create irregular, poorly debrided prepa-rations, particularly in curved canals. These ag-gressive instruments also generate large amountsof debris, which packs apically. Their use is notrecommended.

Engine-Driven Nickel-Titanium Files: Nickel-titanium engine-driven files allow greater control intiny, curved canals. These instruments do not havea cutting end and have less tendency to transportthe apical preparation .31,32 The files are available in avariety of shapes and designs (Figure 10-9). Utiliza-tion of these instruments by dental students intechnique laboratories have demonstrated fewerpreparation errors than with use of stainless steelinstruments in the same courses. 33-3 s

I ntracanal UsageHAND INSTRUMENTS

Broaches: Removal of pulp requires a broach thatwill not bind and yet is large enough to ensnarethe tissue. Binding should be minimized becauseof possible breakage.

Reamers and Files: Two types of motion(Figure 10-10) are common in root canal prepa-ration, reaming and filing." Reaming consists ofrotating the instrument clockwise and scribingan arc from one cutting edge to the next. For ex-ample, a triangular reamer has three 60-degreecutting edges and therefore requires 120 degreesof rotation (one-third of a turn), whereas a filewith a 90-degree angle necessitates only a quar-ter turn before withdrawal. Rhomboidal filesrequire a 180-degree turn to make an edge-to-edge arc.

Filing requires a series of repetitive motions.First, the instrument is advanced to its full


15 9

FIGURE 10-10Filing and reaming motions. Tooth structure is removed pri-marily on the pull stroke with filing and on rotation withreaming.

FIGURE 10-11Defects created during instrumentation. Each file shownmust be discarded because of possible breakage. A, Unwind-ing of the flutes. B, "Roll-up" of the flutes. C, Unwound andbent instrument.

length into the canal space using a passive "twid-dling" (teasing without planing) motion. Next,the file is rotated (a quarter turn or more) andthen withdrawn from the canal space while thetip is pushed against a canal wall, much as apaintbrush is applied to a wall when painting.The twiddling, reaming, and withdrawal mo-tions are repeated with the file tip pushedagainst a different portion of the canal wall oneach outstroke until all walls have been planed(circumferential filing).

Hedstrom and similar design (S or U) files areused only with a filing motion because they haveless torsional resistance to breakage. In otherwords, Hedstrom-type files are more prone to sep-aration because of the decreased cross-sectionaldiameter of equivalent-sized instruments. Also,their design does not facilitate reaming.

Avoidance of Instrument Separation: Sepa-ration of hand files in the canal is prevented byregularly inspecting the instrument for defects(Figure 10-11) such as (1) unwinding of theflutes (twisting clockwise and opening of theflutes); (2) roll-up of the flutes (excessive contin-ued clockwise twisting after unwinding); (3) tipdistortion (the tip has been bent excessively);and (4) corrosion. If an instrument exhibits anysigns of wear, it should be discarded immedi-ately. Prevention is the key to avoiding untimelyinstrument separation.

ROTARY INSTRUMENTS

All of the engine-driven nickel-titanium files relyon rotational motion only and therefore have areaming action.

Avoidance of Instrument Separation

The manufacturer of the nickel-titanium 0.04and 0.06 mm taper rotary files suggest usingthem in high-torque slow-speed handpieces thatrotate at 150 to 300 rpm. The number of canalsthat can be prepared with a nickel-titanium in-strument varies from 4 to 16, depending on thesize and curvature of the canals and pressureused with the files. The smaller and more curvedthe canal, the more wear and tear on the instru-ment. All manufacturers suggest discarding thefiles if any deformation occurs. Recent studieshave suggested that lower speeds reduce the like-lihood of instrument fracture . 37-39 Figure 10-12shows instrument fatigue and "roll-up" andbreakage of nickel-titanium instruments afteruse in canals.

The Lightspeed nickel-titanium instrumentsare also used in high-torque slow-speed hand-pieces at 750 to 2000 rpm. Within this limit,faster rotational speed does not appear to increasethe likelihood of fracture." The manufacturersuggests discarding each file after 10 uses.

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FIGURE 10-12Overused rotary nickel-titanium files exhibiting "roll-up"(small arrow), and "unwinding" (large arrow).

ObturationSeveral filling techniques are available. The in-struments used for the two most practiced tech-niques, lateral and vertical condensation, are de-scribed here.

LATERAL CONDENSATION

The instruments used for lateral condensation arespreaders and small pluggers (Figure 10-13). Theyare used for condensing and adapting gutta-percha and creating space for accessory cones.They are either handled, having a shank attachedto a metal handle, or finger-type, having only aplastic handle (Figure 10-14). The handled instru-ments are stiff because they are generally made ofannealed stainless steel. Finger spreaders andpluggers are not annealed and therefore are deadsoft, giving them more flexibility. Handled instru-ments do not negotiate curved canals. Fingerspreaders and pluggers are best suited for obtu-rating curved canals.

Finger spreaders and pluggers have differenttips (see Figure 10-13). Pluggers are flat, whereasspreaders are pointed. Finger spreaders and plug-gets behave similarly and are used interchange-ably in lateral condensation.

The taper of spreaders varies among instru-ments. Highly tapered spreaders increase in diam-eter at a greater rate than do standardized instru-ments, which increase 0.02 mm per mm of length.The greater the taper, the more the canal space

FIGURE 10-13Fine finger spreader (left) and fine finger plugger (right). Bothare used similarly for lateral condensation. Spreaders arepointed and pluggers are flat at the tip.

FIGURE 10-14D11 handled spreader (left) and a fine finger spreader (right).Both are designed for lateral condensation. The fingerspreader (or plugger) is more versatile and safer.

must be enlarged or flared to facilitate spreaderpenetration.

Both stainless steel and nickel-titaniumspreaders are available. The obvious advantage ofnickel-titanium spreaders over stainless steelspreaders is greater spreader penetration in highlycurved canals .41 Nickel-titanium spreaders alsocreate less stress in curved canals compared withstainless steel spreaders . 42 The disadvantage ofnickel-titanium spreader is the inability to pre-curve it for patients with limited interocclusalspace.

VERTICAL CONDENSATION

In this obturation technique the filling material isalternately softened (with heat) and then verticallycompacted with pluggers. The softened gutta-percha filling material is pushed into the intersticesof the canal, but this technique offers less apicalcontrol of the material than lateral condensation.

Vertical condensation instruments can be di-vided into two categories: those that are heatedto transfer heat to the gutta-percha, and thosethat condense the gutta-percha (pluggers) (Fig-ure 10-15). Heat transfer instruments have han-dles, as do most pluggers. Finger pluggers maybe used in lieu of handled instruments in smallcurved canals.

Adjunctive InstrumentsDIAGNOSTIC INSTRUMENTS

The conventional explorer, periodontal probe,and mouth mirror are pulpal, periradicular, andperiodontal diagnostic aids that have special en-dodontic applications (Figure 10-16).

INSTRUMENTS UNIQUE TOROOT CANAL TREATMENT

Explorers are double-ended instruments with longtapered tines at either a right or an obtuse angle.This design facilitates the location of canal ori-fices. They are very stiff and should not be in-serted into canals or used for condensing gutta-percha. Explorers should never be heated.

The spoon excavator is another long-shank in-strument. The excavator is used to remove caries,deep temporary cement, or coronal pulp tissue.The endodontic excavator has a right or left orien-tation similar to that of operative hand excavators.

The Glick No. 1 instrument is used for place-ment of temporary restorations with the paddleend and removal (and then condensation) of ex-cess gutta-percha with the heated plugger end.


161

The rod-shaped plugger is graduated in 5-mmincrements.

Lentulo spiral drills are twisted wire instrumentsused in the slow-speed handpiece (Figure 10-17).They have been used to spin pastes, sealer, ce-ments, or calcium hydroxide into the canal. Theymust be used with care to avoid "throwing" quan-tities of unset material out of the apex. In fact,there is no reason to use lentulo drills other than

FIGURE 10-15Heat transfer (left) and condenser (heater-plugger) (right) forvertical condensation of gutta-percha.

162


FIGURE 10-16Specialized endodontic instruments. A, D16 explorer. B, 31 Lspoon excavator. C, Glick No. 1. The plugger end (bottom) isfor heating and removal of gutta-percha; the paddle (top) isfor placing temporary materials.

FIGURE 70-77Lentulo spiral drill is used to spin calcium hydroxide intocanals.

to place calcium hydroxide paste. The drill mustbe rotated so that it will not "screw" itself into thecanal; they may lock and separate.

Sterilization and DisinfectionEndodontic instruments are contaminated withblood, soft and hard tissue remnants, and bacte-ria and bacterial byproducts. Thus they must becleaned often and disinfected during the proce-dure and then sterilized. Also, because the instru-ments may be contaminated when new, they must

be sterilized before initial use. Different tech-niques are available.

Small kits such as those used for examinationmay conveniently be bagged, sterilized, and storedin the package until needed. Larger kits for treat-ment may be more rapidly and easily handled incassettes for sterilization and storage.

STERILIZATION

Cold- or heat-labile instruments such as some rub-ber dam frames may be immersed for a sufficientlylong period of time in solutions such as glu-


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taraldehyde. Generally, 24 hours are required toachieve cold sterilization. Immersion may be effec-tive for disinfection but will fail to kill all organ-isms. Because this method of sterilization is notpresently verifiable with biologic indicators, it isleast desirable in the office and should be reservedfor instruments that cannot withstand heat.

Pressure Sterilization

A common method of sterilizing all files and com-mon hand instruments is the steam or chemicalautoclave. Instruments that have been wrappedin gauze should be autoclaved for 20 minutes at121' C and 15 psi. 43 This will kill all bacteria,spores, and viruses. Various sodium nitrite dipswill retard rust. These "milk baths" help spare thecarbon steel Gates-Glidden drills.

Pressure sterilizers using a chemical rather thanwater have the advantage of causing less rusting.However, both steam and chemical autoclavingwill dull the edges of all cutting instruments owingto expansion with heat and contraction with cool-ing, resulting in permanent edge deformation.

Dry Heat Sterilization

Dry heat is superior for sterilizing sharp-edged in-struments such as scissors to best preserve theircutting edge. The time cycle for dry heat steriliza-tion is temperature dependent. After the tempera-ture reaches 160° C, the instruments should beleft undisturbed for 60 minutes. The disadvan-tage of this method is the substantial time re-quired, both for sterilization and subsequently forcooling. If the temperature falls below 160' C, thefull 60-minute heat cycle must be repeated.43

probe, (3) an explorer, such as the double-endedNo. 5 explorer, and (4) cotton forceps.

CLEANING AND SHAPING

Instruments used for access and cleaning andshaping include (1) a 5- to 6-ml Luer-Lok syringewith a 27-gauge needle, (2) locking cotton pliers,(3) rotary instruments (Gates-Glidden drills), (4) aplastic instrument (Glick No. 1) for temporaryplacement, (5) broaches and files, (6) a lentulo spi-ral drill; and 7) a millimeter rule.

OBTURATION

Instruments used for obturation include (1) spread-ers or pluggers, (2) Glick No. 1 for heat transfer andtemporary placement, (3) locking cotton pliers,and (4) 5/7 plugger or pluggers used for verticalcondensation.

EMERGENCY

The instruments necessary for emergency treat-ment are dictated by the diagnosis. For instance,irreversible pulpitis requires pulpotomy or pulpec-tomy. An acute apical abscess may require incisionand drainage.

Basic instrumentation for most emergencyprocedures includes (1) an examination kit, (2) ananesthetic armamentarium, (3) canal preparation(cleaning and shaping) system, and (4) occasion-ally, an incision for drainage kit. Incision anddrainage instruments include (1) scalpel handleand blade; (2) periosteal elevator; (3) rubber damdrain; (4) needle holder; and (5) irrigating syringewith an 18-gauge needle, sterile saline, and suc-tion tip.

DISINFECTION

Surface disinfectann during canal debridement isaccomplished by using a banker's sponge soakedin 70% isopropyl alcohol or proprietary quater-nary ammonium solutions. Files can be thrustbriskly in and out of this sponge to dislodge de-bris and contact the disinfectant. This procedurecleans but does not sterilize the instrument.

BLEACHING

Bleaching usually is done with the instrumentsincluded with the cleaning and shaping tray. Awalking bleach technique requires only the plasticinstrument to place the sodium perborate mix-ture in the chamber and then to temporize.

I nstruments for DifferentProceduresEXAMINATION

A kit for examination and diagnosis includes (1) afront surface mouth mirror, (2) a periodontal

REFERENCES

1. Weinberger B: An introduction to the history of dentistry,St Louis, 1948, Mosby.

2. Luks S: The myth of standardized instruments, NYJDent 43:109, 1973.

3. Walton RE: Histologic evaluation of different meth-ods of enlarging the pulp canal space, J Endod 2:304,1976.

164

1 0 I Endodontic Instruments

4. Short JA, Morgan LA, Baumgartner JC: A comparison

of canal centering ability of four instrumentation

techniques, JEndod 23:503, 1997.5. Luiten DJ, Morgan LA, Baugartner JC, Marshall JG: A

comparison of four instrumentation techniques on

apical canal transportation, JEndod 21: 26, 1995.

6. Peters O, Schonenberger K, Laib A: Effects of four Ni-

Ti preparation techniques on root canal geometry ass-

esed by micro computed tomography, Int Endod J

34:221, 2001.

7. Rhodes JS, Pitt Ford TR, Lynch JA, et al: A comparison

of two nickel-titanium instrumentation techniques in

teeth using microcomputed tomography, Int Endod J

33:279, 2000.

S. Seto BG, Nicholls JI, Harrington GW: Torsional prop-

erties of twisted and machined endodontic files,

JEndod 16:355, 1990.

9. Southard DW, Oswald RJ, Natkin E: Instrumentation

of curved molar root canals with the Roane technique,

JEndod 13:479, 1987.10. Felt RA, Moser JB, Heuer MA: Flute design of en-

dodontic instruments: its influence on cutting effi-

ciency, JEndod 8:253, 1982.

11. Miserendino LJ, Moser JB, Heuer MA, Osetek EM: Cut-

ting efficiency of endodontic instruments. Part 1: a

quantitative comparison of the tip and fluted regions,

JEndod 11:435, 1985.

12. Miserendino LJ, Moser JB, Heuer MA, Osetek EM: Cut-

ting efficiency of endodontic instruments. Part II:

analysis of tip design, JEndod 12:8, 1986.

13. American Dental Association Council on Dental Ma-

terials: New American Dental Association specifica-

tion No. 28 for endodontic files and reamers, J Am Dent

Assoc 93:813, 1976.

14. Oliet S, Sorin SM: Cutting efficiency of endodontic

reamers, Oral Surg Oral Med Oral Pathol 36:243, 1973.

15. Mueller HJ: Corrosion determination techniques ap-

plied to endodontic instruments-irrigating solutions

systems, JEndod 8:246, 1982.

16. Walia HM, Brantley WA, Gerstein H: An initial investi-

gation of the bending and torsional properties of Niti-

nol root canal files, J Endod 14:346, 1988.


terials, Instruments and Equipment: Revised ADA

specification No. 28 for endodontic files and reamers,

J Am Dent Assoc 104:506, 1982.

18. American National Standards Institute-AmericanDental Association: Specification No. 58 for root

canal files, type H (Hedstrom), J Am Dent Assoc

104:88, 1982.


terials, Instruments and Equipment: Revised

ANSI/ADA specification No. 28 for root canal files and

reamers, type K and no. 58 for root canal files, type H

( Hedstrom), J Am Dent Assoc 118:239, 1989.

20. Stenman E, Spangberg LS: Root canal instruments are

poorly standardized, J Endod 19:327, 1993.

21. Felcher T, Stiles M, Walton R: A comparison of en-

dodontic file tip designs as to their effect in instru-

mentation of curved canals (Abstract 1899), J Dent Res

66(Spec Issue):344, 1987.

22. Powell SE, Simon JH, Maze BB: A comparison of the

effect of modified and nonmodified instrument tips

on apical canal configuration, JEndod 12:293, 1986.

23. Yared GM, Bou Dagher FE, Machtou P: Cyclic fatigue

of profile rotary instruments after clinical use, Int

Endod J 33:204, 2000.

24. American Dental Association Council on Scientific Af-

fairs: Proposed American National Standard/Ameri-can Dental Association specification no. 95, root canalenlargers, pp 1-16, Chicago, 2000, American DentalAssociation.

25. Glosson CR, Haller RH, Dove SB, del Rio CE: A com-

parison of root canal preparations using Ni-Ti hand,

Ni-Ti engine-driven, and K-Flex endodontic instru-

ments,J Endod 21:146, 1995.

26. Ramirez-Salomon M, Soler-Bientz R, de la Garza-

Gonzalez R, Palacios-Garza CM: Incidence of Light-

speed separation and the potential for bypassing,

JEndod 23:586, 1997.

27. Pruett JP, Clement DJ, Carnes DL, Jr: Cyclic fatigue

testing of nickel-titanium endodontic instruments,

JEndod 23:77, 1997.28. Luebke NH, Brantley WA: Physical dimensions and

torsional properties of rotary endodontic instruments.

1. Gates Glidden drills, JEndod 16:438, 1990.

29. Luebke NH, Brantley WA: Torsional and metallurgical

properties of rotary endodontic instruments. 2. Stain-

less steel Gates Glidden drills, JEndod 17:319, 1991.

30. Luebke NH, Brantley WA, Sabri ZI, Luebke JH: Physi-

cal dimensions, torsional performance, and metallur-

gical properties of rotary endodontic instruments. 3.

Peeso drills, JEndod 18:13, 1992.

31. Coleman CL, Svec TA: Analysis of Ni-Ti versus stain-

less steel instrumentation in resin simulated canals,

JEndod 23:232, 1997.

32. Kuhn WG, Carnes DL, Jr, Clement DJ, Walker WA:

Effect of tip design of nickel-titanium and stainless

steel files on root canal preparation, J Endod 23:735,

1997.

33. Himel VT, Ahmed KM, Wood DM, Alhadainy HA: An

evaluation of Nitinol and stainless steel files used by

dental students during a laboratory proficiency exam,Oral Surg Oral Med Oral Pathol Oral Radiol Endod 79:232,

1995.

34. Pettiette MT, Metzger Z, Phillips C, Trope M: End-

odontic complications of root canal therapy per-

formed by dental students with stainless-steel K-files

and nickel-titanium hand files, JEndod 25:230, 1999.

35. Baumann MA, Roth A: Effect of experience on quality

of canal preparation with rotary nickel-titanium files,

Oral Surg Oral Med Oral Pathol Oral Radiol Endod 88:714,

1999.

36. Webber J, Moser JB, Heuer MA: A method to determinethe cutting efficiency of root canal instruments in lin-

ear motion, J Endod 6:829, 1980.

37. Gabel WP, Hoen M, Steiman HR, et al: Effect of rota-

tional speed on nickel-titanium file distortion, JEndod

25:752, 1999.

38. Gambarini G: Rationale for the use of low-torque en-

dodontic motors in root canal instrumentation, Endod


39. Dietz DB, Di Fiore PM, Bahcall JK, Lautenschlager EP:

Effect of rotational speed on the breakage of nickel-

titanium rotary files, j Endod 26:68, 2000.

40. Poulsen WB, Dove SB, del Rio CE: Effect of nickel-

titanium engine-driven instrument rotational speed

on root canal morphology, J Endod 21:609, 1995.

41. Berry KA, Loushine RJ, Primack PD, Runyan DA:

Nickel-titanium versus stainless-steel finger spreaders

in curved canals,J Endod 24:752, 1998.

42. Joyce AP, Loushine RJ, West LA, et al: Photoelastic

comparison of stress induced by using stainless-steel

versus nickel-titanium spreaders in vitro, J Endod24:714, 1998.

43. Council on Dental Therapeutics: Sterilization or dis-

infection of dental instruments. In Accepted dental ther-apeutics, ed 40, p 136, Chicago, 1984, American Dental

Association.


165

Internal Anatomy

LEARNING OBJECTIVES

After reading this chapter and the Appendix, the student should be able to.

1 / Recognize errors that may cause difficulties or failures in root canal treatment owing to lack of knowledge

of pulp anatomy.

2 / List ways that help to determine the type of pulp canal system.

a / Draw common shapes of roots in cross section and common canal configurations in these roots.

4 / Describe the most common root and pulp anatomy of each tooth.

5 / List, for each tooth type, the average length, number of roots, and most common root curvatures.

6 / Characterize the more frequent variations in root and pulp anatomy of each tooth.

7 / Explain why standard periapical radiographs do not present the complete picture of root and pulp anatomy.

8 / Draw a representative example of the most common internal and external anatomy of each tooth and rooti n the following planes: (1) sagittal section of mesiodistal and faciolingual planes and (2) cross section

through the cervical, middle, and apical thirds.

9/ Suggest methods for determining whether roots and canals are curved as well as the severity of the curvature.

10/

State the tenet of the relationship of pulp-root anatomy.

11 / List each tooth and the root(s) that require a search for more than one canal.

12 / List and recognize the significance of iatrogenic or pathologic factors that may cause alterations in pulp

anatomy.

13 / Define the pulp space and list and describe its major components.

14 / Describe variations in the pulp system in the apical third, including the apical foramen region.

15 / Describe how to determine clinically the distance from the occlusal-incisal surface to the roof of the chamber.

16 / Discuss location, morphology, frequency, and importance of accessory (lateral) canals.

17/ Describe relationships between anatomic apex, radiographic apex, and actual location of the apical foramen.

Describe common variations in pulp anatomy resulting from developmental abnormalities and state theirsignificance.

19 / Describe why many root curvatures are not apparent on standard radiographs.

Methods of Determining Pulp AnatomyTextbook KnowledgeRadiographic EvidenceExploration

General ConsiderationsRoot and Canal AnatomyI dentification of Canals and Roots

Alterations in Internal AnatomyAgeI rritantsCalcificationsI nternal Resorption

Components of Pulp SystemPulp HornsPulp ChamberRoot CanalsAccessory CanalsApical Region

Variations of Root and Pulp AnatomyDens Invaginatus (Dens in Dente)Dens EvaginatusHigh Pulp HornsLingual GrooveDilacerationOther Variations

11 / Internal Anatomy

167

n terms of success of treatment,knowledge of pulp anatomy cannot beoverstated. As a cause of treatment fail

ures, lack of a working knowledge of pulpanatomy ranks second only to errors in diagnosisand treatment planning. It is critical to know thenormal or usual configuration of the pulp and tobe aware of variations. Special techniques are re-quired to determine the internal anatomy of thetooth under treatment.

Knowledge of the pulp anatomy must be three-dimensional. The pulp cavity must be mentally vi-sualized both longitudinally (from coronal aspectto apical foramen) and in cross section. In addi-tion to general morphologic features, irregulari-ties and "hidden" regions of pulp are presentwithin each canal. To clean and shape the pulpsystem maximally, intracanal instruments mustreach as many of these regions as possible to planethe walls to loosen tissue and tissue remmants.1Lack of attention to this important principle maylead to treatment failure.

Methods of DeterminingPulp AnatomyTEXTBOOK KNOWLEDGE

Knowledge of anatomy gained from textbooks isthe most important and most useful method.Common and frequent variations must be memo-rized for each tooth. This means having a workingknowledge of the number of roots, number ofcanals per root and their location, longitudinaland cross-sectional shapes, most frequent curva-tures (particularly in the faciolingual plane), androot outlines in all dimensions.2-6 It is useful toknow the approximate percentage of each.

Anatomic features are diagrammed in theAppendix.

RADIOGRAPHIC EVIDENCE

Certainly radiographs are useful, but they aresomewhat overrated for this purpose, particu-larly conventional periapical films.' The standardparallel facial projection gives just two dimen-sions; a common error is to examine only thisview, overlooking the important third dimension(Figure 11-1). In addition, radiographs tend tomake the canals look relatively uniform in shapeand taper. In fact, the aberrations often found aregenerally not visible (Figure 11-2).

Standard projections indicate general anatomicfeatures. Special radiographic techniques disclose

168


FIGURE TVIA, Facial projection. Both the second premolar and the first molar appear to have fairly straight roots and an un-complicated anatomy. B, Mesial angled projection. The more proximal view shows severe "bayonet" dilacerationof the second premolar with marked buccal curve in the apex (arrow). Sharp curves of molar roots and two de-finitive canals in the mesiobuccal root are now evident. Both are difficult problems to treat.

FIGURE 11-2A, The impression of pulp anatomy received from viewinga radiograph. B, The reality: internal anatomy actually

has many aberrations and intercommunications. (CourtesyDr. A. Goerig.)

missed canals and determine curvatures.' ,' Thesetechniques are discussed in detail in Chapter 9.

and root. 11,12 In other words, because the pulptends to form the surrounding dentin uniformlyon opposite walls, the pulp is generally a minia-ture version of the tooth and conforms to thetooth surface. `3

ROOT AND CANAL ANATOMY

Although root shape in cross section is variable,there are seven general configurations: round, oval,long oval, bowling pin, kidney bean, ribbon, and hour-glass (Figure 11-3). Shape and location of canalsare governed by root shape (in cross section). Dif-ferent shapes may appear at any level in a singleroot. For example, a root may be hourglass-shaped in cross section at the cervical third, taperto a deep oval in the middle third, and blend tooval in the apical third; the number and shape ofcanals in each level will vary accordingly." Impor-tantly though, a canal is seldom round at anylevel. To assume that it is may result in impropercanal preparation.

EXPLORATION

Additional determinations of pulp anatomy aremade during access preparation and when search-ing for canals. These methods also have limita-tions because canals often are neither readily ap-parent nor easily discovered with instruments."

General ConsiderationsA basic tenet in pulp-root anatomy is the shape ofthe pulp system reflects the surface outline of the crown

I DENTIFICATION OF CANALS AND

ROOTS

Obviously, to clean, shape, and obturate a canal, itmust be located." In roots that may contain twocanals, a basic rule is to assume that the root containstwo canals until proved otherwise. Rather than mem-orize roots that often contain two canals, it is eas-ier to remember those few that are unlikely tohave two canals. Maxillary teeth contain rootsthat rarely have two canals: anterior root, premo-lars with two or three roots, and distobuccal andlingual roots of molars. All other maxillary roots


169

FIGURE 11-3Common variations in root or pulp cross-sectional anatomy.Note that the pulp outline tends to reflect the root outline.Deep concave roots have a greater variety of pulp anatomies.

FIGURE 11-4Note the disclike configuration of the pulp chamber in thefirst molar because of the predominance of dentin formationi n the roof and floor of the chamber. These chambers are dif-ficult to locate during access preparation.

FIGURE 11-5Severe attrition has resulted in tertiary dentin formation onthe roof and floor of the chamber.

and all mandibular roots require a careful searchfor two (or possibly more) canals.

Alterations in Internal Anatomy

floor of the chamber show more dentin forma-tion, eventually making the chamber almostdisclike in configuration (Figure 11-4). Treatmentimplications (difficulty in locating chamber andcanals) are obvious.

Again, initial pulp shape reflects root shape. How-ever, because pulp and dentin react to their envi-ronment, changes in shape occur with increasingtooth age and in response to irritation.

Although dentin formation tends to occur withage on all surfaces, it occurs predominately in cer-tain areas. For example, in molars, the roof and

IRRITANTS

Anything that exposes dentin to the oral cavitycan potentially stimulate increased dentin forma-tion at the base of tubules in the underlyingpulp." Causes of such dentin exposure includecaries, periodontal disease, abrasion, erosion, at-trition, cavity preparations, root planing, andcusp fractures (Figure 11-5). Vital pulp therapysuch as pulpotomy, pulp capping, or placement of

AGE

170

11

/ Internal Anatomy

irritating materials in a deep cavity may cause anincrease in dentin formation, occlusion, calcificmetamorphosis, resorption, or other unusualconfigurations in the chamber or canals. Thesetertiary (irregular secondary) dentin formationstend to occur directly under the involved tubules(Figure 11-G).

It is imperative that the clinician study radi-ographs and visually examine the tooth beingtreated to identify factors that may cause alter-ations in anatomy. Failure to do so may result inserious errors, lost time, and inadequate treatment.

CALCIFICATIONS

Calcifications take two basic forms within thepulp: pulp stones (denticles) and diffuse calcifica-tions. Although pulp stones are usually found in

the chamber and diffuse calcifications within theradicular pulp, the reverse may also occur. Thesecalcifications may form either normally or in re-sponse to irritation. Pulp stones are often seen onradiographs 16; diffuse calcifications are visibleonly histologically.

Pulp stones in the chamber may reach con-siderable size and can markedly alter the inter-nal chamber anatomy (Figure 11-7). Althoughthey do not totally block a canal orifice, theyoften make the process of locating an orificechallenging. These large pulp stones may be at-tached or free and are often removed during ac-cess preparation. Although pulp stones are notcommon in canals, if present, they are usuallyattached or embedded in the canal wall in theapical region. Rarely do they form a barrier toinstrument passage.

FIGURE 11-6As shown on this micrograph, tertiaryor irregular secondary dentin (10) hasformed in large amounts in the pulp (P)directly under the caries (C. At timesthis may significantly alter internalanatomy. (Courtesy Dr. W. Dowden.)

FIGURE 11-7Calcifications (pulp stones [or denticles]) are visu-alized in the chambers. Their discrete appearancesurrounded by radiolucent spaces shows these cal-cifications to be natural and not formed in re-sponse to irritation. (Courtesy Dr. T. Gound.)


171

INTERNAL RESORPTION Components of Pulp SystemSuch resorptions are uncommon and when presentare usually not extensive. They also are a response toirritation that is sufficient to cause inflammation.Most resorptions are small and are not detectableon radiographs or during canal preparation. Whenvisible radiographically, they are usually extensiveand often perforate. Internal resorptions usuallycreate operative difficulties (Figure 11-8).

The pulp cavity is divided into a coronal (the pulpchamber) and a radicular portion (the root canal).Other features include pulp horns, canal orifices, ac-cessory (lateral) canals, and the apical foramen (Fig-ure 11-9). The internal anatomy of these pulpcomponents is altered by secondary dentin or ce-mentum formation.

FIGURE 11-8A, Extensive internal resorption defect (arrow). B, Four years after treatment. Special cleaning, shaping, and ob-turating techniques (lateral condensation plus thermoplasticized) were required, resulting in successful treatment.

FIGURE 11-9Major anatomic components of the pulp cavity. A, Anterior tooth. B, Posterior tooth.

172


FIGURE 11-10A technique for determining the distance from the occlusalsurface to the roof of the pulp chamber. This is of obviousbenefit during access preparation to prevent perforation.

PULP HORNS

Pulp horns represent what the dentist does notwant to locate during restorative procedures butdoes want to locate during access preparation. Al-though they may vary in height and location, asingle pulp horn tends to be associated with eachcusp in a posterior tooth, and mesial and distalhorns tend to be in incisors. Generally, the oc-clusal extent of the pulp horns corresponds to theheight of contour in a younger tooth but liescloser to the cervical margin in an older tooth.Occasionally, an aberrant horn extends occlusallyand is exposed as a result of caries or routine cav-ity preparation. Such abnormally high pulp hornsmay or may not be visible on radiographs.

During access preparation, the height and lo-cation of pulp horns may be more accurately de-termined by measuring from cusp tip to pulphorn or chamber roof using a bur and a handpiece(Figure 11-10).

PULP CHAMBER

The pulp chamber occupies the center of thecrown and trunk of the root. Again, its shape, inboth longitudinal and cross-sectional dimen-sions, depends on the shape of the crown andtrunk; this configuration varies with tooth ageand/or irritation."

FIGURE 11-11Maxillary first premolar roots. A common finding: cross sec-tion through buccal (e) and lingual (L) roots shows a concav-ity on the lingual surface and an irregular canal shape in themiddle third of the buccal root. (Courtesy Dr. A. Tamse.)

ROOT CANALS

Root canals extend the length of the root, begin-ning as a funneled orifice and exiting as the apicalforamen. Significantly, most canals are curved,often in a facial-lingual direction. Therefore acurved canal is often undetectable on facial pro-jection radiographs. As a result, the uninitiated oruninformed clinician may assume that a canal isstraight and may overenlarge what is, in reality, afacial or lingual curvature, resulting in ledging orperforation. The operator should always assume that acanal is curved.

Canal shape varies with root shape and size, de-gree of curvature, and the age and condition ofthe tooth (see Figures 11-2 and 11-3). As a rule,


173

FIGURE 11-12Three-dimensional reconstruction from histologic sections shows complex anatomic structure of apical pulpanatomy. (Adapted from Meyer W: Dtsch Zahnaertzl Z 25:1064, 1970.)

when two canals occur in a root, they tend to bemore oval. In the deep facial-lingual root withmesial or distal (or both) concavities (hourglass-or kidney bean-shaped), a single canal may have abowling pin, kidney-bean, hourglass, or ribbonshape. Regardless of the shape in the cervicalthird, in the apical curvature the root (and canal)tends to become more oval but may be somewhatflattened.17

The shape and number of canals in a root re-flects the facial-lingual depth and shape of theroot at each level (Figure 11-11); the deeper theroot, the more likely that there are two separate,definitive canals. If the root tapers toward the api-cal third, there is a greater likelihood that thecanals will converge to exit as a single canal.

Irregularities and aberrations are common-place. This is particularly true in posterior teeth.Such aberrations include hills and valleys in canalwalls, intercanal communications (isthmuses be-tween two canals), cul-de-sacs, fins, and other vari-ations (Figure 11-12). Again, these aberrations areusually not accessible to instruments or irrigants.

Remember that the chamber tends to occupythe center of the crown; a canal occupies the cen-ter of the root. When there are two canals in aroot, each will often occupy the center of its ownroot "bulge."

ACCESSORY CANALS

Accessory (or lateral) canals are lateral branches ofthe main canal that form a communication be-tween the pulp and periodontium. They containconnective tissue and vessels and may be locatedat any level from funation18,19 to apex, but tend tobe more common in the apical third and in poste-rior teeth .z° In other words, the more apical andthe farther posterior the tooth, the more likelythat accessory canals will be present. The relation-

ship of accessory canals to pulp health and dis-ease as well as to treatment is debatable . ' They donot supply collateral circulation and thereforecontribute little to pulp function and probablyrepresent an anomaly that occurred during rootformation.

These canals do form an exit for irritants fromthe pulp space to the lateral periodontium. Theyprobably cannot be debrided during cleaning andshaping' but are occasionally filled with obturat-ing materials during canal filling (Figure 11-13).The importance of obturating accessory canals isunknown.22

APICAL REGION

Development: The apex is the root terminus. It isrelatively straight in the young mature tooth buttends to curve more distally with time. This cur-vature results from continued apical-distal appo-sition of cementum in response to continuedmesial-occlusal eruption. Alterations in the apicalregion may also result from resorption and irreg-ular cementum apposition. Thus apical anatomytends to be nonuniform and unpredictable."

Apical Foramen: The apical foramen varies insize and configuration with maturity. Before mat-uration, the apical foramen is open. With timeand deposition of dentin and cementum, it be-comes smaller and funneled. Significantly, theforamen usually does not exit at the true(anatomic) root apex" , -' but is offset approxi-mately 0.5 mm and seldom more than 1.0 mmfrom the true apex. The degree of deviation is un-predictable and may vary considerably from theaverage, particularly in the older tooth that hasundergone cementum apposition (Figure 11-14).For this reason, root canal preparation and obtu-ration end short of the anatomic root apex (Fig-ure 11-15) as seen in the radiograph.26 Usually, the

174


FIGURE 11-13A, Resorptive bony lesion is visible (arrow); this usually indicates an accessory canal (not visible) that is a path-way for irritants. B, The accessory canal is now obvious after obturation.

apical foramen is not visible radiographically. Theclinician relies on averages or on electronic mea-suring devices to determine the extent of canalpreparation and obturation.23,24

Variations in Anatomy: The only consistentaspect of the apex region is its inconsistency.2 7,28The canal may take twists and turns, divide intoseveral canals to form a delta with ramifications onthe apical root surface, or exhibit irregularities inthe canal wall (Figure 11-16). Generally, these aber-rations are neither detectable nor predictably nego-tiable and are neither well debrided nor obturated.

A common concept is that canals round out inthis apical region. This is not always true. Canalsare frequently a long oval or even ribbon-shapedapically. 29 These nonround canals cannot be en-larged to a round shape without perforating orweakening the roots. 29

Apical Constriction: The presence of an api-cal constriction is unpredictable. It has been pro-posed that the cementodentinal junction formsthe apical constriction; this is an incorrect con-cept. In fact, the junction is difficult to determineclinically with accuracy,24 and the intracanal ex-tent of cementum is variable. If an apical constric-tion is present, it is not visible on a radiographand usually is not detectable by touch, even by themost skilled practitioner.

Variations of Rootand Pulp Anatomy

Representative examples of the tooth groups arediagrammed in the Appendix, where both cross-sectional and longitudinal aspects are outlined. Inaddition, the pulp anatomy of each is shown in re-lation to the design of the access preparation.

Occasionally, teeth vary significantly in root or,more likely, in pulp anatomy. Such variations andabnormalities are most common in the maxillarylateral incisors, maxillary30,31 and mandibular pre-molars," and maxillary molars .

33,34 Unusual rootmorphology tends to be bilateral . 3s

DENS INVAGINATUS(DENS IN DENTE)

Dens invaginatus is most common in maxillarylateral incisors36 that results from an infolding ofthe enamel organ during proliferation and is anerror in morphodifferentiation (Figure 11-17). Itoften results in an early pulp-oral cavity commu-nication requiring root canal treatment. 37 Densinvaginatus is most common in the maxillary lat-eral incisor and shows varying degrees of severityand complexity.38 39 The more severe cases shouldbe referred to a specialist because special treat-


175

FIGURE 71- 14Variations in apical canal anatomy. A, The radiograph oftendoes not demonstrate the size, shape, or curvature of canalsapically. B, Mesial root apex showing abrupt curve and api-cal foramen exiting on the mesial well short of the anatomicapex. C, Distal root apex showing uniform canal with no con-striction and variable levels (arrows) of cementodentinalj unctions; these variabilities are common. (Cadaver specimencourtesy Dr. D. Holtzmann.)

176


FIGURE 11-15A, Note that the apical foramina (smallarrows) do not correspond to the trueanatomic apex (large arrows). B, inmost situations the apical terminus orseat of the preparation will vary fromthe apical foramen and radiographicapex. (A courtesy Dr. D. Melton.)

DENS EVAGINATUS

FIGURE 11-16The apical region of the canal and apical foramen (AF) areoften very irregular.

A variation of invaginatus,4° dens evaginatus ismost common in mandibular premolars and inindividuals with Oriental ancestry (this includesNative Americans and Hispanics). Clinically, densevaginatus initially appears as a small tubercle"bulge" on the occlusal surface, but it may not beobvious radiographically (Figure 11-18). Thesemalformations often contain an extension of thepulp. When these fragile tubercles fracture off, thepulp is exposed and will become necrotic, requir-ing apexification. They are generally not difficultto treat, prophylactically, by removing the tuber-cle and capping, then restoring with amalgam."

HIGH PULP HORNS

Occasionally, a pulp horn extends far into a cuspregion, resulting in premature exposure by cariesor accidental exposure during cavity preparation.

LINGUAL GROOVE

Usually found in maxillary lateral incisors, a lin-gual groove appears as a surface infolding of dentinoriented from the cervical toward the apical direc-tion (Figure 11-19). 42 Frequently, this results in adeep narrow periodontal defect that occasionallycommunicates with the pulp, causing an endodon-tic/periodontal problem (Figure 11-20). Treatmentis difficult and unpredictable; prognosis is poor.

DILACERATION

ment, such as surgery, is frequently required. Theprognosis of any treatment often is questionable.The invagination is usually visible on radi-ographs; however, it is often small and obscure.The lingual pit on maxillary anterior teeth repre-sents a minor form of dens invaginatus.

By definition, dilaceration is a severe or complexroot curvature (see Figure 11-1). During root for-mation, structures such as the cortical bone of themaxillary sinus or mandibular canal or nasal fossamay deflect the epithelial diaphragm, resulting ina severe curvature. Many of these curvatures are


177

FIGURE 11- 17Dens invaginatus. A, The invagination is visible on the lingual surface (arrow) of this abnormally shaped incisor.B, The invagination is lined internally by enamel (arrow). By communicating with the pulp, the exposure resultedi n pulp necrosis, apical pathosis, and arrested root development. These situations are difficult to treat.

FIGURE 11-18Dens evaginatus. The chamber extends to the occlusal surface. A, The defect is visible from the occlusal surface(arrow). B, There is a communication through this to the pulp space (arrow), with resultant necrosis and apicalperiodontitis. (Courtesy Dr. R. Johnson.)

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FIGURE 11-19Lingual groove, which is an apparent infolding during root andcrown formation. A, The groove is faintly visible on the periapicalradiograph (arrow). B, The groove is often detected on the surfacewith probing and is usually untreatable.

FIGURE 11-20A, Lingual groove defect proved untreatable periodontallyand endodontically. B, Cross section shows that the groovei nvagination (arroM communicates with the pulp.


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FIGURE 11-21Premolar with three canals-a challenge to treat.

found in a facial-lingual plane and are not obvi-ous on standard radiographic projections.

OTHER VARIATIONS

Many other pulp and root anomalies mayoccur ...... Some occur in association with geneticdisorders,48 such as variations in the number ofcanals or roots (Figure 11-21), and teeth with un-usual root canal configurations have an impacton treatment. 49,5° The astute clinician will be alertto these possibilities and will study radiographsand occlusal anatomy carefully. A not uncommonabnormality is the C-shaped canal (Figure 11-22).This usually occurs in mandibular molars. Be-cause of the complex internal anatomy, prognosisof root canal treatment is questionable owing todifficulty in adequate debridement and obtura-tion.s ' Additional treatment measures may be re-quired, and patients with such canals should beconsidered for referral.

New technologies, using computer reconstruc-tion of microtomography, are able to providethree-dimensional morphologic information ontooth and pulp anatomy. ' z °s2

FIGURE 11-22A, C-shaped pulp chamber. The C-shaped space may be continuous throughout the length of the root but is vari-able anatomically. More commonly, three separate canal orifices may be found within the groove. B, ObturatedC-shaped molar with three canals joined by an interconnecting isthmus.

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REFERENCES

1. Walton RE: Histologic comparison of different meth-ods of pulp canal enlargement, J Endod 2:304, 1976.

2. Pineda F, Kuttler Y: Mesiodistal and buccolingualroentgenographic investigation of 7,275 root canals,Oral Surg Oral Med Oral Pathol 33:101, 1972.

3. Mueller AH: Anatomy of the root canals of the in-cisors, cuspids and bicuspids of the permanent teeth, J

Am Dent Assoc 20:1361, 1933.

4. Vertucci F: Root canal anatomy of the human perma-nent teeth, Oral Surg Oral Med Oral Pathol 58:589, 1984.

5. Vertucci FJ: Root canal anatomy of the mandibular an-terior teeth, J Am DentAssoc 89:369, 1974.

6. Green D: Morphology of the pulp cavity of the perma-nent teeth, Oral Surg Oral Med Oral Pathol 8:743, 1955.

7. Kaffe I, Kaufman A, Littner MM, et al: Radiographicstudy of the root canal system of mandibular anteriorteeth, Int Endod J 18:235, 1985.

8. Walton RE: Endodontic radiographic techniques, DentRadiog Pbotog 46:51, 1973.

9. Skidmore A: The importance of pre-operative radi-ographs and determination of root canal configura-tion, Quintessence Int 10:55, 1979.

10. Johnson WT: Difficulties in locating the mesiobuccalcanal in molars, Quintessence Int 16:169, 1985.

11. Stambaugh RV, Wittrock JW: The relationship of thepulp chamber to the external surface of the tooth, J

Prosthet Dent37:537, 1977.12. Bjorndal L, Carlsen O, Thuesen G, et al: External and

internal macromorphology in 3D-reconstructed max-illary molars using computerized X-ray microtomog-raphy, Int Endod J 32:3, 1999.

13. Bhaskar S: Orban's oral histology, ed 10, St Louis, 1986,Mosby.

14. Mauger M, Schindler W, Walker W III: An evaluation

of canal morphology at different levels of root resec-tion in mandibular incisors, JEndod 24:607, 1998.

15. Fogel H, Peikoff M, Christie W: Canal configuration inthe mesiobuccal root of the maxillary first molar: aclinical study,JEndod 20:135, 1994.

16. Tamse A, Kaffe I, Littner MM, Shani R: Statistical eval-uation of radiologic survey of pulp stones, J Endod8:81, 1982.

17. Gani O, Visvisian C: Apical canal diameter in the firstupper molar at various ages, JEndod 25:689, 1999.

18. Guttman J: Prevalence, location, and patency of acces-sory canals in the furcation of molars, J Periodontol49:21, 1978.

19. Vertucci FJ, Anthony RL: A scanning electron micro-scopic investigation of accessory foramina in the fur-cation and pulp chamber floor of molar teeth, OralSurg Oral Med Oral Pathol 62:319, 1986.

20. DeDeus WD: Frequency, location, and direction of thelateral, secondary, and accessory canals, JEndod 1:361,

1975.21. Sinai IH, Soltanoff W: The transmission of pathologic

changes between the pulp and the periodontal struc-tures, Oral Surg Oral Med Oral Pathol 36:558, 1973.

22. Weine F: The enigma of the lateral canal, Dent Clin

North Am 28:833, 1984.23. Kuttler Y: Microscope investigation of root apexes, J

Am Dent Assoc 50:544, 1955.

24. Dummer PM, McGinn JH, Rees DG: The position andtopography of the apical canal constriction and apicalforamen, Int Endod J 17:192, 1984.

25. Miyashita M, Kasahara E, Yasuda E, et al: Root canalsystem of the mandibular incisor,J Endod 23:479, 1997.

26. Wu M, Wesselink P, Walton R: Apical terminus loca-tion of root canal treatment procedures, Oral Surg OralMed Oral Pathol Oral Radiol Endod 89:99, 2000.

27. Morfis A, Sylaras N, Georgopoulou M, et al: Study ofthe apices of human permanent teeth with the use of ascanning electron microscope, Oral Surg Oral Med Oral

Pathol Endod 77:172, 1994.28. Guttman J, Regan J: Historical and contemporary per-

spectives of the root apex, Arab Dent) 3:9, 1998.

29. Wu M, R'Oris A, Barkin D: Prevalence and extent of

long oval canals in the apical third, Oral Surg Oral Med

Oral Pathol Oral Radiol Endod 89:739, 2000.

30. Kartel N, Ozcelik B, Cimilli H: Root canal morphology

of maxillary premolars,J Endod 24:417, 1998.

31. Tamse A, Katz A, Pilo R: Furcation groove of buccalroot of maxillary first premolars-a morphometric

study, JEndod 26:359, 2000.32. Baisden MK, Kulild JC, Weller RN: Root canal config-

uration of the mandibular first premolar, J Endod18:505, 1992.

33. Libfeld H, Rotstein 1: Incidence of four-rooted maxil-lary second molars: literature review and radiographicsurvey of 1,200 teeth, JEndod 15:129, 1989.

34. Stropko J: Canal morphology of maxillary molars:clinical observations of canal configurations, J Endod25:446,1999.

35. Sabala CL, Benenati FW, Neas BR: Bilateral root orroot canal aberrations in a dental school patient pop-ulation, J Endod 20:38, 1994.

36. Hulsmann M: Dens invaginatus. aetiology, classifica-tion, prevalence, diagnosis, and treatment considera-tions, Int Endod J 30:79, 1997.

37. Piatelli A, Trisi P: Dens invaginatus: a histologicalstudy of undemineralized material, Endod Dent Trau-

matol 9:191, 1993.38. Oehlers F: Dens invaginatus. I. Variations of the in-

vagination process and associated crown forms, Oral

Surg Oral Med Oral Pathol 10:1204, 1957.39. Gound TG: Dens invaginatus-a pathway to pulpal

pathology: a literature review, Pract Periodontics Aesthet

Dent 9:585, 1997.40. Reichart PA, Methah D, Sukasem M: Morphologic

findings in dens evaginatus, Int J Oral Surg Oral MedOral Pathol 11:59, 1982.

41. McCulloch K, Mills C, Greenfield R, Coil J: Dens evagi-natus: review of the literature and report of severalclinical cases, J Can DentAssoc 64:104, 1998.

42. Lara V, Consolaro A, Bruce R: Macroscopic and micro-scopic analysis of the palato-gingival groove, J Endod26:345, 2000.

43. Beatty RG, Krell K: Mandibular molars with five canals.Report of two cases, J Am DentAssoc 114:802, 1987.

44. Yang Z-P, Yang S-F, Lee G: The root and root canalanatomy of maxillary molars in a Chinese population,Endod Dent Traumatol 4:215, 1988.

45. Sieraski SM, Taylor GN, Kohn RA: Identification andendodontic management of three canalled maxillarypremolars, J Endod 15:29, 1989.

46. Manning SA: Root canal anatomy of mandibular sec-ond molars, Int Endod J 23:34, 1990.

47. Melton DC, Krell KV Fuller MW: Anatomical and his-tological features of C-shaped canals in mandibularsecond molars, J Endod 17:384, 1991.

48. Kelsen A, Love R, Kieser J, Herbison P: Root canalanatomy of anterior and premolar teeth in Down'ssyndrome, Int Endod J 32:211, 1999.

49. Sharma R, Pecora J, Lumley P, Walmsley A: The externaland internal anatomy of human mandibular canineteeth with two roots, Endod Dent Traumatol 14:88, 1998.

50. Ferreira C, Gomes de Moraes 1, Bernardineli N: Three-rooted maxillary second premolar, J Endod 26:105,2000.

51. Fava L, Otani A, Otani 1: The C-shaped root canal sys-tem and its endodontic implications: a clinical review,Endod Pract 2:18, 1999.

52. Mikrogeorgis G, Lyroudia K, Nikopoulos, et al: 3Dcomputer-aided reconstruction of six teeth with mor-phological abnormalities, Int Endod J 32:88, 1999.


181

Access Preparationand length Determination

LEARNING OBJECTIVES


1 / I dentify major objectives of access preparation in both anterior and posterior teeth.

2 / Describe why straight-line access is critical.

3 / Explain why removal of pulp horns in anterior teeth is important.

4 / Relate reasons and indications for removing caries or restorations during access preparation.

5/ Explain the reason and technique for removing the dentin shelf in anterior and posterior teeth.

6 / Describe the procedure, burs used, and sequence of operations to start and complete access preparations

on various teeth.

7 / Identify common errors for specific teeth that may occur during access preparation.

8 / Recognize when these errors occur and know how to correct them (if they are correctable).

9/ Describe techniques for locating difficult-to-find chambers or canals.

10 / Account for conditions under which working length (distance from radiographic apex) varies.

11

/ Demonstrate the step-by-step technique for obtaining estimated and final working lengths.

12 / Describe how to designate and maintain (and create, when necessary) a stable reference point.

13 / Describe electronic apex locators-how they function and when they are useful.

Refer to the Appendix:

14 / Diagram the portions of the tooth that must be removed to attain straight-line access to the canals.

Illustrate this on sagittal sections of both anterior and posterior teeth.

15 / Diagram the outline form of the access preparation for all teeth.

16 / Show the location of each canal orifice relative to the occlusal or lingual surface.

182

Access Preparation

Major Objectives

Access in Special Situations

Access Techniques

Errors

Working Length Determination

Reference Point

Technique for Determination


12 / Access Preparation and Length Determination

183

his chapter and the following twochapters (Chapters 13 and 14) cover thetechnical aspects of root canal treat

ment. Discussed are access and working length,cleaning and shaping, and obturation. These pro-cedures occupy much of the clinician's effort; thesteps involved are critical for success.

There are many ways to accomplish varioustasks. A variety of techniques, instruments, andmaterials can be used to perform root canal treat-ment successfully. These three chapters representbasically one general approach. The recom-mended methods follow a sequence of proceduresthat have proved to be successful based on re-search and clinical usage. Other approaches ormodifications may also result in success. There isnot enough space here to describe all variations;these will be found in individual courses on en-dodontics or in other publications.

Access Preparation

MAJOR OBJECTIVES

Access preparation is the most important phase of thetechnical aspects of root canal treatment! Access is thekey that opens the door to maximize cleaning,shaping, and obturation. These three proceduresare difficult at best; without adequate accesspreparation, instruments and materials are diffi-cult to control within the pulp system. Impor-tantly, the time and effort devoted to accesspreparation pay dividends in the treatment stepsthat follow.

The three major objectives of access prepara-tion are (1) attainment of straight-line access, (2) con-servation of tooth structure, and (3) unroofing of thechamber to expose orifices and to remove pulphorns in anterior teeth. Of course, the approachand specific details for each of these vary in differ-ent teeth.

Straight-Line Access

As stated earlier, access preparation is very impor-tant; straight-line access is the most critical aspect.The ideal procedure would be to have instrumentspass through the chamber without touching thewalls and through the straight part of the canalundeflected. The initial curve of the instrumentwould then occur at the first bend of the canal,usually in the apical third of the root. This, ofcourse, is not always possible because of crown-root relationships; however, this straight-line access tothe first canal curvature is attempted (Figure 12-1).

I mproved Instrument Control. Minimizing in-strument curvature and deflection increases the

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FIGURE 12-1I n the ideal straight-line accesspreparation, the instrument isnot deflected until it reachesthe first curve of the canal.

FIGURE 12-2A, Small hand instruments (No. 20 or less) usually negotiatecurves. B, Larger files overcome dentin resistance by straight-ening themselves and cutting raw dentin on the outside ofthe curve. Adequate straight-line access decreases this ten-dency for files to transport a curved canal.

operator's ability to manipulate files in as manyareas of the canal as possible without grossly al-tering the internal canal anatomy.' Stainless steelfiles are relatively inflexible and resist deforma-tion, particularly those of size 25 or above. Nickel-titanium files have more flexibility in larger sizes.In either case, any instrument in a curved canal al-ways tries to straighten itself. A sharp stainlesssteel file larger than size 25 in a curved canal over-comes the resistance of confining dentin. It there-fore cuts straight ahead and does most of its workremoving raw dentin on the outside of the curve(Figure 12-2). This straight-ahead cutting is ac-centuated according to the severity of the curveand the size of the file. Therefore less curve in thecoronal portion of the instrument makes thestraightening effect toward the tip less pro-nounced. The end result is improved instrumentcontrol, resulting in better cleaning and shapingof the canal system with less chance of undesir-able internal alterations such as transportation,ledging, and "zipping. "Z,3

Another advantage of straight-line access is theease of introducing instruments into canals.Achieving straight-line access involves controlledfunneling of canal orifices. These funnels guidethe instrument tips into the canals, minimizingthe frustration of repeated tap tap tapping of thefile on the chamber floor while attempting to lo-cate the canal orifice(s).

I mproved Obturation. The same principles statedunder instrument control apply to obturation.Straighter access to the apical portion (and the

greater the funneling of the canal orifice),makes the obturation easier and more effective.Because spreader or plugger depth is criticalfor a better seal throughout the length of thecanal, it is important to introduce these instru-ments (with minimal curve) close to the apicalpreparation.'

Decreased Procedural Errors. The principle of im-proved instrument control through reduced cur-vature also applies to decreased procedural errors.The curved instrument straightens itself. Largerinstruments have greater stiffness; therefore theymore readily cut straight ahead (Figure 12-2).Straight-line access decreases canal curvature andprovides better instrument control. There arethree potential unfortunate accidents that may beresult from inadequate straight-line access, whichresults in more transportation.

Ledge Formation.' The canal is straightened.Suddenly the file no longer negotiates the curvebut bumps into a dead end. A radiograph madewith the file in place shows the tip of the instru-ment now straight and pointing toward the out-side of the curve.' It is now difficult (usually im-possible) to renegotiate the original curve tocomplete debridement and obturation.

Apical Perforation. If the operator persists, theinstrument will continue to straighten both itselfand the canal; the eventual outcome will be a zip-ping perforation. Again, this possibility is reducedwith straight-line access.

Furcal (Stripping) Perforation. Stripping resultsusually from over-rigorous planing and forcing in-


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FIGURE 12-3Using large rotary instruments such as this No. 5 Gates-Glidden bur against the furcation wall of a canal in molarsi s dangerous.

FIGURE 12-4A, Totally inadequate access. The instrument tends to do all itswork by cutting toward the facial aspect and will never reach

i nto and debride portions of the canal toward the lingual as-pect (arrows). Straight-line access is achieved by removing thelingual dentin shelf (8) and the enamel triangle (A). B, The re-sult is straight access and improved instrument control.

struments or burs toward the furcation wall.' Strip-ping perforation of the furcation is usually devas-tating and is difficult to repair with predictablelong-term success. Of course, stripping may also re-sult from improper use of rotary instruments toachieve straight-line access (Figure 12-3). Files andburs should not be overused against the furcationportion of canal walls (the so-called danger zone)but directed toward the periphery (the safetyzone).7,8

Tooth Structure Removal. Straight-line accessconsists of removal of dentin and enamel in se-lected regions (Figure 12-4). Dentin is removed in-ternally at or just apical to the canal orifice(dentin or lingual shelf). Enamel is removed fromthe incisal surface of anterior teeth (enamel trian-gle) and toward the crown periphery (cusp tips)on posterior teeth.

The preferred site for removal and the most efficientin terms of improved instrument control and straight ac-cess is reduction of the dentin shelf. Not only does this

provide the desired decrease in instrument curva-ture, but it also "opens up" regions of the canalthat would otherwise be sequestered. Such hiddenareas tend to occur in roots that contain only asingle canal. Because of canal constriction nearthe orifice, concavities will be found (usually to-ward the lingual aspect) in the midroor that arenot otherwise accessible (Figure 12-4).

An axiom of canal preparation is that instru-ments must physically contact and plane the walls toloosen the tissue and debris for removal. Unplanedareas often retain existing or potential irritants.Removal of a constriction or shelf duringstraight-line access permits files to reach moresurface areas.

Conservation of Tooth Structure

Removal of excess enamel and dentin (in particu-lar) weakens the tooth and increases the possibilityof fracture or perforation. Generally, a preparation

186


that allows adequate straight-line access need notrequire removal of much tooth structure. The keyis to remove dentin and enamel in strategic areas,leaving other areas intact. A properly designed ac-cess preparation generally has little effect on de-creasing cusp strength.'o

Minimal Weakening of Tooth. Gouging out por-tions of the dentin wall invariably weakens thecusps and compromises the integrity of themarginal ridges, leading to diminished cuspalstrength and an increased incidence of fracture."In molars, the orifice location and access outlinesshow that it is generally unnecessary to extend thepreparation into marginal ridges. 'z Marginalridges with their underlying dentin are the basicfacial-lingual strength of the tooth.13 Unless theyare already involved with caries or restorations,marginal ridges should be left alone!

Excessive removal of dentin apically beyondthe orifice increases the chances of vertical rootfracture. Extreme lateral forces may be createdduring condensation or placement of posts. With-out doubt, the key factor affecting the strength ofthe crown and root is the amount of dentin re-maining and not the so-called brittleness ofdentin per se.13,14

The design and extent of permanent restora-tions are also affected by the amount of toothstructure removed during access preparation. Ex-cessive removal may require a more complexrestoration than would otherwise have been nec-essary. At times, a cusp that has adequate dentin

support and is bound by a strong, intact marginalridge need not be covered.

Prevention of Accidents. Accidents mean perfo-rations! Obviously, excessive removal of toothstructure in any region increases the likelihood ofperforation. Except for vertical root fracture, per-foration is the most devastating occurrence. Spe-cific details on root perforations and their prog-nosis and repair are discussed in Chapter 18.

Unroofing of Chamber and Exposureof Pulp Horns

Unroofing of the chamber in all teeth is importantto locate canals and permit adequate access tothem. It also decreases the incidence of discol-oration in anterior teeth. An attempt to economizeon unroofing the chamber in an effort to preservea small amount of dentin only increases the frus-tration level. However, unroofing the chamberdoes vary according to tooth groups, as follows.

Maximal Visibility. It is counterproductive towork through a "mousehole." Inadequate open-ings (Figure 12-5) through the occlusal surface orchamber roof do not permit adequate light toenter the chamber. In addition, clear visualizationis compromised in all aspects of the chamberfloor. Visibility is important in the posterior teeth.Molars, in particular, present difficulties in iden-tifying canal orifices.

Location of Canals. Unroofing the chamber inmolars is a prerequisite for locating canals, partic-

FIGURE 12-5

A, Inadequate opening would permit neither good visibility to locate canals nor adequate straight-line access.B, Wide opening through occlusal surface of crown is correct. Note that the access does not extend to the porce-lain to prevent its chipping.


187

ularly those that have displaced orifices. An exam-ple is the mesiobuccal (MB) canal in both maxil-lary and mandibular molars. These canals are themost difficult to locate because they lie farthest atthe periphery and under the mesiobuccal cusp.

A particular challenge is the second (mesiolin-gual [ML]) canal in the MB root of maxillarymolars." This orifice is usually obscured by ashelf of dentin and requires special techniques ofexposure. 16,17

I mprove Straight-Line Access. Areas of the roof ofthe chamber and dentin shelves that overlie canalorifices are particularly likely to impede straight-line access. They must be removed (Figure 12-6).

Exposure of Pulp Horns. Exposure of pulp hornsin all teeth is critical, particularly in anteriorteeth, because of future aesthetic considerations.Pulp horns contain debris and trap sealer rem-nants; both are liable to cause eventual discol-oration, which may become manifest months oryears after treatment. Pulp horns should beopened conservatively and with care. It is not nec-essary to remove excessive amounts of enamel ordentin to obtain access for removal of debris andsealer. The technique is described later in thischapter.

ACCESS IN SPECIAL SITUATIONS

Usually, access preparation is done under lessthan ideal conditions. Most teeth requiring rootcanal treatment have been affected by caries,

restorations, fractures, attrition, and so on. Fre-quently, these irritants have promoted depositionof dentin. This means that the preparation itselfwill not be "ideal" and must be altered to accom-modate variations. It is critical for the operator to rec-ognize these variations and plan the access accordingly(Figure 12-7) before picking up the handpiece!

Caries

Ordinarily, all caries are removed early in the ac-cess preparation phase. Ideally, caries are exca-vated before the chamber is entered to avoid con-taminating the chamber and canals with latercaries removal. The reason for not leaving caries isobvious; the pulp chamber will be heavily conta-minated with bacteria, which may be introducedinto the pulp system during canal preparation.Also, a temporary seal is not obtained unless thesealing material is in direct contact with clean andnoncarious dentin.

There is one exception. When caries removalmay lacerate the gingiva or compromise isola-tion, it is advisable to leave a very small remnantof caries temporarily. This thin band of caries atthe gingival margin may remain until root canaltreatment is complete (Figure 12-8). Then thecarious remnants are removed before the postob-turation temporary restoration is placed. How-ever, to repeat, all caries internal to this regionmust be removed, preferably before the chamber isunroofed.

FIGURE 72-6A, Inadequate access opening because dentin shelves obscure orifices, particularly the mesiobuccal and mesi-olingual orifices (arrows). B, Removal of these shelves gives good straight-line access to the canals in this max-illary molar.

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FIGURE 12-7Unusual situations. A, Extensive caries permits accessfrom the facial surface. B, The dentist did not recognizethat the retainer was misoriented on the tooth; the burwas misaligned and perforated the mesial surface.

A hint: When caries under enamel are re-moved, a portion of enamel is left undermined.This undermining should be at the proximaledges, not under a cusp. These undercuts in thefacial and lingual aid in retaining the temporaryrestoration.

Existing Permanent Restoration

There is a general idea that when a restoration ispresent, a textbook outline access preparationshould be done through the restoration. This isnot the case! A restoration generally providesmore flexibility in designing the preparation be-cause of the opportunity for a wider opening.Tooth structure is not being removed, only therestorative materials.

I deal Situations. Removal of the entire restora-tion, whether a small occlusal amalgam or a fullcrown, is preferred. Total removal increases visi-bility and simplifies the search for and prepara-tion of canals. However, total removal is often nei-ther feasible nor desirable. Retaining the proximalcomponent of an intact class II restoration thatextends subgingivally will aid in isolation. Acrown that is still serviceable and that will not bereplaced ordinarily is retained because the castingmay be destroyed on removal.

Extent of Opening. When the existing restora-tion will not be removed entirely, the openingshould be expanded. This allows the operator towiden the access to attain better visibility andstraighter access (see Figure 12-5). Obviously, adecision must be made early in treatment (prefer-ably as a first consideration) whether to replace orrepair the restoration (see Chapter IS). If it is tobe repaired, the opening is minimized. An excep-

tion is a full gold crown, which permits a verywide access.

Porcelain Restorations. Access through thesepresents some special problems. Edge chippingand cracks are common; shattering or loss of seg-ments of porcelain occasionally occurs. 18 To min-imize these effects, preparations should be doneslowly, with copious water spray.

Restoration Repair. Restoring the access open-ing through a crown with amalgam is permanentand maintains crown retention at original levels.19Therefore access usually does not ultimately com-promise retention or strength.

Defective Restoration. Before access is begun andthe rubber dam is placed, the margins of therestoration are checked carefully with an explorer.This is particularly important subgingivally. Openmargins, recurrent caries, or other factors thatmay lead to communication with the pulp spaceafter access preparation may jeopardize isolationduring treatment and between appointments. Ifdefective, the restoration must be removed en-tirely. It is very important not to discover a defec-tive restoration after the access preparation is com-plete! This wastes time and compromisestreatment. Such a determination is made beforethe rubber dam is placed and access is begun.

Existing Temporary Restoration

Frequently, a tooth requiring root canal treatmenthas been restored temporarily. The same basic prin-ciples apply as with the permanent restoration;that is, the entire temporary restoration is removedwhen feasible. When the entire temporary restora-tion will not be removed, the opening is overpre-pared at the expense of the material. Occasionally,


189

FIGURE 12-8A, A band of caries may be left peripherally at the gin-gival margin (arrow to prevent laceration during cariesremoval and loss of isolation. B, Caries (arrow) shouldbe totally removed when treatment is complete.

a portion (usually proximal) of the temporaryrestoration may remain to improve isolation.

Temporary Crowns. Unless there are extenuatingcircumstances, temporary crowns are removed be-fore isolation. This improves visibility, enhancesaccess and canal preparation, and facilitates obtu-ration. When left in place, temporary crowns fre-quently become loose and are displaced by therubber dam clamp or leak during treatment andbetween appointments.

Bands. Ordinarily it is safer to remove bandsbecause of their potential for leakage. However, ifa band has been placed to help retain a temporarycrown, it may aid in isolation. A well-fitting or-thodontic band may remain and does not im-pinge on or hamper occlusal access. However, arubber dam clamp may displace a band during theprocedure. If the band is not removed, the clampshould be placed on an adjacent tooth.

Copper bands are notoriously poor for main-taining a seal (Figure 12-9). If they are already inplace, the adequacy of adaptation should be de-termined. If in doubt, the band is removed andanother isolation system is used (see Chapter 8).

Previous Partial Treatment

Root canal treatment started by another operatoroffers special challenges. The practitioner must

make a periapical radiograph before institutingtreatment (Figure 12-10). This is done for two rea-sons: first, to become aware of the situation andany previous mishaps (e.g., perforations, sepa-rated instruments, or misoriented access); andsecond, if such a mishap was caused by the firstoperator, the patient is made aware of the situa-tion. Radiographs are made partly for protection;otherwise, responsibility for the mishap may beattributed to the second operator by the patientor by a jury.

Although some phases of treatment have beencompleted, it should not be assumed that treat-ment has been satisfactory to that point. For ex-ample, if access preparation and partial canal in-strumentation have been done, the access may nothave good straight-line preparation. The operatorshould be ready to correct another's faults orerrors.

Timing and Reasons for Removalof a Restoration

Restoration removal, either total or partial,should be completed before the opening into thechamber is made. This saves time and also helpsto prevent particles of the temporary or perma-nent restoration from precipitating into andblocking the canals. If it becomes necessary to

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FIGURE 12-9A, Two teeth requiring retreatment that will present isolation and access problems. B, Two methods of isolationfor access are shown. The copper band on the premolar is poorly adapted and will irritate the gingiva and prob-ably leak. The IRM on the molar is the preferred approach for temporary isolation.

FIGURE 12-10The reason for making preoperative radiographs is evident. Atreatment attempt by an earlier operator left amalgam shav-

i ng (arrows) in the canals of the first molar. The shavingscould easily be packed deeper and could block the canals.

(Courtesy G. Obermayr.)

remove more restoration after unroofing thechamber, a cotton pellet is packed tightly onto thechamber floor to protect the orifices. This is onlypartially satisfactory; frequently the bur grabs anddisplaces the cotton pellet.

Altered Internal Anatomy

External irritants and age change the morphologyof the pulp space. Anything that exposes dentin tothe oral cavity often results in formation of addi-tional layers of dentin in the chamber.

Dentin Formation. Generally, dentin that formsin response to surface irritants is irregular, thusgiving rise to the term "irregular secondary (ortertiary) dentin". This dentin results from eitherthe stimulation of existing odontoblasts or thedestruction and replacement of odontoblasts bya unique cell that forms a hard tissue. Invariably,this irregular dentin forms at the base of tubulesthat communicate with the exposure or theirritation.

Areas of Altered Dentin. In most cases, the irri-tants responsible for dentin formation are obvi-ous. These include things such as caries, restora-tions, areas of attrition or abrasion, andfractures. Each results in dentin exposure and ir-ritation of the underlying pulp. A second meansof identification is careful viewing of radio-graphs, directing particular attention to the pulpregions under areas of dentin irritation or expo-sure (Figure 12-11). Access should be designedaccordingly.


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Difficult-to-Locate Canals

Difficulty in locating canals is common; a canal orcanals are certainly present in the root (as they al-ways are) but cannot be located. Frequently, thisdifficulty can be anticipated. Isolation and radi-ographs assist in finding the canal.

Delay Isolation. Teeth may have extensiverestorations or caries or may contain canals notvisible on radiographs; these and other factorssuggest difficulties in orientation and location oforifices. Occasionally, placement of a rubber dammay be delayed until the chamber or canals are lo-cated; this permits improved bur orientation tothe long axis of the crown and root. Radiographsare studied to determine root direction, and thealveolus is examined to detect root prominence.The inclination of the root relative to the crownand to adjacent teeth is noted. A canal (if single) islocated in the approximate center of the root. Allthese factors serve as a guide for the operator andthe bur.

Although the best means of searching for anddetermining the location of a canal is to use asmall file as an explorer, caution is needed becausethe airway is not protected unless a rubber dam isin place. A piece of floss is placed through the holein the handle of the file or a gauze pack posi-tioned at the back of the tongue for protection.

Once a canal is discovered or suspected, therubber dam is placed immediately. A confirma-tory radiograph with a file in place is recom-mended if there is a possibility that the "canal"might, in fact, be a perforation.

Exploratory Radiographs. Occasionally, as the bursearch goes deeper into the root, radiographs aremade to determine the position of the accesspreparation in the root. Two radiographs aremade, one from the straight facial perspective andanother from a mesial or a distal perspective. Thecanal is centered, and therefore the preparationshould also be directed toward the center of theroot. The facial projection gives a mesiodistal ori-entation; the angled radiograph provides a facial-lingual direction relative to where the canal shouldlie. Appropriate adjustments are made to directthe bur toward the center of the root. For specificdetails of this technique, refer to Chapter 9.

FIGURE 12-11Caries, restorations, and pins on the premolar all alter the in-ternal anatomy by stimulating formation of irregular sec-ondary dentin. Thus, access is difficult and must be modifiedaccordingly.

lyze each situation, formulate an approach, andthen proceed with caution. If on initial assess-ment the case seems complex, the clinician shouldnot attempt access preparation and thus create er-rors. The patient should initially be referred to anendodontist.

Burs

ACCESS TECHNIQUES

There is a basic approach to access preparationthat applies in principle to all situations. Varia-tions occur according to position, orientation,restoration, extent of caries, and other factors.Specific details for all situations are not discussedin this chapter. The operator must carefully ana-

Although different designs and types of burs havebeen advocated, none has been demonstrated tobe superior.20 Special burs are manufactured pri-marily for access (Figure 12-12). These are effec-tive but require practice. Conventional burs thatfunction well include the straight and tapered fis-sure burs (Figure 12-13), occasionally supple-mented by round burs.

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FIGURE 12-12Access burs. A, Gates-Glidden drills; size is identified by the grooves on the shank. The drills also are available in two

l engths. The shorter are useful in molars. B, These special end-cutting burs are good for opening through porcelain or

metal. Left to right. Beaver by Dentsply Midwest, GW#2 by S S White, Transmetal by Dentsply Maillefer, H34L by

Braessler. C, Non-end-cutting burs are for removing dentin shelves and finishing the outline. Left to right Endo Access

Bur, Endo Z, Multipurpose Bur-all three by Dentsply Maillefer; 269GK by Braessler. (B and C courtesy Dr. W. Johnson.)

Procedure

To repeat, there are three general objectives. (1)Expose and unroof the chamber for visibility. Thisincludes removal of pulp horns in anterior teeth;removal of pulp horns is not always necessary inposterior teeth. (2) Conserve tooth structure byremoving only the portions that must be re-moved. Restorations should be removed or atleast opened widely. (3) Most important is to ob-tain straight-line access.

These objectives are accomplished as follows(Figure 12-13):

1. Rough out the access cavity well into thedentin, close to the chamber, with a high-speed handpiece (Figure 12-13, A).

2. Penetrate and unroof the chamber with ahigh-speed bur (Figure 12-13, B). It is pru-dent to measure on the radiograph the dis-tance between the occlusal or incisal sur-face and the roof of the chamber. Thismarking is transferred onto the bur toserve as a landmark. It indicates the ap-proximate bur depth to the chamber roof.When difficulty in locating the chamber isanticipated, a search should be made forthe chamber region of greatest dimension(for example, over the lingual canal regionin maxillary molars and over the distalcanal in mandibular molars).

3. Locate canal orifices with the endodonticexplorer. These are confirmed as canals by


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FIGURE 12-13Basic steps in access preparation. A, The access cavity is outlined deep in the dentin and close to the chamberroof by the high-speed bur. B, Penetration and unroofing are achieved by low-speed latch-type burs or, as in thisexample, a tapered fissure high-speed bur. Other shaped burs are suitable also. C, Canal orifices are located withan endodontic explorer and are identified and negotiated to their estimated length with small files. D, The dentinshelves that overlie and obscure the orifices are removed.

penetrating them with small (No. 15 and25) files (Figure 12-13, C). If there is doubtabout which canal has been discovered, anangled radiograph is made with a file orfiles in place before proceeding. Frequentlya canal that is thought to be of one typeturns out to be another.

4. Remove dentin shelves that usually overlieand obscure canal orifices in molars withlong-shank, small round, or small taperedfissure or diamond burs (Figure 12-13, D).Standard-length burs may be converted tosurgical length by extension in the hand-piece chuck. Gates-Glidden burs are notfor removal of dentin from the chamber;these are for use at or beyond the orificeand in the canal.

5. Before obtaining straight-line access,canals are explored with small files to de-termine patency and whether the canal islarge enough to accommodate Gates-Glidden burs. This evaluation is carriedout as follows:a. A series of small files ( No. 10 to 25) is

set at the estimated working length foreach canal.

b. Each canal is explored starting with thesmallest and progressing to the largerfiles at estimated length to establishpatency.

G. Occasionally small instruments cannot beinserted to length; this may be caused byone of two problems:a. Blockage. The file passes easily but

strikes a dead end, possibly owing to asmall ledge or calcification deep in thecanal. A small curve or bend is made atthe tip of the file and an attempt ismade to wiggle and tease the file tippast the blockage.

b. Constriction. The instrument increas-ingly binds and then stops in the smallcanal. A lubricant (glycerin, liquid sur-gical soap, or topical anesthetic) isplaced at the orifice with the tip of cot-ton pliers or with a small syringe. Thelubricant is worked ahead of the file bypumping and spinning counterclock-wise. This usually permits the file toslide several millimeters farther. Lubri-cant is also useful in initial enlargementand in placing larger files in the canalafter the corrected working length is de-termined. Also, opening a canal coro-nally often facilitates passage to the api-cal end of the canal. More informationon managing constrictions and block-ages is found in Chapter 13.

7. Small canals must be sufficiently large andpatent to permit passage of Gates-Glidden

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FIGURE 12-14Gates-Glidden drill usage. A, No. 3 extends well past the orifice. B, No. 4 is usedshorter than the No. 3 and can be used peripherally for straight-line preparation.

C, These burs must be used only on peripheral walls and away from the furcation.

burs. In these smaller canals, this is bestachieved by a "passive step-back" (preflaring)of the canals.21 This provides nonforcedenlargement and slight canal flaring; thereis a reduction in procedural errors, whichallows use of larger working length files,with more control.22 The technique is asfollows:a. The estimated working length (EWL) is

determined (radiographic tooth lengthminus 3 mm).

b. Irrigant (in larger canals) or a lubricant(in smaller canals) is worked apically.

c. Small files that will pass without forceto or close to EWL are then rotated(reamed) a few times to remove a smallamount of dentin.

d. Progressively larger files at successivelyshorter lengths are again rotated to re-move small amounts of dentin. Thisis continued through several sizedinstruments.

8. After passive step-back preparation insmall canals or in already larger canals, thecoronal segment of the canal is ready forGates-Glidden burs. These burs will nowhave a definite canal to follow and are lesslikely to bind or create a blind ending.Gates-Glidden burs (see Figure 12-12, A)for most situations are stainless steel in

sizes 2, 3, and 4 (as indicated by the num-ber of bands on the shank). No. 1 burs aretoo small to be effective, dull quickly, andbreak easily.23 Sizes 5 and 6 are overly largeand dangerous.

9. The No. 2 or 3 bur is run at medium speedand with light force several millimeters(the distance depends on canal size andcurvature) into the canal, allowing the burto make its own way, but away from thedanger zone. The bur should be inserted inthe same direction as the canal exits thechamber. It should not be forced laterally,and no attempt to gain straight-line accessshould be made with the No. 2 or 3 bur(Figure 12-14, A).

10. Use of the No. 4 bur follows almost to thedepth of the No. 3 bur. To obtain straight-line access, the No. 4 bur is worked on theoutstroke (Figure 12-14, B). This motion isdirected toward the lingual aspect in ante-rior teeth and toward the periphery (or lineangles) in posterior teeth, staying awayfrom the danger zone (Figure 12-14, C).

NOTE: Gates-Glidden burs are always workedaway from the furcation in molars to avoida stripping perforation. For example, to ob-tain straight-line access on the mesiobuccalcanal of a maxillary molar, the No. 4 bur isworked toward a "standing up" position


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FIGURE 12-15A, The dashed lines show where dentin must be removed to achieve straight-line access. B, The access so at-tained. C, The original canal (a) is modified by Gates-Glidden burs by removing tooth structure at Band C.

(safety zone region) on the mesiobuccalwall (Figure 12-15).

11. Straight-line access is checked with files,which should pass undeflected deep intothe canals. Smaller (No. 3) Gates-Gliddenburs carefully used in the canal close tothe curve facilitate straight-line access(Figure 12-16).

Anterior Teeth

The procedure followed is basically that outlinedin the preceding section, with the following spe-cial considerations.

Straight-Line Access. Access is evaluated with afile. When placed deep in the canal, the file shouldnot be deflected from the incisal enamel. Ideally,the file should sit passively in the canal. If it doesnot, tooth structure may be removed from the in-cisal triangle' or, preferably, from the lingual shelf(see Figure 12-4). Usually lingual access extendsdeep under the cingulum. Also, a lingual canal inmandibular anterior teeth or premolars is oftenmissed because of inadequate lingual extensionand lack of straight-line access. In some cases (es-pecially in mandibular anterior teeth), the prepa-ration is extended close to the incisal edge to gaindirect access .24

Pulp Horns Removed. Removal of pulp horns isevaluated with the small hooked end of an ex-plorer (Figure 12-17). There should be no incisal

FIGURE 12-16Gates-Glidden burs may be used deep in the canal or until re-sistance is felt at the curvature. The more these burs improvethe access, the more efficient is the overall preparation of thecanal.

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FIGURE 12-17The hook end of an explorer detects unremoved pulp horns.This preparation requires opening and exposure of the hornsand removal of the lingual shelf.

FIGURE 12-18Mesial and distal files demonstrate good straight-line access.The middle file (arrow) is deflected by dentin shelves and of-fers poor straight-line access.

catch. The remaining pulp horns are opened andremoved with small round burs.

Posterior Teeth

Straight-Line Access. Access is evaluated withfiles, which should not deflect off the enamel. In asingle-canal premolar, the file should passstraight into the canal. 25 In a multicanaled tooth,the file handles ideally are parallel when all areplaced in their respective canals simultaneously(Figure 12-18). This result is usually not totallyfeasible, but at least the file shaft should not de-flect from the enamel on an opposite wall. A cur-vature on the thicker upper portion of the file im-parts more straightening force on the apicalportion of the file. Therefore a straighter approach ofthe file in the curved canal decreases the probability ofpreparation error in the apical region.

In other words, straight-line access to the canalin a curved root provides an opportunity to reachthe apical region and to prepare the apical curva-ture more efficiently (by having to deal with onlyone curvature rather than two).

Pulp Horns Removed. It is not necessary to openthe access excessively to remove pulp horns in mo-lars and premolars.

Specific Preparations

In the diagrams of molar access (see the Appen-dix), the outline is centered mesiodistally. Canalorifices and chamber are centered and are not lo-cated mesially as commonly reported.12 The Ap-pendix illustrates pulp morphology and accesspreparations for each tooth group.

ERRORS

Unfortunately, mistakes occur. Most result frominadequate diagnosis and failure to recognizeproblems early. Others reflect a lack of knowledgeeither of internal anatomy or the desired endpoint of access preparation.

Misorien to tion

I nternal Excess Removal. Excess removal ofdentin constitutes needless destruction of dentineither in searching for the chamber or canals or inplacing the access improperly.

Anterior Teeth. Usually the bur is directed toofar labially or lingually and gouges the dentin in-ternally (Figure 12-19).

Premolars. As with anterior teeth, the bur is di-rected too far labially or lingually as well as


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FIGURE 12- 19A common error encountered in achiev-i ng access on mandibular anteriorteeth: gouging the facial or lingualsurface internally.

FIGURE 12-20A common error encountered onmaxillary premolars: misdirectionand gouging internally towardthe mesial concavity. D, Distal;M, mesial.

FIGURE 12-21Common errors in access preparation of mandibularmolars. A, Gouging toward the lingual surface be-cause of the lingual inclination of the crown and lin-gual tipping of the tooth. L, lingual; B, buccal. B, Un-dermining of the marginal ridge and near-perforationon the mesial surface. The error was created by start-i ng access too far mesially and directing the bursstraight inferiorly. D, distal; M, mesial. C, Example ofmisdirected access preparations.

mesially or distally.25 These teeth leave little roomfor error, particularly toward the mesial or distalaspect, which is narrow with cervical concavities(Figure 12-20).

Mandibular Molars. Two regions tend to beabused: the mesial aspect under the marginalridge and the lingual surface beneath the lingualcusps. The teeth and the crowns tip mesially and

lingually. A bur directed straight inferior willgouge these areas (Figure 12-21).

Maxillary Molars. As in mandibular molars,there is a tendency to remove dentin beneath themesial marginal ridge (Figure 12-22).

Mistaken Canal. As stated earlier, it is commonto become misoriented during molar accesspreparation and mistake one canal for another.

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12 I Access Preparation and Length Determination

When in doubt, a file is placed and then an ap-propriate angled radiograph is made to identifythe discovered canal.

Perforation

Perforation usually results from misorientation(Figure 12-23) or while searching for a canal. Allperforations adversely affect prognosis; somedoom the tooth to extraction.

Causes. The major cause for perforation is lackof knowledge of the internal tooth anatomy andfailure to consider alterations. The second major

FIGURE 12-22A maxillary molar error: direct-i ng access too far mesially withundermining of the marginridge. D, Distal; M, mesial.

cause is rushing to treat without careful evalua-tion. These considerations were described earlierin this chapter and are related to restorations, al-tered tooth position, or changes in internalanatomy caused by caries. When the practitioneris searching for canals in molars, most perfora-tions occur into the furcation.

Treatment. Techniques for repairing perforationsdepend on their location, size, and other factors.Specific techniques are described in Chapter 18.

Prevention. Many errors can be prevented, min-imized, or corrected before they become serious.One such preventive technique is to make a bitew-ing radiograph, which often identifies an impend-ing problem (Figure 12-24).

Two tricks can be used to minimize misorien-tation by staying in the long axis of the root andcrown during initial access: (1) A rubber dam isnot placed until the canal is located; and (2) a pen-cil line is scribed on the crown, showing the longaxis of the root (Figure 12-2S).

Bur Separation

Using burs or drills improperly may result inbreakage in the canal. Delicate tapered fissureburs should not be used deep into an orifice.Gates-Glidden drills should be worked into canalswith continuous rotation; stopping probably willcause the drill to bind and then separate. Theseoften lock in the canal and cannot be removed(Figure 12-26).

FIGURE 12-23Misorientation resulting in perforation. A, Molar is inclined mesially and lingually. 8, Incorrect access approachresulting in severe perforation on mesial and into furcation.


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FIGURE 12-24Misorientation of the access is obvious(arrow) on the bitewing radiograph.Identifying such an error early often pre-vents a serious consequence and permitscorrection. (Courtesy Dr. C. Koloffon.)

FIGURE 12-25Techniques that help with difficult access. A line is scribed onthe facial surface in the long axis of the tooth. Preparation isstarted without a rubber dam (until the canal is located); thisaids in orientation.

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FIGURE 12-26Gates-Glidden drill separation. A, Drill was stopped, causing binding and breakage up the shaft. B, The drill couldnot be removed, but was bypassed. C, The canal was prepared and obturated; the prognosis is good becausecanal is sealed apically and coronally.

Working Length Determination

The objective is to establish the length (distancefrom the apex) at which canal preparation andsubsequent obturation are to be completed. Opti-mal length is 1 to 2 mm short of the apex, al-though this may vary slightly with different diag-noses. 26 Procedures may be terminated 0 to 2 mmfrom the apex if the pulp is necrotic and 0 to3 mm if the pulp is vital . 21 Of course, lengths willvary according to many factors; these ideals arenot always attainable. Apex location varies; thesevariations can be approximated but not usuallydetermined using only a diagnostic radiograph. 28-so

Therefore this determination must be an esti-mate, using average measurements of distancesfrom the apical foramen to the true apex andfrom the apical constriction (or within the canal)to the apical foramen." Electronic apex locatorsare also helpful with length determination inmany situations.

Prognosis and microbiologic studies as well ashistologic experiments involving healing after ob-turation consistently show that it is preferable to

confine instruments, chemicals, and obturatingmaterials to the canal space. 12-11

REFERENCE POINT

The reference point is the site on the occlusal orincisal surface from which measurements aremade. This point is used throughout canal prepa-ration and obturation.

Selection

A reference point is chosen that is stable and eas-ily visualized during preparation. Usually this isthe highest point on the incisal edge on anteriorteeth and a buccal cusp tip on posterior teeth. Thesame reference point is best used for all canals inmultirooted teeth. The mesiobuccal cusp tip ispreferred in molars.

Stability

A reference point that will not change during orbetween appointments is selected. Examples of


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unstable reference points are undermined cuspsor cements. If it is necessary to use an underminedcusp, it should be reduced considerably before ac-cess preparation. Areas other than cusp tips, suchas marginal ridges or the floor of the chamber, areunreliable or difficult to visualize.

TECHNIQUE FOR DETERMINATION

After coronal access preparation and passive step-back, the working length is determined . 38

Different techniques have been used, studied,and advocated for determining working length,including radiographic (conventional or digital),electronic, and tactile methods; none are totallyaccurate or infallible . 39 Electronic techniques arebest used in certain situations, but must be con-firmed radiographically; tactile methods are toounreliable. Radiographs are usually made to de-termine the working length. A workable tech-nique is as follows.

Estimated Working Length

and are usually not visible. On molar radi-ographs, No. 15 file tips are often obscure.

5. In a multicanaled tooth, files are usuallyplaced in all canals.

6. If a root contains two canals (or may havean undiscovered canal), the cone should bepositioned at a 20-to 30-degree horizontaldeviation from the standard facial projec-tion. (Exceptions are maxillary molars, forwhich at least a facial radiograph should beprovided.)

7. A film is exposed with the instruments inplace. Either conventional or digital radiog-raphy is suitable.'"' Usually one radi-ograph is sufficient; occasionally an addi-tional film is necessary.

Corrected Working Length

The corrected working length is determined bymeasuring the discrepancy between the tip of thefile and the radiographic apex. The file is then ad-justed to 1 to 2 mm short of the radiographic apex.

1. The diagnostic film, which is made using aparalleling technique, is measured from thereference point to the apex with a millime-ter endodontic ruler.

2. From the radiographic tooth measure-ment, 3 mm is subtracted for the estimatedworking length. This takes into accountthe following:

a. The relation of the radiographic apexto the actual apical foramen or con-striction (approximately 1 mm).

b. The magnification effect of the radi-ograph. Magnification of 2 mm (be-cause of divergence of the centralbeam) is allowed for all teeth.

c. This 3-mm decrease should generallyleave the initial instrument placementslightly short of working length (agood "fudge" factor).

3. An instrument stop measured to the esti-mated working length is placed on each of aseries of small files.

4. These files are used in successively largersizes to explore the canal until a size isreached that binds (locks) at or slightlyshort of the estimated working length. Ifthis is No. 25 or larger, a working lengthfilm is made with this file in place. If smallerthan this, passive step-back is performed(described earlier). A radiograph is thenmade with a file binding tight. No. 8 or 10files should not be used to take workinglength radiographs; small file tips fade out

Variations

The proper working length distance from the ra-diographic apex varies (Figure 12-27). A periradic-ular lesion resorbs bone and apical tooth struc-ture .'Z The apical resorption may or may not bevisible radiographically, but significantly altersapical anatomy (Figure 12-28). Working lengthdistance from the apex is determined when thefollowing are seen radiograpbically:`

1. No bone or root resorption: 1 mm fromapex.

2. Bone but no root resorption: 1.5 mm fromapex.

3. Bone and root resorption: 2 mm from apex.

The distance from the file to the apex is mea-sured and then the file is adjusted to obtain thecorrect working length. An additional radiographis not necessary for verification unless there is adiscrepancy greater than 3 mm. If so, a confirma-tory radiograph should be made.

ALTERNATIVE TECHNIQUESElectronic Apex Locators

Electronic devices have been designed to deter-mine canal length by "reading" when periodontalligament has been reached by the file tip at the api-cal foramen. The electronic principle is relativelysimple and is based on electrical resistance; when acircuit is complete (tissue is contacted by the tip ofthe file), resistance decreases markedly and current

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suddenly begins to flow (Figure 12-29). 4 " Accord-ing to the device, this event is signaled by a beep, abuzz, a flashing light, digital readouts, or a pointeron a dial.

The original electronic apex locators operatedon the direct current principle. A problem withthese devices was that conductive fluids such as he-morrhage, exudate, or irrigant in the canal wouldpermit current flow and therefore a false reading.Newer devices (Figure 12-30) are impedance-based,using alternating current of two frequencies; thesemeasure and compare two electrical impedances

that change as the file moves apically. The benefitis that these devices are much less affected by fluidconductive media in the canal." The impedance-type apex locators have been demonstrated to be80 to 95% accurate in identifying the apical fora-men. 46,47 Therefore after obtaining a reading, 1 to2 mm is subtracted as the corrected workinglength.

Although there are some variations with newerdevices, most operate similarly. One electrode isattached to the patient (commonly a lip clip); theother electrode is clipped to the file. The patient

FIGURE 12-27Determination of proper working length distance from apex. This distance varies according to radiographic find-i ngs: A, When there is no bone or root resorption: 1 mm from apex. B, Bone but no root resorption: 1.5 mm fromapex. C, Both bone and root resorption: 2 mm from apex. (Courtesy Dr. A. Goerig.)

FIGURE 12-28Apical resorption. A, Bone and root resorption at theapex. B, Viewing this histologically, the apex appearsblunt and the canal has funneling resorption (arrow).The working length must be decreased to confine in-struments to the canal. (Cadaver specimen, courtesyDr. D. Holtzmann.)


203

therefore forms part of the circuit. When currentflows, the operator is notified by one of the afore-mentioned signals. After the length adjustment ismade, a confirmatory radiograph is made (angledwhen indicated) with an appropriate size file atthis length.

These heavily marketed devices have engen-dered the interest and attention of clinicians andhave been the subject of considerable research."The apex locators are most useful for determiningor confirming lengths on apices that are notclearly visible radiographically (Figure 12-31).They also are a good supplement to working radi-ographs and may improve length determina-tion." Importantly, this method does not replaceradiographic techniques." Radiographs not onlydetermine working lengths, but angled workingfilms also provide information regarding toothand canal anatomy, curvatures, and relationships.

Electronic apex locators are also useful foridentifying the presence and location of a perfora-tions' If a perforation is suspected, a file may beclipped to an apex locator. The file tip is thenteased into the area of the suspected perforation.A positive reading would indicate contact withlateral periodontium.

Feeling the Apical Constriction

A popular belief is that a dentist with well-developed fingertip tactile sense can detect

when the file tip has reached the apical constric-tion. In most instances, this is unreliable."Many apical regions do not in fact have a con-striction; even those that do are at variable dis-tances from the apical foramen.

FIGURE 12-29Electronic apex locators (EALs) operate on direct current,which is supplied by the unit on the upper right. One electrode

is in contact with the metal shaft of the file; the other contactssoft tissue, usually by a lip clip. When the tip of the file touchestissue at the apical foramen, current begins to flow.

FIGURE 12-30Examples of impedance-based electronic apex locators. These will function fairly accurately in either a wet or dry canal.

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FIGURE 72-37An apex locator would be very useful in determining the work-i ng length of this molar; all apices cannot be visualized radi-ographically because of superimposition over the other molar.

Patient Response

Another fallacious belief is that if the pulp isnecrotic or if canal preparation is complete, anunanesthetized patient will detect the file tipwhen it reaches and contacts the vital tissue at theapical foramen. Supposedly, the patient then sig-nals this event with an "eye blink" or other painresponse. There are problems with this approachalso. First, the procedure is painful for the pa-tient. Second, a necrotic pulp frequently containsvital inflamed tissue that extends several millime-ters into the canal . 34 This tissue may be very sensi-tive and respond to instrument contact short ofthe apex. Third, a patient feels pain after canalpreparation is complete from hydraulic pressureeven though instruments do not reach the apicalregion.

The opposite of pain with instruments short oflength is lack of pain response when instrumentsare beyond the apex. This has been observed insome situations when, in an unanesthetized pa-tient, an instrument has passed several millime-ters out of the apex without being detected.

REFERENCES

1. LaTurno SA, Zillich RM: Straight-line endodontic ac-cess to anterior teeth, Oral Surg Oral Med Oral Pathol59:418, 1985.

2. Leeb J: Canal orifice enlargement as related to biome-chanical preparation, JEndod 9:463, 1983.

3. Abou-Bass M, Patoni FJ: The effects of decreasing sur-face tension on the flow of irrigating solutions in nar-row root canals, Oral Surg Oral Med Oral Pathol 53:524,1982.

4. Allison D, Michelich R, Walton R: The influence ofmethod of canal preparation on the quality of apicaland coronal obturation, JEndod 5:298, 1979.

5. Weine F, Kelly R, Lio P: The effect of preparation pro-cedures on original canal shape and on apical foramenshape,JEndod 1:255, 1975.

6. Greene KJ, Krell KV: Clinical factors associated withledged canals in maxillary and mandibular molars,Oral Surg Oral Med Oral Pathol 70:490, 1990.

7. Montgomery S: Root canal wall thickness of mandibu-lar molars after biomechanical preparation, J Endod

11:257, 1985.8. Abou-Rass M, Frank AL, Glick DH: Anticurvature fil-

ing method to prepare the root canal, J Am Dent Assoc

101:792, 1980.9. Walton R: Histologic evaluation of different methods

of enlarging the pulp canal space, JEndod 2:304, 1976.10. Reeh E, Messer H, Douglas W: Reduction in tooth

stiffness as a result of endodontic and restorative pro-cedures,JEndod 15:512, 1989.

11. Panitvisai P, Messer H: Cuspal deflection in molars inrelation to endodontic and restorative procedures, JEndod 21:57,1995.

12. Wilcox L, Walton R, Case W: Molar access shape andoutline according to orifice location, J Endod 15:315,1989.

13. Sedgley C, Messer H: Are endodontically treated teethmore brittle?JEndod 18:332, 1992.

14. Wilcox L, Roskelley C, Sutton T: Relationship of rootcanal enlargement to finger-spreader induced verticalfracture,JEndod 23:533, 1997.

15. Stropko J: Canal morphology of maxillary molars:clinical observations of canal configurations, J Endod

25:447, 1999.16. Weller R, Hartwell G: Impact of improved access and

searching techniques on detection of the mesiolingualcanal in maxillary molars, JEndod 15:2, 1989.

17. Ting P, Nga L: Clinical detection of the minormesiobuccal canal of maxillary first molars, Int Endod J

25:304, 1992.18. Haselton D, Lloyd P, Johnson W: A comparison of the

effects of two burs on endodontic access in all-ceramichigh Lucite crowns, Oral Surg Oral Med Oral Pathol89:486, 2000.

19. McMullen A, Himel V, Sarkar N: An in vitro study ofthe effects endodontic access preparation and amal-gam restoration have upon incisor crown retention, J

Endod 16:269, 1990.20. Stokes A, Tidmarsh B: Comparison of diamond and

tungsten carbide burs for preparing endodontic accesscavities through crowns,JEndod 14:550, 1988.

21. Torabinejad M: Passive step-back technique, Oral SurgOral Med Oral Pathol 77:398, 1994.

22. Stabholz A, Rotstein I, Torabinejad M: Effect of pre-flaring on tactile detection of the apical constriction, JEndod 21:92, 1995.


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23. Leubke N, Brantley W: Torsional and metallurgicalproperties of rotary endodontic instruments. II. Stain-less steel Gates-Glidden drills, J Endod 17:319, 1991.

24. Manger M, Waite R, Alexander J, Schindler W: Ideal en-dodontic access in mandibular incisors, J Endod25:206, 1999.

25. Wilcox L, Walton R: The shape and location ofmandibular premolar access openings, Int Endodon J20:223, 1987.

26. Taintor J, Biesterfeld R, Valle G: Termination of theroot canal filling, Dent Surg 3:54, 1979.

27. Wu M-K, Wesselink P, Walton R: Apical terminus loca-tion of root canal treatment procedures, Oral Surg OralMed Oral Pathol 89:99, 2000.

28. Burch J, Hulen S: The relationship of the apical fora-men to the anatomic apex of the tooth root, Oral SurgOral Med Oral Pathol 34:262, 1972.

29. Mizutani T, Ohno N, Nakamura H: Anatomical studyof the root apex in the maxillary anterior teeth, JEndod18:344, 1992.

30. Olson AK, Goerig A, Cavataio R: The ability of the ra-diograph to determine the location of the apical fora-men, Int Endod J 24:28, 1991.

31. Morfis A, Sylaras S, Georgopoulou M, et al: Study ofapices of human permanent teeth with the use of ascanning electron microscope, Oral Surg Oral Med OralPathol77:172, 1994.

32. Matsumoto T, Nagai T, Ida K: Factors affecting suc-cessful prognosis of root canal treatment, J Endod13:239, 1987.

33. Debelian G, Olsen I, Tronstad L: Anaerobic bacteremiaand fungemia in patients undergoing endodontictherapy: an overview, Ann Periodontol 3:281, 1998.

34. Ricucci D: Apical limit of root canal instrumentationand obturation. Part 1. Literature review, Int Endod J31:384, 1998.

35. Ricucci D, Langeland K: Apical limit of root canal in-strumentation and obturation, part 2. A histologicalstudy, IntEndod j 31:394, 1998.

36. Seltzer S, Soltanoff W, Sinai I, et al: Biologic aspects ofendodontics. III. Periapical reactions to root canal in-struments, Oral Surg Oral Med Oral Pathol 26:534, 1968.

37. Seltzer S, Solanoff W, Smith J: Biologic aspects of en-dodontics. V. Periapical tissue reactions to root canal

instrumentation beyond the apex and root canal fill-i ngs short of and beyond the apex, Oral Surg Oral MedOral Pathol 36:725, 1973.

38. Ibarrola J, Chapman B, Howard J, et al: Effect of pre-flaring on Root ZX apex locators, JEndod 25:625, 1999.

39. Katz A, et al: Tooth length determination: a review,Oral Surg Oral Med Oral Patho172:238, 1991.

40. Cederberg R, Tidwell E, Frederiksen N, Benson B: En-dodontic working length assessment: comparison ofstorage phosphor digital imaging and radiographicfilm, Oral Surg Oral Med Oral Pathol 85:325, 1998.

41. Burger C, Mork T, Hutter J, Nicoll B: Direct digital ra-diography versus conventional radiography for esti-mation of canal length in curved canals, J Endod25:260, 1999.

42. Malueg L, Wilcox L, Johnson W: Examination of exter-nal apical root resorption with scanning electron mi-croscopy, Oral Surg Oral Med Oral Pathol 82:89, 1996.

43. Weine F: Endodontic therapy, ed 5, pp 395-405, StLouis, 1996, Mosby.

44. Sunada I: New method for measuring the length of theroot canal, J Dent Res 41:375, 1962.

45. Lumley P: Impedance type electronic apex locators,Endod Pract 2:6, 1999.

46. Pagavino G, Pace R, Baccetti T: A SEM study of in vivoaccuracy of the Root ZX electronic apex locator, JEndod 24:438, 1998.

47. Dunlap C, Remeikis N, BeGole E, Rauschenberger C:An in vivo evaluation of an electronic apex locator thatuses the ratio method in vital and necrotic canals, JEndod 24:48, 1998.

48. Rivera E, Seraji M: Effect of recapitulation on accuracyof electronically determined canal length, Oral SurgOral Med Oral Pathol 76:225, 1993.

49. Fouad A, Reid L: Effect of using electronic apex loca-tors on selected endodontic treatment parameters, JEndod 26:364, 2000.

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51. Fuss Z, Assooline L, Kaufman A: Determination of lo-cation of root perforations by electronic apex locators,Oral Surg Oral Med Oral Radiol 82:324, 1996.

Cleaning and Shaping

LEARNING OBJECTIVES


1/ State reasons and describe situations for enlarging the cervical portion of the canal before performing

straight-line access.

2/ Define how to determine the appropriate size of the master apical file.

3 / Describe objectives for both cleaning and shaping; explain how to determine when these have been achieved.

4/ Diagram "perfect" shapes of flared (step-back) and standardized preparations; draw these both in

l ongitudinal and cross-sectional diagrams.

5/ Diagram probable actual shapes of flared (step-back) and standardized preparations in curved canals.

6/ Describe techniques for shaping canals that are irregular, such as round, oval, hourglass, bowling-pin,

kidney-bean, or ribbon-shaped.

7/ Describe techniques, step-by-step, for standardized and flaring (step-back and/or crown-down) preparations.

8/ Distinguish between apical stop, apical seat, and open apex and discuss how to manage obturation in each.

9/ Describe the technique of pulp extirpation.

10 / Characterize the difficulties of preparation in the presence of anatomic aberrations that make complete

debridement difficult.

11/ list properties of the "ideal" irrigant and identify which irrigant meets most of these criteria.

12/ Describe the needles and techniques that provide the maximal irrigant effect.

13/ Discuss the properties and role of chelating and decalcifying agents.

14/ Explain how to minimize preparation errors in small curved canals.

15/ Describe techniques for negotiating severely curved, "blocked," or constricted canals.

16/ Describe, in general, the principles of application of ultrasonic devices for cleaning and shaping.

17/ Evaluate, in general, alternative means of cleaning and shaping and list their advantages and disadvantages.

18/ Discuss nickel-titanium hand and rotary instruments and how the physical properties of this metal affect

cleaning and shaping.

19/ Discuss the properties and role of intracanal, interappointment medicaments.

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http://disadvantages.is



Objectives

Cleaning

Shaping

Master Apical File Determination

Apical Preparation

Techniques of Pulp Extirpation and Cleaning

and Shaping

Pulp Extirpation

Standardized Preparation

Flaring Preparation

Passive Step-Back

Apical Clearing

Anatomic Aberrations

Chemical Adjuncts

I rrigation

Dentin Softening

Lubricants

Desiccants

Avoidance of Preparation Errors

Problems

Prevention

Other Errors

Review of Basic Principles of

I nstrumentation

Nickel-Titanium Instrumentation

Hand

Engine-Driven Rotary

Combination of Passive Step-Back and Rotary

I nstrumentation

Alternative Techniques of Cleaning and

Shaping

Balanced Forces

Energized Vibratory Systems

Other Mechanized Techniques

Lasers

I ntracanal Medicaments

Applications

Limitations and Contraindications

Calcium Hydroxide

ObjectivesThe end points of cleaning and shaping must berecognized. In other words, is canal preparationcomplete, and what criteria are used to make thatdetermination? Schilder' defined the general ob-jectives of canal preparation as follows: "Rootcanal systems must be cleaned and shaped:cleaned of their organic remnants and shaped toreceive a three dimensional hermetic filling of theentire root canal space."

Cleaning and shaping are action words thatidentify precisely the two major goals of canalpreparation. In fact, the goals are quite different,even though both are accomplished simultane-ously and with the same instruments and agents.Therefore, criteria for each are considered sepa-rately. In addition to cleaning and shaping, apicalpreparation is also an important goal.

CLEANING

Debridement

By definition, debridement is the removal of exist-ing or potential irritants from the root canal sys-tem. The goal is elimination; in actual practice,there is usually only a significant reduction. Theseirritants consist of the following, either singly orin combination: bacteria, bacterial byproducts,necrotic tissue, organic debris, vital tissue, salivarybyproducts, hemorrhage, and other contami-nants. The components in a necrotic pulp spacerepresent a potent irritant.

Technique. The principle of debridement is sim-ple. Ideally, instruments contact and plane allwalls to loosen debris. The chemical action of irri-gants further dissolves organic remnants and de-stroys microorganisms. Irrigants then flush theloosened and suspended debris from the canalspace. This rids the canal space of irritants. How-ever, experiments have shown clearly that with thecanal preparation techniques currently available,such complete debridement is very difficult and inmost cases nearly impossible.` Despite a practi-tioner's best efforts, remnants usually persist afterthe most careful chemomechanical preparation ofthe canal (Figure 13-1). So, realistically, the objec-tives are (1) to reduce these irritants to a subsig-nificant level and (2) to obturate so that the rem-nants are sequestered within the canal. Histologicand ultrastructural studies have demonstrated thepresence of tissue elements and debris at all levelsand in all areas of the canal, particularly in regionsinaccessible to files (Figures 13-1 and 13-2).

Limitations. The root canal system is a very dif-ficult environment in which to operate. To reem-phasize an important concept, files must contact and

13 / Cleaning and Shaping

207

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FIGURE 13-1A, Remnants of tissue and debris are present in apical ramifications (arrows) and in a concavity in the canal wall.B, Remnants in the concavity comprise a mixture of connective tissue, dentin chips, and other debris. This is a re-gion in which the wall was not contacted by files during canal preparation.

plane the walls to debride effectively (see Figure 13-1).Such contact is often impossible owing to the de-sign and physical properties of instruments and theirregularities of the pulp system.

Intracanal instruments were designed origi-nally without consideration to the space in whichthey were to do their work. Reamers and files arebest suited to enlarge a relatively straight, slightlytapered canal for post space. Their design andphysical properties preclude effective debride-ment of actual canals. The interior of canals isbumpy with dips, concavities, intercanal commu-nications, cul-de-sacs, inaccessible fins, apicalramifications, and other sequestered regions thatthese instruments have no chance of reaching. Anadditional complication is the usually curvedcanal that must be negotiated with relatively in-flexible intracanal instruments.

It would seem that these debridement prob-lems could be overcome by enlarging canals togreater sizes and by using irrigants or other chem-icals that would break down tissue and bacterialremnants. However, increasing canal enlargement

may not improve debridement and has other dis-advantages, such as weakening the tooth.' Irrigat-ing solutions also have limitations; these are dis-cussed in detail later in this chapter.

Because of the difficulties with and inadequa-cies of instruments, irrigants, and techniques, theoutcome is usually incomplete debridement ofcanals. There may be sufficient debris to compro-mise success, however, obturation may sequesterthese irritants, but this sequestration may not lastindefinitely. With time, sealer may be washed out,or other communications may develop. Thus, thedebris may now harbor and feed bacteria. Then ir-ritants are produced that pass via the main or lat-eral canals to the periodontium. The result maybe short-term treatment success but long-termfailure. Thus, it is important to maximize canaldebridement during cleaning and shaping.

Criteria. Unfortunately, there are no totally re-liable, easily definable criteria for determining theend point of debridement. One suggestion hasbeen to obtain clean shavings. However, shavingsare difficult to see on files at all, whether clean or

FIGURE 13-2Facial-lingual section through the mesial root of a first molar.The intercommunicating isthmus (arrow) contains tissue aftercanal preparation. These regions are common and are inac-cessible to instruments and irrigants.

dirty. When this criterion has been used in studiesevaluating canal debridement, there is little rela-tionship between clean shavings and the qualityof debridement.' Attainment of clean irrigatingsolution is another criterion. However, this is alsoinaccurate and serves only as a crude indictor.

Achievement of glassy smooth walls is the pre-ferred result.' Smoothness is evaluated by firmlypushing the side of the tip of a small instrumentalong each wall on the outstroke. The wallsshould become and feel smooth in all dimensions.Although the best indicator to date, this criterionis not totally accurate either. Other and better de-terminants are yet to be identified.

SHAPING

Schilder' outlined the principles of shaping as fol-lows: "To develop a continuously shaped conicalform from apical to coronal. The apical prepara-tion should be as small as is practical and in itsoriginal position spatially." In addition, removal ofa uniform layer of dentin in all dimensions and allregions of the canal is also desirable. Is such uni-form removal of dentin from all canal walls achiev-able? The answer is "seldom" for either straight orslightly curved canals and "almost never" for more


209

FIGURE 13-3Canal cross section (after preparation) shows the ineffective-ness of debridement at times. The dashed line indicates theapproximate dimension of the original canal. Residue in-cludes intact tissue with blood vessels (BV) mixed withdentin chips (DC). Note that instruments have done most oftheir work by stripping away the dentin outside the originalcanal and have left other areas untouched.

curved canals. The same problem occurs in shap-ing as in cleaning. The nature of canal dimensions,shape, and curves as well as the physical propertiesof shaping instruments prevents the possibility ofa uniform, tapered, flowing preparation.

Essentially all canals are curved, and most in-struments are relatively inflexible. It has been sug-gested that instruments be precurved to fit thecanal. However, the files will cut to the outside ofthe curvature ("transportation") regardless ofwhether files are precurved 7 ' and whether the filesare stainless steel or nickel- titanium. 9 In curvedcanals, files do most of their work by strippingaway layers of raw dentin from one or two walls incertain areas (Figure 13-3); they may not touch ormay enlarge many other regions of the canal."Recognizing these deficiencies, the dentist at-tempts to minimize this action by using certaintechniques of preparation.

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Enlargement

The eternal question is, how much should thecanal be enlarged? The answer is simple (althoughimplementation is difficult): enough to permitadequate debridement as well as manipulationand control of obturating materials and instru-ments, but not so much that the chances of mak-ing procedural errors and needlessly weakeningthe root are increased.

taper is sufficient to permit spreader penetrationdeep into the canal (0 to 1 mm from the apicalstop) with some space adjacent for gutta-percha,the flare is adequate (Figure 13-4)." With lateralcondensation, the deeper the spreader penetratesduring its initial insertion alongside the gutta-percha, the better the apical seal." With verticalcondensation, sufficient flare is required to allowplacement of pluggers within 3 to 5 mm of work-ing length.

Taper

Generally, taper should be sufficient to permitdeep penetration of spreaders or pluggers whenobturating with gutta-percha. Excessive tapermay result in unnecessary removal of dentin andweakening of the root.

Criteria

Adequate shaping basically reflects adequacy ofpreparation for obturation. That is, whether thetechnique is lateral or vertical condensation, thecanal must be flared and enlarged to permit con-trol and to achieve adequate depth for spreader orplugger insertion during obturation."

To test adequacy, selected obturating instru-ments are "tried-in" during canal shaping. When

MASTER APICAL FILEDETERMINATION

The master apical file (MAF) is by definition thelargest file that binds slightly at the correctedworking length. The MAF is determined by pas-sively placing successively larger files at the cor-rect working length until a size is reached thatslightly binds at the tip. This determination ismade after straight-line access (see Chapter 12).Straight-line access allows files to be introducedwithout binding through the chamber and intothe canal until the first canal curve is reached,thus eliminating interference cervical to theapical constriction." After MAF determination,the next procedure is step-back cleaning andshaping.

FIGURE 13-4A, Canal preparation has inadequate flare, limiting spreader penetration. B, Canal preparation has greater taperto allow deep spreader penetration and better obturation.


211

APICAL PREPARATION

An additional objective is adequate preparationof the apical region. Length is important, buteven more critical is the creation of an apical"matrix" or constriction. The apical matrix hastwo purposes: (1) to help confine instruments,materials, and chemicals to the canal space; and(2) to create (or retain) a barrier against whichgutta-percha can be condensed. Depending onapical foramen configuration and canal shapeand size, an apical stop, apical seat, or open apexwill be created (Figure 13-5). Whichever of thesethree occurs, the result will influence the choiceof the obturation technique and possibly affectthe ultimate prognosis."

The apical patency concept has been proposedas another means of managing the apex.'-' Thetechnique is to perform apical "trephination,"i.e., to pass small files through the apical fora-men (without widening it) at times during canalpreparation. The idea is that this will preventhard or soft tissue blockage of the foramen,thereby improving debridement and reducingirritants. There is no experimental support forthe apical patency approach. In fact, repeateduse of files through the apex and extruded sealerwill damage periradicular tissues and causeinflammation.

Variations

Apical Stop. A barrier at the preparation end isan apical stop.

Apical Seat. Lack of a complete barrier but thepresence of a constriction represents an apical seat.

Open Apex. The apical preparation resemblesan open cylinder (neither barrier nor constric-tion). Open apex is undesirable and will probablynot confine materials to the canal space. In addi-tion, there is no semblance of a matrix againstwhich to condense gutta-percha; often, no apicalseal will be created.

Criteria

An instrument one or two sizes smaller than thatused for apical preparation (i.e., the MAP) is theinstrument used for evaluation. If this smaller in-strument is placed to length, tapped around, andhits a dead end in all areas, this is an apical stop. Ifthe file meets some resistance but can be passedthrough the constriction, this is an apical seat. Ifthe instrument passes unimpeded through theapical preparation, neither seat nor stop is pre-sent; this represents an open apex. Lack of a stop orseat is undesirable and is usually preventable.

A mnemonic that can be used to rememberstop, seat, and open is as follows: Santa Claus at-tempts to go down the chimney. If the damper isclosed, his feet strike that impediment and heproceeds no farther; that is a stop. If the damper isopen but small, his feet and legs will pass throughbut not his seat. If a damper is not present, his feet,legs, seat, and torso pass through with ease (anopen apex); the same thing tends to occur withgutta-percha and sealer during condensation.

FIGURE 73-5Apical preparations. A, Apical stop: Creation of a small ledge at working length. B, Apical seat: Permits passageof a small instrument through the apical foramen. C, Open apex: Preparation is wide open with no barrier or con-striction. It is difficult to obtain a seal and to contain obturating materials. (Courtesy Dr. A. Goerig.)

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Techniques of Pulp Extirpationand Cleaning and ShapingPreparation includes removal of vital pulp (extirpa-tion) as well as cleaning and shaping. Cleaning andshaping methods have historically varied accordingto the situation and the obturating material se-lected. However, at present, two basic approachesare used: the standardized taper and the flaring (step-back or crown-down) taper. There are several varia-tions in methods used to achieve these.

The broach is measured at estimated lengthand teased into the canal short of working length.The handle is rotated a few times and then with-drawn. The broach is not reused if it is bent or hasbound in the canal-a new instrument is selected.If tissue is not removed, a larger size is tried. Atechnique used in larger canals is the "broachwrap." Two smaller broaches are inserted, andthen the handles are wrapped several timesaround each other; this often engages and dis-lodges the pulp.

PULP EXTIRPATIONBulk Removal

Pulpotomy is removal of the coronal vital pulp.Extirpation of the vital radicular pulp with a

broach does not represent pulpectomy, which istotal removal of pulp tissue. Rather, portions ofpulp are dislodged and pulled out, leaving shred-ded remnants. This is a partial pulpectomy. Com-plete removal is not accomplished until workinglength is established and considerable canalpreparation has been done.

Complete removal of necrotic and vital radicu-lar pulp is referred to as debridement (cleaningand shaping). To perform a pulpotomy or pulpec-tomy, there must be vital pulp tissue present.There is no descriptive term for the removal ofnecrotic pulp tissue; however debridement of thecanal space is necessary. The description "accesswith no vital pulp" or "debridement with no vitalpulp" should be used instead of "pulpotomy" or"pulpectomy" to describe situations in which thepulp is necrotic.

The preferred time for pulp extirpation is dur-ing access. Completion of access preparation isdifficult without good visibility, which is difficultwith continuous hemorrhage into the chamberfrom a torn pulp stump. The best time to extir-pate is when the chamber is unroofed and canalsare discovered. Another indication for extirpationis persistent tissue sensitivity in a particular canal.The hyperreactive pulp is broached out quickly,facilitating canal preparation if the patient iscomfortable.

Technique

A barbed broach should fit the canal dimensionsapproximately (according to radiographic size)but does not bind. The larger the instrument, thebetter it will "grab" tissue. However, a too-large in-strument risks binding in dentin with possiblebreakage. Caution must be used with broaches be-cause they are somewhat fragile instruments andare difficult to remove when separated.

STANDARDIZED PREPARATION

This is the classic technique initially described asthe preferred method of cleaning and shaping. ' 6

Objective

The desired end result is the creation of a prepara-tion that has the same size, shape, and taper as astandardized instrument. The technique was anoutgrowth of size standardization, which was intro-duced in the 1950s as a guide for endodontic in-strument manufacturers." At that time, an attemptwas made to apply these standards as a guide tocanal enlargement. In fact, creating a true standard-ized tapered preparation is difficult in ideal situa-tions and impossible in curved canals.10,18,19

Standardized preparation is indicated for silvercone obturation but may also be used for gutta-percha.20 However, the operator must exercisecare, particularly in curved canals. Preparationwith large instruments around curves transportsthe preparation, which tends to create irregulari-ties (ledges and zips) and subsequent problems.

Method

The technique is shown in Figure 13-6.

FLARING PREPARATION

This is a tapered preparation, using a step-back orcrown-down technique or a combination of thetwo. The concept of the step-back (also known asflaring or serial preparation) technique is rela-tively recent. It was first described by Clem" in1969 and became popular when a series of re-search reportS2,4 indicated its superiority over thestandardized preparation techniques. In addition,the step-back technique creates a smoother flowand a more tapered preparation from apical tocoronal direction. The step-back technique withstainless steel instruments is currently the mostwidely taught and used technique . 22 The crown-down (also known as step-down) technique is also

relatively new and also creates a tapered prepara-tion. Flaring techniques that use nickel-titaniumhand or engine-driven rotary instruments are be-coming increasingly popular. Also popular aretechniques that use a combination of step-backand crown-down with hand and/or rotary instru-mentation. These will be further discussed later inthis chapter.

Objective

The objective is to keep the apical preparation assmall as practical (but well debrided) with an in-creasing taper throughout the canal. Also, thefinal apical preparation should be at or close tothe original canal position. It is desirable to re-move a layer of dentin from all canal walls fromapical to coronal. Such removal has been shownto be difficult but is more achievable with the flar-ing techniques.

Method

The basic method of canal preparation for anyflaring technique is as follows:

1. Negotiate the canal space with small files tolength.

2. Remove coronal dentin (enlarge the coronalcanal) to facilitate placement of larger filesin the middle and apical regions. This is per-formed with Gates-Glidden burs, orificeopeners, or hand files.

3. Determine the size of the file that corre-sponds with the size of the most apicalcanal space. This is the "master apical file."


21 3

FIGURE 13-6Standardized technique. A to C, The objective is to at-tempt to prepare the canal to uniform size using suc-cessively larger instruments to working length. D, In re-ality, instruments larger than No. 20 or 25 (dependingon curvature) tend to cut straight ahead, resulting inapical "transportation," ledges, or creation of a newcanal, as indicated by the dotted and dashed lines.

FIGURE 13-7Step-back technique. A, Canals are prepared to a smallsize at the apical length. B and C, Larger files are usedsequentially to decreasing lengths. D, The result is apreparation with small apical enlargement and a markedtaper from apical to coronal. Small steps usually remaini n the apical area.

4. Enlarge the apical and middle canal spaceswith a flaring preparation (step-back orcrown-down) to clean and shape.

The description to follow is a hand prepara-tion technique with stainless steel and/or nickel-titanium files. First, access preparation, passivestep-back ,23 and working length are performed asdetailed in Chapter 12.

Straight-line access is also completed and MAFsize is determined. The step-back technique (Fig-ure 13-7) is then executed as follows. Note thatapical preparation has two phases, initial andfinal. The initial phase is small to minimize trans-portation. In the final phase the apical prepara-tion is increased three to four sizes larger duringapical clearing; this will improve debridement andobturation. The apical clearing technique is ex-plained later in this chapter.

Apical Preparation. This is the next step afterstraight-line access is made and the MAF size isdetermined. To keep the canal small but debrided,the apical 1 to 2 mm of the canal is enlarged byreaming (cutting by rotation), generally to onlyone or two sizes larger than the MAR Care is re-quired to not overprepare the apical region, particularlyin the curved canal!

As the curvature becomes greater, a smallerapical preparation is needed. If the canal is smalland the curvature is more than slight, the MAF isusually no larger than a No. 20 file. A straight orslightly curved canal allows more latitude for alarger MAR

If the apical portion of the curved canal isanatomically larger than a No. 25 file, to minimizetransportation, no attempt should be made to enlarge

21 4


this region further than the size of the file that shows slightbinding. Again, whichever instrument binds slightlyat length is used; this will be the MAF. Step-back isbegun from this point.

Taper. After apical preparation, tapering ofthe remaining canal is created by shorteningthe working length of each successively largerinstrument by 0.5 mm and by performing pe-ripheral filing (Figure 13-8)." This creates thestep-back.

Recapitulation. After each step-back file is used,recapitulation is performed by returning to lengthwith the MAF (or smaller file) (Figure 13-9)." Theinstrument is rotated carefully to loosen debrisbut not enlarge the apical canal.

I rrigation. At least 2 ml of irrigant is usedbetween each file size after recapitulation (Fig-ure 13-9).

Size of Preparation. Step-back instrumentationup to at least a size 70 file is usually necessary. Thisshould give adequate debridement of most of thecanal as well as sufficient taper to permit deepspreader (or plugger) penetration. A larger step-back is indicated in larger canals.

Final Apical Enlargement. This will improvedebridement of the apical portion of the canal.See the upcoming section on "Apical Clearing."

Crown-Down

The "crown-down pressureless" technique26 andthe step-down technique27 are modifications ofthe step-back technique. Crown-down, step-down, and step-back procedures produce a simi-lar outcome, resulting in a flaring preparationwith small apical enlargement. Like the step-back,these techniques are particularly useful in finecurved canals of maxillary and mandibular mo-lars (Figure 13-10). Advocates propose that thecanals will be somewhat debrided before the in-struments are placed in the apical region, therebydecreasing the chance of debris extrusion.

The crown-down is often suggested as a basicapproach using nickel-titanium rotary instru-ments. Although there is some evidence that thesetechniques are effective and result in a desirablepreparation shape ,26.27 there is no proof that theyare superior clinically to step-back instrumenta-tion with hand files. However, the logic of theseapproaches makes them good alternatives.

PASSIVE STEP-BACK

The passive step-back technique uses a combina-tion of hand instruments (files) and rotary instru-ments (Gates-Glidden drills and Peeso reamers) toachieve adequate coronal flare before apical rootcanal preparation.

The passive step-back technique provides anunforceful and gradual enlargement of canals inan apical-coronal direction. In addition, it is ap-plicable in every canal type, is easy to master, re-duces procedural accidents, and is convenient forboth operator and patient.

Instruments

No. 10 to 40 K-type files, No. 2 and 3 Gates-Gliddendrills, and Peeso engine reamers as well as high-speed round and diamond burs will suffice for mostsituations.

FIGURE 13-8Peripheral filing. The end portions of the files are pressed suc-cessively against each of the four walls (arrows). The actioni s similar to that used with a paintbrush. (Courtesy Dr. G.Scott.)

Clinical Techniques and Rationale

Step One: Access Preparation. With the use of anappropriate sized bur in a high-speed handpiece,

FIGURE 13-9Sequencing during preparation.


21 5

the pulp chamber is penetrated and unroofed.After the canal orifice is located, the access cavitywall(s) are flared adjacent to the orifice with athin, tapered diamond bur. With use of the diag-nostic film, a No. 15 file is placed in the canal atthe estimated working length of the root canal ei-ther as determined radiographically or with anelectronic apex locator.

Step Two: Passive Step-Back Hand Instrumentation.

After depositing sodium hypochlorite in the pulpchamber, a No. 10 or 15 K-type file is placed to theradiographic apex with a very light one eighth toone quarter turn and push-pull strokes to establishapical canal patency with little or no resistance.With the same motion, No. 20,2S, 30,3S, and 40 K-type files are carried into the canal as far as they canbe inserted passively to remove small amounts ofdentin. After passage of these files, the canal is irri-gated with sodium hypochlorite solution.

Step Three: Passive Use of Gates-Glidden Drills. ANo. 2 Gates-Glidden drill is inserted into themildly flared canal to a point where it bindsslightly. It is then pulled back about 1 to 1.5 mmand the slow-speed handpiece is activated. Withan up-and-down motion and slight pressure, thedesired canal wall(s) is planed and flared. A simi-lar technique is used to plane and flare the coro-nal region with No. 3 Gates-Glidden drill. A No. 4Gates-Glidden drill is used in large canals. Theroot canals should be irrigated with sodiumhypochlorite solution between the engine-driveninstrument.

Step Four: Passive Use of Peeso Reamers. A No. 2Peeso reamer is placed into the canal to a point

where it binds slightly. It is then pulled backabout 1 to 1.5 mm and the slow-speed handpieceis activated. With a gentle up-and-down motion,the coronal portion of the canal is shaped andflared further. With the use of a similar technique,the coronal 2 to 3 mm can be flared with a No. 3Peeso reamer.

Step Five: Confirmation of Working Length. Be-cause flaring and removal of curvatures reducethe working length, it is essential to confirm thecorrected working length before apical prepara-tion. After placing a No. 15 (patency file) orNo. 20 file in the canal, the working length shouldbe confirmed either with a radiograph or an elec-tronic apex locator.

Step Six: Apical Preparation. After the canal isflared and the corrected working length is deter-mined, a No. 20 file should penetrate to the work-ing length without any resistance. The canal is thenprepared with sequential use of progressively largerinstruments placed successively short of the work-ing length. Narrow or curved root canals shouldnot be enlarged beyond the size of No. 25 or 30 files.

Evaluation Criteria

There are basically three criteria for evaluation ofcanal preparation.

1. Dibridement. After preparation, the MAF tipis pressed firmly against each wall on theoutstroke. All walls should feel smooth.

2. Taper. The selected spreader passes easily toor within 1 mm of the working length with

FIGURE 73-10A summary of the step-down preparation. Thediagram indicates the instruments or burs used

i n each region. Other combinations of burs andhand and/or rotary instruments can be used.This approach is designed for straight unim-peded access to the apical region. (CourtesyDr. A. Goerig.)

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13 I Cleaning and Shaping

APICAL CLEARING

FIGURE 13-77Apical clearing has two steps: finalapical enlargement and dry reaming.Note removal of dentin chips apicallyand accentuation of the apical stop.The last instrument used is the finalapical file (upper right lower center).

space alongside for the master gutta-perchacone.

3. Apical Preparation. A seat or a stop or neither(open apex) is identified by using a filesmaller than the MAF at the workinglength.

These three criteria were described earlier inthis chapter.

APICAL CLEARING

Apical clearing results in (1) better debridement,(2) enhanced obturation, and (3) a more definedapical stop.28 Performed in a prepared canal with anapical stop, apical clearing enlarges the apical re-gion at the corrected working length (Figure 13-11).There are two steps: final apical enlargement and dryreaming.

Apical clearing is indicated only if there is anapical stop. Further apical enlargement in thepresence of an apical seat or open apex configura-tion increases the chance of an overfill by remov-ing dentin chips that are forming a partial plug orseal, or it may actually open the apex further.

Final Apical Enlargement. This step is performedafter canal preparation is complete and has metthe criteria of adequate cleaning and shaping. In-stead of final recapitulation, instruments three tofour sizes larger than the MAF are carefully spun(reamed) in a clockwise manner at the workinglength in the wet canal. Therefore, the final apicalsize in a smaller canal would be No. 35 or 40. Finalirrigation with 2 to 3 ml of irrigant per canal is

followed by drying with paper points. This mini-mal, careful use of files in a tapered (flared) canalwill better debride the apical few millimeters andwill not cause transportation or ledging.28

Final apical enlargement is not done in canalsgreater than a size 40. If MAF size is alreadygreater than 40 and there is an apical stop, dryreaming is done with the MAF only.

Dry Reaming. The files used will remove dentinchips that pack apically during drying (Fig-ure 13-12). Dry reaming is done after final apicalenlargement and irrigation and drying with paperpoints. The last size file used for final apical en-largement (or the MAF if larger than a size 40) isthen spun carefully in a clockwise manner tolength. This is the final apical file.

ANATOMIC ABERRATIONS

The root canal system, contrary to the usual dia-grammatic representation, is irregular. MotherNature does not form dentin internally with auniform pattern; therefore, there are many re-gions containing tissue that lie outside the maincanal. These relatively inaccessible areas must beconsidered during preparation and are recognizedas potential causes of long-term failure.

Types

These aberrations are subclassified as intercanalisthmi, cul-de-sacs, lateral canals, apical ramifica-tions, and concavities. Numbers and irregularitiesof anatomic aberrations increase in the posterior


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FIGURE 13-12Apical clearing. Apical enlargement has been done with Nos.25, 30, and 35 files (left to right). Note the dentin shavings(arrows) on the apical regions of the files.

teeth,29 reflecting the larger roots of molars and

most premolars as well as their complex patternof formation.

Significance

All these aberrations are relatively inaccessible tointracanal instruments . 3° Regardless of the tech-nique or chemicals used, isthmi (see Figure 13-2),cul-de-sacs, lateral canals (Figure 13-13), and apicalramifications (Figures 13-1 and 13-14) are gener-ally not debrided at all. Fins and concavities, if ex-posed to irrigants, may be partially cleaned, proba-bly owing to the surface solvent or flushing actionof the irrigant. Not only are all these aberrationslargely undebrided, but also bits of tissue anddentin chips may actually be pushed into theseareas after being loosened from the main canal.

NOTE: Maximal debridement will occur pre-dictably only when the files contact and plane allwalls. The ability to achieve maximum instru-ment contact is enhanced with good straight-lineaccess (Figure 13-15).

FIGURE 13-13A lateral canal (arrow) in this cross section of a root in the api-cal third. Although the main canal has been well debrided, tis-sue remains intact in the lateral canal. This is a typical finding.

FIGURE 13-14Apical ramifications. These are similar to the lateral canals inthat they communicate pulp-to-periodontium. These regionsalso contain tissue and preparation debris (arrow) that is notremoved by instruments and irrigants.

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FIGURE 13-15I nadequate straight-line access on the mesial canals (A) hasbeen corrected (B). C, The resultant preparation and obtura-tion shows small apical enlargement and continuous flaring.

The importance of minimizing the volume oftissue remnants in canals after preparation is obvi-ous. If these irritants are sufficiently large and po-tent, have access to the periodontium, and are nototherwise "neutralized" by host defenses, diseaseand eventual failure will occur because of inflam-mation. This principle was discussed in detail ear-lier in this chapter. The bottom line is that thereare regions that cannot be debrided and these maycompromise treatment and, ultimately, success.Therefore, some factors that cause failure are be-yond the capability of the dentist to manage.

Chemical AdjunctsAs man does not live by bread alone, the pulp sys-tem is not cleaned and shaped by instrumentsalone. Important adjuncts are irrigants and agentsthat aid in debridement and that may alter dentinto facilitate enlargement. All vary in relative effec-tiveness. Other adjuncts are lubricants, which facil-

irate the negotiation of small canals, and desic-cants, which aid in drying before obturation.

I RRIGATION

With filing, the other important process in canaldebridement is irrigation. In theory, files loosenand disrupt materials within canals and removedentin from the walls as shavings; the wholesludge is then flushed out with an irrigant. Thisprocess is more theoretical than actual. Irrigantsand irrigation are only moderately effective. Themost important factor is the delivery system ofthe irrigant and not the solution per se.

Irrigants

Many types of solutions have been used, such asdistilled water, concentrated acids, and antimicro-bials. Unfortunately, although numerous studieshave been done in vitro (not in a clinical mode),the relative effectiveness of different irrigants has

not been clearly demonstrated in clinical usage.Therefore, much information is theoretical.

Although the major function of an irrigant isto flush debris from the canal, the irrigant mayhave additional properties that aid in cleaningand shaping. Below are outlined the characteris-tics of an ideal irrigant.

Properties of Ideal Irrigant

Tissue or Debris Solvent. In regions inaccessibleto instruments, the irrigant could dissolve ordisrupt soft tissue or hard tissue remnants topermit their removal . 31-33

Toxicity. The irrigant should be noninjurious toperiradicular tissues.Low Surface Tension. This property promotesflow into tubules34 and into inaccessibleareas . 3 ' Alcohol added to an irrigant de-creases surface tension and increases penetra-bility36 ; whether this enhances debridementis unknown.Lubricant. Lubrication helps instruments toslide down the canal. All liquids have this ef-fect, some more than others.Sterilization (or at Least Disinfection).37.38Removal of Smear Layer. The smear layer is alayer of microcrystalline and organic particledebris spread on the walls after canal prepara-tion. There are solutions that chelate and de-calcify remove the smear layer .39-41 At present itis not known whether the smear layer shouldbe removed. One advantage is that the smearlayer seems to inhibit bacterial colonization."Other Factors. Other factors relate to irrigant util-ity and include availability, moderate cost, userfriendliness, convenience, adequate shelf life,and ease of storage. An additional important re-quirement is that the chemical not be easily neu-tralized in the canal to retain effectiveness.

Solutions. Sodium hypochlorite, in variousconcentrations, is the most popular and most ad-vocated irrigant. This inexpensive, readily avail-able, easily used chemical usually rates the best inresearch. However, experimental evidence doesnot necessarily correspond directly to clinical ef-fectiveness. Although in vitro studies" indicatethat sodium hypochlorite dissolves tissues read-ily, experiments in extracted teeth and clinicalusage in patients are less impressive. Most histo-logic and scanning electron microscope studies" -" do not show that the tissue dissolution or ster-ilization properties of sodium hypochlorite areconsistently effective.

The difference between in vitro and in vivostudies may be that in the clinical situation, irri-


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gating solutions have limited surface contact andare buffered (neutralized). In the canal, irrigantswould not have extensive and intimate contactwith all areas of tissue.47 In addition, the irriganthas little access to sequestered areas and aberra-tions and, therefore, leaves regions undebrided.46

The same phenomenon of noncontact maylimit the antibacterial action of irrigants. Al-though experiments have shown that sodiumhypochlorite is very effective in vitro48 and doesreduce bacterial populations in canals and intubules," bacteria usually are not totally elimi-nated. 50-52 The same problem of limited contact inhidden areas compromises bactericidal action.

Another disadvantage of sodium hypochloriteis toxicity. It is capable of causing tissue damageand has access to periradicular tissue in smallamounts .53,54 However, the limited extrusion ofsodium hypochlorite is unlikely to be significantbecause it is diluted and buffered by tissue fluidsapically.

Chelators (calcium removers), such as ethylene-diaminetetraacetic acid (EDTA) or citric acid, re-move the smear layer. The combination of chela-tors alternating with sodium hypochlorite haspotential as the ultimate clinical debriding agentto soften dentin'-' and to reduce the smear layerand organic debris." As yet, this theory has beentested only in bench-top studies and not in clini-cal trials.

The use ofhydrogen peroxide (H2O2), alone or al-ternating with sodium hypochlorite, is not benefi-cial. This once popular method was thought tohave a nascent bubbling action to facilitate debrisremoval; however, improved debridement doesnot occur.56,57

Other sterilizing agents have been tested. A com-mon antimicrobial solution used in dentistry ischlorhexidine. In both in vivo and in vitro experi-ments chlorhexidine has been shown to signifi-cantly reduce numbers of bacteria." However,sodium hypochlorite is probably more effective"and offers the distinct advantages of ease of use,some tissue dissolution, and much lower cost.

Recommendation. A suggested concentration ofsodium hypochlorite is common householdbleach (5.25%) diluted with equal parts of waterfor a 2.6% solution. This is just as effective as fullstrength and is safer and more pleasant for bothnatient and dentist.

Technique

Needles. Different types of needles are avail-able, but none has a demonstrated advantage.What is important is the gauge, which should besmall. A 27- or 28-gauge needle is preferred. These

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needles have the potential to pass farther into thecanal for better delivery and flushing. Smaller nee-dles tend to clog; this tendency is minimized byaspirating air into the needle after each irrigation.

Usage. Needle penetration and volume of irrig-ant are the most important factors. The needle in-troduces irrigant to flush the canal only coronal tothe extent of penetration .57,60 Therefore, a smallergauge needle, in conjunction with canal enlarge-ment and copious and frequent irrigation, willproduce better flushing (Figure 13-16).

An interesting recent innovation is the use ofnickel-titanium needles. These are flexible and re-portedly can be inserted deeply into small, curvedcanals. If this claim proves to be correct, theyshould provide improved flushing of canals.

Safety. To avoid forcing irrigant or debris outof the apex, the needle tip must not bind in thecanal. Careful insertion and slight withdrawalafter binding (or a slight pumping action duringirrigation) minimizes this potentially serious oc-currence that creates a "hypochlorite accident.""This free backflow is particularly important whenthere is no apical stop or when the apical foramenopens directly into the maxillary sinus.

FIGURE 13-76Depth of irrigating needle penetration is critical. A 27-gaugeneedle (left) is closer to length (preferred) than the 25-gaugeneedle (right). No flushing occurs except coronal to the needle.

DENTIN SOFTENING

Dentin softeners can potentially facilitate instru-ment passage and canal enlargement by removingmineral components from the dentin walls oreliminating obstructions .

62,63 Whether dentinsofteners are clinically advantageous is doubtful.

Chelators

By definition, the organic substances called chela-tors remove metallic ions (such as calcium) bybinding them chemically. These agents have beenpromoted as commercial products, usually incombination with lubricating or bubbling agents(oxygen releasers).

Types. The two most common chelators areEDTA and dilute (10%) citric acid.64

Action. As dentin-softening agents, chelatorshave not provided impressive results in either invitro or in vivo studies. EDTA works very slowly,65probably more slowly than the cutting action ofthe file. This is particularly true in the apical re-gions of small canals, where the amount of chelat-ing agent that can be introduced is limited.66 Thecombination of EDTA and bubbling agents alsodoes not seem to increase the volume of tissue re-moved or aid in flushing. Limited information isavailable about citric acid .64

Effectiveness. A time and motion study67demonstrated that chelators alone or in combina-tion with sodium hypochlorite did not reduce thetime required for canal preparation. EDTA was in-effective; the combination of 10% citric acid usedalternately with sodium hypochlorite slightly de-creased the time needed for enlargement.

There is no proof that chelators soften or re-move canal obstructions sufficiently to permitpassage of instruments. In fact, softening agentsfor this purpose are contraindicated because theyslightly alter the walls, thereby limiting the abilityof instruments to be guided along hard dentin. Ifthese softening chemicals are used, they should beplaced in canals only after instruments have beenused to length and the canal preparation has beenstarted. As a further precaution, these chemicalsshould not remain in the canal for any period oftime without instrumentation.

Decalcifiers

By definition, decalcifiers are chemicals that re-move mineral salts in solution. Decalcifyingagents are commonly used in histologic prepara-tion of mineralized tissues, but they have not beendemonstrated to be useful in canal enlargement.

Acids. Strong inorganic acids, such as hy-drochloric and sulfuric acids, have been used as


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enlargement aids. Organic acids such as concen-trated citric acid (30% to 50%) have also been pro-posed for irrigation and softening. These concen-trated acids are too potent. Therefore, theirtoxicity is high and their decalcifying action toorapid to control. They are not recommended.

LUBRICANTS

Lubricants are helpful in passing of instrumentsto length during exploration and negotiation ofsmall constricted canals. If small files bind pro-gressively tighter and stop short of workinglength, this indicates a need for a lubricating sub-stance. Lubricants may not be beneficial when thefile stops abruptly, which indicates a ledge or ob-struction that must be bypassed.

Types

Glycerin is a good lubricant. This mild alcohol isvery slippery, self-sterilizing, inexpensive, andnontoxic. Also it is slightly soluble, permitting re-moval once it has completed its function. Soap(liquid or bar) or topical anesthetic may also beused. However, liquid soap (unless sterile) or barsoap may be contaminated with bacteria.

Commercial preparations of EDTA usuallycontain lubricants (wax or glycerin). These aresuitable as lubricants but should be used withcaution when one is negotiating a tight canal;EDTA may soften the walls slightly, thus permit-ting the file tips to gouge and ledge.

Usage

For glycerin or sterile liquid soap, a drop is placedat the orifice by picking up a small amount withcotton pliers, placing the tip at the orifice, andopening the pliers slightly. This introduces small,controlled amounts of the liquid (Figure 13-17).Another method is to introduce glycerin with atuberculin (or other small) syringe.

The file is worked up and down through theglycerin and into the canal using a pumping ac-tion and counterclockwise spin. This carries thelubricant ahead of the file. Usually the file canthen be worked (teased) closer to length. Lubri-cant may even be used to facilitate initial enlarge-ment through two or three file sizes.

DESICCANTS

determined. The same irrigating syringe used inthe same manner as that used for chemical irriga-tion is indicated for alcohol. Only a small amountof alcohol (1 to 2 ml per canal) is needed.

Avoidance of Preparation Errors

Preparation errors are most common in small,round, curved, long canals. As stated earlier, instru-ments are not designed to enlarge small curves; theyattempt to straighten themselves68 and cut the out-side of the curve in the apical region . 7,69 Histologicsections of these curved canals after preparation aredramatic. The files have done most of their work bystripping away layers of raw dentin from certainareas but accomplishing nothing in other regions(see Figure 13-3) .'° Using increasingly larger instru-ments only aggravates the effect. The outcome willbe largely undesirable. Careful instrument use is thekey. 71 In addition, a flaring (step-back or crown-down) technique involves small instruments in theapical curvature and larger, less flexible instrumentsin the straighter portion of the canal. This prepara-tion tends to create fewer problems. More informa-

Concentrated solutions of 70% to 90% alcohol( methanol or ethanol) may be used as a final irri-gant to dry the canal and remove traces of otherchemicals. Whether this is beneficial has not been

FIGURE 13-17Glycerin is an excellent lubricant. A drop (arrow) is trans-ported from a dappen dish to the canal orifice in the beaks ofcotton pliers or may be introduced with a syringe.

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FIGURE 13-18Hazards of overenlarging the apical curvature. A, Correct preparation is maintained when small flexible instru-ments, less than No. 25, are used to negotiate the curvature. B, Larger instruments increase stiffness and cuttingefficiency and transport the apical preparation. C, Continued enlargement results in perforation. D, Apical regioni s zipped when large instruments are continually forced apically.

FIGURE 73-19Transportation, creating a small ledge. The apical region of acurved canal shows too-large file overpreparation andstraightening of the canal with creation of a small ledge out-side the curvature. (Courtesy Dr. P. Ardines.)

tion on preventing and managing canal prepara-tion problems is found in Chapter 18.

PROBLEMS

Overinstrumentation

A major mistake is overenlargement of small,curved canals. The files cut to the outside of thecurvature (a process called transportation) in an at-tempt to straighten themselves and cut to the in-side of the curve in the cervical region. This re-sults from using too-large instruments oroverusing smaller instruments in the apicalcurved portion of the canal (Figure 13-18). Thegreater the curvature72 and the longer and smallerthe canal, the higher is the potential for the fol-

FIGURE 13-20Both mesial and distal canals were straightened, ledged, andobturated short of working length. The preparation and theobturation are not centered in the root. The long-term prog-nosis is compromised; significant areas of canals remainundebrided and unobturated.

lowing unfortunate occurrences.69,73 Each prob-lem adversely affects short-term or long-termprognosis by compromising obturation74 or bycreating a frank perforation.

Ledge Formation

Degree of curvature is the problem: the greater thecurve, the more likely is the formation of a ledge .'zAs the instrument straightens, the tip begins togouge into raw dentin (Figure 13-19). It also tendsto cut straight ahead; the operator may accentuatethis action by boring deeper in dentin in an at-tempt to regain lost length. The file now has thesensation of banging into a dead end short oflength; this is the feeling of a ledge. A radiograph


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FIGURE 13-21The consequences of ledging and "bor-i ng" a new canal. A, Not only did per-foration occur, but also an area of thecanal (arrow) remains undebrided andunobturated. B, At 2-year recall, theperiradicular lesion remains, thus consti-tuting a treatment failure.

FIGURE 73-22Correcting a ledge. A, Ledges or obstructions are occasionally bypassed by placing asmall bend at the instrument tip. B, To negotiate the file past blockages or ledges, thetip is teased along the canal wall to attempt to locate the original canal.

shows that the instrument or obturation nolonger follows the original curve (Figure 13-20).Relocating and renegotiating the original canal isa problem; correcting the ledge is difficult, even ifthe original canal is renegotiated (Figure 13-21).

Trying to regain the original working lengthwill result in boring straight ahead into raw

dentin. Continued boring will create a perfora-tion away from the apical foramen.

A technique (usually unsuccessful, but worth atry) that may aid in relocating the main canal is toplace a bend in the apical 1 to 2 mm of a No. 15,20, or 25 file (Figure 13-22). The tip is teasedalong the wall in the direction of the original

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FIGURE 13-23A and B, Safety zones and danger zones of molar roots. Rotary and hand instruments should be used in the canaltoward the safety zone. (Adapted courtesy Dr. M. Abou-Rass.)

FIGURE 13-24I nadequate access and overzealousenlargement in the danger zoneare evident in this mesial root ofa mandibular molar. Dashed lines(arrows) indicate approximate originalcanal dimensions. (Courtesy Dr. H.Rodriguez.)

canal. Also, this technique is helpful in bypassingcreated blockages.

Zipping of the Apical Canal

Transportation may create a reverse funnel of theapical preparation as the file straightens thecurved canal. If the preparation is continued pastthe apex and is straightened, a long or "zipping"perforation results. It is then difficult to controlobturating materials adequately to obtain a goodseal" owing to the reverse funnel shape.

Stripping Perforation

Strip perforation is, in most cases, very damaging.The cervical portion of the instrument (file orGates-Glidden bur) straightens the canal in multi-rooted teeth, leading eventually to communicationwith the furcation. The canal and dentin facing thefurcation constitute a "danger" zone (Figure 13-23).

In the danger zone there is less tooth structurecompared with the more peripheral portion (safetyzone) of the root dentin.75 There is a tendency, par-ticularly in canals without straight-line access, to re-move dentin from the danger zone (Figure 13-24).' 6


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FIGURE 13-25Stripping perforation. Overpreparation in the danger zoneperforated the furcation. Obturating materials are forced in-terradicularly. Prognosis is very poor.

FIGURE 13-26Recapitulation. Small files are used often to working lengthto loosen debris to permit removal by irrigation.

Recapitulation is another preventive technique(Figure 13-26).25 This removal of debris with smallfiles helps to avoid canal straightening. Also, fre-quent and copious irrigation, particularly after re-capitulation, minimizes packing of dentin chips.This apical accumulation of chips promotes de-flection and straightening of the instrument tip.

OTHER ERRORS

A stripping perforation may also occur duringstraight-line access preparation by overusing Gates-Glidden burs into the danger zone.

A stripping perforation into the furcation gen-erally results in failure" if obturating material ex-trudes into the periodontium (Figure 13-25). Pre-vention is the key; these types of perforations arevery difficult to correct.

Mistakes such as separated instruments, canalblockages, overpreparation beyond the apex, andthe preceding procedural errors are discussed inmore detail in Chapter 18. Also discussed are pre-vention and management.

Review of Basic Principlesof Instrumentation

PREVENTION

These problems are easy to create; to preventthem is a challenge. The most important steps arepassive step-back for preflaring, then goodstraight-line access, and then judicious use of in-struments around curves to maintain a small api-cal preparation! Larger files used around curvesaccomplish relatively little debridement. To re-peat, small canals with more than a slight curva-ture should usually undergo apical preparationwith no larger than a size 20 MAR

Another approach for more curved canals is arepeat step-back technique. This involves minimaldentin removal (about 1-mm increments) aroundthe curve during the first step-back. Then moreaggressive dentin removal is done at 0.5-mm in-crements during the second step-back.

Some principles apply regardless of the techniqueof instrumentation used.

1. Files are always worked in a canal filledwith irrigant.

2. Copious irrigation is done between eachfile size.

3. Exploration is always done with smallerfiles to gauge canal size and configuration.

4. Passive step-back (preflaring) with handinstruments will facilitate placing largerworking length files (either hand or rotary)and will reduce transportation.

5. Canal enlargement is gradual, using se-quentially larger files from apical to coro-nal, regardless of flaring technique.

6. Debris is loosened and dentin is removedfrom all walls on the outstroke (circumfer-

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FIGURE 13-27Extrusion of a "worm" of debris through the apical foramen.This represents an irritant that may be sufficient to initiate orexacerbate existing periapical inflammation.

ential filing) or with a rotating (reaming)action at or close to working length.

7. Instrument binding or dentin removal oninsertion should be avoided. Files areteased to length using a "twiddling" ac-tion. Twiddling is a back-and-forth rotat-ing motion of the files (giving a quarterturn) between the thumb and forefinger,continually working apically. Careful fileinsertion (twiddling) followed by planingon the outstroke will help to avoid apicalpacking of debris and minimize extrusionof debris apically (Figure 13-27).

8. Reaming is accomplished by twiddling theinstrument to length and then working itback and forth until it rotates freely andcontinuously in a clockwise direction.Reaming is accomplished using eitherreamers or K-type files.

9. Filing is a dentin stripping or planing mo-tion accomplished on the pull stroke. Thefile is twiddled to length, rotated clockwiseuntil it locks (the amount of rotationneeded depends on the size of the canaland the instrument), and then withdrawnwhile the instrument tip is pushed alter-nately against all walls (Figure 13-28). Thepushing motion is analogous to the actionof a paintbrush. Overall, this is a turn andpull motion.

FIGURE 13-28Files should be used peripherally in an attempt to remove alayer of dentin from all walls, recognizing that the canals areusually irregular in shape.

10. After each insertion and planing pull ofthe file, the file is removed and the flutesare cleaned of debris; the file is then rein-serted into the canal to plane the next wall.

11. Debris is removed from the file by wipingit with an alcohol-soaked gauze or cottonroll." An alternative but less effective tech-nique is to spear the file up and down inthe alcohol-soaked sponge or in othersponge systems used for instrument stor-age (Figure 13-29).

12. The canal is effectively cleaned onlywhere the files actually contact and planethe walls. Inaccessible regions are poorlydebrided.

13. Recapitulation is done to loosen debris byoften returning to working length and ro-tating the MAF or a smaller size (see Figure 13-2G). The walls should not beplaned, nor should the canal be enlargedduring recapitulation.

14. Small, long, curved, round canals arethe most difficult and tedious to en-large. They require extra caution duringpreparation, being the most prone totransportation.

15. Too-aggressive overenlargement of curvedcanals by files attempting to straightenthemselves is likely to lead to proceduralerrors (Figure 13-30).

16. Overpreparation of canal walls toward thefurcation leads into the danger zone; rootdentin is thinner in this area.


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FIGURE 13-29A, A sponge in a glass or plastic dish soaked with alcohol isideal for organizing, cleaning, and storing files and Gates-Glidden burs during the appointment. B, A special storageand measuring device is conveniently fit on the index finger.(B courtesy Dr. G. Glickman.)

17. It is neither desirable nor necessary totry to remove created steps or otherslight irregularities created during canalpreparation.

18. Everything (instruments, irrigants, debris,and obturating materials) should be con-tained within the canal. These are allknown physical or chemical irritants thatwill induce inflammation and may delay orcompromise healing.

19. Creation of an apical stop may be impossi-ble if the apical foramen is already verylarge. An apical taper (seat) is attempted,but with care. Overusing large files aggra-vates the problem by creating an evenlarger apical opening.

20. Forcing or continuing to rotate (eitherclockwise or counterclockwise) a file thatbinds is dangerous. This tends to untwist,wrap-up, weaken, and break the instrument.

Nickel-Titanium Instrumentation

FIGURE 13-30Overenlargement has resulted in perforation (arrow) and anopen apex. The canal contains blood, a frequent finding afterapical perforation.

The importance of nickel-titanium (NiTi) instru-ments has recently become significant.79 Thismetal, when cut to the shape of a file, has desirablephysical properties .

80 These relate to the flexibilityof the instrument without memory (the instru-ment can be bent significantly, but returns to itsoriginal shape). In contrast to stainless steel

(which is less flexible), NiTi may be used in a ro-tary, slow speed (150 to 300 rpm) handpiece. Thephysical properties of NiTi instruments (variabletapering cross-sectional flat radial land design,noncutting tips, and parallel core) are discussed in

22 8


greater detail in Chapter 10. NiTi is used for bothhand and engine-driven rotary instruments."

HAND

NiTi hand files have advantages and disadvan-tages compared with more commonly used stain-less steel files . 82 The major advantages are flexibil-ity and superelastic behavior (memory) upondeformation. These are useful when a small,curved canal is prepared; there is evidence of lesstransportation.83 Other claimed advantages in-clude strength, anticorrosive properties, and noweakening after sterilization.

Disadvantages include cost (much more ex-pensive), inability to precurve, lack of some stiff-ness (stiffness is desirable when trying to locate ornegotiate a small canal), and a tendency for break-age if overused. NiTi hand instruments seem to beless efficient in removing dentin compared withstainless steel files because of their cross-sectionaland flute designs.

NiTl hand files are used in a manner similar tothat used for stainless steel files. These techniquesare described earlier in this chapter.

ENGINE-DRIVEN ROTARY

Systems

A variety of NiTi rotary file systems have been de-veloped by different manufacturers (each with itsown instrumentation technique). General featureswill be described in this chapter; specific features

and techniques are described in promotional ma-terials, videotapes, and other publications for eachsystem.

Many designs ofNiTi instruments are available.Most resemble a basic file, with flutes along thelength and a latching or attaching system to affixthe file to a handpiece. Some are available in differ-ent tapers and with noncutting tips (Figure 13-31).Another unique design (Lightspeed) resembles aGates-Glidden drill, with a small shaft and a short,flame-shaped cutting head; this instrument alsohas a latch to attach to a rotary handpiece (seeChapter 10, Figure 10-7). Both types can be usedwith either conventional or special low-torque,controlled speed motor systems, (Figure 13-32) in-cluding battery-operated handpieces.84

Techniques

After negotiating the canals and determining thecorrected working length, NiTi rotary instru-ments are used to flare either with the step-backor the crown-down methods. Straight-line accessto the canal space is established (usually withGates-Glidden drills or with special orificeshapers). A small hand file ( No. 10 stainless steel)is used to explore the canal to the correctedlength. Hand instrumentation (reaming) is per-formed at the corrected length through two orthree sizes with either stainless steel or NiTi files.This is followed by rotary instrumentation.

The rotary NiTi instruments are used in theapical portion of the canal at or short (usually

FIGURE 73-37Nickel-titanium rotary file. One designshows a flat "land" area (arrow) and a non-cutting tip. These help the file stay morecentered in the canal during preparation.(Courtesy Tulsa Dentsply Dental.)


229

2 to 4 mm) of the corrected working length. Thefiles are continuously rotated with the foot pedalof the electric or air turbine motor handpiecefully depressed for constant speed and torque.Very light pressure is used along with lubrication(irrigant) to place the NiTi rotary instrumentinto the canal until resistance is felt. The in-strument is then immediately withdrawn in asmooth motion from the canal space, althoughrecommendations of advancement of the instru-ment apically in an up-and-down "pecking" mo-tion have also been made. Slow speed is preferredto minimize instrument distortion . 85,86 Lightpressure (force is never used!) is applied; the in-strument is withdrawn when resistance is felt toprevent breakage . 87 After each withdrawal, theflutes are cleaned with wet gauze or an alcoholsponge, and the file is examined for distortionsand/or deformations (unwinding or wrapping-up of the flutes).

This process is repeated by using a sequence oflarger instruments to the desired length, with re-capitulation and irrigation between each instru-ment size. Patience and careful insertion withlight pressure is necessary, allowing the system todo the work, particularly in canals with calcific

metamorphosis. Instrumentation of the apicalportion of the canal space is usually performed ina step-back manner with hand (stainless steel orNiTi) instruments to form an apical matrix.

The Lightspeed technique has a somewhat dif-ferent approach, using only the "pecking" actionto prepare the canal; this is also done in a crown-down mode." Debridement effectiveness withthese unique instruments seems similar to thatwith hand preparation. 89

NiTi rotary instrumentation has advantages aswell as disadvantages compared with stainless steelhand instrumentation. Because of their flexibility,the files have less tendency to transport curvedcanals. Finger fatigue is less because the handpieceis doing much of the work. Somewhat less time isrequired to prepare the canal. Preliminary evidenceindicates that debridement effectiveness is compa-rable to that with hand instrumentation.90 Thereare also disadvantages. Expense is greater if one ofthe special motor systems is purchased; in addi-tion, the files are costly. Files are prone to breakage,without warning, particularly if overused. 91 Over-all, no difference is seen with NiTi rotary instru-ments for either quality of debridement or progno-sis; there are no substantive data on either.

FIGURE 73-32Two control units ("motors") for handpieces that drive nickel-titanium rotary files. The unit on the left allows controlof speed and torque; that on the right is programmable for these two functions plus a variety of other functions.

230


COMBINATION OF PASSIVESTEP-BACK AND ROTARYINSTRUMENTATION

The crown down or step down technique with ro-tary instruments is advocated by the manufacturersfor shaping of canals with rotary NiTi files. The maindisadvantage of this recommendation is the possi-bility of instrument separation. To reduce the fre-quency of this procedural accident, coronal flaringas recommended for the passive step-back tech-nique (as described earlier in this chapter) is usedbefore rotary instruments are used to shape the api-cal portion of the canal. This flaring enhances irri-gation of the apical third and removes irritants. Inaddition, the use of this technique before the use ofrotary instruments creates straighter line access tothe apical canal and less transportation during api-cal preparation with rotary instruments. 23 This pro-cedure reduces the chances for instrument separa-tion, packing debris, ledging, straightening theapical portion of the canal, and root perforation.

The steps are as follows:

1. After the pulp chamber is completely un-roofed, an estimated working length is de-termined from a preoperative radiograph.After apical-canal patency is establishedwith a No. 10 or 15 K-type file, the canal ispassively (without binding) flared using No.15 to 45 K-type files.

2. After filing, Gates-Glidden drills (Nos. 2 and3 and in large canals No. 4) are used in anup-and-down motion without lateral pres-sure. To further enlarge and flare the coro-nal portion of the canal, Nos. 2 and 3 Peesoreamers are used passively.

3. After copious irrigation with sodiumhypochlorite, a new working length with anapex locator is determined and confirmedradiographically.

4. With the use of rotary NiTi files (sizes 15to 25) and a "pecking" motion, the apical por-tion of the canal is enlarged to the workinglength. With the use of larger rotary NiTi files(sizes 30 to 40), the coronal portion of thecanal is flared progressively at successivelyshorter lengths (increments of 0.5 to 1mm).

5. The canal is irrigated with sodium hypo-chlorite, and the working length is con-firmed by a radiograph or an apex locatorbefore obturation.

Alternative Techniquesof Cleaning and Shaping

est and enthusiasm, whereas others have attractedlittle attention. Because conventional preparationwith hand instruments is somewhat difficult andtime-consuming, the search continues for some-thing more effective and less involved. Interest-ingly, automated devices that create cavitationand hydrodynamic turbulence with continuousirrigant exchange are being tested.92 These orother devices probably will evolve in the future tosimplify treatment modalities.

Some unique approaches have been intro-duced, including ultrasonic and sonic devices aswell as the newer engine-driven, slow-speed hand-pieces that make use of special nickel-titaniumfiles; these techniques and devices have generatedmuch interest. Other, older mechanical devices(handpieces) are also in use. These, including al-ternative hand techniques, are briefly reviewedhere.

BALANCED FORCES

The balanced forces method is a somewhat differ-ent approach; the technique also uses an alteredinstrument design.•' The files used have a modi-fied tip that is noncutting. Canal preparation in-volves counterclockwise rotation combined withapical pressure. There is evidence that thismethod allows the instrument to stay more cen-tered in the canal during preparation, causing lesstransportation.94,95 However, it has not beendemonstrated whether this ultimately results inbetter clinical success or whether there is a signif-icant advantage in cleaning and shaping with thistechnique or instruments. 96

ENERGIZED VIBRATORY SYSTEMS

Sonic and ultrasonic techniques were introducedin the 1980s. Some authors proposed that thesetechniques were the "wave of the future." Theyhave not, however, proved to be panaceas. In addi-tion, some questions remain unanswered andthere has been insufficient clinical usage over timeto allow endorsement with or without reserva-tions. Ultrasonic and sonic techniques have beensuggested to have a role when used in combina-tion with hand instruments..'

These vibratory systems were developed in thehope of replacing or supplementing hand instru-mentation. Nickel-titanium rotary instrumentsseem to be filling that role; the vibratory systemscurrently are little used for canal preparation.

Ultrasonic Instruments

Other approaches to canal preparation have beendevised. Some of these have generated great inter-

Physics. Essentially, endosonic machines are anadaptation of the ultrasound apparatus used for


231

scaling. The power source (either electromagneticor piezoelectric) is transferred to a special insertthat holds an instrument similar to a file. The fileis energized as ultrasonic energy is transmittedthrough the insert. The file then vibrates at ap-proximately 25,000 vibrations per second.

The energy from the file is transmitted to afluid medium (irrigant) within the canal, whichtransfers the energy to the dentin walls. This en-ergized solution shows acoustic streaming, whichis the "rapid movement of particles of fluid invortex-like motion about a vibrating object.""The swirls and whirlpools of moving fluid sup-posedly help loosen debris from the canal walls.

Application. The devices seem to be most effec-tive for cleaning and shaping canals that are eas-ier to prepare. 99 For more difficult situations,such as small curved canals, ultrasonic instru-ments are no more or less effective than standardhand instrument techniques.100-103 In more uni-form canals, where the instrument can be fully en-ergized, ultrasonic devices may provide superiordebriding qualities. However, if the instrument iscurved or binds in the canal, it may not have the

FIGURE 13-33Theory of the difference in ultrasonic vibrations noted in astraight versus a curved canal. Instrument and irrigation pat-terns may be very active in the straight canal (left). The curvedampens the energy of the file and reduces or eliminates itsvibratory action (right).

same vibratory activity and therefore is less ener-gized (Figure 13-33).' 0'

Effectiveness. Research and clinical usage haveled to the following conclusions. Debridement maybe quite good in the straighter canals but less soin small, curved canals. Flushing seems to be effec-tive, with irrigant flowing to the tip of the filewhen it is energized properly.105 Whether thistechnique is superior to conventional irrigationwith a syringe has not been shown.

Endodontists have found ultrasonic instru-ments useful for removing posts, silver points,paste fills, and separated instruments. 103,106-108

Sonic Instrumentation

Special handpieces have been developed that vi-brate root canal instruments of various designs.The handpiece is run from the standard high-speedair line of the dental unit. When activated, the in-struments whip in an oval, whirling motion at afrequency of approximately 1500 to 8000 vibra-tions per second (Figure 13-34). The file vibratesagainst and scrapes the canal walls. Irrigating solu-tion (water) is delivered to and directed along thefile into the canal. In limited tests, the sonic instru-ment appeared to enlarge and debride the canalsafely and effectively.109,110 In usage tests under rig-orous conditions (in small curved canals), sonichandpieces did not perform as well as the step-back

FIGURE 13-34A sonic handpiece transmits a whipping vibration and an ir-rigant to a specially designed file.

232


preparation but results were approximately equalto those with ultrasonic devices.100,101

Sonic handpieces seem to have fallen into dis-use because of their limitations.

OTHER MECHANIZED TECHNIQUES

Stainless Steel Rotary. It seems like a great ideato adapt conventional stainless steel instrumentsto standard handpieces that would mechanicallyclean and shape canals. This should be faster andless tedious than manipulating files with fingers.However, because of the relative inflexibility ofstainless steel, these techniques are ineffectiveand fraught with danger, particularly in curvedcanals.

Many approaches, instruments, and specialhandpieces have been designed to perform canalpreparation. Reamers have added latches for at-tachment to standard handpieces. Instrumentssimilar to a broach are latched to fit into a specialhandpiece that vibrates alternately back andforth. Handpieces that rotate back and forth in aquarter circle and up and down a few millimetersare available; these also grasp the handles of cer-tain files.

There are problems with these devices that usestainless steel instruments. First, they generallydo not debride well. 76,111 Second, they tend topush debris in an apical direction, particularly theinstruments using an up-and-down motion."'Third, they tend to markedly straighten and ledgecurved canals without creating a taper.76,111 Theseare not recommended.

LASERS

phorated monochlorophenol (CMCP), formocre-sol, and Cresatin. Calcium hydroxide (Ca(OH)2) isof a different class and is promising as an antimi-crobial agent.

Uses and actions of most of these agents arelargely based on empiricism and opinion.114 Clin-icians and lecturers in the past applied theseagents without investigation. Thus, popular In-tracanal medicaments were designed and pro-posed for (1) antimicrobial activity in the pulpand periapex, (2) neutralization of canal rem-nants to render them inert, and (3) control orprevention of post-treatment pain. Again, thephenolic and fixative agents have no beneficial ef-fects when used as Intracanal medicaments be-tween appointments.

Habits, beliefs, and clinical impressions are po-tent influences. Pressured by the focus of infec-tion theories of the early 1900s, practitionersadapted strong antimicrobial agents for rootcanal treatment. The goal was to render the canalsand periradicular tissues sterile and to preventsupposed dissemination of dangerous bacteriathroughout the body.

As the focal infection theory diminished in im-portance, the use as well as the significance of an-timicrobial medicaments also diminished. Intra-canal bacterial populations are best reduced or eveneliminated by careful instrumentation and irriga-tion.,","-' Thus, the use of traditional medicaments,

Groupings of Commonly UsedI ntracanal Medicaments

Lasers have been experimentally applied as aids inroot canal treatment. As yet, there are no demon-strated useful applications in canal preparation.

I ntracanal MedicamentsIntracanal medicaments have traditionally beenintegral to root canal treatment and have beenconsidered important to success (Box 13-1). Infact, at one time, a common assumption that suc-cess, both short-term and long-term, dependedon the chemical placed in the canal between ap-pointments. It was also recognized that medica-ments possess potentially harmful side effects;each is an active, toxic chemical or therapeuticagent. The question was and still is, Are the bene-fits worth the risks? The answer is mainly no. 113

There is no demonstrated usefulness for the tra-ditional phenolic or fixative agents such as cam-

From Walton R: Intracanal medicaments, Dent Clin North Am 28:783,1984.

owing to lack of evidence of usefulness and toxicity,is in decline. In contrast, calcium hydroxide(Ca(OH) 2) usage is increasing because of its demon-strated antimicrobial properties, coupled withsome initial evidence of its aiding in reducing peri-apical inflammation. 116 However, the long-termoutcome (success or failure) with the use Ca(OH)2as an intracanal medicament is uncertain.' 17

APPLICATIONS

Studies to test medicament effectiveness showthat they either do not perform as expected or oc-casionally have the opposite effect. There are,however, exceptions, including steroids and cal-cium hydroxide.

Antibacterial Action. The most popular antimi-crobials are calcium hydroxide, CMCP, andformocresol. These are potent microbe killersunder ideal laboratory test conditions; their effec-tiveness in clinical use is doubtful,"' althoughcalcium hydroxide does inhibit intracanal bacter-ial growth119 and alters the biologic properties ofbacterial lipopolysaccharide. 120

Pain Relief. Certain intracanal medicaments areclaimed to reduce pain by anodyne, antimicrobialeffect, or both. Reducing or preventing inflamma-tion presumably decreases its byproduct, pain.

Clinical studies on phenolics, formocresol, andcalcium hydroxide show that routine use as intra-canal medicaments has no effect on prevention orcontrol of pain. 121-124 However, steroids have beendemonstrated to decrease post-treatment painsomewhat, but with mixed results. These drugs,whether applied topically (for example, throughthe canal) 125 or systemically, alter the inflamma-tory or vascular response sufficiently to affectlower levels of pain.126 However, steroids do notreduce the incidence of flare-ups (severe pain).124In endodontic applications their action seems tobe minor and affects only milder degrees of pain.

Canal Contents Rendered Inert. Chemicals usedfor this purpose are fixatives, or aldehyde deriva-tives. They fix fresh tissues for histologic study;however, aldehydes do not effectively fix necroticor decomposed tissues. Fixed tissues are notinert."' In fact, when both necrotic and vital tis-sues are fixed with aldehydes, they become moretoxic and antigenic.

LIMITATIONS ANDCONTRAINDICATIONS

I ntracanal Environment. The chemical or thera-peutic action of medicaments depends on directcontact of the agent with microbes or tissue. Thisis a drawback to chemicals used in the pulp space;

13 1 Cleaning and Shaping

233

these substances probably do not reach all areasin the canal and into dentinal tubules where bac-teria or tissues are hidden and their action is lim-ited to the surface only.

Duration. To be effective, most agents shouldremain chemically active during the time betweenappointments. Phenolics dissipate and may losetheir activity within 24 hours."' Calcium hydrox-ide retains antimicrobial activity for prolongedperiods and can inhibit regrowth of bacteria. Theduration of steroid activity is unknown.

Sustained-release delivery systems of variousintracanal medicaments have been evaluated invitro, but their clinical effectiveness has not beenclearly demonstrated. 1 28-130

Toxicity. Any chemical that kills bacteria willalso kill host cells. Both in vitro (bench type) andin vivo (animal and clinical use) studies show thatphenolics and aldehydes are generally potent cellkillers. 131,132 Another potential adverse side effectis allergeniciry. Some medicaments act as haptensand alter tissues to become foreign substances,which then elicit an immune response. '33 This ac-tion may be responsible for their localized adverseeffects on pulp or periapical tissues.134 Neithercalcium hydroxide nor steroid compounds havesignificant toxicity.

Distribution. There is ample evidence that sub-stances placed in the pulp, with or without tissue,have ready access to periradicular tissues and evento the systemic circulation. 135-137 Although thedangers of this distribution are unknown, 131 theuse of potent chemicals that have no demon-strated beneficial effects is questionable.

Taste and Smell. The phenolics in particularpossess a pungent odor and foul taste. Thesemedicaments soak into and through the tempo-rary restoration into the oral cavity. Patients re-port a disagreeable medicinal taste; many find thismost objectionable. Some dentists believe that if apatient reports a bad taste, the temporary seal isdefective and will leak saliva into the canal; thereis no evidence to support this presumption.

CALCIUM HYDROXIDE

Properties. Calcium hydroxide is available indifferent forms, combinations, and proprietarycompounds."' When sealed in the canal for eithershort- or long-term use, a number of actions havebeen attributed to it.119 ,140 Most have not beenclearly substantiated in clinical trials. Calcium hy-droxide may be used as a canal dressing betweenappointments, particularly when pulp necrosishas been diagnosed.

Although the antibacterial properties of cal-cium hydroxide pastes are effective when evalu-

234


FIGURE 13-35Calcium hydroxide placement. Powder is mixed with glycerin to toothpaste consistency (A) and placed with al entulo spiral (B). Proper fill appears dense (C). Slight overfill is not a problem.

ated over short time periods, 119,140 little is knownconcerning their long-term antimicrobial efficacy.This is a clinically relevant concern, because highnumbers of bacteria within the canal space and/or tubules may represent a source of continualmicrobial challenge to originally placed calciumhydroxide." 9

Calcium hydroxide also has some tissue-alteringeffects, 1 41-143 but it does not aid in debridementwhen placed in the canal space 46

Placement. Calcium hydroxide should ideally beplaced deep and densely in the canal space so thatits biological effect can be exerted in close proxim-ity to the appropriate tissues. Techniques that de-liver dry calcium hydroxide powder alone are diffi-

cult or impossible in smaller, more curved canals.In most cases, the calcium hydroxide must bemixed with a liquid such as anesthetic solutionwater, glycerin, other intracanal medicaments, ormethyl cellulose to facilitate placement. 144 To use,calcium hydroxide is mixed with glycerin (water isless effective in terms of density to length) to athick paste and placed in the canal with either aplugger or spun into a lentulo spiral (Figure 13-35)using a counter-clockwise motion.145 The lentulospiral (use with caution!) is most effective devicefor carrying calcium hydroxide paste to length insmall, curved canals. 145,146 The powder alone may beplaced with a Messing gun or pluggers in large,straight canals. 147


235

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Obturation

LEARNING OBJECTIVES


1 / Recognize the clinical criteria that determine when to obturate.

2 / List the criteria for the ideal obturating material.

3 / Describe the purpose of obturation and the reasons why inadequate obturation may result in treatment failure.

4 / Identify the two core obturating materials most commonly used and list their constituents and physicalproperties.

5/ Describe the advantages and disadvantages of each core material.

6 / Discuss the indications and contraindications for obturating with each core material.

7 / Differentiate between "standardized" and "conventional" sizes of gutta-percha cones and discuss wheneach is indicated.

8/ Define and differentiate between lateral and vertical condensation and suggest where each is indicated.

9 / Describe the lateral condensation technique.

10/ Discuss the significance of depth of spreader penetration during condensation.11 / Describe the vertical condensation technique.

12 / Describe briefly other techniques used for obturation, including thermoplasticization, thermocompaction,

paste injection, gutta-percha carrier systems, and sectional obturation.

13 / Describe the custom cone (chloroform-softened) technique and discuss when it is indicated.

14 / Describe the preparation of the canal for obturation.

15 / Review the techniques for final drying and apical clearing.

16 / Discuss the technique for fitting the master cone.

17 / List criteria for the ideal sealer.

18 / Describe a technique for mixing and placing sealer.

19 / Discuss the technique for removing excess sealer and obturating material from the chamber and why thisprocess is necessary.

20 / Discuss the clinical and radiographic criteria for evaluating the quality of obturation.

239

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1 4 / Obturation

Objectives of Obturation

Objectives of Obturation

Potential Causes of FailureApical SealCoronal SealLateral SealLength of ObturationLateral CanalsVertical Root Fractures

Timing of ObturationPatient SymptomsPulp and Periradicular StatusDegree of DifficultyCulture ResultsNumber of Appointments

Core Obturating MaterialsSolid MaterialsPastes (Semisolids)

SealersDesirable PropertiesTypesMixingPlacement

Obturation Techniques with Gutta-PerchaSelection of TechniqueLateral CondensationSolvent-Softened Custom ConesVertical CondensationAlternative Techniques

Evaluation of ObturationSymptomsRadiographic Criteria

The obturation phase of root canal treatment re-ceives a great deal of attention. Historically, obtu-ration has been accorded the role of the most crit-ical step and the cause of most treatment failures.An early and often quoted report' stated thatmost treatment failures could be attributed to in-adequate obturation. Such retrospective surveyshave major limitations. This study consisted ofradiographic assessment of healing at various pe-riods of time after root canal treatment.' The ob-served failures were correlated with apparentlypoorly obturated canals (as evaluated on radi-ographs). The fallacy in this reasoning is evident;just because two events are associated does notprove cause and effect.

In other words, although canals in thesefailed treatments may not have demonstrateddense fills, other factors may have caused irrita-tion of the periradicular tissues and failure.These include (1) loss of the corona' seal, (2) in-adequate debridement, (3) missed canals, (4)vertical root fractures, (5) significant periodon-tal disease, (6) corona' fractures, and (7) proce-dural errors such as loss of length, ledging, zip-ping, and perforations.

Significantly, a periradicular lesion may healafter debridement without obturation. Althoughthis is not an acceptable treatment option (an un-obturated canal would result in long-term treat-ment failure), it does demonstrate an importantconcept: What is removed from the root canal system ismore important than what is inserted in the system. Ob-turation is important, but not the most signifi-cant factor for success.

The objective of obturation is to create a com-plete seal along the length of the root canal sys-tem from the corona' opening to the apical termi-nation. The importance of establishing andmaintaining a corona' seal has been overlooked;the corona' seal is probably more important thanthe apical seal in long-term success. 2

Potential Causes of FailureMost treatment failures related to deficienciesin obturation are long-term failures. A low vol-ume of irritant or slow release of irritant intoperiradicular tissues produces damage that isnot apparent in the short term. Persistence or de-velopment ofperiradicular patbosis may not be evidentfor months or even years after treatment. Therefore,recall evaluation to assess the response to treat-ment is important.

Obturation-related failures occur in differentways.

APICAL SEALIrritating Remnants in Canals

Bacteria, tissue debris, and other irritants are usu-ally not totally removed during cleaning andshaping (refer to Chapter 13). These constitute apotential source of irritation that may lead to fail-ure. It is likely, and there is evidence, that sealingin these irritants during obturation may preventtheir escape into the surrounding tissues. Obvi-ously, this seal must remain intact indefinitely be-cause this reservoir of irritants persists forever. In-terestingly, some bacteria sealed in the canal maylose viability, probably because of lack of sub-strate.3 Possibly, other bacteria remain dormant,waiting for the introduction of substrate, to pro-liferate and create havoc. Even dead bacteria ortheir remnants can be irritating or antigenic andcause inflammation.

Percolation

By definition, percolation is movement of fluidsinto a small space, usually by capillary action. Thepotential for communication exists between thepulp space and the periapex.1,4-7 Tissue fluids withplasma proteins may seep into this space and thendegrade into irritating chemicals; these irritantsmay then diffuse back into the periapical tissuesand induce inflammation. Another possibility isthat periradicular tissue fluids supply substrate(growth medium) to bacteria remaining in theroot canal space. With proliferation, bacteria andtheir toxins could then return to periapical tissuesto cause inflammation.

A vicious cycle is established. Periapical inflam-mation produces exudation and transudation offluid as well as an accumulation of cellular debriscomposed primarily of inflammatory and tissuecells. These irritants and inflammatory fluids thenpass into the canal space, and the cycle is repeated.

CORONAL SEALIrritants from Oral Cavity

A coronal seal is important. If the myriad of irri-tants in the oral cavity gain access to periradiculartissues, they may cause inflammation and treat-ment failure. Irritants include substances in salivasuch as microorganisms, food, chemicals, or otheragents that pass through the mouth.

If coronal gutta-percha or sealer obturation isexposed to saliva, dissolution of sealer and leak-

age over a relatively short period of time mayoccur.8-11 This results in leakage of bacteria, tox-ins, and chemicals into and around the gutta-percha.12,13 The consequences of sealer loss are ob-vious; communication from the oral cavity to theperiapex or periodontium will eventually be com-plete via a lateral canal or apical foramen.

It is not possible to determine clinicallywhether communication from the oral cavity tothe periapex has been established. Therefore, it isunwise to restore a tooth with a canal that maycontain saliva, bacteria, food debris, or other irri-tants. Coronal exposure of the obturating mater-ial for more than a short period of time throughloss of restoration, recurrent caries, or open mar-gins requires retreatment. The time of exposurerequiring retreatment is undetermined, but prob-ably depends on varied factors, such as quality ofobturation, length of canal(s) and surface area ofexposure.

Restoration

Both design and placement of the final restora-tion are critical. This aspect of treatment is an in-tegral part of obturation. The restoration acts as aprotector and is the primary coronal seal, whethertemporary or final. 14 These factors are discussedin detail in Chapter 15.

LATERAL SEAL

Although not as critical as the apical and coronalseals, establishment of a seal in the inner middleaspect of the canal is also important. Lateralcanals are occasionally found in these regions;they constitute a potential communication for ir-ritants or, possibly, percolation from the canal in-terior to the lateral periodontium (Figure 14-1).

LENGTH OF OBTURATION

Extent of obturation relative to the apex is alsoimportant. Ideally, obturating materials shouldremain within the canal.

Overfill

Overfills are undesirable. Prognosis studies con-sistently show that failures increase with timewhen the primary obturating material has beenextruded. 12-17 Histologic examination of periapi-cal tissues after overfilling typically shows in-creased inflammation with delayed or impairedhealing.", " Patients probably experience morepostobturation discomfort after overfills. Two

14l Obturation

241

242

14 / Obturation

FIGURE 14-1A, Pulp necrosis with apical and lateral radiolucent lesions. B, On obturation, a lateral canal was detected com-municating with periodontium. This lesion should heal after removal of necrotic pulp tissue in the main canal andthen obturation.

other problems with overfills are irritation fromthe material itself and lack of an apical seal.

Obturating Materials. Whether the obturatingmaterial is core or sealer, both are irritants to agreater or lesser degree.'"' Silver points andgutta-percha (slightly) as well as sealers (in partic-ular) are toxic when they are in contact with tis-sues. Sealers invoke a foreign body response andinflammation .21-23

Lack of Apical Seal Secondary to Overfill. This maybe even more important than irritation from thematerials. Gutta-percha, like amalgam, requires amatrix to condense against. Imagine trying tocondense and form amalgam into a class II prepa-ration without a metal matrix! The same is true ofgutta-percha and sealer. Absence of an apical ma-trix may prevent lateral spreading and sealingduring condensation.

A tapered apical preparation with no core ma-terials and a small amount of sealer passing out ofthe foramen is not a significant problem. Thetaper forms an adequate matrix for gutta-perchacondensation; irritation from the sealer shouldresolve. However, when there is gross overfill ofboth primary obturating materials and sealer, per-

sistent inflammation" and failure often ensue(Figure 14-2).

Underfill

Underfill results when both preparation and ob-turation are short of the desired working lengthor when the obturation does not extend to theprepared length. Either instance may contributeto treatment failure, particularly long term (Fig-ure 14-3).

The "ideal" preparation or obturation lengthis 1 to 2 mm short of the apex (Figure 14-4). 24Preparation or obturation short of this lengthleaves existing or potential irritants in the apicalcanal. Periapical inflammation may developover an extended period of time, dependingon the volume of irritants or the balance estab-lished between irritants and the immunesystem.

Compared with overfill, underfill is less of aproblem, as indicated by prognosis and histologicstudies. Therefore, the axiom is, ifthere isgoing to bean error, err on the short side; try to confine every-thing to the canal space.

14 / Obturation

243

FIGURE 14-2Gross overfill. A, The mass of gutta-percha has been extruded, indicating lack of an apical stop or seat. B, At1 0-year recall, persistent pathosis (arrow) suggests a poor apical seal (lack of an apical matrix).

FIGURE 14-3Failure caused by operator errors. The mesial canals are un-derprepared (inadequate debridement) and incompletely ob-turated; the distal (arrow) has a poorly adapted restoration(coronal leakage).

FIGURE 14-4Desired lengths and preparations. The canals are preparedand obturated to a tapered shape approximately 2 mm fromeach apex.

244

14 / Obturation

LATERAL CANALS VERTICAL ROOT FRACTURES

The role of lateral (accessory) canals in rootcanal treatment has been a subject of debate . 2s

These canals connect pulp space and periodon-tium. Irritants in the root canal system, such asbacteria and necrotic debris, may leak into thelateral periodontium and initiate inflammation(see Figure 14-1).

Histologic examination of roots after debride-ment shows that lateral canals are rarely if everdebrided. 26 There is no significant difference inthe ability of various obturation techniques tofill the main canal. However, certain techniquestend to force materials into the lateral canals(Figure 14-5) .27

When the main canal space is adequatelydebrided and obturated, lateral lesions adjacentto lateral canals heal as readily as periapical le-sions. This occurs whether or not obturating ma-terial has been expressed into the lateral canal.

The conclusion is that obturation of lateralcanals is inconsequential to the outcome ofmost root canal treatments despite proponentsof certain techniques that claim to fill lateralcanals .28

Vertical root fracture is a devastating occurrencethat usually requires removal of the tooth or frac-tured root. Signs and symptoms as well as radi-ographic findings show that bone loss and softtissue lesions are common." ," Lateral forces ex-erted during obturation or postplacement aremajor etiologic factors owing to their wedging ac-tion. 31-37 The pathogenesis, findings, and preven-tion of vertical fractures are discussed further inChapter 28.

Timing of ObturationTo answer the questions, When is treatment to becompleted? Is it time to obturate?, the followingfactors are considered: signs and symptoms, pulpand periapical status, and difficulty of procedure.Combinations of these factors affect decisionsmade about number of appointments and timingof obturation.

PATIENT SYMPTOMS

FIGURE 14-5This premolar was obturated using a procedure (the diffusiontechnique) that involves dissolving the gutta-percha in chlo-roform. This tends to obturate the accessory and lateralcanals but provides a poor apical seal.

In general, if the patient presents with severesymptoms and the diagnosis is acute apical peri-odontitis or abscess, obturation is contraindi-cated. These are emergency situations, and it ispreferable to manage the immediate problem anddelay definitive treatment. Even an acute apicalabscess may be treated in a single appointment. 38However, this is not good treatment; if the patientcontinues to have problems, management is moredifficult if the canal is filled.

Painful irreversible pulpitis is a different situ-ation. Because the inflamed pulp (which is thepain source) is to be removed, obturation may becompleted at the same appointment. However,treatment of these problems requires caution be-cause of difficulties in management of a patientin pain.

PULP AND PERIRADICULAR STATUS

Vital Pulp

Regardless of the inflammatory status of thepulp, and if time permits, the procedure may becompleted in a single visit.

Necrotic Pulp

Without significant symptoms, obturation may becompleted during the same appointment as canalpreparation. Pulp necrosis with asymptomaticperiradicular pathosis (that is, chronic apical peri-

odontitis, suppurative apical periodontitis, or con-densing osteitis) alone is not necessarily a con-traindication to single-appointment treatment atleast as related to postobturation symptoms.

There may be an advantage, however, to mul-tiple appointments related to healing of apicalpathosis. Recent studies indicate the benefits oftreating these patients in two visits. 39-41 Place-ment of an intracanal antimicrobial dressingsuch as calcium hydroxide reduces bacteria andreduces inflammation somewhat. Calcium hy-droxide in the canal for 7 days can effectivelyinhibit bacteria.42 A recent prognosis study com-paring single-visit versus two-visit with intra-canal calcium hydroxide treatment did notdemonstrate differences in long-term prognosis,however. 13 At present, there are no definitiveconclusions about when single- or multiple-visitprocedures are indicated.

One situation that contraindicates single-visitcare is the presence and persistence of exudationin the canal during preparation. The potentialfor post-treatment exacerbation is increased ifthe periapical lesion is productive and generatescontinual suppuration. If the canal is sealed,pressure and corresponding tissue destructionmay proceed rapidly. In these cases, canal prepa-ration is completed, followed by calcium hydrox-ide placement. A dry cotton pellet is placed overthe calcium hydroxide and the access is sealedwith a temporary restoration. Generally, exuda-tion will be diminished and controllable at asubsequent appointment; obturation may thenbe completed.

DEGREE OF DIFFICULTY

Complex cases are time consuming and are bettermanaged in multiple appointments.

CULTURE RESULTS

Some practitioners rely on culturing canal con-tents to indicate timing of completion of treat-ment. Although the evidence is not clear aboutthe value of cultures as an aid in increasing suc-cess in root canal treatment, culture results are anindicator of long-term prognosis." 44,4S Somepractitioners believe that persistent positive cul-tures may indicate a poorly debrided canal,missed canals, or resistant strains of bacteria;these conclusions have not been proved and aredebatable. However, proponents recommend thatat least one negative culture be obtained beforeobturation, which requires more than one ap-pointment. Currently, this approach is seldomused.


The decision about the number of appointmentsneeded usually occurs during initial treatmentplanning. The decision to schedule another ap-pointment, when made during an appointment,reflects a change of circumstances such as the pa-tient or dentist is tired or has lost patience.

Core Obturating MaterialsPrimary obturating materials are usually solid orsemisolid (paste or softened form). They comprisethe bulk of material that will fill the canal spaceand may or may not be used with a sealer. How-ever, a sealer is essential with all core obturatingmaterials.

These materials may be introduced into thecanals in different forms and may be manipulatedby different means once inside. Imaginations (andmarketing) run rampant, resulting in a variety ofmaterials and techniques. However, a small num-ber of widely accepted and taught materials andtechniques are used for obturation. These are dis-cussed in some detail; alternatives are mentionedbriefly.

SOLID MATERIALS

Solids have major advantages over semisolids(pastes). Although various materials have beentried, the only one universally accepted currentlyis gutta-percha as the primary material. This haswithstood the test of time and research, and is byfar the most commonly used material .47-49A major

Desirable Properties of ObturatingMaterials

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advantage of gutta-percha over semi-solid pastetypes is the ability to control length as well as thereasonable ability to adapt to irregularities and tocreate an adequate seal.

Gutta-Percha

Composition. The primary ingredient of agutta-percha cone is zinc oxide (±75 percent).Gutta-percha accounts for approximately 20 per-cent and gives the cone its unique properties suchas plasticity. The remaining ingredients arebinders, opaquers, and coloring agents.

Shapes. Gutta-percha cones are available intwo basic shapes: the "standardized" and the"conventional" (Figure 14-6). Standardized conesare designed to have the same size and taper as thecorresponding endodontic instruments. That is, aNo. 40 cone should correspond to a No. 40 file.

Interestingly, there is no uniformity in gutta-percha sizing. For example, the contents of a box

FIGURE 74-6Comparison of conventional with standardized cones. Thethree conventional cones (from left to right. fine fine,medium fine, and fine) have a heavier body and a finer tipand are easier to manipulate than the small, standardized,color-coded cones (sizes 35 and 40) on the right. (CourtesyDr. W. Johnson.)

or vial ofNo. 40 standardized gutta-percha conesvary in size from No. 35 to No. 45 and has incon-sistent tips and shapes.50 This lack of uniformityis not critical; canal shape after preparation is alsovariable.

Conventional cones use a different sizing sys-tem. The tip of the cone has one size and the bodyof the cone another. They are available in variouscombinations. For example, a fine tip end-medium body would be referred to as a fine-medium cone. Generally, conventional cones havea smaller tip with a relatively wider body com-pared with standardized cones.

Gutta-percha master cones tend to be selectedaccording to the method of canal preparation orto match the master apical fill size. This is notuniversal, however; operator preferences vary con-siderably, indicating that size and shape of thecone are relatively unimportant.

Advantages. Gutta-percha has withstood thetest of time, having been introduced as an obtu-rating material more than 160 years ago. It is thestandard to which other obturating materials arecompared. First, because of plasticity, gutta-percha adapts with compaction to irregularities inprepared canals; second, it is relatively easy tomanage and manipulate despite some complexobturation techniques; third, gutta-percha is easyto remove from the canal, either partially to allowpost placement or totally for retreatment; andlast, gutta-percha has relatively little toxicity,being nearly inert over time when in contact withconnective tissue.20,51 Another advantage of gutta-percha is that it tends to be self-sterilizing, as itwill not support bacterial growth. If there is a pos-sibility of cones being contaminated, they are pre-dictably sterilized by immersion in 1% (or greater)sodium hypochloride for 1 minute.52

Sealability. Regardless of the technique used(condensation or plasticization), studies haveconsistently shown that gutta-percha withoutsealer will not seal .4,53-55 Disadvantages of gutta-percha are a lack of adhesion to dentin and aslight elasticity, which causes a rebound andpulling away from the canal walls. Warmedgutta-percha shrinks during cooling. Gutta-percha mixed with solvents such as chloroformor eucalyptol shrinks with evaporation of thesolvent.56 Therefore, a sealer must be used to filland seal the spaces between the gutta-perchacones and between the gutta-percha and thecanal wall. Also gutta-percha should be added tothe canal in increments.

Methods of Placement. As stated earlier, place-ment methods are varied and imaginative. Mostpopular is lateral condensation, followed by verti-cal condensation. Other techniques involve either

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chemical or physical alteration of the gutta-perchain an attempt to render the material more plasticor more adaptable.

Another variation is a system that includes asolid core (carrier) surrounded by a cone of gutta-percha. The carrier may be stainless steel, tita-nium, plastic, or a segment of a file. After prepa-ration, the carrier and gutta-percha are warmedand placed in the canal as a unit.

Other devices have been introduced that involvewarming to plasticize and inject gutta-percha.These will be discussed in more detail later in thischapter.

I ndications. Gutta-percha is the material ofchoice in most situations. Some exceptions are se-verely curved, inaccessible canals in which gutta-percha or obturating instruments would be diffi-cult or impossible to manage. However, if curva-tures of canals are that severe, the patient should bereferred to an endodontist.

Silver Points

Silver points were designed to correspond to thelast file size used in preparation, to presumably fillthe canal precisely in all dimensions. Because ofthe complexity of shape of the root canals, this isfallacious; it is impossible to predictably preparecanals to a uniform size and shape .57

Although the short term sealability success ofsilver points seemed comparable to that of gutta-percha, silver points are a poor long-term choice asa routine obturating material . 11,16,58,59 Their majorproblems relate to nonadaptability (Figure 14-7)and toxicity from corrosion.60 Also, because of theirtight frictional fit and hardness, silver cones are dif-ficult to remove totally (retreatment) or partially(post space preparation) .6 1 Also, if silver cones arecontacted with a bur, their seal may be broken.

In summary, silver cones are contraindicated as anobturating material.

Files as Core Materials

Files used as core materials are an interesting con-cept. Because preparation is accomplished withfiles, why not fill the canal with sealer, force or"screw" a file into place at the correct workinglength, and then cut it at the canal orifice? Thistechnique has not gained popular acceptance, al-though there have been advocates.

A major disadvantage is that, because of theirdesign and the complexity of root canals, files donot provide a complete seal.59 Their fluting pre-cludes a close fit, and sealer will not occupy therest of the space. In addition, retrieval is difficultif retreatment or a post space is needed. Files as aprimary core material are contraindicated.

FIGURE 14-7A, Apparent good obturation, but a persistent lesion (arrow) is seen on the lateral incisor, indicating treatmentfailure. B, The reason for the failure is poor adaptation; a No. 25 file readily passes lingual to the silver point.

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PASTES (SEMISOLIDS)

Why not develop a paste or cement that can bemixed in a liquid or putty form, inject the mate-rial to length, fill the entire canal, and then allowthe material to set? This would be fast, the pastewould fill the entire canal space, and obturationwould be much simpler. In addition, this methodwould permit use of a material that would adhereto dentin and create an absolute seal.

Although the concept is appealing, there aresignificant practical difficulties. However, it cer-tainly has been attempted, and work on develop-ing such a material continues. The major disad-vantages of paste materials are lack of lengthcontrol, unpredictability, and shrinkage.

Types

Zinc Oxide and Eugenol. Zinc oxide and eugenolmay be mixed pure (no additives) to intermediatethickness. Other formulations combine zincoxide-eugenol (ZnOE) with various additives. Thetypes known as N2 or RC2B are most common.These are derivations of Sargenti's formula andcontain opaquers, metallic oxides (lead) or chlo-rides (mercuric), steroids (at times), plasticizers,paraformaldehyde, and various other ingredients.Claims of antimicrobial properties, biologic ther-apeutic activity, and superiority are made forthese paste formulations; no proof exists thatthey contribute any beneficial aspects to obtura-tion. In fact, most of these additives are quitetoxic.62

Plastics. It has been suggested that a resin-based sealer such as AH26 and Diaket be used asthe sole obturating material. These sealers havethe same disadvantages as pastes and, therefore,have not attained popular use.

coated, and then it is placed and spun deep inthe canal. As with the syringe device, the canal issupposedly filled with paste as the drill is slowlywithdrawn.

Both techniques are more attractive in theorythan in fact. Neither technique has demonstratedan ability to seal effectively or to fill the root canalsystem. Because of lack of control, both injectionand placement by lentulo spiral drill have majordeficiencies and are contraindicated.

Advantages and Disadvantages of Pastes

The advantages are obvious: paste techniques arefast and relativity easy to use and involve the useof a single material. The equipment needed, atleast with the lentulo spiral technique, is relativelysimple, comprising only a limited assortment ofspecial drills.

The disadvantages outweigh the advantagesby far. First, the universal problem with any non-solid core material is length control. It is difficultto avoid overfills (Figure 14-8) or underfills (Fig-ure 14-9). Theoretically, radiographs should bemade many times during obturation to assesslength and density as the material is being in-jected or placed. Obviously, this is time consum-ing and subjects the patient to needless radiation.

Another major disadvantage is sealability.These techniques seal inconsistently: sometimeswell, other times poorly. 64,65 This unpredictabilitymay be related to three factors: (1) large voids ordiscrepancies within the material or adjacent tothe walls; (2) shrinkage of ZnOE on setting, whichleaves a space for microleakage; and (3) solubilityof pastes in tissue or oral fluids. In addition, in-jection devices are difficult to clean and maintain.

Techniques of Placement SealersVarious approaches and instruments have beendevised or modified for insertion of pastes or seal-ers. Two popular methods are injection and place-ment with a lentulo spiral.

Injection is accomplished using a syringe-typedevice with a barrel and special needles.63 Thepaste is mixed and placed in the barrel, a screwhandle is inserted and twisted, and the paste is ex-truded through the special needle-like tips. Theneedles are placed deep in the canal, and the pasteis expressed as the needles are slowly backed outof the canal. Advocates claim that this methodcompletely fills the canal from the apical portionto the canal orifice.

Instrument placement is done with lentulospiral drills. The paste is mixed, the drill is

A basic concept is that sealer is more importantthan the core obturating material. Sealer accom-plishes the objective of providing a fluid-tightseal; the core occupies space, serving as a vehiclefor the sealer . 66 Sealer must be used in conjunc-tion with the obturating material regardless ofthe technique or material used. This makes thephysical properties and placement of the sealerimportant.

DESIRABLE PROPERTIES

Grossman outlined the criteria for an idealsealer . 66 None of the currently available sealerspossesses all these ideal properties, but some havemore than others. His criteria are as follows.

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FIGURE 14-8Mandibular paresthesia after treatment. A, Using an injection technique, unset paste was forced out the apex intothe mandibular canal causing chemical damage to the inferior alveolar nerve. B, Periradicular surgery correctedthe endodontic problem, but failed to resolve the paresthesia.

Tissue Tolerance

The sealer and its components should cause nei-ther tissue destruction nor cell death. All com-monly used sealers show a degree of toxicity.21This toxicity is greatest when the sealer is unsetbut tends to diminish after setting and withtime.67,68

No Shrinkage with Setting

Sealer should remain dimensionally stable or evenexpand slightly on setting.

Slow Setting Time

Sealer should provide adequate working time forplacement and manipulation of obturating mate-rial, then set reasonably soon after obturation iscomplete. It is desirable to have sealer unset ifpost space is made immediately.

FIGURE 14-9Frequent problems with inadequate preparation combinedwith paste fills: gross underfill and numerous voids, leadingto long-term failure.

Adhesiveness

Adhesiveness is a most desirable property. A trulyadhesive material would form an absolute bond

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between the core material and dentin, closing offany spaces. ZnOE-based sealers have no adhesion;plastics have some.

Radiopacity

Sealer should be readily visible on radiographs.However, the more radiopaque the sealer, themore it obscures voids in the obturation. Someclinicians prefer a highly radiopaque sealer tomask discrepancies.

Absence of Staining

Remnants should not cause future staining of thecrown. Currently, all tested sealers, particularlyZnOE-based sealers or those containing heavymetals, stain dentin. 69,70

Solubility in Solvent

Occasionally post space or retreatment may benecessary days, months, or years after obturation.The sealer should be soluble in a solvent. Differ-ent sealers have different degrees of solubility indifferent solvents and with varying mechanicaltechniques . 71,72

Insolubility to Oral and Tissue Fluids

Sealer should not disintegrate when in contactwith tissue fluids. Sealers are somewhat soluble,particularly when in contact with oral fluids. 9,73

tion. This has withstood the test of time andusage, although some of plastics (resins) also noware widely used and have many desirable proper-ties. Calcium hydroxide and glass ionomer typesare newer and have interesting properties but alsosignificant drawbacks.

Zinc Oxide-Eugenol-Based

The major advantage of ZnOE-based sealer typesis their long history of successful usage. Obvi-ously, their positive qualities outweigh their nega-tive aspects (staining, very slow setting time, non-adhesion, and solubility).

Grossman's Formulation. The formula is as fol-lows:

Powder: zinc oxide (body), 42 parts, stabelliteresin (setting time and consistency), 27 parts;bismuth subcarbonate, 15 parts; bariumsulfate (radiopacity), 15 parts; sodium bo-rate, 1 part

Liquid: eugenol

Most ZnOE sealers in use and available todayare variations of this original formula. A problemwith this formulation is the very slow settingtime, more than 2 months, as studied in a usagetest.75

Other Types. ZnOE forms the base for othersealers, some of which have been used more com-monly than others. These will not be discussedfurther here.

Bacteriostatic Properties

Although a bactericidal sealer would seem to bedesirable, a substance that kills bacteria will alsobe toxic to host tissues. At a minimum, the sealershould not encourage bacterial growth .74

Creation of a Seal

This is an obviously important physical property.The material must create and maintain a seal api-cally, laterally, and coronally.

TYPES

Generally, there are four major types of sealers:ZnOE-based, plastics, glass ionomer, and thosecontaining calcium hydroxide. Other variationsand compounds have been proposed or are mar-keted as sealers; these should be consideredexperimental.

Certainly, the standard sealer with which allothers are compared is the Grossman formula-

Plastics

Plastics are much less commonly used and ac-cepted, at least in the United States. Some havevery desirable properties, however.

Epoxy. Epoxy is available in a powder-liquidformula (AH26). Its properties include antimicro-bial action, adhesion, long working time, ease ofmixing, and very good sealability.76,77 Its disadvan-tages are staining, relative insolubility in solvents,some toxicity when unset, and some solubility tooral fluids. A recently introduced variation (AH-Plus) has similar physical properties, but betterbiocompatibility because it releases less formalde-hyde and a supposed decrease in dentin stainingby elimination of silver from the formula . 71

Other Plastics. These are primarily of the methylmethacrylate type and are not commonly used.

Calcium Hydroxide

Calcium hydroxide sealers have been introducedin which the calcium hydroxide is incorporatedi n a ZnOE or plastic base. These sealers suppos-

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edly have biologic properties that stimulate a cal-cific barrier at the apex; however, these propertieshave not been conclusively demonstrated in clin-ical or experimental use. Calcium hydroxide seal-ers show antimicrobial properties79 and adequateshort-term sealability." Questions have beenraised about their long-term stability (greater sol-ubility) and tissue toxicity.81 Until further experi-mental and clinical data are available, these seal-ers have no demonstrated advantages and are notrecommended.

Glass lonomer

Endodontic formulations of glass ionomer" havebeen introduced recently. This material has theadvantage of bonding to dentin, seems to providean adequate apical and coronal seal, and is bio-compatible.83-86 However, its hardness and insolu-bility make retreatment and post space prepara-tion more difficult.$'

Others

Various luting agents and basing and restorativematerials have been tried and tested as endodon-tic sealers.88 " Examples are zinc phosphate ce-ment, composite, and polycarboxylate cement.These materials have not proved satisfactory.

MIXING

The common sealer types should be mixed care-fully to a thick consistency. They should stringapproximately 2 to 3 inches. The thicker the mix,the better are the properties of the sealer, particu-larly in regard to stability, superiority of seal, anddiminished toxicity. 90

PLACEMENT

Various techniques have been advocated forplacement of sealer, which is done before inser-tion of the core material. The sealer may beplaced with paper points, with files, with ultra-sonic activation of files, with special drills(lentulo), as a coating on the primary cone, or byinjecting with special syringes. Although differ-ent methods have shown varying degrees of effec-tiveness in sealer application, no technique hasproved superior.91-94 I n fact, sealers may not com-pletely cover the interface between gutta-perchaand canal wall after obturation. 95

A simple and effective technique is to coat thewalls by picking up sealer on the final apical file ora one-size smaller file (Figure 14-10). The file isteased to length and spun counterclockwise,

FIGURE 14-10An easy, effective method of sealer application. The file cov-ered with sealer will be inserted and spun counterclockwiseto coat the canal walls.

which has the effect of carrying the sealer apicallyand coating the walls. Flooding the canal withsealer is neither necessary nor desirable.

Sealer is not placed in all canals at once unlessit gives a long working time. Removing sealer thathas set is difficult. The Grossman formulationsand epoxy resins are slow setting and may beplaced in all canal S.75

Obturation Techniques withGutta-PerchaDifferent approaches are available, depending onthe size of the prepared canal, the final shape of thepreparation, and irregularities within the canal.The overriding factor is operator preference. 96

SELECTION OF TECHNIQUE

The two traditional techniques are lateral andvertical condensation; sealability is similar inboth.97,98 Again, the choice is dictated primarily

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by preference and custom, although there maybe special situations indicating a particular useof each technique. Both must be used with asealer.

More recent approaches have been introducedthat depend upon warming and softening formu-lations of gutta-percha with special devices andinstruments and then placing the gutta-perchaincrementally. Some of these techniques and de-vices are heavily promoted and will be discussedlater in the chapter.

Other methods are also used; most involve al-teration of the entire gutta-percha cone with a sol-vent such as chloroform or eucalyptol. These aretechnique sensitive and therefore are not widelyused or taught in the United States. They are notdiscussed in this textbook; details are found inother published sources.

A variation of lateral condensation is the solvent-softened (or custom-fitted tip) technique, which isoutlined later in this chapter.

LATERAL CONDENSATION

Lateral condensation is the most popular tech-nique of obturation, both in practice and astaught in most institutions.99 Therefore, this tech-nique will be described in detail.

Indications

Lateral condensation of gutta-percha may beused in most situations. Exceptions are severelycurved or abnormally shaped canals or thosewith gross irregularities such as internal resorp-tion. However, lateral condensation may be com-bined with other obturation approaches. In gen-eral, if the situation is not amenable to lateral (orvertical, if that is the usual approach) condensa-tion, it is too difficult for the general practi-tioner and the patient should be referred to anendodontist.

Advantages

Lateral condensation is relatively uncomplicated,requires a simple armamentarium, and seals andobturates as well as any other technique in con-ventional situations.100,101 A major advantage ithas over most other techniques is length con-trol." With an apical stop and with careful use ofthe spreader, the length of the gutta-percha fillingis managed well. Additional advantages includeease of retreatment, adaptation to the canal walls,positive dimensional stability, and the ability toprepare post space.100,101

Disadvantages

There are no major disadvantages to lateral con-densation other than difficulties in obturating se-verely curved canals, an open apex, and canalswith internal resorptive defects.

Technique

Although there are variations, a workable and ac-ceptable technique is presented here. Variations oflateral condensation are described in other text-books and manuals.

Spreader or Plugger Selection. Selection and try-in should be performed during the cleaning andshaping of the canal. Finger spreaders or plug-gets are preferred over standard (long-handled)spreaders because of better tactile sensations,improved apical seal, better instrument control(Figure 14-11), and reduced dentin stress duringobturation.3 4,102 Use of these finger instruments

FIGURE 14-77Hand spreaders may be precurved to improve manipulationinto curved canals.

likely decreases the incidence of vertical rootfractures during obturation. Finger spreaders/pluggers also can be inserted more deeply thanstandard hand spreaders (Figure 14-12).

Nickel-titanium finger spreaders have been in-troduced recently. Because of their flexibility,these spreaders seem to produce less wedgingforce while penetrating deeper. 103,104 Their advan-tage may be less tendency to produce vertical rootfractures. These spreaders do behave differentlybecause of their flexibility and require practice forefficient use.

Master Cone Selection. Either a standardized ora conventionally shaped, fine gutta-percha conemay be adapted as a master cone. Apical prepara-tions that are very irregular in shape, are largerthan a No. 50 file, have no apical stop, or have anapical seat greater than a No. 40 file should havethe custom solvent-softened cone (describedlater).

Large standardized cones (No. 50 and above)are used in the custom cone technique in canalslarger than a No. 50 file. Conventional cones arecut and adapted to canals less than a No. 50 file.

Fitting the Master Cone. Apical clearing (whenindicated) is important before the master cone is

fitted (see Chapter 13). After apical clearing is:ompleted, the steps are as follows:

1. Because the master cone fits only in the api-cal portion of the apically cleared, flaredcanal, the amount of resistance shown to re-moval is slight (Figure 14-13). A slight fric-tional fit is acceptable; the so-called tugbackis unnecessary."' However, there should bea definite stop when the cone fits into place.The cone is fitted to within 1 mm of work-ing length.

FIGURE 14-13The master cone needs only a slight frictional fit in the veryapical region. This permits deep spreader penetration be-tween the gutta-percha and the canal wall.

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FIGURE 14-12Comparison of hand spreader with finger pluggers or spreaders. A, The stiff, more tapered hand spreader will notnegotiate the curve. B, The smaller, more flexible finger spreader permits deeper penetration and produces a su-

perior apical seal.

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2. A cone may be too small as indicated by abuckling in the apical few millimeters (Fig-ure 14-14, A). A larger sized apical end ismade by cutting 1-mm segments off the mas-ter cone until the slight fit is obtained (Fig-ure 14-14, B). Frequently, the cone cannot beinserted quite to working length. This is ac-ceptable only if (a) the apical area has beencleared of debris and (b) the spreader pene-

trates to within 1 mm of the prepared length.A cleared apical area and deep spreader pene-tration will usually push the gutta-perchaand sealer apically to fill the remaining 1 mm(Figure 14-15).106

3. The master cone is removed by grasping itat the reference point, and the length is ver-ified by measuring it on a ruler, then cor-rected if necessary.

4. Master cone length (not lateral fit) is evalu-ated radiographically. Again, the coneshould be no more than 1 mm short of theprepared length. The traditional close radi-ographic fit of the master cone in the apicalthird is unrelated to the quality of the finalSeal.' °s

5. If the master cone length is not within1 mm of the prepared canal length, either(a) dry reaming is repeated to be certainthere is no debris, or (b) another, smallercone is adapted.

FIGURE 14-14A, A cone that appears buckled on the radiograph or on re-moval is much too small. B, A larger cone should be selectedor clipped to form a larger size at the tip.

FIGURE 14-15A, The master cone need not extend along the entire lengthi f the preparation (arrow) has been apically cleared. B, Deepspreader penetration then often pushes the gutta-perchaand sealer apically to fill the prepared space. (Courtesy Dr. J.Parsons.)

6. A gutta-percha cone that extends beyondthe apical foramen shows the lack of an api-cal stop. This requires a custom solvent-softened cone or selection and modificationof a shorter, larger cone.

FIGURE 14-16An assortment of obturation instruments and gutta-perchacones. From left to right: A 21-mm fine plugger with measure-ment markings on the shaft; a 25-mm medium fine plugger; a25-mm fine plugger; a conventional fine gutta-percha point;and No. 35 and No. 40 standardized gutta-percha cones. Agood combination for most situations is the fine gutta-perchapoint (right arrow) and the fine finger plugger (left arrow).

Steps in Obturation. Although there are manycombinations of obturating instruments and dif-ferent types of gutta-percha, a suggested combi-nation for routine situations is a fine finger plug-ger and fine accessory cone (Figure 14-16). Thereis no precise correlation between size of accessorypoint and size of finger spreader.'°' Specific stepsare as follows (Figure 14-17):

1. Sealer is mixed and applied to canal walls.2. The master cone (without sealer coating) is

inserted slowly to allow air and excess ce-ment to escape.

3. Before the spreader is inserted and re-moved, an accessory cone is picked up withlocking pliers at the measured length, readyto be inserted.

4. The measured spreader is inserted betweenthe master cone and the canal wall usingfirm (apical only) pressure (5 to 7 pounds asfor amalgam condensation) to within 1 to2 mm from working length. Spreader taperis the mechanical force that laterally com-presses and spreads gutta-percha, creating aspace for an additional accessory cone.

5. The spreader is freed for removal by back-and-forth rotation around its axis. Thespreader is removed and the measured ac-cessory (fine) gutta-percha cone is immedi-ately inserted into the space created.

6. ( Optional) A radiograph may be made afterone or two cones are placed. If there arelength problems, the cones are retrieved. Anew master cone is fit at a connected length.

7. This procedure is repeated until thespreader can no longer be pressed beyond

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25 5

FIGURE 14-17The steps of lateral condensation. A, The master cone is fitted. B, A finger spreader or plugger is inserted, ideallyto 1 to 2 mm of the prepared length. C, The spreader is rotated and removed, and an accessory cone is placed inthe space created. D, The process is repeated.

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the apical third of the canal (approximatelythree to seven accessory cones). The last in-sertion is an accessory cone, not thespreader! The spreader need not be steppedall the way out of the canal, adding acces-sory cones. Obturation may be evaluatedwith a radiograph at this time.

8. Excess gutta-percha is seared off with a hotinstrument (Glick No. 1, a heated plugger,or a battery-controlled heating device (Fig-ure 14-18). This is done approximately1 mm apical to the gingival margin in ante-rior teeth and 1 mm apical to the canal ori-fice in posterior teeth.

9. The cervical portion of the warm gutta-perchais vertically condensed firmly using the GlickNo. 1 or a No. 5-7 heater-plugger.108

Finishing Touches

The procedure is completed as follows:

1. The chamber is cleaned thoroughly withcotton pellets soaked in alcohol or chloro-form; unset sealers are soluble in these solu-tions. Remnants of gutta-percha or sealer(in particular) may cause future discol-oration (Figure 14-19).

2. A temporary or permanent restoration isplaced. Appropriate temporization orrestoration (semipermanent or permanent)is discussed in Chapter 15.

3. A radiograph is made with the restorationin place and the clamp removed.

Correcting Obturation Problems

Ultrasonic Condensation. A variation is lateralcondensation with ultrasonic activation of thespreader. With this technique the spreader isplaced next to the master cone and activated with-out a water coolant. Apical pressure is exerted, andthe spreader is inserted to a predetermined length.Advantages are that the ultrasonic action mayspread the sealer, the friction of the spreader maythermoplasticize the gutta-percha, and the forcerequired to place the spreader may be less. 109,110

Occasionally, voids or length problems will be ap-parent on the radiograph taken during or afterobturation. These should be corrected now, beforethe sealer sets!

For voids, gutta-percha is removed with hotpluggers until the spreader can be reinserted justbeyond the void or discrepancy. Then, a freshmix of sealer is prepared. Lateral condensation isperformed as described previously; sealer isadded back to the canal by coating each acces-sory cone.

An advantage of making an obturation verifi-cation radiograph before the excess gutta-perchais seared off is that the entire mass can usually beremoved by grasping the cones with the fingers.

FIGURE 14-18A, A convenient battery-controlled heating deviceholds an assortment of tips. B, The tip is rapidly heatedfor removal of excess gutta-percha from the chamber,or from the canal when creating a post space.

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Fitting a new master cone and reobturation isthen possible.

If the excess gutta-percha has been seared off,an overfill can sometimes be corrected before thesealer sets by removing all gutta-percha with filesor broaches. When extruded beyond the apex, theoverfilled gutta-percha is difficult to recoverthrough the canal, particularly after the sealer sets.Extruded sealer can only be retrieved surgically.

Obturating materials extruded beyond the apexare irritants and affect healing, but generally theydo not completely prevent resolution (Figure 14-20)unless there is gross overfill of core material.ZnOE-based sealers often resorb from periapical tis-sues over time.111 These situations should not betreated surgically unless failure to heal is evident onrecall examination.

An impression of the apical 3 or 4 mm of thecanal is made in the gutta-percha master cone. Itis basically a "cone within a cone," as only thecone surface is softened and then shaped. The ob-jective is to fit the cone closely into the apical por-tion to try to create a better seal but primarily toprevent extrusion of gutta-percha beyond theapex. In fact, solvent softening does not result ul-timately in a better apical seal. 114-116

Indications

Basically there are two indications: (1) an apicalstop is lacking or (2) a stop is present but the api-cal portion of the canal is very large or irregular.

Technique

SOLVENT-SOFTENED CUSTOM

CONES

Different solvents have been proposed andtested. The two that have been proven to be use-ful clinically and that are used most often arechloroform and halothane; however, concernsabout toxicity have been expressed. Some con-cerns about chloroform are unfounded; recentevaluations show that, if used judiciously, chlo-roform is safe for retreatment and for the forma-tion of custom cones.112,113 Described here is atechnique using chloroform; halothane is used ina similar manner.

The steps are as follows:

1. The master cone selected is usually a largerstandardized cone that, when inserted, stops2 to 4 mm short of the working length.

2. The master cone tip (apical 3 to 4 mm) issoftened by dipping it in chloroform for 1to 2 seconds (Figure 14-21). Halothane dip-ping is done for 3 to 4 seconds.

3. The cone is tamped apically in the canal sev-eral times. Then, the cone is grasped at thereference point, removed, and measured.Softening and tamping are repeated untilthe cone goes to working length. The cone is

FIGURE 14-19Often discoloration is caused by improper technique and is preventable. A, A too-frequent unfortunate occur-rence: gradual discoloration after root canal treatment. B, Causes include sealer remnants and a silver point ex-tending into the chamber and amalgam restoring the lingual access. This tooth will be difficult to bleach because

the stains are from metallic ions.

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FIGURE 14-20A, This is not a serious overfill. The core obturating material is confined to the canal. B, Recall examination showshealing and resorption of sealer.

FIGURE 14-21The softened custom cone technique. The apical portion (3 to4 mm) is dipped in chloroform for 1 to 2 seconds and thentamped in the canal.

marked or bent for orientation; it must bereplaced exactly in the same position duringobturation.

4. The cone is removed, and the solvent is al-lowed to evaporate. The cone should not beleft in the canal for any length of time whilesoft; the softening will continue and the tipmay separate when the master cone is re-moved. The cone tip should show an impres-sion of the apical preparation (Figure 14-22).

S. The cone is replaced and a confirmatory ra-diograph is made. The cone need not extendto working length but may be slightlyshorter, up to 1 mm.

G. Sealer is mixed thick. The canal walls are notcoated, only the apical third of the mastercone. The cone is carefully inserted to lengthwithout wiping off all the sealer on the walls.

7. The standard lateral condensation proce-dure follows with spreader insertion, rota-tion, removal, accessory cone placement,and so on. More sealer is added by coatingeach accessory cone before placement.

8. A radiograph may be made to evaluate theobturation before the excess is seared off.

FIGURE 14-22After the softened cone has been tamped into the canal andremoved, it should show an impression of the apical region(arrow).

The mass can be pulled out and reobtura-tion done if necessary.

VERTICAL CONDENSATION

Vertical condensation is also an effective technique;studies show its sealability is comparable to that oflateral condensation. Although vertical condensa-tion is not widely taught in dental schools, thetechnique is becoming more popular. With the in-troduction of new devices and techniques, thewarm vertical compaction technique is somewhatmore user friendly and is less time consuming.

Indications

In general, vertical condensation can be used inthe same situations as lateral condensation. It ispreferred in a few circumstances, such as with in-ternal resorption and with root end induction.

Advantages and Disadvantages

Its principal advantage over lateral condensationis the ability to adapt the warmed and softened

FIGURE 74-23Warm vertical condensation. Larger canal preparations arei ndicated to accommodate obturating instruments (heater-pluggers). Also, this technique tends to apically extrude

sealer and softened gutta-percha.

gutta-percha to the irregular root canal sys-tem.' 'e" 8 Disadvantages include difficulty oflength control, a more complicated procedure,and a larger assortment of required instruments.Also, a somewhat larger canal preparation is nec-essary to allow manipulation of the instruments(Figure 14-23).

Technique

The warm vertical compaction technique requiresa heat source and various sized pluggers for com-paction of the thermoplasticized gutta-percha.Schilder pluggers begin at 0.4 mm in diameterand increase by 0.1 mm for each of the successiveinstruments with 1.1 mm being the largest instru-ment. Pluggers are also available in ISO standard-ized sizes.

The technique consists of fitting a gutta-perchacone with a taper similar to the canal, short of theapex and applying heat using a flame-heated car-rier. The gutta-percha is softened by the heat andbecomes plastic. Pluggers are then placed in thecanal with apical pressure to produce a hydraulicforce that moves the gutta-percha apically, against

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259

260

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the canal walls, and into canal irregularities suchas accessory canals. Gutta-percha is then added insmall increments; each increment of gutta-perchais heated and softened and packed vertically untilthe entire canal is filled. Detailed descriptions ofthe technique appear elsewhere.119

FIGURE 74-24Device for heating gutta-percha. A controlled current causesrapid heating of the plugger, which then softens a prefitgutta-percha cone in the canal.

Other Warm Vertical Approaches

A recent modification of the warm vertical com-paction technique is termed the "continuouswave of condensation." Prerequisites for this tech-nique are a tapering canal preparation, a con-stricted apical preparation, and an accurate conefit. The technique is often used after preparationwith nickel-titanium rotary files of greater taper.The heat source is an electric device that suppliesheat to a plugger on demand (Figure 14-24). Plug-gets are available in nonstandardized sizes thatmatch the nonstandardized gutta-percha conesor in standardized sizes that match files of greatertaper (Figure 14-25). In addition, two hand plug-gets of differing diameters are used to sustain andcondense the gutta-percha apically.

Heat is applied at a prescribed temperature(200° C) for a short period of time as determinedby the operator. By applying a constant source ofheat to a prefitted gutta-percha cone, hydraulicpressure can be applied in one continuous motion.As the plugger moves apically, the fit becomes moreprecise and the hydraulic pressure is increased,forcing the gutta-percha into canal irregularities.Details of the continuous wave of condensationtechnique are available in other publications. 120

There are inherent risks. When thermoplasti-cization or any technique that physically altersgutta-percha is used, there is the potential for ex-trusion into the periradicular tissues as well aspossible damage to the periodontal ligament andsupporting alveolar bone from heat. An increaseof 10° C above body temperature appears to be acritical threshold for damaging osseous tis-sues .96,121 Flame-heated carriers reach high tem-peratures and pose the greatest threat of damageto the periodontal structures. 122-125 When usedproperly, the injectable gutta-percha techniqueand the continuous wave condensation tech-nique appear to produce temperature changesthat are below the critical threshold. 1 2s -127

Sectional Obturation

A recent innovation, this technique involves a two-phased sectional approach. A small apical segmentof gutta-percha is placed ("downpacked"), fol-lowed by a backfilling of gutta-percha. This tech-nique seems relatively fast and may prove useful,but requires more investigation. 128 Details of thetechnique appear elsewhere. 129

FIGURE 14-25"Continuous wave of condensation" plugger is designed tosize-match the rotary file used to prepare the canal. Pluggersare also approximately matched to nonstandardized gutta-percha in an attempt to obturate the apical portion of a canalwith a single cone.

Thermoplasticized Injection

With this technique, specially formulated gutta-percha is warmed and then injected into the pre-pared canal with a device (Figure 14-26) that

14 / Obturation

26 1

works like a caulking gun.130 When used in con-junction with a sealer, thermoplasticized injectionprovides an adequate seal. 131 This technique isuseful in special situations (Figure 14-27). How-ever, lack of length control and shrinkage uponcooling are disadvantages.

Solvent Techniques

Solvent techniques involve the total or partial dis-solution of gutta-percha in solvents, primarilychloroform or eucalyptol (see Figure 14-5). Thesehave names such as chloropercha, eucapercha,diffusion technique, or chloroform resin. Often,

FIGURE 14-26A thermoplasticizing device. A high-heat gun softens gutta-percha (arrow)

i nto an injectable plastic mass.

FIGURE 14-27A, Internal resorptive defect is a good indication for B, obturation with a thermoplasticized gutta-perchatechnique. (Courtesy Dr. M Gomez.)

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these techniques are not used in conjunction witha standard sealer but depend on softened gutta-percha to adapt closely. The problem is thatgutta-percha shrinks away from the walls as thesolvents evaporate. Extensive leakage is generallyseen with these techniques,56 and some have apoorer long-term prognosis. 132

Gutta-Percha Carrier Systems

These systems use a central carrier (stainless steel,titanium, or plastic) coated with gutta-percha.The carrier is flexible yet it provides rigidity forthe overlying gutta-percha. The obturators arestandardized, so the carriers correspond to thesize of instruments. After canal preparation, thecanal is dried and lightly coated with sealer.The appropriate size obturator is heated in a spe-cial oven and firmly placed to working length. Thecarrier is then sectioned 1 to 2 mm above the ori-fice to the canal. These carrier/gutta-percha sys-tems are equivalent to conventional gutta-perchaobturation with apical sealing, but do not consis-tently create a coronal seal. 133,131

Advantages of the technique include ease ofplacement and the potential for the plasticizedgutta-percha to flow into canal irregularities. Dis-advantages include a tendency for extrusion ofmaterial periapically, an inability to control thedensity of fill in irregularly shaped canals, diffi-culties in removing carrier and gutta-percha dur-ing retreatment, and variable adaptation of com-ponents in the canal. 131,131 Overall, there are nodemonstrated advantages to routine use of thesesystems.

term toxicity than the standard accepted materi-als.l38-140 Although there are advocates for the so-called Sargenti technique, which continues to bepracticed, experimental and clinical evidenceweighs heavily against this approach. In addition,there are warnings and, in some countries andstates, bans against it. There is also a federal banon importation and interstate sales of the N2 orRC2B paste. Perhaps for these and other reasons,malpractice lawsuits and out-of-court settlementshave consistently been decided for the plaintiffand against the dentist employing the Sargentitechnique and the paste.

However, on the horizon are some interestingand radical approaches to preparation and obtu-ration using hydrodynamics and vacuum tech-niques.141 These are still experimental, lackingclinical verification, but show promise.

Evaluation of ObturationSurprisingly, evaluation of obturation is difficult.The only means of immediate assessment is radi-ographic, which is imprecise at best. However, ra-diographic evaluation has been the standard andat least provides some criteria with which to judgeobturation quality.

SYMPTOMS

The presence of symptoms for a few days after ob-turation is common and probably is unrelatedto an inadequate seal. This reflects a differentphenomenon.

ALTERNATIVE TECHNIQUES RADIOGRAPHIC CRITERIA

Other techniques involve primarily mixing andplacement of unset material into the canal. Eitherchemical or physical changes cause the materialto set into a semisolid or solid form. Many mate-rials have been tried, clinical validation researchon them usually is sparse or absent. None have yetproved feasible for various reasons related to ei-ther the material or the techniques of insertion.Again, length control and obturation voids aremajor difficulties."' Included with some of thesetechniques are materials as such amalgam, glassionomer, composites, silicone pastes, semisoftacrylics N2 or RC2B paste ("Sargenti" technique),and ZnOE paste with various additives.

In addition to problems with physical proper-ties, generally there are many biologic disadvan-tages as well."' In particular, the pastes with for-maldehyde or heavy metal additives (e.g., Sargentiformulations) show more short-term and long-

Good obturation (fluid-tight seal) cannot be seenon a radiograph. Only fairly gross discrepanciesare visible; these voids or deficiencies may or maynot relate to lack of seal and may result in long-term failure. 142 The evaluative criteria as deter-mined by studying the obturation radiograph(Figure 14-28) are as follows.

Radiolucencies

Voids within the body or at the interface of obtu-rating material and dentin wall represent incom-plete obturation.

Density

Material should be of uniform density fromcoronal to apical aspects. The coronal region(and large canals) are more radiopaque than the

1 41 Obturation

263

FIGURE 74-28Evaluation of obturation: an example showing several deficiencies and correction. A, Length: apical portion showsslight overfill; shape: there is not consistent taper (the fill is narrower in the cervical region); density: voids arepresent throughout; coronal removal: material remains in the chamber. B, Improved access, cleaning and shap-i ng, correct obturation, and restoration. Healing is evident. (Courtesy Dr. A. Stabholz.)

apical region because of differences in mass ofmaterial. The margins of gutta-percha should besharp and distinct with no fuzziness, indicatingclose adaptation.

Restoration

Whether permanent or temporary, the restorationshould be contacting enough dentin surface toensure a coronal seal.

Length

The material should extend to the preparedlength and be removed apical to the gingival mar-gin (anterior teeth) and orifices (posterior teeth).

Taper

The gutta-percha should reflect the canal shape;that is, it should be tapered from coronal to api-cal regions. Taper need not be uniform bur shouldbe consistent. Ideally, the apical region shouldtaper nearly to a point unless the canal in this re-gion was not small before preparation.

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101. Amditis C, Blackler SM, Bryant RW, Hewitt GH: The

adaptation achieved by four root canal filling tech-

niques as assessed by three methods, Aust Dent J

37:439, 1992.

102. Simons J, lbanez B, Friedman S, Trope M: Leakage

after lateral condensation with finger spreaders and

D-1 1-T spreaders, JEndod 17:101, 1991.

103. Joyce A, Loushine R, West L, et al: Photoelastic compar-

ison of stress induced by using stainless-steel versus

nickel-titanium spreaders in vitro,JEndod 24:714,1998.

104. Schmidt K, Walker T, Johnson J, Nicoll B: Compari-

son of nickel-titanium and stainless-steel spreader

penetration and accessory cone fit in curved canals, J

Endod 26:42, 2000.

105. Allison DA, Michelich RJ, Walton RE: The influenceof master cone adaptation on the quality of the api-cal seal, JEndod 11:166, 1981.

106. Yared GM, Bou Dagher FE: Elongation and move-

ment of the gutta-percha master cone during initial

lateral condensation, JEndod 19:395, 1993.

107. Hartwell GR, Barbieri SJ, Gerard SE, Gunsolley JC:

Evaluation of size variation between endodontic fin-

ger spreaders and accessory gutta-percha cones, J

Endod 17:8, 1991.

108. Yared G, Bou Dagher F, Machtou P: Influence of theremoval of coronal gutta-percha on the seal of rootcanal obturation, JEndod 23:146, 1997.

109. Baumgardner K, Krell K: Ultrasonic condensation of

gutta-percha: an in vitro dye penetration and scan-

ning electron microscopic study, J Endod 16:253,

1990.

110. Zmener O, Banegas G: Clinical experience of root

canal filling by ultrasonic condensation of gutta-

percha, Endod Dent Traumatol 15:57, 1999.

111. Augsberger RA, Peters DD: Radiographic evaluation

of extruded obturation materials, J Endod 16:492,

1990.112. McDonald MN, Vire DE: Chloroform in the en-

dodontic operatory J Endod 18:301, 1992.113. Allard U, Andersson L: Exposure of dental personnel

to chloroform in root-filling procedures, Endod DentTraumatol8:155, 1992.

114. Keane KM, Harrington GW: The use of chloroformsoftened gutta-percha master cone and its effects on

the apical seal, JEndod 10:57, 1984.

115. Smith JJ, Montgomery S: A comparison of apical seal:

chloroform versus halothane-dipped gutta-percha

cones,JEndod 18:156, 1992.

116. Yancich PP, Hartwell GR, Portell FR: A comparison of

apical seal: chloroform versus eucalyptol-dipped

gutta-percha obturation, JEndod 15:257, 1989.

117. Wolcott J, Himel V, Powell W: Effect of two obtura-

tion techniques on the filling of lateral canals and the

main canal, J Endod 23:632, 1997.

118. DuLac K, Nielsen C, Tomazic T, et al: Comparison of

the obturation of lateral canals by six techniques, J

Endod 25:376, 1999.

119. Schilder H: Vertical comparison of warm gutta-

percha. In Gerstein H, editor, Techniques in clinical en-

dodontics, Philadelphia, 1983, WB Saunders.

120. Buchanan S: Continuous wave of condensation tech-

nique, Endod Pract 2:7, 1998.

121. Eriksson A, Albbrektsson T: Temperature threshold

levels for heat-induced bone tissue injury; a vital mi-

croscopic study in the rabbit, J Prostbet Dent

50:101,1983.

122. Hand R, Hugel E, Tsaknis P: Effects of a warm gutta

percha technique on the lateral periodontium, OralSurg Oral Med Oral Patbol 36:872, 1973.

123. Marciano J, Michailesco P: Dental gutta percha;

chemical composition, x-ray identification, enthalpicstudies and clinical i mplications, J Endod

15:149,1989.

124. Lee F, VanCura J, BeGole E: A comparison of root sur-

face temperatures using different obturation heat

sources, JEndod 24:617, 1998.

125. Silver G, Love R, Purton D: Comparison of two verti-cal condensation obturation techniques: Touch 'n

Heat modified and System B, Int Endod J 32:287,

1999.

126. Weller RN, Koch K: In vitro radicular temperatures

produced by injectable thermoplasticized gutta-

percha, IntEndodJ25:593, 1999.

127. Floren J, Weller RN, Pashly D, Kimbrough W:

Changes in root surface temperatures with in vitro

use of the System B HeatSource, JEndod 25:593, 1999.

128. Santos M, Walker W, Carnes D: Evaluation of apical

seal in straight canals after obturation using the

Lightspeed sectional method, JEndod 25:609, 1999.

129. Senia S: Canal diameter: the forgotten dimension,

Endod Pract 3:34, 2000.

130. Marlin J, Krakow A, Desilets R, Gron P: Clinical use

of injection-molded thermoplasticized gutta-percha

for obturation of the root canal systems: a prelimi-

nary report, JEndod 7:277, 1981.

131. Evans JT, Simon JHS: Evaluation of the apical seal

produced by injected thermoplasticized gutta-percha

i n the absence of smear layer and root canal sealer, J

Endod 12:101, 1986.132. Orstavik D, Kerekes K, Eriksen HM: Clinical perfor-

mance of three endodontic sealers, Endod Dent Trau-

matol3:178, 1987.133. Dummer PM, Kelly T, Meghji A, et al: An in vitro

study of the quality of root fillings in teeth obturated

by lateral condensation of gutta-percha or Thermafil

obturators, Int EndodJ 26:99, 1993.

1 4 / Obturation

267

134. Baumgardner K, Taylor J, Walton R: Canal adapta-

tion and coronal leakage: lateral condensation com-

pared to Thermafil, JAm Dent Assoc 126:351, 1995.

135. Juhlin J, Walton RE, Dovgan JS: Adaptation of Ther-

mafil components to canal walls, J Endod 19:130,

1993.

136. Kothari P, Hanson N, Cannell H: Bilateral mandibu-

lar nerve damage following root canal therapy, Br

DentJ 180:189, 1996.

137. Langeland K, Walton R: Sargenti (N2) technique. In

Clark J, editor. Clinical dentistry, Philadelphia, 1982,

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138. Newton CW, Patterson SS, Kafrawy AH: Studies ofSargenti's technique of endodontic treatment: six-

month and one year responses, J Endod 6:509, 1980.

139. West NM, England MC, Safavi K, Green DB: Level of

lead in blood of dogs with RC-2B root canal fillings, J

Endod 6:598, 1980.

140. Pitt Ford T: Tissue reactions to two root canal sealers

containing formaldehyde, Oral Surg Oral Med Oral

Pathol 60:661, 1985.

141. Lussi A, Imwinkelried S, Stich H: Obturation of root

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voids within obturated root canals, Int EndodJ 28:77,

1995.

Preparation for Restorationand Temporization

LEARNING OBJECTIVES


1 / Describe the role of the restoration in longevity of endodontically treated teeth.

2 / Explain the importance of coronal seal in successful root canal treatment.

3/ Summarize factors contributing to loss of tooth strength, and describe the structural importance ofremaining tooth tissue.

4 / Describe requirements of an adequate restoration and how it protects and seals coronally.

5 / Outline postoperative risks to the unrestored tooth.

6 / Discuss the rationale for immediate restoration and list indications for delaying final restoration.

7 / Identify restorative options before commencing root canal treatment.

8 / Discuss advantages and disadvantages of direct and indirect restorations.

9 / Outline indications for post placement in anterior and posterior teeth.

10 / Describe common post systems and advantages and disadvantages of each.

11 / Describe core materials and their placement.

12 / Describe techniques for restoring an access opening through an existing restoration.

13 / List the principal temporary filling materials and describe techniques for their placement and removal.

14 / Describe temporization of extensively damaged teeth.

15 / Outline techniques and materials used for long-term temporization.

268

15 / Preparation for Restoration and Temporization

269

Longevity of Endodontically Treated Teeth

CoronalSeal

Structural and Biomechanical

Considerations

Structural Changes in Dentin

Loss of Tooth Structure

Biomechanical Considerations

Requirements for an Adequate Restoration

Restoration Timing

The Ideal: Immediate Restoration

I ndications for Delaying Final Restoration

Semipermanent Temporary Restoration

Restoration Design

Principles and Concepts

Planning the Definitive Restoration

Preparation of Canal Space and Tooth

Post Selection

Post Space Preparation

Retention and Core Systems

Anterior Teeth

Posterior Teeth

Pins

Restoring Access Through an Existing

Restoration

Temporary Restorations

Objectives of Temporization

Routine Access Cavities

Extensive Coronal Breakdown

Temporary Post Crowns

Long-Term Temporary Restorations

he need for careful restoration is re-flected in the fact that more endodonti-cally treated teeth are lost because of

restorative factors than because of failure of theroot canal treatment itself.1,2 Options for restora-tion are considered before root canal treatment isbegun, although the final decision on the mostappropriate restoration is often made only astreatment progresses. The profusion of restora-tive techniques and materials makes planning ap-pear complex; however, in most cases restorationis usually straightforward.

This chapter considers principles of restora-tion rather than detailed techniques, which arebeyond the scope of this textbook. Conservationof tooth structure is emphasized, though not atthe expense of preserving the treated tooth as afunctional unit.

Longevity of EndodonticallyTreated TeethThe effort and expense of root canal treatment andrestoration require that the tooth function effec-tively for a prolonged period. Surprisingly few clin-ical studies have addressed the question of howlong endodontically treated teeth survive. The nu-merous studies evaluating treatment success andfailure have focused on endodontic aspects (devel-opment or persistence of a periapical lesion, withaccompanying signs and symptoms), which aregenerally amenable to further management . 3 Fewretrospective clinical studies have evaluated ratesand causes of tooth loss; these have consistentlydemonstrated the importance of the restoration.

An 8- to 9-year follow-up study reported that11% of root canal treated teeth were extracted,most for restorative or periodontal reasons.' Sur-vival rates in excess of 90% after 10 years have beenreported .45 Many restorative variables influencethe success rate achieved in clinical practice, andmuch lower survival rates can be expected with in-adequate restoration.6,7 Many endodonticallytreated teeth require extraction because of crownfracture from inadequate restoration, but inap-propriate use of posts also leads to an unaccept-ably high rate of clinical failure.' Under ideal con-ditions, a loss rate from restorative failures of 1%to 2% per year may be achievable.

Coronal SealRoot canal treatment will ultimately fail if the ob-turating materials become exposed to oral fluids.Coronal leakage is a major cause of failure. 8,9 Evena well-obturated canal with appropriate use of

270


sealer cement does not provide an enduring bar-rier to bacterial penetration; the restoration (bothtemporary and permanent) provides the coronalseal.'° Exposure of obturating materials to oralfluids through a lost restoration, marginal dis-crepancy, or recurrent caries leads eventually tosealer disintegration and bacterial contaminationof the canal system. The restoration must pro-vide the coronal seal either as a separate step (forexample, placing a barrier over canal orifices) ormore commonly as an integral part of the restora-tion by virtue of its marginal sealing abihty. 9,11Posts (particularly prefabricated posts) and coresdo not create a seal until the crown is placed. 'z,'3

Lack of an intact sealing restoration is an im-portant factor in assessing the cause of a persis-tent or developing periapical lesion. Fortunately,this is usually correctable by endodontic andrestorative retreatment. Another concern is an in-adequate temporary seal, both during treatmentand after treatment is complete but before finalrestoration. There is not sufficient information toknow how much exposure time to oral fluidsmandates retreatment, although 3 months maxi-mum exposure has been suggested as a generalguideline."

Structural and BiomechanicalConsiderationsRestorative failures commonly include cusp frac-tures or some form of crown-root fracture (splittooth)' (Figure 15-1). It is important to under-stand the basis for this fracture susceptibilitywhen designing restorations. Access preparationsuperimposed on an extensively carious or re-stored tooth leads to further loss of tooth struc-ture. Unsupported cusps (particularly those with-out an adjacent intact marginal ridge) associatedwith a large access opening are more prone tofracture. Excessive preparation of the canal spacefor a post further weakens the root and intro-duces significant stress areas.14,15

STRUCTURAL CHANGES IN DENTIN

A deeply entrenched clinical perception persiststhat root canal treated teeth become brittle, sup-posedly losing resilience as the moisture contentof dentin declines after pulp loss. This perceptionis unsupported experimentally. Few studies havecompared physical properties of endodonticallytreated versus nontreated human teeth with vitalpulps. The moisture content of endodonticallytreated teeth was not reduced, even after 10 years.16Also, a comparison of these two groups revealedno significant differences in strength, toughness,

FIGURE 15-1Crown-root fracture (split tooth) of a root canal treatedtooth restored with amalgam but lacking cusp protection.(Courtesy Dr. H. Colman.)

and hardness of dentin.17,18 Thus, susceptibility tofracture cannot be reliably attributed to structuralchanges in dentin after loss of pulp vitality or afterroot canal treatment.

LOSS OF TOOTH STRUCTURE

Teeth are measurably weakened even by occlusalcavity preparation; greater loss of tooth structurefurther compromises strength. Loss of one or bothmarginal ridges is a major contributor to reducedcuspal stiffness (strength), which predisposes teethto fracture. 19,20 Access has only a minor effect on de-creasing cuspal strength when the access cavity issurrounded by solid walls of dentin. In a tooth al-ready seriously compromised by caries, trauma, orlarge restorations, the access cavity is more signifi-cant, particularly if the adjacent marginal ridge hasbeen lost.21 Excessive coronal flaring results ingreater susceptibility to cusp fractures . 2Z

BIOMECHANICAL CONSIDERATIONS

Cuspal flexure (movement under loading) willweaken premolars and molars over time .20,2 1 Ascavity preparations become larger and deeper, un-supported cusps become weaker and show moredeflection under occlusal loads. Greater cuspal

flexure leads to cyclic opening of margins betweenthe tooth and the restorative material. Fatigue isalso a factor; cusps become progressively weakerwith repetitive flexing. Hence, the restorationmust be designed to minimize cuspal flexure toprotect against fracture and marginal leakage.

Requirements for an AdequateRestorationThe permanent restoration must (1) provide acoronal seal, (2) protect the remaining toothstructure, (3) minimize cuspal flexure, and (4) sat-isfy function and esthetics.

Restoration TimingThe unrestored, temporized tooth without a perma-nent restoration is a candidate for problems! Unlessthere are specific reasons for delay, final restorationis completed as soon as practical after root canaltreatment.8,23 In teeth requiring restoration of onlythe access (for example, minimally restored anteriorteeth), the final restoration is best placed immedi-ately after obturation. It may be necessary to deferrestoration, but the delay should be minimal ratherthan to wait until after recall examination.

THE IDEAL: IMMEDIATERESTORATION

The tooth is at its weakest after access and remainsso until it is appropriately restored. The temporaryrestoration will not provide complete protectionagainst occlusal forces even when the tooth is outof occlusion or splinted with an orthodontic band.Fracture during or soon after treatment is all toocommon (Figure 15-2) and is usually preventable.

Most temporary restorative materials have lowwear and fracture resistance; substantial occlusalwear or material fracture may occur within weeks.Immediate restoration is preferred. It is unneces-sary to wait for radiographic evidence of healingbefore the final restoration is placed. Even formany teeth having a guarded prognosis, promptpermanent restoration may improve the progno-sis because of the better protection. In the event offailure, retreatment is usually possible throughthe restoration. Surgical management will notdisturb the permanent restoration either.

INDICATIONS FOR DELAYING FINALRESTORATION

Almost the only reason to delay the permanentrestoration is a questionable prognosis where fail-


271

FIGURE 15-2I nterappointment fracture of a weakened tooth associatedwith incomplete removal of the previous restoration. Cuspprotection and/or cusp reduction usually will prevent thisoccurrence.

ure would lead to extraction. A compromisedprognosis may exist because of procedural diffi-culties or for nonendodontic reasons. These in-clude canals that are not negotiable or incom-pletely obturated and procedural problems (forexample, a broken instrument or perforation).The proposed use of the tooth as a bridge abut-ment may demand evidence of healing before anexpensive prosthesis is placed. However, few indi-cations justify delaying restoration.

With a guarded prognosis, the rationale forpostponing final restoration is based on the natureof further management if failure occurs. Decision-making for managing failure is covered in Chap-ter 20. If failure is likely to result in extraction, theexpense of a final restoration may dictate delay untilthe outcome is more certain. If correction requiressurgery, there is no reason to delay restoration.

SEMIPERMANENT TEMPORARYRESTORATION

If final restoration is delayed, the temporary restora-tion must last as long as necessary (up to a year). Itmust protect, seal, and meet functional and estheticdemands. A good semipermanent posterior tempo-rary restoration is an amalcore that onlays weak-ened cusps, thus providing functional and sealingprotection. If a crown is to be placed later, the finalcrown preparation can be completed without

272

15 I Preparation for Restoration and Temporization

FIGURE 15-3Chamber and canal orifices retain an amalgam core, takingadvantage of natural undercuts. The teeth can be preparedfor crowns without removing the amalcore, or the amalgamsmay be the permanent restoration if the cusps are ade-quately protected. (Courtesy Dr. P. Parashos.)

removing the core (Figure 15-3). Comparable ante-rior restorations are more challenging owing to es-thetic factors and difficulties with coronal seal. Atemporary post crown will not provide an adequateseal. 13 It is preferable to place a cast post and coreimmediately (which provides a better coronal seal)when a temporary crown is indicated.12,13

Restoration DesignPRINCIPLES AND CONCEPTS

Three practical principles for function and dura-bility are the following:

transmit functional loads through thetooth to the suspensory apparatus.

PLANNING THE DEFINITIVERESTORATION

Restoration planning begins before root canaltreatment is started. The plan may be modifiedafter the restoration and/or after caries is re-moved and the access is prepared and as treat-ment progresses. Visualizing the restorativepreparation in advance ensures that structural re-quirements of the core will be preserved.

For anterior teeth, the choice of final restorationis somewhat limited. Wherever possible, restorationof the access (e.g., acid-etch composite) is used; thisis sufficient for teeth that are otherwise largely in-tact. For more extensively damaged teeth (trauma,large proximal restorations), full coronal coveragesupported by a post/core is indicated. The choicesfor premolars and molars are more varied. 2s

Direct Restoration

Restorations inserted directly into the preparedcavity (amalgam or composite) may be conserva-tive, but a requirement is that the restoration pro-tects against coronal fracture. Indications includethe following:

1. Minimal tooth structure has been lost be-fore and during root canal treatment. Aconventional access cavity in a tooth withintact marginal ridges is restored withoutfurther preparation.

2. Prognosis is uncertain, requiring a durablesemipermanent restoration.

3. Ease of placement and cost.

1. Conservation of tooth structure. Most teeth re-quiring treatment are already compromisedstructurally; further dentin removal shouldbe minimized .

22,24 On the other hand, cus-pal reduction and capping may be neces-sary. Routinely decoronating and rebuild-ing an endodontically treated tooth is anoutdated measure.

2. Retention. The coronal restoration is re-tained by the core and remaining dentin. Ifthe core requires retention, then the canalsystem is used, with provision of a post. Thepost weakens and may perforate the rootand should be placed only to retain thecore. 14,24

3. Protection of remaining tooth structure. In pos-terior teeth, this applies to protecting un-supported cusps to minimize flexure andfracture. The restoration is designed to

Many posterior teeth may be restored withamalgam if unsupported cusps are adequatelyprotected .26 A conventional class 11 amalgam willnot achieve this, and ordinarily should not beused.6,27 As a general guideline, cusps adjacent to alost marginal ridge should be onlaid, with suffi-cient thickness of amalgam (at least 3 to 4 mm) toresist occlusal forces. This is a significant reduc-tion. Premolars are more vulnerable to fracturethan molars and should have both cusps onlaidwhen a marginal ridge is involved . 6 In molars, cov-erage only of cusps adjacent to a lost marginalridge will generally be adequate if the remainingcusps and marginal ridge are not undermined.The amalgam should extend into the pulp cham-ber and canal orifices to aid retention.

Advantages of amalgam as a permanentrestoration include significantly less cost andfewer appointments; the longevity of extensiveamalgam restorations is similar to that of cast

FIGURE 15-4Cast gold onlay incorporates a reverse bevel for additionalprotection against cuspal flexure.

restorations.28 The amalgam may subsequentlyserve as a core for indirect cast restoration if indi-cated (see Figure 15-3).

Composite resins have a limited role in directrestoration of posterior teeth.29 With an occlusalaccess surrounded by enamel, acid-etch compos-ites may prove sufficient. Bonded restorations(amalgam and composite) will probably be morewidely used in the future, as bonding materialsand techniques continue to improve.'"' However,at present amalgam bonding has few documentedbenefits in long-term clinical usage, and bond fail-ure is likely to be catastrophic for otherwise un-supported cusps.31,32

Indirect restorations

Cast restorations (onlays, 3/, and full crowns) pro-vide the greatest occlusal protection and are opti-mal if there is extensive loss of tooth structure. Theattractiveness of onlays is that the cavity designusually requires little additional tooth tissue re-moval other than for the cusp onlays (Figure 15-4).The access cavity should be sealed with an amal-core or glass ionomer, which forms a base for thecasting. The strength of gold allows conservativetooth reduction and a reverse bevel for greater cuspreinforcement.

A full crown is a reliable, strong restorationthat protects against crown-root fracture .4,24,33

Tooth reduction often removes most remainingcoronal tooth structure; for retention, a coremust be placed (and occasionally a post) to retainthe core. To plan the core shape, there must be


273

FIGURE 15-5A, The gingival margin of the premolar is obscured by gingi-val overgrowth. B, The margins have been exposed by elec-trosurgery, and the core has been fabricated and cemented.

complete exposure of the margins. Gingival re-traction cord and electrosurgery are useful for ex-posure, and prevent undersized cores being madebecause of incomplete viewing of the margins(Figure 15-5).

274


Full crowns should be used only when there isinsufficient coronal tooth structure present for amore conservative restoration or if functional orparafunctional stresses require the splinting ef-fect of full coronal coverage. Full crowns havebeen overused based on the mistaken conceptthat the treated tooth is weak and requires maxi-mal protection.

Preparation of Canal Spaceand ToothPOST SELECTION

A post retains the core; the need for a post is dic-tated by the amount of remaining coronal toothstructure. A major disadvantage is that posts donot reinforce the tooth, but further weaken it byadditional removal of dentin and by creatingstresses that predispose to root fracture. 7,14,24

A post system should be selected that fits therequirements of the tooth and restoration. Thetooth and restoration should not be prepared andadapted to the post system; rather, the post sys-tem and preparation design should be selected asappropriate to the situation.

There is much debate on how the post shouldinteract with the tooth under load. Should thepost material be similar in stiffness to rootdentin (carbon fiber), somewhat stiffer (titaniumand gold), or much stiffer (stainless steel andcobalt-chromium alloys) ?14 Stiffer posts may leadto tooth fracture, whereas the more flexible postsdeform with the tooth, and tend to fail withoutfracturing the tooth . 35 Bonding between the postand the tooth may allow the restored tooth to de-form more with loading, compared with the con-ventional approach of the indirect restorationbeing much more rigid than the tooth. Long-term clinical trials will determine how postsshould interact with teeth, and what degree ofstiffness functions best.

A further consideration is that of radiopacity; ti-tanium posts have a radiopacity similar to that ofgutta-percha, which can create clinical uncer-tainty. 36 All post designs are predisposed to leakage,particularly temporary post/core/crown systems."

POST SPACE PREPARATION

Both chamber and canal may retain the restora-tion, and, in many instances, are essential. When apost is required for core retention, the minimumpost space (length, diameter, and taper) should beprepared consistent with that need. Preparationconsists of removing gutta-percha to the required

FIGURE 15-6Post space preparation has led to a perforation in one incisorand unnecessary weakening of the other as a result of diver-gence from the canal space during gutta-percha removal byrotary instruments.

length, followed by enlargement and shaping toreceive the post. Caution is required; removing ex-cess gutta-percha results in a defective apicalseal . 37,38 Also, excessive dentin removal seriouslyweakens the root, which may predispose to rootfracture . 39 A perforation may occur if the cuttinginstrument deviates from the canal or if thepreparation is too large or extends beyond thestraight portion of the canal (Figure 15-6). Radio-graphs may be deceptive as a guide to root curva-ture and diameter by disguising root concavitiesand faciolingual curves." As a general rule, postdiameter should be minimal, particularly apically,and not more than one third of the root diame-ter." Tapered post preparation prevents a step atthe apical post space, which predisposes to wedg-ing and root fracture.

Removal of Gutta-Percha

Whenever possible, gutta-percha is removed im-mediately after obturation to ensure the mostpredictable apical seal.42 At this stage the dentistis most familiar with the canal features, includingshape, length, size, and curvature. Depending onthe obturation technique, the canal may be filledonly to the desired length, or gutta-percha may beremoved to length using a hot instrument. The re-

FIGURE 15-7Gutta-percha removal. A, Enough remains in the distal canal to preserve the apical seal. B, Excessive removalfrom the palatal canal. This probably eliminated the apical seal and left a space between the post and gutta-percha. A radiograph taken before post placement would have allowed correction.

maining gutta-percha is then vertically condensedin the apical canal before the sealer has set. Theobturation radiograph will confirm that suffi-cient gutta-percha remains (4 to S mm).

Gutta-percha removal at a subsequent ap-pointment is satisfactory. Again, the safest proce-dure is use of a heated instrument. Gutta-perchais removed in increments to the desired length,using a heat carrier or plugger. Any instrumentthat penetrates to the desired depth can be used,so long as it has sufficient heat capacity. An alter-native means of removal include solvents and me-chanical. Problems with solvents such as chloro-form, xylene, or eucalyptol include messiness andunpredictable depth of penetration. Use of rotaryinstruments, especially Peeso reamers, requirescaution because of their tendency to diverge andperforate or at least seriously damage the root.They may also "grab" and displace the apicalgutta-percha. Specially designed rotary nickel-titanium instruments rotating at low speeds maybe more effective.

Whatever technique of removal is used, suffi-cient gutta-percha must remain to preserve theseal. At least 4 mm of gutta-percha is recom-mended (Figure 1S-7), and this should be con-firmed radiographically before the post iscemented .37,38

Finishing the Post Space

The post space is then further refined. If gutta-percha has been adequately removed, use of rotaryinstruments for final canal shaping should not be


275

a problem. The bulk of the canal preparation hasbeen achieved by the endodontic treatment, re-quiring only small refinements. Parallel sideddrills generate significant temperature increase;final shaping should be by hand manipulation ofthe cutting instrument, since only small amountsof tooth need be removed.43.

Retention and Core SystemsANTERIOR TEETH

These teeth must withstand lateral forces frommandibular excursive movements, which if trans-mitted via a post, tend to split the root. Consider-ation should be given to the occlusal scheme.Where possible, the excursive load should be lim-ited, with more force being borne by adjacent,more structurally sound teeth.

The optimal design is a cast metal post andcore, prepared as a single unit. The post portionprovides unit strength and retention, and the corecannot separate from the post. Custom fitting ofthe post and core permits minimal dentin re-moval both from canal space and coronally, plusmaximum ferrule effect without crown lengthen-ing (Figure 1S-8). 44 Importantly, core shapeshould conform to the remaining coronal toothstructure, rather than machining the tooth for astandard core or technique. The small cross-sectional area of posts for mandibular incisorsmay result in casting porosities; it is possible touse a wrought gold alloy post as a basis for the ad-dition of a cast core.

276


FIGURE 15-8Cast post/cores in maxillary incisors. The preparation on theleft shows extensive coronal dentin providing maximal fer-rule effect; the preparation on the right illustrates minimalcoronal dentin and little ferrule effect.

FIGURE 15-9Molar correctly restored without a post and with a full crown.The decision to use a post depends on remaining coronaltooth structure and the retention provided by the chamber.

Use of a prefabricated post with direct corebuildup is a last resort for an anterior tooth and isgenerally contraindicated. If used, a preformedpost should be passive to minimize wedgingforces. Also, passive fit facilitates removing the

post for retreatment. Screw-retained posts arecontraindicated-they predispose to vertical rootfracture and are difficult to remove.

POSTERIOR TEETH

Premolars with substantial loss of coronal struc-ture are also generally best restored with a castpost and core. Narrow mesiodistal root widthdoes not permit adequate core thickness in asso-ciation with a prefabricated post. Minimal en-largement during post space preparation is essen-tial to preserve sufficient dentin thickness.41 Inmaxillary premolars with two roots, only thepalatal canal should be used for the post; the buc-cal furcation groove and narrow root preclude useof the buccal root.41,45 A small, short (2 to 3 mm)post in the buccal canal provides some retentionand antirotation.

Molars, which have larger pulp chambers, per-mit direct core options; the volume of the core isgreater and the chamber shape provides reten-tion. Most molars are restored with the direct coreonly, without a post (Figure 15-9). However, withminimal remaining coronal tooth structure and asmall pulp chamber, a post may be placed in onecanal for additional retention. Cast post/core sys-tems are rarely necessary and should be consid-ered only when essentially no coronal tooth struc-ture remains.

The longest and straightest canal is preferredfor the post, usually the palatal canal of maxillarymolars and the distal canal of mandibular mo-lars.40 Other canals are narrower and more curvedand are in weaker roots with surface concavities.These should be used only (and cautiously) ifother factors preclude placement in the largercanals. Core retention is supplemented by extend-ing the core material 2 to 3 mm into the remain-ing canal orifices.

A wide variety of passively seated prefabricatedposts is available. Parallel-sided posts providegreater retention than tapered posts and do notwedge. They require more post space preparation;matching post size to canal size is important tominimize dentin removal. The post need not con-tact dentin throughout its length to achieve ade-quate retention (this is important in distal canalsof mandibular molars, which are often broad cer-vically). Threaded screw posts should not be used.

Molar core design is simple and placement ofthe core requires little removal of tooth structure.A coronoradicular core of amalgam (amalcore)condensed into the chamber and slightly intocanal orifices is preferred and provides a passive,strong core; an amalgam bonding agent may alsobe used." ," With fast-setting amalgam, the crownmay be prepared at the same visit, although


27 7

preparation is easier when the material is fullyset. An alternative is resin composite, which doesnot have the strength or long-term sealability ofamalgam. However, composite resin has the ad-vantage of allowing immediate crown prepara-tion" (Figure 15-10). Glass ionomer cements donot have sufficient shear strength.

PINS

There is no need for retentive pins. The stressesand microfractures generated in dentin and therisk of perforation by pins outweigh any potentialgain in retention of the restoration. Pins havebeen suggested for antirotation of the post/core;this is best achieved by other means such as aslightly out-of-round preparation.

Restoring Access Throughan Existing Restoration

Occasionally, pulps undergo irreversible pulpitisor necrosis after placement of a crown, requiringroot canal treatment (Figure 15-11). 33 Accessthrough the restoration, with subsequent perma-nent repair of the opening is often preferred.

For the restoration to remain functional, threeconditions must be met: (1) the interface betweenthe restoration and the repair material must pro-vide a good coronal seal; (2) retention of therestoration must not be compromised; and (3) thefinal core structure must support the restorationagainst functional or minor traumatic stresses. Ac-cess, particularly if overextended, may leave only athin shell of dentin, especially in anterior teeth andpremolars. Retention then depends almost entirelyon the repair material. Fortunately, the chamberand canal are available to create a core that pro-vides adequate retention and support in most in-stances. Placement of a dowel or post through anaccess or through an existing restoration adds nosupport and little retention and is rarely indicated.

The repair material should have high compres-sive and shear strength. In most situations, amal-gam is preferred. It improves retention, maintainsand even improves its seal with time, and is easilycondensed into the entire chamber and access cav-ity as a single unit.48 Composite resins, glassionomer cements, and glass cermets do not havethe requisite shear strength. Amalgam also func-tions well in anterior teeth with porcelain-fused-to-metal restorations. If esthetics is a problem, a newrestoration is the first choice. A layer of compositecan be placed over the amalgam core but servesonly as a short-term repair. Inlays or gold foil to re-store access openings through gold castings offerno advantage and do not merit the effort and cost.

FIGURE 15-10Restoration of a decoronated mandibular molar. Cementedparallel-sided posts retain a composite core. Inability to con-dense amalgam dictated the use of composite resin, placedand cured in many increments.

FIGURE 15-11Pulp necrosis several years after preparation and placementof a cantilever bridge. Root canal treatment is requiredthrough the crown, with attendant risks of perforation and/orl oss of retention.

Temporary Restorations

Many endodontic procedures involve multiplevisits. Also, unless the final restoration is limitedto a routine access cavity, root canal treatmentand final restoration are usually not completed inthe same appointment. A temporary restoration is

278


thus required. The temporary restoration is nor-mally in place for 1 to 4 weeks. In special situa-tions such as apexification or delayed permanentrestoration, the temporary restoration must lastseveral months.

OBJECTIVES OF TEMPORIZATION

Objectives depend on the intended duration ofuse. Thus different materials are required, de-pending on time, occlusal load and wear, com-plexity of access, and loss of tooth structure.

ROUTINE ACCESS CAVITIES

Most access cavities involve only one surface andare surrounded by dentin walls or by porcelain ormetal (if the restoration is retained). The tempo-rary restoration must last from several days to sev-eral weeks. Numerous types are available, includingpremixed cements that set on contact with mois-ture (Cavit), intermediate restorative materials(IRM), glass ionomer cements, and specially for-mulated light-cured composite materials such astemporary endodontic restorative material(TERM)49 -51 Ease of use and good sealing abilitymake Cavit a good routine material, but lowstrength and rapid occlusal wear limit its use toshort-term sealing of simple access cavities. Inter-mediate restorative materials provide improvedwear resistance. TERM undergoes polymerizationshrinkage followed by expansion resulting fromwater sorption. Its seal is comparable to that ofCavit, with superior strength and wear limits. Moredurable restorative materials (composites and glassionomer cements) tend to provide the best seal.51 Itis not known whether experimental leakage differ-ences based on bacterial leakage or dye penetrationare significant clinically. Most critical are the thick-ness and placement of the material.

Techniques of Placement

The quality of the coronal seal depends on thethickness of the material, how it is compacted

Cotton Pellet

FIGURE 15-12Techniques for temporization. Shown on the left are the cor-rect techniques; either minimal space is occupied by cotton orno cotton pellet is used, particularly if the proximal surface isto be restored. It is wrong to nearly fill the chamber withcotton, which leaves inadequate space and strength for thetemporary restorative material (3 to 4 mm are required).(Courtesy Dr. L. Wilcox.)

into the cavity, and the extent of contact withsound tooth structure or restoration. A minimumdepth of 3 to 4 mm is required around the pe-riphery and preferably 4 mm or more to allow forwear. In anterior teeth, the access is oblique to thetooth surface; care must be taken to ensure thatthe material is at least 3 mm thick in the cingu-Ium area.

IRM and Cavit (or a similar material) areplaced as follows. The chamber and cavity wallsshould be dry, with a thin layer of cotton (exceptin a class II situation) over the canal orifices toprevent canal blockage (Figure 15-12). Cavit ispacked into the access opening with a plastic in-strument in increments from the bottom up andpressed against the cavity walls and into under-cuts (Figure 15-13). The excess is removed, andthe surface is smoothed with moist cotton. Thepatient should avoid chewing on the tooth for atleast 1 hour. TERM is prepackaged by the manu-facturer in compules, ready for injection into theaccess. The material is inserted, packed with aplastic instrument, adjusted occlusally, and thenlight-cured.

EXTENSIVE CORONAL BREAKDOWN

Teeth without marginal ridges or with under-mined cusps may require a stronger filling mate-rial (high-strength glass ionomer cement), withcare being taken to ensure adequate thicknessand good marginal adaptation proximally. Re-ducing the height of undermined cusps reduces

FIGURE 15-13Techniques for placing temporary restoration material. A, The "blob" technique is wrong because it does not sealthe walls. B, The incremental technique, which adds successive layers, pressing each against the chamber walls,i s correct. (Courtesy Dr. L. Wilcox.)

the risk of fracture. For severely broken-downteeth, a cusp-onlay amalgam or occasionally awell-fitting orthodontic band cemented onto thetooth (restored with glass ionomer cement) pro-vides a durable temporary restoration. At thenext appointment, access is cut through therestoration.

TEMPORARY POST CROWNS

Interappointment temporary crowns are gener-ally contraindicated. In most situations if a crownis in place, it must be removed during the rootcanal procedure and then recemented after tem-porization of the access.

Esthetic restoration of anterior teeth is chal-lenging if little coronal structure remains. A tem-porary crown retained with a post (preformed alu-minum post, paper clip, or a sectioned largeendodontic file) has inherent problems. Using thecanal space for a temporary post precludes use ofan intracanal medicament, and the coronal sealdepends entirely on the temporary cement. Thecoronal seal is generally inadequate with a looselyfitting and mobile temporary post and crown. 13 Ifa temporary crown is placed, fabrication shouldpreferably be done under rubber dam, with adja-cent teeth also isolated to assist in preparingcontacts.

The temporary post should fit the canal snugly(not binding) and extend apically 4 to 5 mm shortof working length and coronally to within 2 to3 mm of the incisal edge. A polycarbonate shell is


279

FIGURE 15-14Technique sequence for anterior temporary post-core-crownfabrication. A, Post space is prepared. B, A temporary post ofthe proper size is fitted. C, A polycarbonate crown is adapted,filled with resin, and seated over the post. Excess resin istrimmed from the margins after the resin has set. D, Thepost/crown is cemented using a temporary cement such asTemp Bond.

trimmed to a good fit; self-curing material then isadded to the inside of the shell to mold to theroot face and attach to the post. The temporaryluting cement (Temp Bond or similar cement) isplaced on the coronal 3 to 4 mm of the post androot face, and the unit is cemented into place(Figure 15-14). A provisional removable partialoverdenture is a useful alternative; access remainsexcellent, and there is little chance of disturbingthe coronal seal between appointments.

I ncremental Technique

Blob Technique

280


LONG-TERM TEMPORARYRESTORATIONS

Restorations for procedures such as apexificationmay last for months, up to 2 years. For routine ac-cess openings, a durable restoration such as amal-gam, glass ionomer cement, or acid-etch compositeshould be used, allowing sufficient thickness to en-sure strength and a long-term seal. If the perma-nent restoration is delayed, these semipermanenttemporary restorations are generally sufficient.

REFERENCES

1. Vire DE: Failure of endodontically treated teeth: classi-fication and evaluation, JEndod 17:338, 1991.

2. Sjogren U, Hagglund B, Sundqvist G, Wing K: Factorsaffecting the long-term results of endodontic treat-ment,JEndod 16:498,1990.

3. Friedman S: Treatment outcome and prognosis of en-dodontic therapy. In Orstavik D, Pitt Ford TR, editors,Essential endodontology, Oxford, 1998, Blackwell Science,p. 368.

4. Sorensen JA, Martinoff JT: Intracoronal reinforcementand coronal coverage: a study of endodonticallytreated teeth, J Prosthet Dent 51:780, 1984.

5. Weine FS, Wax AH, Wenckus CS: Retrospective studyof tapered, smooth post systems in place for 10 yearsor more, JEndod 17:293, 1991.

6. Hansen EK, Asmussen E, Christiansen NC: In vivofractures of endodontically treated posterior teeth re-stored with amalgam, Endod Dent Traumatol 6:49, 1990.

7. Goodacre CJ, Spolnik KJ: The prosthodontic manage-ment of endodontically treated teeth: a literature re-view. Part I. Success and failure data, treatment con-cepts, J Prosthodont 3:243, 1994.

8. Saunders WP, Saunders EM: Corona] leakage as acause of failure in root-canal therapy: a review, EndodDent Traumatol 10:105, 1994.

9. Ray H, Trope M: Periapical status of endodonticallytreated teeth in relation to the technical quality of theroot filling and the coronal restoration, Int Endod J28:12, 1995.

10. Magura ME, Kafrawy AH, Brown CE Jr, Newton CW:Human saliva coronal microleakage in obturated rootcanals: an in vitro study, J Endod 17:324, 1991.

11. Wolcott JF, Hicks ML, Himel VT: Evaluation of pig-mented intraorifice barriers in endodontically treatedteeth, JEndod 25:589, 1999.

12. Fogel HM: Microleakage of posts used to restore en-dodontically treated teeth, JEndod 21:376, 1995.

13. Fox K, Gutteridge DL: An in vitro study of coronal mi-croleakage in root-canal-treated teeth restored by thepost and core technique, Int Endod J 30:361, 1997.

14. Gutmann JL: The dentin-root complex: anatomic andbiologic considerations in restoring endodonticallytreated teeth, j Prosthet Dent 67:458, 1992.

15. Sorensen JA, Engelman MJ: Effect of post adaptationon fracture resistance of endodontically treated teeth,JProsthet Dent 64:419, 1990.

16. Papa J, Cain C, Messer HH: Moisture content of en-dodontically treated vs vital teeth, Endod Dent Trauma-tol 10:91, 1994.

17. Huang T -J, Schilder H, Nathanson D: Effects of mois-ture content and endodontic treatment on some me-chanical properties of human dentin, J Endod 18:209,1992.

18. Sedgley CM, Messer HH: Are endodontically treatedteeth more brittle? JEndod 18:332, 1992.

19. Reeh ES, Messer HH, Douglas WH: Reduction intooth stiffness as a result of endodontic and restora-tive procedures, JEndod 15:512, 1989.

20. Hood JAA: Biomechanics of the intact, prepared andrestored tooth: some clinical implications, Int Dentj41:25, 1991.

21. Panitvisai P, Messer HH: Cuspal deflection in molarsin relation to endodontic and restorative procedures, jEndod 21:57, 1995.

22. Hansen EK, Asmussen E: Cusp fracture of endodonti-cally treated posterior teeth restored with amalgam.Teeth restored in Denmark before 1975 versus after1979, Acta Odont Scand 51:73, 1993.

23. Safavi KE, Dowden WE, Langeland K: Influence of de-layed coronal permanent restoration on endodonticprognosis, Endod Dent Traumatol 3:187, 1987.

24. Assif D, Gorfil C: Biomechanical considerations inrestoring endodontically treated teeth, JProsthet Dent71:565, 1994.

25. Morgano SM, Brackett SE: Foundation restorations infixed prosthodontics: current knowledge and futureneeds, JProsthetDent 82:643, 1999.

26. Plasmans PJJM, Creugers NHJ, Mulder J: Long-termsurvival of extensive amalgam restorations, J Dent Res77:453, 1998.

27. Linn J, Messer HH: Effect of restorative procedures onthe strength of endodontically treated molars, JEndod20:479, 1994.

28. Martin JA, Bader JD: Five year treatment outcomes forteeth with large amalgams and crowns, Oper Dent22:72, 1997.

29. Steele A, Johnson BR: In vitro fracture strength of en-dodontically premolars, JEndod 25:6, 1999.

30. Roulet J-F: Benefits and disadvantages of tooth-coloured alternatives to amalgam, J Dent 25:459, 1997.

31. Mahler DB, Engle JH: Clinical evaluation of amalgambonding in class I and II restorations, J Am Dent Assoc131:43, 2000.

32. Davis R, Overton JD: Efficacy of bonded and non-bonded amalgam in the treatment of teeth with in-complete fractures, JAm DentAssoc 131:469, 2000.

33. Valderhaug J, Jokstad A, Ambjornsen E, Norheim PW:Assessment of the periapical and clinical status ofcrowned teeth over 25 years, JDent 25:97, 1997.

34. Asmussen E, Peutzfeld A, Heitmann T: Stiffness, elas-tic limit, and strength of newer types of endodonticposts, J Dent 27:275, 1999.

35. Martinez-Insua A, da Silva L, Santana U: Comparisonof the fracture resistances of pulpless teeth restoredwith a cast post and core or carbon-fiber post with acomposite core, JProsthet Dent 80:527, 1998.


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36. Kleier D, Shibilski K, Averbach RE: Radiographic ap-

pearance of titanium posts in endodontically treated

teeth, JEndod 25:128, 1999.

37. Gish SP, Drake DR, Walton RE, Wilcox L: Coronal

leakage: bacterial penetration through obturated

canals following post preparation, J Am Dent Assoc

125:1369, 1994.

38. Kvist T, Rydin E, Reit C: The relative frequency of peri-

apical lesions in teeth with root canal-retained posts, J

Endod 12:578, 1989.

39. Wilcox LR, Roskelley C, Sutton T: The relationship of

root canal enlargement to finger-spreader induced ver-

tical root fracture,J Endod 23:533, 1997.

40. Perez E, Zillich R, Yaman P: Root curvature localiza-

tions as indicators of post length in various tooth

groups, Endod Dent Traumatol 2:58, 1986.

41. Raiden G, Costa L, Koss S, Hernandez JL: Residual

thickness of root in first maxillary premolars with post

space preparation, J Endod 25; 502, 1999.

42. Fan B, Wu M-K, Wesselink PR: Coronal leakage along

apical root fillings after immediate and delayed post

space preparation, Endod Dent Traumatol 15:124, 1999.

43. Hussey DL, Biagioni PA, McCullagh JJP, Lamey P-J:

Thermographic assessment of heat generated on the

root surface during post space preparation, Int Endod J

30:187, 1997.

44. Sorensen JA. Engelman MJ: Ferrule design and frac-

ture resistance of endodontically treated teeth, J Pros-

thetDent 63:529, 1990.

45. Tamse A, Katz A, Pilo R: Furcation groove of buccal

root of maxillary first premolars-a morphometric

study, JEndod 26:359, 2000.

46. Nayyar A, Walton RE, Leonard LA: An amalgam coronal-

radicular dowel and core technique for endodontically

treated posterior teeth, J Prosthet Dent 43:511, 1980.

47. Davalou S, Gutmann JL, Nunn MH: Assessment ofapical and coronal root canal seals using contempo-

rary endodontic obturation and restorative materials

and techniques, Int Endod J 32:388, 1999.

48. Mulvay PG, Abbott PV: The effect of endodontic ac-

cess cavity preparation and subsequent restorative

procedures on molar crown retention, Aust Dent J

41:134, 1996.

49. Deveaux E, Hildelbert P, Neut C, Romond C: Bacterial

microleakage of Cavit, IRM, TERM, and Fermit: a

21-day in vitro study,JEndod 25:653, 1999.

50. Barthel CR, Strobach A, Briedigkeit H, et al: Leakage in

roots coronally sealed with different temporary fill-

ings,J Endod 25:731, 1999.

51. Uranga A, Blum J-Y, Esher S, et al: A comparative study

of four coronal obturation materials in endodontic

treatment, J Endod 25:178, 1999.


1 / Define terms associated with endodontic microbiology.

2 /

Describe portals of entry of microorganisms to the pulp and periradicular tissues.

3/

Understand the significance of bacteria in pulpal and periradicular diseases.

4 /

Describe the predominant bacteria and discuss microbial virulence factors and the microbial ecosystem

associated with endodontic infections.

5 /

Describe the reaction of pulp and periradicular tissues to bacteria.

6 /

Understand infection control as applied to endodontic practice.

7 /

Discuss the rationale for debridement of the root canal system.

8 /

Understand the importance of drainage in treating acute apical infections (abscess).

9 /

Describe the indications and methods for microbial sampling of endodontic infections.

282

LEARNING OBJECTIVES

Endodontic Microbiology

Bacteria Associated with Endodontic

Infections

Terminology

Portals of Entry to the Pulp

Caries and Pulpal Disease

Reaction of Pulp to Bacteria

Polymicrobial Infections

Microbial Ecosystem in the Root Canal

Association of Bacteria with Periradicular

Disease

Virulence Factors

Correlations with Pathoses and Treatment

I nfection Control

Treatment of Endodontic Infections

Debridement of the Root Canal System

I ntracanal Medication

Drainage

When and How to Culture

16 / Endodontic Microbiology

283

ost pathoses of the dental pulp andPeriradicular tissues are either directlyor indirectly related to microorganisms.

Knowledge of the bacteria associated with en-dodontic pathoses is important in understandingthe disease process and in developing a sound ra-tionale for treatment. This chapter discusses mi-croorganisms associated with pulpal and Peri-radicular diseases, infection control, and theprinciples of treatment of endodontic infections.

Bacteria Associated withEndodontic InfectionsTERMINOLOGY

Colonization is the establishment of bacteria orother microorganisms in a living host. Coloniza-tion occurs if appropriate biochemical and physi-cal conditions are available for growth and in-hibitory factors are inadequate to destroy theorganisms. Permanent colonization in a symbioticrelationship with the host results in establish-ment of normal oral flora. These organisms par-ticipate in many beneficial relationships but areconsidered opportunistic pathogens if they gain ac-cess to a normally sterile area of the body and pro-duce disease.

Infectious disease (infection) results if microor-ganisms damage the host and produce clinicalsigns and symptoms. Pulpal and Periradicularpathoses (diseases) result from opportunisticpathogens infecting the pulp cavity and, at times,Periradicular tissues.

Pathogenicity is the capacity of organisms toproduce disease within a particular host. Virulenceexpresses the degree of pathogenicity in a hostunder defined circumstances. Stages in develop-ment of an endodontic infection include micro-bial invasion, colonization, multiplication, andpathogenic activity.

PORTALS OF ENTRY TO THE PULP

Microbes may take several routes to invade and in-fect the pulp. If enamel or cementum is missing,microorganisms may invade the pulp through ex-posed dentinal tubules. Caries are the most com-mon source of bacterial penetration through thetubules. Bacteria can invade and multiply withinpermeable tubules. Importantly, bacterial penetra-tion into dentinal tubules has been shown to begreater in teeth with necrotic pulps than in teethwith vital pulps.' Tubule permeability is reducedby the presence of various components of thedentinal fluid, the living odontoblastic processes,

284

16 / Encloclontic Microbiology

and the formation of peritubular dentin or ter-tiary dentin. Bacteria are preceded through thetubules by their byproducts and breakdown prod-ucts, which may be pulp irritants. An example ofthis is the positive correlation between the pres-ence of bacteria under restorations with pulpalinflammation.

Microorganisms may reach the pulp after di-rect pulpal exposure associated with caries,restorative procedures, or a traumatic injury thatfractures, cracks, or displaces the tooth.2 Pulp sta-tus is an important factor in susceptibility to mi-crobial invasion. Vital pulp is very resistant to mi-crobial invasion. Penetration of the surface of ahealthy pulp by oral flora is relatively slow or maybe blocked entirely. For example, if the pulp is ex-posed to the oral cavity following tooth fracture,the resulting inflammation, necrosis, and bacter-ial penetration extend no more than 2 mm intothe pulp after 2 weeks. In contrast, a necrotic pulpis rapidly invaded and colonized by bacteria.'

There is also an intimate relationship betweenthe pulp and periodontium via tubules, lateral oraccessory canals, furcation canals, and the apicalforamen. Pulpal necrosis and the egress of irritantsby these routes may affect the periodontal liga-ment and surrounding attachment apparatus. Thereverse seems less likely. It is debatable whether peri-odontal pathoses directly cause significant pulpaldisease.4,5 However, if periodontal disease involvesthe apex of a tooth, the pulp may become necrotic.6Presumably, pulpal inflammation results if bacte-ria can penetrate the lateral canals, furcationcanals, or denuded dentin after periodontal treat-ment. The removal of cementum during periodon-tal therapy exposes dentinal tubules to oral flora. Astudy in humans after root planing demonstratedthe presence of pulpitis, bacterial penetration intoexposed dentinal tubules, and thermal sensitivity.'

Anachoresis is a process by which microorgan-isms are transported in the blood to an area of in-flammation where they establish an infection. In-vestigators using animals have demonstrated thelocalization of blood-borne bacteria in inflamedpulp but not in instrumented unfilled canals."How often (or whether) anachoresis contributesto pulpal or periradicular infections in humanshas not been determined.

tococcus sobrinus) have been associated with smoothsurface and pit-fissure caries, whereas Actinomycesspp. have been associated with root caries. Al-though mutans streptococci are important in ini-tiating caries, they may not be as important in theprogression of deep caries. Bacteria in the deepestlayers of caries are predominantly strict anaer-obes.10 After exposure of the dental pulp by caries,numerous species of opportunistic oral flora mayinvade and colonize necrotic tissue. This allowsmicrobial selection by the ecosystem associatedwith infections of endodontic origin. 11,12

REACTION OF PULP TO BACTERIA

Like other connective tissues, pulp responds to ir-ritants with (1) nonspecific inflammation and (2)specific immunologic reactions. Pulpal inflamma-tion from caries begins as an insidious chronic cel-lular response characterized by the presence oflymphocytes, plasma cells, and macrophages. Theresponse to caries by the pulp-dentin complex in-cludes the formation of peritubular dentin, de-creased permeability of dentinal tubules, andoften, production of tertiary dentin." , " This irreg-ular tertiary dentin is less tubular and presumablyacts as a barrier to the invading caries. Generally,the pulp is not severely (not irreversibly) inflamedwhen caries do not penetrate to the pulp.

After pulp exposure by caries, numerousspecies of opportunistic oral flora may colonizethe exposed tissue. Polymorphonuclear (PMN)leukocytes characteristic of acute inflammationare chemotactically attracted to the area. An accu-mulation of PMN leukocytes results in abscessformation. The pulp may remain inflamed for along time or may undergo rapid necrosis. The dy-namics of the pulpal reaction is related to the vir-ulence of the bacteria, host response, amount ofpulpal circulation, and degree of drainage. Be-cause it is surrounded by hard tissue, the inflamedpulp is located in a unique low-compliance envi-ronment.15 This low compliance causes increasedintrapulpal pressure when extravascular inflam-matory cells and fluids accumulate. The increasedpressure further interferes with normal circula-tion and cell function, making the cells more sus-ceptible to injury or death.

CARIES AND PULPAL DISEASE POLYMICROBIAL INFECTIONS

The most common source of bacteria to the pulpis from caries. Bacteria associated with caries arenot motile but apparently advance through thedentinal tubules by dividing (binary fission) andby dentinal fluid movement. In humans, mutansstreptococci (mainly Streptococcus mutans and Strep-

The intimate association between microorgan-isms and endodontic pathoses was demonstratedin rats by Kakehashi and associates.16 After expo-sure of the dental pulp to the oral cavity, ab-scesses, pulpal necrosis, and periradicular inflam-matory lesions developed in rats with normal

1 6 / Endodontic Microbiology

28 5

microbial flora but not in germ-free rats. In thegerm-free animals, pulpal inflammation resultingfrom exposure was minimal.16 In humans, whenbacteria reach the pulp, it may become inflamedbut stay vital for some time, or quickly becomenecrotic. Microorganisms invade the necroticpulp, multiply, and infect the root canal system,including the dentinal tubules (Figure 16-1).Once the pulp becomes necrotic, it becomes areservoir for microorganisms, microbial byprod-ucts, and microbial breakdown products. En-dodontic infections include infections of both thepulp cavity and the periradicular diseased tissues.

Of about 500 species of bacteria recognized asnormal oral flora, only a relatively small group arecommonly isolated from infected pulp cavities.Strict anaerobic bacteria predominate, with somefacultative anaerobes and, rarely, aerobes. Manybacteria (especially strict anaerobes) are difficultto cultivate. Differences in frequency of isolationfrom one study to another may be related to anumber of variables including sampling tech-nique, transport medium, culture medium, typeof incubation, and method of identification.

Modern culturing techniques have demon-strated the association of polymicrobial oppor-tunistic oral bacteria with pulpal and periradicu-lar diseases. Sophisticated anaerobic technologyprovides an environment conducive to the growthof strict anaerobes. For example, in one study ex-

amining intact teeth with infected root canals,more than 90% of the bacteria were strict anaer-obes (Table 16-1)." Another study isolated andidentified bacteria from the apical 5 mm of in-fected root canals in teeth with carious pulpal ex-posures and associated periradicular lesions. 17 Itwas found that most (68%) of the isolates werestrict anaerobes. The predominance of strictanaerobes suggests a selective process favoring the

FIGURE 16-1Cocci observed with scanning election microscopy in a tubulefrom a fractured root through a canal containing necrotic de-bris. Bacteria such as these, deep in tubules, may not be re-moved or killed during canal preparation or by intracanalmedicaments.

Predominant Isolates from the Root Canals of 65 Teeth with Periapical Lesions

Adapted from Sundqvist G: Oral Microbiol Immunol7:257, 1992.*Species isolated in low number or not identified to species level.

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16 1 Endodontic Microbiology

growth of anaerobes." Importantly, the relativeproportion of strict anaerobic bacteria to faculta-tive bacteria increases with time, as does the totalnumber of bacteria. 18

The anaerobic genus Bacteroides has undergonemajor taxonomic revision, which has changed thenomenclature for the black-pigmented bacteria(BPB) associated with endodontic infections.Species of BPB were previously located in thegenus Bacteroides. These species are nonmotile,non-spore-forming, Gram-negative rods. Threeasaccharolytic species of BPB have been reclassi-fied into a separate genus named Porphyromonas

(Box 16-1). 19 Species of saccharolytic BPB havebeen reclassified into a separate genus named Pre-

votella (Box 16-1).20 Several nonpigmented oralspecies of bacteria previously classified as Bac-

teroides have also been placed in the genus Pre-votella (Box 16-1). The current nomenclature isused in this chapter.

Although no absolute correlation has beenmade between any species of bacteria and the clini-cal signs or symptoms of endodontic pathosis, BPB

have been the most often implicated. 21-26 Otherstudies have found that Porphyromonas gingivalisand Porphyromonas endodontalis were isolated only

Recent Taxonomic Changes forPrevious Bacteroides Species

Studies have associated species with clinical signs and symptoms.tMost commonly isolated black-pigmented bacteria from endodon-tic infections.

from acute infections, whereas Prevotella intermediawas found with both symptomatic and asympto-matic infections.27 Recently, with DNA methods,Prevotella nigrescens has been characterized as aspecies separate from P. intermedia. 2s Studies con-firmed that P. nigrescens is the BPB most commonlycultivated from endodontic infections . 28-30

Molecular methods have also been used to de-tect and identify the presence of another BPB, Pre-

votella tannerae, in endodontic infections. Whenthe polymerase chain reaction was used to evalu-ate 118 microbial samples from endodontic infec-tions, 60% of the samples tested positive for thepresence of P. tannerae, although only 5 strainswere cultivable.31 Molecular methods will proba-bly detect numerous other presently uncultivablemicroorganisms.

Other bacteria often associated with clinicalsigns and symptoms include Prevotella buccae andspecies of Peptococcus, Peptostreptococcus, Eubacterium, Actinomyces, and Fusobacterium.24.26,32,33 Ani-mal studies have demonstrated that purulent le-sions may be induced with specific combinationsof bacteria, especially strains of BPB. 18,34-36 How-ever, no absolute causative relationship betweenspecific microorganisms and endodontic diseasehave been defined.

Actinomyces and Propionibacterium species are ableto persist in periradicular tissues in the presence ofchronic inflammatory tissue .37-39 Most of these in-fections apparently respond to conventional rootcanal treatment; however, surgery or antibioticsmay be needed to resolve these infections .37- 39

Recent studies have found a high incidence ofthe facultative anaerobe, Streptococcus faecalis, inroot canals of teeth requiring retreatment of pre-vious root canal therapy because of persistent in-flammation .40-42 A recent study found healing in94% of the cases after a negative culture at the ob-turation appointment but only a 68% rate of heal-ing if the cultures were positive at the time of ob-turation.40 These studies support previousinvestigations that demonstrated absence of heal-ing when canals are obturated in the presence ofmicrobes in the root canal . 43

Yeasts and viruses are also found in the pulpcavity. Fungi have been identified in root canalsand in teeth refractory to endodontic treat-ment.42-47 Viruses, including the human immun-odeficiency virus (HIV), are present in the pulpand may be associated with endodontic dis-ease .48,49 The significance of intrapulpal viruses isunknown. A case report recently associated a her-pes zoster infection with periodontal and en-dodontic disease.50

In summary, the microbial population in vari-ous endodontic pathoses and conditions has been

identified as being important, but is not yet thor-oughly understood. This includes both the typesof microorganisms and their significance. Futureresearch should continue to clarify these issues.

MICROBIAL ECOSYSTEMIN THE ROOT CANAL

When a necrotic pulp is sampled, a mix of bacter-ial species are recovered. Because of the lack of cir-culation within a necrotic pulp, normal host de-fense mechanisms (inflammation and immunity)are absent or compromised. The pulp cavity sup-plies substrate and becomes a reservoir for invad-ing microbes. The root canal system also is a spe-cial environment where selection results in arestricted group of bacteria. Tissue fluid and dis-integrated cells from necrotic tissue form a sub-strate of nutrients (especially polypeptides andamino acids) essential for microorganisms. Thesenutrients, low oxygen tension, and bacterial inter-actions are the key ecologic determinants ofwhich bacteria will predominate. Conditionsfavor the growth of anaerobes able to metabolizepeptides and amino acids rather than carbohy-drates. The growth of one bacterial species maydepend on another commensal species, whichsupplies an essential nutrient as a metabolicbyproduct. Figure 16-2 shows some of the possi-ble complex nutritional relationships among bac-teria in an infected root canal. 12

Likewise, antagonistic relationships may de-velop among bacteria. Some by-products (e.g.,ammonia) may be either a nutrient or a toxin, de-pending on the species of bacteria and the con-centration of its by-products in the ecosystem.Bacteiiocins are antibiotic-like proteins producedby one species of bacteria that inhibit the growthof other species.

Root canal treatment uses chemomechanicalmethods of debridement to disrupt, destroy, andremove the microbial ecosystem. This is accom-plished through the cleaning and shaping processand the adjunctive use of antimicrobials withinthe pulp system. Effective obturation of the rootcanal space and coronal restoration prevents api-cal and coronal leakage and eliminates the pulpcavity as a reservoir of infection.

Association of Bacteria withPeriradicular DiseaseAs stated earlier, the contents of infected rootcanals are potent irritants. The importance of bac-teria and the development of apical periodontitishave been demonstrated. 16 Periradicular lesions

(disease) develop when the canal contains bacte-ria. 18 22,36,51 Evidence indicates that bacteria and bac-terial by-products emanating from the root canalare the major irritants associated with periradicu-lar inflammation. Bacterial by-products alone arecapable of causing periradicular pathosis. 5 2

VIRULENCE FACTORS

Bacterial virulence factors include fimbriae (pili),capsules, extracellular vesicles, lipopolysaccha-rides (LPSs), enzymes, short-chain fatty acids,polyamines, and low-molecular-weight productssuch as ammonia and hydrogen sulfide. Bacterialfimbriae are important for attachment to surfacesand to other bacteria. Fimbriae may be importantin synergistic relationships between bacteria. Cap-sules are a significant resistance factor for bacte-ria, enabling them to avoid phagocytosis. BPB as-sociated with endodontic infections may havesuch capsules.

Lipopolysaccharides

LPSs are found on the surface of Gram-negativebacteria and have numerous biologic effects that in-duce periradicular pathosis. LPSs have nonspecificantigens that are not well neutralized by antibodies.LPS antigens activate the complement cascadethrough both the classic and alternative pathways.When released from the cell wall, LPSs are known asendotoxins. A relationship has been established be-tween the presence of endotoxins and the extent ofperiradicular inflammation . 11,53 Endotoxin is capa-ble of diffusing across dentin. The content of LPSsin canals of symptomatic teeth with radiographi-cally evident lesions and exudate is higher than thatof asymptomatic teeth .53-55


287

FIGURE 16-2Possible nutritional relationships between bacteria in an in-fected root canal. A mixed microbial flora is necessary. Then,the dynamic interrelationships between the bacteria and hostdetermine the degree of pathosis. (From Sundqvist G: J Endod1 8:428, 1992.)

288


Enzymes

Bacteria produce enzymes (proteases) that neu-tralize immunoglobulins and complement com-ponents.56-58 Recently the gene for collagenase, ametalloprotease associated with the spread of cel-lulitis, was detected in strains of Porphyromonasgingivalis isolated from endodontic infections."'In addition, hydrolytic enzymes released fromPMN leukocytes in purulent infections have anadverse effect on surrounding tissues.

Extracellular Vesicles

Another type of irritant produced by Gram-neg-ative bacteria is extracellular vesicles. These maybe free endotoxin, blebs, and outer membranefragments . 62 They have a trilaminar structure sim-ilar to that of the outer membrane of a Gram-negative bacterium (Figure 16-3). The vesiclescontain enzymes or other products that affecthost cells. These vesicles may be involved inhemagglutination, hemolysis, bacterial adhesion,and proteolytic activities .62,63 They have the sameantigenic determinants on their surface as theirparent bacteria. They may protect the bacteria byneutralizing specific antibodies.

affect neutrophil chemotaxis, degranulation,chemiluminescence, phagocytosis, and other in-tracellular changes. Research has shown that bu-tyric acid offers greater inhibition of T-cell blasto-genesis than does propionate or isobutyrate. 64Butyric acid has been shown to stimulate produc-tion of interleukin-1, which is associated withbone resorption and periradicular path OSiS.64

Polyamines

Biologically active polyamines have been found ininfected canals.65 Host cells and most bacteria, es-pecially Gram-negative bacteria, contain largeamounts of polyamines. Polyamines such as pu-trescine, cadaverine, spermidine, and spermine areinvolved in the regulation of cell growth, regener-ation of tissues, and modulation of inflamma-tion. Amounts of putrescine and total polyaminesare higher in the necrotic pulps of teeth that arepainful to percussion or those that have sponta-neous pain. Teeth with a sinus tract have a signif-icantly greater amount of cadaverine in the pulpspace. 6s Although correlations such as these havebeen demonstrated, cause and effect relationshipshave not been proved for all virulence factors.

Fatty AcidsCORRELATIONS WITH PATHOSES

AND TREATMENT

Anaerobic bacteria produce short-chain fattyacids such as propionic, butyric, and isobutyricacids. These acids are active virulence factors that

FIGURE 76-3Extracellular vesicles (arrows) from the budding outer mem-brane of a strain of black-pigmented Prevotella intermedia, asuspected pathogen. The trilaminar structure is similar to thatof the outer membrane of Gram-negative bacteria includingli popolysaccharides. These vesicles may be involved inhemagglutination, hemolysis, bacterial adhesion, and prote-olytic activities (original magnification x20,000).

The association of specific species of bacteria withpulpal and periapical pathoses as well as withclinical signs and symptoms is not absolute. En-dodontic infections are polymicrobial, with eachspecies of bacteria having variable virulence fac-tors. No single microorganism or group of bacte-ria has been proven to be more pathogenic thananother. From a treatment point of view, all en-dodontic infections are considered polymicrobialand are treated accordingly. Root canal treatmentof a necrotic pulp will disrupt the microbialecosystem by removing bacteria, bacterial byprod-ucts, and substrate from the root canal system.

In contrast to the necrotic debris and microbessequestered in a pulp cavity, periradicular tissueshave an excellent collateral blood supply, lym-phatic drainage, and a large pool of undifferenti-ated cells. Eventually, periradicular pathoses de-velop primarily in response to microorganisms,microbial byproducts, and microbial breakdownproducts. The extent of the periradicular inflam-matory reaction will depend on the severity of theirritation, its duration, and the host response. Me-diators of both nonspecific inflammatory reac-tions and specific immunologic reactions partici-pate in the formation and perpetuation ofperiradicular lesions (see Chapter 3).

Acute apical periodontitis (AAP) is the initialresponse that results from extension of pulpal in-flammation to the periradicular tissues. Bacteriaand their byproducts are usually involved in theprocess. Other factors that may be involved inAAP include inflammatory mediators from pulp,instrument trauma, and chemicals used duringroot canal treatment.

Microbiologic, histologic, and immunologicmethods have been used to determine whetherbacteria persist in the inflammatory tissue ofasymptomatic chronic apical periodontitis( CAP). Whether bacteria can invade, colonize,and multiply in CAP is controversial. Differentopinions result from different investigative tech-niques and interpretation of results. One prob-

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lem with microbial sampling of periradicular le-sions at the time of either periradicular surgeryor tooth extraction is contamination of the sam-ple by oral flora or by bacteria in the infected rootcanal. Results of culturing studies have been con-troversial and inconclusive . 66-69 Histologic evalua-tion of periradicular samples diagnosed as CAPrarely demonstrates bacteria in the tissue .38,68,70,71

A scanning electron microscopic study demon-strated bacterial plaque on surgically resectedroot tips of teeth that were refractory to rootcanal treatment. 66 Other studies have shown abarrier of neutrophils or epithelium or an amor-phous (necrotic) tissue between the bacteria inthe canal and the periradicular inflammatory tis-sue (Figure 16-4). 38 7 0

FIGURE 16-4A, Resected apical third (D) of a human tooth with pulp necrosis and chronic apical periodontitis (GR). B, The bac-

teria appear to be blocked by a wall of neutrophils (NG) or by (C) an epithelial plug (EP) i n the apical foramen.

Note dense aggregates of bacteria ( AB i n B) adherent to the dentin wall. Bacteria may clump (SB i n B) or form

l oose collections (BA in inset i n C) in the root canal. The infected canal becomes a sequestered reservoir for sub-

strate and bacteria. (From Nair R: l Endod 13:31, 1987.)

290


Immunocytochemical methods have provideda means of identifying bacteria present in chronicperiradicular lesions through the use of specificantisera to identify bacteria in the histologic sec-tions. Only Actinomyces israelii, Actinomyces naes-lundii, Propionibacterium (Aracbnia) propionica, andP. intermedia have been identified using immuno-cytochemical methods in sections of periradicularlesions . 3 ', 7 2,73 Any study that disturbs the peri-radicular tissues may allow their contaminationwith oral (or possibly intracanal) flora; also, thepresence of a species of bacteria does not prove anetiologic relationship (cause and effect) with theperiradicular pathosis.

Acute apical abscesses (AAAs), acute exacerba-tion of CAP (so-called "phoenix" abscesses), andsuppurative apical periodontitis are characterizedby large numbers of PMN leukocytes, necrotic tis-sue, and bacteria. Under certain circumstances (re-lated to host resistance and virulence of bacteria)periradicular tissues are invaded and become in-volved in progressive infections (abscesses and cel-lulitis). The bacteria are polymicrobial and are sim-ilar to those isolated from infected root canals .74-76The number of strains of bacteria isolated fromperiradicular abscesses are on average more thanfive per sample, with most being strict anaer-obes.11,75,77 Thus, in both root canal infections andperiradicular abscesses, a predominance of mixedstrict anaerobes contributes to the disease.

I nfection ControlToday's practice of dentistry, including endodonticprocedures, requires universal precautions. All pa-tients must be treated as if they have a transmissi-ble disease. Precautions include preventing crosscontamination between patients and health careproviders. Not all exposures to microorganisms re-sult in disease. Whether a disease is transmitteddepends on the dose of the infective agent, thevirulence of the microorganism, and the hostresistance.

An effective way to reduce the dose of microor-ganisms is the use of physical barriers, which in-clude the rubber dam, safety glasses or face shields,masks, gowns, and gloves. Once a rubber dam thatseals against salivary contamination has been po-sitioned, the tooth surface and surrounding rub-ber dam should be disinfected using sodiumhypochlorite (NaOCI) or other accepted disinfec-tant. Irrigation of canals with sodium hypochlo-rite provides an additional chemical barrieragainst microorganisms for health care providers.

Endodontic procedures pose a risk for acciden-tal percutaneous exposure to body fluids for bothpatient and dentist by burs, files, contaminatedneedles, instruments, spreaders and pluggers,Gates-Glidden drills, and so on. Techniques mustbe used to avoid accidental exposure to thesesharp instruments. Disposable items are availableto minimize the chances of contamination.

FIGURE 76-SProtective role of activated macrophages and T-lymphocytesi n periapical inflammatory granulomas. T-lymphocyte activa-tion leads to antigen-specific B-lymphocyte activation andl ocal production of specific antibodies. Healing will not occuruntil the bacteria are removed. (From Metzger ZV: EndodDent Traumatol16:3, 2000. C Munksgaard.)

Treatment of EndodonticI nfectionsThe microbial ecosystem of an infected root canalsystem and the subsequent inflammatory re-sponse of the periradicular tissue will persist untilthe source of irritation is removed (Figure 16-5).Treatment should establish an environment fa-vorable for the host to resolve the disease. The keyto successful treatment of periradicular disease isremoval of the reservoir of infection (necrotic tis-sue, bacteria, and bacterial by-products) by thor-ough debridement.

DEBRIDEMENT OF THE ROOT

CANAL SYSTEM

Root canal debridement, as a part of the cleaningand shaping process, is the removal of substratesthat support microorganisms. Because the rootcanal system is irregular, instruments do notreach all the fins, cul-de-sacs, indentations, andareas between the main canals. Irrigants flush outloose debris, provide lubrication, exert antimicro-bial action, and dissolve some debris in the canal.

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Sodium hypochlorite (NaOCI) (0.5% to 5.25%)is considered the irrigant of choice. NaOCI willdissolve some organic debris in areas not reachedby instruments and is an excellent antimicrobialagent against those bacteria reached by the chem-ical .78,86 The chemical activity of NaOCI should bemaintained by frequent irrigation of the canalsbeing instrumented.78,84 A root canal system withnecrotic pulpal debris may harbor bacteria in finsand other uninstrumented areas. Instrumenta-tion combined with NaOCI irrigation accountsfor tissue removal in the main canal but remainsrelatively ineffective in isthmi and fins.87 Irrigantsmust reach the debris in these areas to be effective.Straight-line access and proper flaring of the rootcanal will enhance debridement and allow moreefficient irrigation (see Chapter 13).

Instruments have been shown to produce anamorphous smear layer of burnished dentin andother debris about 1 to 4 Mm thick on the rootcanal surface with plugs of the material extendingup to 40 Mm into the dentinal tubules.88 The pres-ence of a smear layer has been shown to affect thepermeability of the dentin and to inhibit bacterialcolonization; however, smear layer could harborbacteria and decrease the effectiveness of intra-canal antimicrobials. 79,89,90

I NTRACANAL MEDICATION

The antimicrobial function of intracanal medica-tion between appointments is an important con-sideration. Microorganisms not removed fromthe canal will multiply. 85,91,92 Placement of a steriledry cotton pellet may allow growth of bacteria.86Historically, intracanal medicaments were usuallyphenolics such as formocresol, camphorated para-chlorophenol, eugenol, metacresylacetate, andhalides (iodine-potassium iodide). These medica-ments (particularly phenolics) are not recom-mended, being antigenic and cytotoxic, and func-tion as antimicrobials for only a short time .93-95

Clindamycin was recently tested as an intracanalmedicament with questionable results.96 There isconcern that antibiotics that are normally usedsystemically may produce allergies or select forresistant organisms when used as intracanalmedicaments.

Use of calcium hydroxide is recommended incanals with necrotic pulps after instrumentation.This chemical has a greater antimicrobial effectbetween appointments than the agents justlisted.97,98 Calcium hydroxide has some ability todissolve pulp tissue in vitro but not in vivo.87,99,100

However, intracanal use of calcium hydroxidemay increase the effectiveness of sodiumhypochlorite at the subsequent appointment,

which should also enhance the effectiveness of an-timicrobial agents.101

Calcium hydroxide powder should be mixedwith water or glycerin to form a thick paste. Thispaste or a commercial preparation is placed in thepulp chamber with a plastic instrument, amalgamcarrier, or syringe and carried down each canal bymeans of a lenrulo spiral, a plugger, or counter-clockwise rotation of files.102 The paste is coveredwith a sterile cotton pellet and the access is sealedwith a temporary restoration at least 3 mm thickto prevent coronal leakage of microbes or micro-bial by-products. 103-109

DRAINAGE

Severe infections require a multifaceted approachincluding debridement, drainage, and pharma-cotherapeutics. Debridement of the pulp space toremove the source of the infection is key alongwith drainage in managing an abscess or cellulitis.An abscess, which itself is a potent irritant, alsohas elevated osmotic pressure. This attracts moretissue fluid, thereby contributing to more edemaand pain. Drainage from the canal or soft tissuedecreases discomfort caused by inflammatory me-diators and particularly the pressure of a fluctu-ant swelling containing purulent material. Inci-sion of an indurated swelling is also effectivebecause it releases blood and serous fluids thatcontain bacteria, bacterial byproducts, and in-flammatory mediators. Good drainage also im-proves circulation to the area and improves deliv-ery of antibiotics so a minimum inhibitoryconcentration may be reached. These proceduresare discussed in detail in Chapter 17.

Antibiotics (antimicrobials) should be consid-ered adjunctive treatment of more severe infectionsand are not a substitute for proper local treatment.The indications and recommendations for the useof antibiotics are discussed in Chapter 30.

WHEN AND HOW TO CULTURE

Because of the wide range of bacteria found in en-dodontic infections, the empirical administrationof antibiotics may not be effective. Although cul-turing is rarely required, at times it may providevaluable information for better antibiotic selec-tion. Great care must be taken to avoid contami-nation of the sample. In addition, the propertransport media must be obtained from the labo-ratory to ensure that the bacteria remain viablefor culturing.

To prevent contamination by oral flora, a sub-mucosal swelling should be sampled by needle as-piration. After anesthesia, the mucosal surface is

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dried and disinfected with Betadine or chlorhexi-dine. A 16- to 20-gauge needle is used to aspiratethe exudate. The aspirate should be immediatelyinjected into a container with prereduced trans-port media. Good communication with the labo-ratory technicians is important.

Gram staining should be performed on thesample to demonstrate which types of microor-ganisms predominate. The culture results shouldidentify the predominant isolated microorgan-isms, which should not be identified merely as"normal oral flora."

Antibiotics are chosen to treat anaerobic infec-tions based on the identification of the promi-nent microorganisms in the culture. A factorcomplicating the culture of anaerobes is that theidentification may not be made for days or evenweeks. In the future, once specific bacteria or com-binations of bacteria are determined to be associ-ated with endodontic pathoses, selective media,precise biochemical tests, immunofluorescence,and molecular methods may provide more rapididentification of pathogens.

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pigmented Bacteroides, J Med Microbial 19:85, 1985.

59. Tamura M, Nagaoka S, Kawagoe M: Interleukin-1

stimulates interstitial collagenase gene expression in

human dental pulp fibroblast, J Endod 22:240, 1996.

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of collagenase in human periapical lesions, J Endod

13:228, 1987.

61. Odell L, Baumgartner J, Xia T, David L: Survey of col-

lagenase gene prtC in porphyromonas gingivalis and Por-

pbyromonas endodontalis isolated from endodontic in-

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62. Shah HH: Biology of the species Porphyromonas gingivalis,

Ann Arbor, Mich, 1993, CRC Press.

63. Kinder SA, Holt SC: Characterization of coaggrega-

tion between Bacteroides gingivalis T22 and Fusobac-

terium nucleatum T18, Infect Immunol 57:3425, 1989.

64. Eftimiadi C, Stashenko P, Tonetti M, et al: Diver-

gent effect of the anaerobic bacteria by-product bu-

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terleukin-1 beta production, Oral Microbial Immunol

6:17, 1991.

65. Maita E, Horiuchi H: Polyamine analysis of infected

root canal contents related to clinical symptoms,

Endod Dent Traumatol6:213, 1990.

66. Tronstad L, Barnett F, Cervone F: Periapical bacterial

plaque in teeth refractory to endodontic treatment,

Endod Dent Traumatol 6:73, 1990.

67. Iwu C, MacFarlane TW, MacKenzie D, Stenhouse D:The microbiology of periapical granulomas, Oral Surg

69:502, 1990.

68. Wayman BE, Murata SM, Almeida RJ, Fowler CB: A

bacteriological and histological evaluation of 58 peri-

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69. Sunde PT, Olsen 1, Lind PO, Tronstad L: Extraradicu-

lar infection: a methodological study, Endod Dent


70. Walton RE, Ardjmand K: Histological evaluation of

the presence of bacteria in induced periapical lesions

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71. Block RM, Bushell A, Rodrigues H, Langeland K: A

histopathologic, histobacteriologic, and radiographic

study of periapical endodontic surgical specimens,

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72. Nair PNR, Schroeder HE: Periapical actinomycosis, J

Endod 10:567, 1984.

73. Barnett F, Stevens R, Tronstad L: Demonstration of

Bacteroides intermedius in periapical tissue using indi-

rect immunofluorescence microscopy, Endod Dent

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dominant microflora associated with human dental

periapical abscesses, J Clin Microbiol 15:964, 1982.75. Van Winkelhoff AJ, Carlee AW, de GraaffJ: Bacteroides en-

dodontalis and other black-pigmented Bacteroides species

in odontogenic abscesses, Infect Immunol 49:494, 1985.

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tion of black-pigmented bacteria with endodontic in-

fections, JEndod 25:413, 1999.

78. Baumgartner JC, Ibay AC: The chemical reactions of

irrigants used for root canal debridement, J Endod13:47, 1987.

79. Baumgartner JC, Mader CL: A scanning electron mi-croscopic evaluation of four root canal irrigation reg-

imens,J Endod 13:147, 1987.

80. Harrison JW, Hand RE: The effect of dilution and or-

ganic matter on the antimicrobial property of 5.25%

sodium hypochlorite, JEndod 7:128, 1981.

81. Hand RE, Smith ML, Harrison JW: Analysis of the ef-

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teeth, Oral Surg 1971:96, 1971.

83. Shih M, Marshall FJ, Rosen S: The bactericidal effi-

ciency of sodium hypochlorite as an endodontic irri-

gant, Oral Surg 29:613, 1970.

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86. Bystrom A, Sundqvist G: Bacteriologic evaluation ofthe efficacy of mechanical root canal instrumentation

in endodontic therapy, ScandJDentRes 89:321, 1981.87. Yang S, Rivera E, Walton R, Baumgardner K: Canal

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and calcium hydroxide as medicaments, J Endod 22:

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88. Mader CL, Baumgartner JC, Peters DD: Scanning elec-

tron microscopic investigation of the smeared layer

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terial retention in canal walls in vitro: effect of smear

layer, JEndod 20:78, 1994.90. Galvan DA, Ciarlone AE, Pashley DH, et al: Effect of

smear layer removal on the diffusion permeability of

human roots,J Endod 20:83, 1994.

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ultrasonic root canal instrumentation, Oral Surg63:366, 1987.

92. Bystrom A, Sundqvist G: Bacteriologic evaluation of

the efficacy of mechanical root canal instrumenta-

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ogous tissue implants,J Endod 3:179, 1977.

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fects of dental materials. 3. Toxicity and antimicrobial

effect of endodontic antiseptics in vitro, Oral Surg

36:856, 1973.95. Walton R: Intracanal medicaments, Dent Clin North

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a clindamycin-impregnated fiber as an intracanal

medication in endodontic therapy, J Endod 25:722,1999.

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comparative antimicrobial effect of calcium hydrox-ide, Oral Surg 72:101, 1991.



dodontic therapy, Int Endod j 1:35, 1985.

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trasonics and calcium hydroxide for the debride-

ment of human mandibular molars, JEndod 15:373,

1989.

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In vitro solubility of human pulp tissue in calcium hy-

droxide and sodium hypochlorite, Endod Dent Trauma-

tol 8:104, 1992.

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102. Sigurdsson A, Stancill R, Madison S: Intracanal place-

ment of Ca(OH)2: a comparison of techniques, JEndod18:367, 1992.

103. Deveaux E, Hildelbert P, Neut C, et al: Bacterial mi-

croleakage of Cavit, IRM, and TERM, Oral Surg74:634, 1992.

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coronal microleakage in endodontically treated teeth.

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24:S87, 1998.

Endodontic Emergencies

LEARNING OBJECTIVES


1/ Identify causes of emergencies as they occur before treatment, between appointments, and afterobturation.

2 / Recognize what constitutes a true emergency as opposed to urgency.

3 / Describe the emotional status of the emergency patient and explain how this complicates diagnosis andtreatment.

4 / Describe the psychologic and physiologic factors that affect pain perception and pain reaction and howthese are managed.

5 / List the factors that relate to greater frequency of interappointment or postobturation flare-ups.

6 / Describe and outline a sequential approach to endodontic emergencies:a. Determine the source of pain (pulpal or periradicular)b. Establish a pulpal and periradicular diagnosisc. Identify the etiologic factor of the pathosisd. Design an emergency (short-term) treatment plane. Design a long-term treatment plan

7 / Outline a system of subjective and objective examinations and radiographic findings to identify the sourceof pain and the pulpal or periradicular diagnosis.

8 / Describe when pretreatment emergencies might occur and how to manage these emergencies.

9 / Outline the steps involved in treatment of painful irreversible pulpitis.

10 / Describe the steps involved in treatment of necrotic pulp with acute apical periodontitis.

11 / Describe treatment of acute apical abscess; include the indications and procedure for incision and drainage.

12 / Describe treatment of acute apical periodontitis after cleaning and shaping (interappointment) or afterobturation (post-treatment).

13 / Detail the pharmacologic supportive therapy (analgesics, antibiotics, and anti-inflammatory agents) used inemergencies and their role in controlling inflammation or infection.

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Definition

Categories

Pretreatment Emergency

I nterappointment and Postobturation

Emergency

The Challenge

Differentiation of Emergency and Urgency

Development of a System

Pain Perception and Pain Reaction

Physical Condition

System of Diagnosis

Medical and Dental Histories

Subjective Examination

Objective Examination

Periodontal Examination

Radiographic Examination

Diagnostic Outcome

Treatment Planning

Pretreatment Emergencies

Patient Management

Profound Anesthesia

Management of Painful Irreversible Pulpitis

Management of Pulp Necrosis with Apical

Pathosis

Postoperative Instructions

Interappointment Emergencies

I ncidence

Causative Factors

Prevention

Diagnosis

Treatment of Flare-ups

Medications

Postobturation Emergencies

Causative Factors

Treatment

ndodontic emergencies are a chal-l enge for both diagnosis and manage-ment. Knowledge and skill in several

aspects of endodontics are required; failure toapply these will result in serious consequences forthe patient. Incorrect diagnosis or incorrect treat-ment will fail to relieve pain and, in fact, may ag-gravate the situation. The clinician must haveknowledge of pain mechanisms, patient manage-ment, diagnosis, anesthesia, therapeutics, and ap-propriate treatment measures for both hard andsoft tissues.

This chapter discusses approaches to the diag-nosis and treatment of various categories of emer-gencies. It includes a review of etiologic factorsand details of a systematic approach to identify-ing and diagnosing the offending cause; then ap-propriate treatment is described.

These emergencies are a matter of concern topatients, dentists, and staff. Varying (but not un-common) frequencies of pain or swelling occur inpatients before, during, and after root canal treat-ment.1-4 Causes of such emergencies are a combi-nation of irritants that induce severe inflamma-tion in the pulp and/or periradicular tissues.

Investigations into the role of host factors (age,gender, tooth type, and so on) contributing to theoccurrence of endodontic emergencies have beeninconclusive; clear cause-and-effect relationshipshave not been established. Most studies of inter-appointment pain have shown little or no directrelationship between emergencies and the factors(intracanal medication, occlusal reduction, and soon) that can be controlled by the operator.1,5 As-sociated factors are those presented by the pa-tient, such as the pulp or periapical diagnosis andthe presenting levels of pain.1 -6

Among major elements, the role of bacteria andtheir by-products in dental emergencies is well es-tablished. Bacteria are important causative agentsof pathosis of the pulpal and periradicular tis-sues.7,8 A mixed flora, including Gram-negativeanaerobic bacteria, is related to clinical signs andsymptoms of periradicular pathosis."' Bacterialby-products (including collagenase, chondroiti-nase, and hyaluronidase) isolated from root canalshave also been related to clinical symptoms."

Irritation of periradicular tissues results in in-flammation and the release of a group of chemicalmediators that initiate inflammation. The con-centrations of some of these substances in thepulp and periradicular tissues are significantlyhigher in symptomatic than in asymptomatic le-sions." Pain results from two factors related to in-flammation: (1) chemical mediators and (2) pressure.Chemical mediators cause pain either directly bylowering the response threshold of the sensory

nerve fibers or indirectly by increasing vascularpermeability and producing edema. Edema re-sults in increased fluid pressure, which directlystimulates pain receptors. Of the two causes ofpain, pressure is the more important.

Definition

By definition, endodontic emergencies are usuallyassociated with pain and/or swelling and requireimmediate diagnosis and treatment. These emer-gencies are caused by pathoses in the pulp or peri-radicular tissues. They also include severe trau-matic injuries that result in luxation, avulsion, orfractures of the hard tissues. Management ofemergencies related to trauma will not be in-cluded in this chapter (see Chapter 25).

CategoriesPRETREATMENT EMERGENCY

These are situations in which the patient is seeninitially with severe pain and/or swelling. Prob-lems occur with both diagnosis and treatment.

I NTERAPPOINTMENT ANDPOSTOBTURATION EMERGENCY

Also referred to as the "flare-up," this problem oc-curs after an endodontic appointment. Althoughan upsetting event, this is easier to manage be-cause the offending tooth has already been identi-fied and a diagnosis has been previously estab-lished. Also, the clinician has knowledge of theprior procedure and will be better able to correctthe problem.

The Challenge

it is satisfying and rewarding to successfully man-age a distraught patient who has an emergency(Figure 17-1). In contrast, how distressing it is tohave a patient with a flare-up after root canaltreatment in a previously asymptomatic tooth!The aim is to increase occurrences in the first cat-egory and decrease those in the second.

DIFFERENTIATION OF EMERGENCYAND URGENCY

Whether a pretreatment, interappointment, orpostobturation problem, it is important to differ-entiate between a true emergency and the less criticalurgency. A true emergency is a condition requiring an


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FIGURE 17-1Patient is distraught from severe pulpal pain. This patient willbe a challenge to diagnose and treat.

unscheduled office visit with diagnosis and treat-ment now! The visit cannot be rescheduled becauseof the severity of the problem. Urgency indicates aless severe problem; a visit may be scheduled formutual convenience of the patient and the dentist.Key questions (that may be asked by telephone) todetermine severity include the following:

1. Does the problem disturb your sleeping,eating, working, concentrating, or otherdaily activities? (A true emergency disruptsthe patient's activities or quality of life.)

2. How long has this problem been botheringyou? (A true emergency has rarely been se-vere for more than a few hours to 2 days.)

3. Have you taken any pain medication? Wasthe medication ineffective? (Analgesics donot relieve the pain of a true emergency.)

An affirmative answer to these questions re-quires an immediate office visit for managementand constitutes a true emergency. Obviously, thepatient's emotional and mental status must alsobe determined. To some patients, even a minorproblem has major proportions and is disruptive.

DEVELOPMENT OF A SYSTEM

Because a misdiagnosis will probably result in im-proper treatment and an exacerbation of theproblem, a systematic approach is mandatory!

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The emotional status of the patient, pressures oftime, and stress on dentist and staff should notaffect such an orderly approach.

cantly, greatly facilitating the procedure. Psycho-logic management of the patient is the most im-portant factor in emergency treatment!

Pain Perception and PainReactionPain is a complex physiologic and psychologicphenomenon. Pain perception levels are not con-stant; pain thresholds as well as reactions to painchange significantly under various circum-stances." Psychologic components of pain percep-tion and pain reaction comprise cognitive, emo-tional, and symbolic factors. The pain reactionthreshold is significantly altered by past experi-ences and by present anxiety levels and emotionalstatus. (Refer to Chapter 29 for more details onpain perception and reaction and pain threshold.)

To reduce anxiety and consequently obtain re-liable information about the chief complaint andto receive cooperation during treatment, the clin-ician should (1) establish and maintain control ofthe situation, (2) gain the confidence of the pa-tient, (3) provide attention and sympathy, and (4)treat the patient as an important individual.13 Bymanaging these pain components, pain percep-tion and reaction thresholds are raised signifi-

FIGURE 77-2Severe submandibular swelling. The patient has limitedmouth opening resulting from trismus.

Physical ConditionIn addition to the emotional factors that compli-cate the diagnosis of endodontic emergencies,physical conditions induced as a result of thesesituations also contribute to the problems. Painor swelling may limit mouth opening, therebyhampering diagnostic procedures as well as treat-ment (Figure 17-2). In addition, hypersensitivityto thermal stimuli or pressure influences diagno-sis and treatment.

System of DiagnosisPatients in pain often provide information and re-sponses that are exaggerated and inaccurate. Theytend to be confused as well as apprehensive. It iseasy (and tempting) to rush through the diagno-sis to institute treatment for a suffering patient.After pertinent information regarding the med-ical and dental histories is obtained, both subjec-tive questioning and an objective examination areperformed carefully and completely."

A rule of the true emergency is one tooth is the of-fender, i.e., the source of pain. In the excitement ofthe moment, the patient might believe that the se-vere pain is emanating from more than a singletooth. The clinician may become convinced also,leading to overtreatment.

MEDICAL AND DENTAL HISTORIES

Medical and dental histories should be reviewedfirst. If the patient is the dentist's own, the med-


299

ical history is briefly reviewed and updated. If thepatient is new, a standard, complete history istaken. An important medical complication maybe easily overlooked in an emergency situation.Either a short or a complete dental history istaken. This includes recalling of dental proce-dures, a chronology of symptoms, or an earlierrelevant comment by a dentist.


When the patient is in pain, the subjective exami-nation comprises careful questioning and is themost important aspect of diagnosis. Questions re-late to the history, location, severity, duration,character, and eliciting stimuli of pain. Questionsrelating to the cause or stimulus that elicits or re-lieves the pain help select appropriate objectivetests to arrive at a final diagnosis.

Pain that is elicited by thermal stimuli and/oris referred is likely to originate from the pulp.Pain that occurs on mastication or tooth contactand is well localized is probably periradicular.

The three important factors constituting thequality and quantity of pain are its spontaneity, in-tensity, and duration (see Chapter 4). If the patientreports any of these symptoms (and assuming thatthe patient is not exaggerating), significant patho-sis is likely to be present. Careful questioning pro-vides important information about the source ofthe pain and whether it is pulpal or periradicular.In fact, a perceptive, clever clinician should be ableto arrive at a tentative diagnosis by means of athorough subjective examination; objective testsand radiographic findings are then used for con-firmation. For example, a reported complaint ofsevere, continuous (lingering) pain when the pa-tient drinks cold beverages and marked tendernesson mastication indicates irreversible pulpitis andacute apical periodontitis. These stimuli are thenrepeated on an objective examination to confirmthe patient's response.

In addition, objective tests include extraoraland intraoral examination. Included are observa-tion for swelling as well as mirror and explorer ex-amination to note the presence of defectiverestorations, discolored crowns, recurrent caries,and fractures.

Periradicular tests include (1) palpation overthe apex, (2) digital pressure on or wiggling ofteeth (preferred if the patient reports severe painon mastication), (3) light percussion with the endof the mirror handle, and (4) selective biting on anobject such as a cotton swab or Tooth Slooth.

Pulp vitality tests are most useful to reproducereported pain. Cold, heat, electricity, and directdentin stimulation, however, usually indicate thepulp status (vital or necrotic).

PERIODONTAL EXAMINATION

A periodontal examination is always necessary.Probing helps in differentiating endodontic fromperiodontal disease. For example, a periodontalabscess can simulate an acute apical abscess (Fig-ure 17-3). However, with a localized periodontalabscess, the pulp is usually vital (see Chapter 26).In contrast, an acute apical abscess is related to anunresponsive (necrotic) pulp. These abscesses oc-casionally communicate with the sulcus and havea deep probing defect. In addition to these tests,when the differential diagnosis is difficult, a testcavity may identify the pulp status and isolate theoffending tooth.

RADIOGRAPHIC EXAMINATION

Radiographs are helpful, but have limitations.There is a tendency to over-rely on radiographs,often with unfortunate consequences. Periapicaland bitewing radiography may detect the presenceof interproximal and recurrent caries, possiblepulpal exposure, internal or external resorption,and periradicular pathosis, among other entities.

OBJECTIVE EXAMINATION DIAGNOSTIC OUTCOME

Again, it is important in identifying the offendingtooth to repeat tests that mimic what the patientreports subjectively. In other words, the best testis to repeat the stimulus that reportedly causesthe pain. As in the previous example, applyingcold and pressure should reproduce pain of basi-cally the same type and magnitude as related bythe patient. If similar subjective symptoms are notreproduced, this may not be a true emergency; thepatient may be "over-reporting" (exaggerating theproblem).

After carefully working through the sequence justdescribed, the clinician should have identified theoffending tooth and the tissue (pulpal or peri-radicular) that is the source of pain and shouldhave recorded a pulpal or periradicular diagnosis.For many reasons, all or none of these conclu-sions may be clear. This may not be a true emer-gency, or the problem may be beyond the capabil-ity of the generalist and the patient should bereferred (Figure 17-4). If the diagnosis is clear,however, treatment planning follows.

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1 7 / Endodontic Emergencies

FIGURE 17-3A, Periodontal abscess, B, Radiographic appearance. Positive responses to pulp testing differentiates this condi-tion from an acute apical abscess.

FIGURE 17-4This patient has a complex problem and should be considered for referral. A and B, Submental space swellingresulting from trauma followed by acute apical abscess. C, Removal of the necrotic tissue was followed by ex-traoral incision and placement of a drain. (Courtesy Dr. V Jones.)

Treatment PlanningAs previously discussed, inflammation and its con-sequences, that is, increased tissue pressure and re-lease of chemical mediators in the pulp or peri-radicular tissues, are the major causes of painfuldental emergencies.15,16 Therefore, reducing the ir-ritant, or reduction of pressure or removal of theinflamed pulp or periradicular tissue should be the

immediate goal; this usually results in pain relief.Of the two, pressure release is the most effective.

Pretreatment EmergenciesThese emergencies require a diagnosis and treat-ment sequencing. Each step is important: (1) cat-egorizing the problem, (2) taking a medical his-


301

tory, (3) identifying the source, (4) making the di-agnosis, (5) planning the treatment, and(6) treat-ing the patient.

PATIENT MANAGEMENT

Patient management is always the most criticalfactor. The frightened patient in pain must haveconfidence that his or her problem is being prop-erly managed.

PROFOUND ANESTHESIA

Obtaining profound anesthesia of inflamedpainful tissue is a challenge. Adequate anesthesia,however, will instill confidence and cooperationand influence the patient's desire to save the of-fending tooth. Maxillary anesthesia is usually ob-tained by infiltration or block injections in thebuccal and palatal regions. With mandibularteeth, in addition to an inferior alveolar and lin-gual nerve block, a long buccal injection may behelpful. Often (particularly with mandibular mo-lars), although all "classic" signs of profoundanesthesia are present, access into the dentin orpulp is painful. Periodontal, intrapulpal, or in-traosseous injection controls the remaining sensi-tivity in most cases." These supplemental injec-tions are often given prophylactically, particularlywith painful irreversible pulpitis.18 Other condi-tions (for example, acute apical abscess) requireother approaches. Chapter 7 contains details.

FIGURE 97-5Removal of coronal pulp. Pulpotomy and placement of a drycotton pellet and a temporary filling result in relief of painfrom irreversible pulpitis.

a dry cotton pellet is placed and the access issealed temporarily. A mild analgesic may be pre-scribed for patients with irreversible pulpitis. An-tibiotics, however, are definitely not indicated.

With Acute Apical Periodontitis

In patients with extreme tenderness on percus-sion, a partial or total pulpectomy (as describedabove) is appropriate. Reducing the occlusion toeliminate contact has been shown to aid in reliefof symptoms. 21 Trephination (artificial fistula-tion) by creating an opening through mucosa andbone is not useful and is contraindicated. 22,23

MANAGEMENT OF PAINFULIRREVERSIBLE PULPITIS

Because the pain is the result of inflammation,primarily in the coronal pulp, removal of the in-flamed tissue will usually reduce the pain.

Without Acute Apical Periodontitis

Complete cleaning and shaping of the root canalsis the preferred treatment if time permits. Withlimited time, most pulpal tissue is extirpated witha broach (partial pulpectomy) in single-rootedteeth. In molars, a partial pulpectomy is per-formed on the largest canals (palatal or distalroot). Pulpotomy (Figure 17-5) is usually effectivein molars when minimal time is available. 19,20

An old but still popular idea is that chemicalmedicaments sealed in chambers help control orprevent additional pain; this is not true. A drycotton pellet alone is as effective in relieving painas a pellet moistened with camphorated mono-chlorophenol (CMCP), formocresol, Cresatin,eugenol, or saline." Therefore, after irrigation ofthe chamber or canals with sodium hypochlorite,

MANAGEMENT OF PULP NECROSISWITH APICAL PATHOSIS

The pain is related to periradicular inflammation,which results from potent irritants in the necrotictissue in the pulp space. Treatment now is bipha-sic: (1) remove or reduce the pulp irritants and (2)relieve the apical fluid pressure (when possible).The diagnosis may be acute apical periodontitis(no significant periradicular resorption) or acuteapical abscess with or without swelling.

Therefore, with pain and pulp necrosis theremay be (1) no swelling, (2) localized swelling, or(3) diffuse, more extensive swelling. Each is man-aged differently. Of these three conditions, dif-fuse swelling is the least common.

Pulp Necrosis Without Swelling

These teeth may contain vital inflamed tissues inthe apical canal and have inflamed painful peri-radicular tissues (acute apical periodontitis). Pro-found local anesthesia may be a problem, requir-ing a supplemental injection.

Alternatively, the lesion may have expandedand formed an abscess that is confined to bone.

302


FIGURE 17-6A, Localized swelling. B, Incision for drainage after cleaning and shaping of offending incisor. (CourtesyDr. E. Rivera.)

FIGURE 17-7After opening into a root canal and establishment ofdrainage, instrumentation should be confined to the rootcanal system. Release of purulence removes a potent irritant(pus) and relieves pressure.

These are often painful, primarily because of fluidpressure in a noncompliant environment. Theaim is to reduce the canal irritants and to try toencourage some drainage through the tooth.

Complete canal debridement, after determin-ing the corrected working length, is the treatmentof choice. If time is limited, partial debridementat the estimated working length is performedwith light instrumentation with a passive step-back or crown-down technique to remove irritat-ing debris. Canals are not enlarged withoutknowledge of the working length. During clean-ing, canals are flooded and flushed with copiousamounts of sodium hypochlorite. Finally, canals

are irrigated with the same solution, dried withpaper points, filled with calcium hydroxide paste(if the preparation is large enough), and sealedwith a dry cotton pellet and a temporary filling.

Some clinicians empirically place a cotton pelletlightly dampened with intracanal chemical med-ication in the pulp chamber before placing a tem-porary filling. There is no value to these medica-ments. Administering a long-acting anesthetic,reassuring the patient, removing (or reducing) theirritant, and prescribing an analgesic will usuallyreduce postoperative pain significantly. Antibioticsare not indicated.24 The patient is told that therewill still be some pain (the inflamed, sensitive tis-sues are still present), but should subside duringthe next 2 or 3 days, as the inflammation decreases.

Pulp Necrosis with Localized Swelling

The abscess has now invaded regional soft tissuesand at times, there is purulence in the canal. Ra-diographic findings range from no periapicalchange (rarely) to a large radiolucency.

Again, treatment is biphasic. First and most im-portant is debridement (complete cleaning andshaping if time permits) of the canal or canals,and second in urgency is drainage (see Color Fig-ure 17-1 immediately following page 308). Local-ized swelling (whether fluctuant or nonfluctuant)should be incised (Figure 17-6). Drainage accom-plishes two things: (1) relief of pressure and painand (2) removal of a very potent irritant-purulence.

In teeth that drain readily after opening, instru-mentation should be confined to the root canalsystem (Figure 17-7). In patients with a periradicu-


303

FIGURE 77-8A, Localized fluctuant abscess as a result of periradicular pathosis after trauma. B, Radiographic appearance. C,Drainage was spontaneous when the tooth was opened. D, Christmas tree-shaped rubber drain placed after softtissue incision. Antibiotics are unnecessary, but analgesics are indicated.

lar abscess but no drainage through the canal,penetration of the apical foramen with small files(up to 25) may initiate drainage and release ofpressure. This release often does not occur becausethe abscess cavity does not communicate directlywith the apical foramen. Occasionally there maybe more than one abscess (Figure 17-8). One com-municates with the apex while another, separateabscess is found in the vestibule. Because they do

not communicate, drainage must occur throughboth the tooth and a mucosal incision. Often, adrain is placed to permit continued drainage for 1or 2 days or until debridement is complete. Severaldesigns of drain are used (Figure 17-9).

Copious irrigation with sodium hypochloriteis performed throughout. The canals are thendried with paper points and filled with calciumhydroxide paste. After placement of a dry cotton

304


FIGURE 17-9Different shapes of rubber drains. From left to right: I drain;Christmas tree drain; T drain; Penrose drain with oblique cuts.These designs are self-retentive and do not require suturingto the incision margins.

FIGURE 17-10Progressively spreading swelling resulting from pulpal necro-sis and acute apical abscess. The abscess moved rapidly intothe buccal space. This patient has systemic signs of infection(elevated temperature). Localized treatment (extraction orpulp space debridement, incision for drainage) and antibi-otics are indicated.

pellet, the access is sealed temporarily. These teethshould not be left open to drain, although leavingteeth open has been a common procedure. A canalexposed to the oral cavity is a potential home forintroduced bacteria, food debris, and evenviruses.24 Occasionally, purulence will continue tofill the canal during the preparation (the so-called"weeping" canal). If this occurs, the patientshould sit for a time. Usually, the flow will ceaseand the access may be closed.

These patients seldom have elevated tempera-tures or other systemic signs. Therefore, in acuteapical abscess with localized swelling, the use ofsystemic antibiotics is not necessary, having beenshown to be of no benefit .25-27

Pulp Necrosis with Diffuse Swelling

These rapidly progressive and spreading swellingsare not localized and may have dissected intothe fascial spaces (Figure 17-10). These patientsoccasionally have elevated temperature or othersystemic signs and usually should be referred to aspecialist.

Most important is removal of the irritant bycanal debridement (cleaning and shaping is com-pleted, if possible) or by extraction. The apicalforamen may then be gently penetrated with a fileto hopefully permit a flow of exudate (see Figure17-8), although drainage often does not occur.Also at this time, swelling may be incised and arubber drain inserted for 1 or 2 days. Occasionallythe abscess localizes extraorally and subcuta-

neously, requiring extraoral incision for drainage(Figure 17-11).

Speed of recovery (whether the swelling is local-ized or diffuse) depends primarily on canaldebridement and drainage. Because edema (fluid)has spread through the tissues, diffuse swelling de-creases slowly, over a period of perhaps 3 to 4 days.As with patients undergoing removal of impactedthird molars, pretreatment with nonsteroidal anti-inflammatory drugs may reduce the frequency andamount of postoperative discomfort.14

After placing calcium hydroxide paste and a drypellet, the access is closed with a temporary filling.Systemic antibiotics are indicated for the diffuse,rapidly spreading swelling. The preferred and first(albeit empirical) choice is penicillin; the causativemicroorganisms are likely to be streptococci.28.29 Analternative for penicillin-allergic patients is clin-damycin.29 Systemic steroids, advocated by some,are probably of no benefit. Analgesics for moderateto severe pain should be prescribed. Specific detailson therapeutics are found in Chapter 30.

POSTOPERATIVE INSTRUCTIONS

Patients must be informed of their responsibili-ties and of what to expect. The pain and swellingwill take time to resolve, proper nutrition and ad-equate intake of fluids are important, and med-ications must be taken as prescribed. The prob-lem may recur or worsen (flare-up), requiringanother emergency visit.' Communication afterthe visit is very important; calling the patient the


305

FIGURE 17-77An acute apical abscess from a mandibular molar hasrapidly spread to bilateral submandibular and cervicalspaces. Also involved is the space of Burns. The result is aLudwig's angina that requires immediate hospitalization.This patient is at risk for airway compromise and requiresspecial procedures, including antibiotics, extraoral drainage,and airway management.

day after the appointment has been shown to re-duce pain perception and analgesic needs 30 and al-lows the clinician the opportunity of monitoringthe progress of the patient.

I nterappointment EmergenciesThe interappointment flare-up is a true emergencyand is so severe that an unscheduled patient visitand treatment are required. Despite judicious andcareful treatment procedures, complications suchas pain, swelling, or both may occur. Regional tem-porary paresthesia has even been reported . 3 ' As withemergencies occurring before root canal therapy,these interappointment emergencies are undesir-able and disruptive events and should be resolvedquickly. Occasionally flare-ups are unexpected, al-though they can often be better predicted accordingto certain patient presenting factors.

teria were examined. The problems with most ofthese studies are that they are retrospective, lackcontrols, have relatively small numbers of pa-tients, or have undefined variables.' Prospectivestudies, which are better controlled, report anoverall incidence of flare-ups of 1.4% to 3%. 1,33

Therefore, overall the occurrence is low, but itvaries in certain situations. Most postoperativediscomfort is in the mild range. 35

CAUSATIVE FACTORS

The causative factors associated with flare-ups havealso been examined. These factors generally can becategorized as related to the patient, to pulpal orperiapical diagnosis, or to treatment procedures.Although many factors have been examined, a his-tory of preoperative pain or swelling is the best pre-dictor of interappointment emergencies., 5,6

In other words, a patient who has a painfulacute apical abscess that requires emergency treat-ment is much more likely to experience a flare-up.A tooth with a vital pulp, on the other hand, is un-likely to demonstrate severe interappointmentsymptoms while under treatment.

PREVENTION

Procedures

Use of long-acting anesthetic solutions, completecleaning and shaping of the root canal system(possibly), analgesics, and psychologic prepara-tion of patients (particularly those with preopera-tive pain) will decrease interappointment symp-toms in the mild to moderate levels . 36 There are,however, no demonstrated treatment or therapeu-tic measures that will reduce the number of inter-appointment flare-ups. In other words, no partic-ular relationship of flare-ups to actual treatmentprocedures has been shown.1.5

Verbal Instructions

Most important is the preparation of patients forwhat to expect after the appointment. Theyshould be told that discomfort is likely; the dis-comfort should subside within a day or two. Anincrease in pain, noticeable swelling, or other ad-verse signs necessitate a call and sometimes a visit.This explanation reduces the number of callsfrom unnecessarily concerned patients.

I NCIDENCE

Studies report varying incidences (1.4% to 2S%) offlare-ups. 1.2,6,12-" These variations may be due tothe fact that different factors, conditions, and cri-

Therapeutic Prophylaxis

A popular preventive approach has been the pre-scribing of antibiotics to minimize postoperativesymptoms. This has been demonstrated to be notuseful and needlessly exposes the patient to expert-

306


sive, potentially dangerous drugs .38.38 In contrast,certain analgesics and anti-inflammatory agentswill reduce post-treatment symptoms. More infor-mation on therapeutics is included in Chapter 30.

DIAGNOSIS

The same basic procedure is followed as outlinedearlier in this chapter for pretreatment emergen-cies, although with modifications. The problemhas already been diagnosed initially; the operatorhas an advantage. However, a step-by-step ap-proach to diagnose the existing condition reducesconfusion and error; most important, it calms apatient who has been shaken by the episode ofpain or swelling. After the underlying complica-tions are identified, treatment is initiated.

TREATMENT OF FLARE-UPS

Reassurance (the "Big R") is the most important aspectof treatment. The patient is generally frightenedand upset and may even assume that extraction isnecessary. The explanation is that the flare-up isneither unusual nor irrevocable and will be man-aged. Next in importance is restoring the patient'scomfort and breaking the pain cycle. For extendedanesthesia or analgesia, administration of ropiva-caine, etidocaine, or bupivacaine hydrochloride isrecommended.

Interappointment emergencies are dividedinto patients with an initial diagnosis of a vital ora necrotic pulp and with or without swelling.

Previously Vital Pulps with CompleteDebridement

then placed followed by a temporary filling, and amild to moderate analgesic is prescribed.

Occasionally, a previously vital pulp (with orwithout complete debridement) will develop intoan acute apical abscess. This will occur some timeafter the appointment and indicates that pulpalremnants have become necrotic and are invadedby bacteria.

Previously Necrotic Pulps with NoSwelling

Occasionally these teeth develop an acute apicalabscess (flare-up) after the appointment.' The ab-scess is confined to bone and can be very painful.

The tooth is opened and the canal is gently re-cleaned and irrigated with sodium hypochlorite.Drainage should be established if possible (see Fig-ure 17-7). If there is active drainage from the toothafter opening, the canal should be recleaned (ordebridement completed) and irrigated with sodiumhypochlorite. The rubber dam is left in place afterthe tooth is opened; the patient is allowed to restpain-free for at least 30 minutes or until drainagestops. Then, the canals are dried, calcium hydroxidepaste is placed, and the access is sealed. The toothshould not be left open! If there is no drainage, thetooth should also be lightly instrumented and gentlyirrigated, medicated with calcium hydroxide paste,and then closed. The symptoms usually subside, butdo so more slowly than if drainage was present.Again, patient education and reassurance are criti-cal. A long-acting anesthetic and a strong analgesicare helpful; antibiotics are not indicated.25.26

Previously Necrotic Pulps with Swelling

Because this situation is unlikely to be a true flare-up, patient reassurance and the prescription of amild to moderate analgesic often will suffice.Generally,. nothing is to be gained by openingthese teeth; the pain will usually regress sponta-neously. Placing corticosteroids in the canal orgiving an intraoral or intramuscular injection ofthese medications after cleaning and shaping re-duces inflammation and somewhat lowers thelevel of moderate pain .39-43 Flare-ups, however,have not been shown to be prevented by steroids,whether administered intracanal or systemically.44

Previously Vital Pulps with IncompleteDebridement

It is likely that tissue remnants have become in-flamed and are now a major irritant. The workinglength should be rechecked, and the canal(s)

should be carefully cleaned with copious irriga-tion of sodium hypochlorite. A dry cotton pellet is

These cases are best managed with incision anddrainage (see Figure 17-6). In addition, it is mostimportant that the canals have been debrided. Ifnot, they should be opened and debrided, med-icated with calcium hydroxide paste, and closed.Then incision and drainage with placement of adrain are completed.

Follow-up Care

With flare-ups, the patient should be contacteddaily until the symptoms abate. Communicationmay be made by telephone; patients with more se-rious problems or those that are not resolving(many do not and require additional measures)should return to the dentist for treatment as de-scribed above, depending on findings. When symp-toms recur or cannot be controlled, these patientsshould be considered for referral. Ultimate treat-ment by a specialist may include extra measures,such as apical surgery, or even hospitalization.

MEDICATIONS

Intracanal

Both local and systemic medications are part ofthe treatment regimen used for flare-ups. Pheno-lic intracanal medications include formocresol,CMCP, Cresatin, and eugenol. Other medicationsused in canals are steroid combinations and cal-cium hydroxide. None of these has been shown toprevent flare-ups; none helps in relieving flare-upsymptoms."

Systemic

Systemic drugs are usually limited to analgesicsand antibiotics. Nonsteroidal anti-inflammatoryagents are indicated if an analgesic effect is de-sired. Narcotics are useful to provide analgesia andsedation. Combinations of an opioid (codeine,oxycodone, pentazocine, and so on) and a non-


307

steroidal agent are most effective for more severepain. Antibiotics are indicated only if there is a dif-fuse, rapidly spreading cellulitis into the fascialspaces. Localized swelling does not indicate a needfor antibiotic administration; surgical or canaldrainage and complete canal debridement are nec-essary. 25,26 See Chapter 30 for more information ontherapeutics.

Occasionally, but rarely, a flare-up or a present-ing acute apical abscess may be serious or evenlife-threatening (Figure 17-12). These situationsmay require hospitalization and aggressive ther-apy with the cooperation of an oral surgeon.

Postobturation EmergenciesTrue emergencies postobturation are infrequentalthough pain at the mild level is common. There-

FIGURE 17-12Progressively spreading swelling from a flare-up resultingi n an acute apical abscess from a mandibular secondmolar. A, The swelling has extended to the temporal, sub-mandibular, pharyngeal, and sublingual spaces. Thiscondition compromised the patient's airway, requiringhospitalization for aggressive therapy including nasal in-tubation (B) and placement of extraoral drains (C). Thesesevere infections are best managed by an oral surgeon.

308

17 1 Endodontic Emergencies

fore, active intervention is seldom necessary; usu-ally symptoms will resolve spontaneously.

CAUSATIVE FACTORS

Little is known about the etiologic factors involvedin postoperative pain after obturation. Approxi-mately one-third of endodontic patients experi-ence some pain after obturation.45 There is a cor-relation between the level of obturation and painincidence, with overextension associated with thehighest incidence of discomfort. 46 Postobturationpain also relates to preobturation pain; levels ofpain reported after obturation tend to correlate tolevels of pain before the appointment.46.47

TREATMENT

Information about possible discomfort for thefirst few days, reassurance about the availability ofemergency services, and administration of mildanalgesics significantly control the patient's anxi-ety and prevent overreaction. This in turn de-creases the incidence of postobturation frantictelephone calls or "emergency" visits. Some pa-tients, however, do develop serious complicationsand require follow-up treatment.

Retreatment is indicated when prior treatmentobviously has been inadequate. Apical surgery isoften required when an acute apical abscess devel-ops, and there is uncorrectable, inadequate rootcanal treatment. If root canal treatment was ac-ceptable, excision and drainage of swelling afterobturation (an occasional occurrence) should beperformed, usually the swelling resolves withoutfurther treatment. At times the patient reports se-vere pain, but there is no evidence of acute apicalabscess, and the root canal treatment has beenwell done. These patients are treated with reassur-ance and analgesics; again, the symptoms usuallysubside spontaneously.

Patients with postobturation emergencies thatdo not respond to therapy should be referred toan endodontist for other treatment modalities,such as surgery.

REFERENCES

1. Walton R, Fouad A: Endodontic interappointmentflare-ups: a prospective study of incidence and relatedfactors, JEndod 18:172, 1992.

2. Mor C, Rotstein I, Friedman S: Incidence of interap-pointment emergency associated with endodontictherapy, JEndod 28:509, 1992.

3. Marshall JG, Liesinger AW: Factors associated with en-dodontic posttreatment pain, JEndod 19:573, 1993.

4. Albashaireh Z, Alnegrish A: Postobturation pain aftersingle- and multiple-visit endodontic therapy. Aprospective study, J Dent 26:227, 1998.

5. Torabinejad M, Kettering JD, McGraw C, et al: Factorsassociated with endodontic interappointment emergen-cies of teeth with necrotic pulps, JEndod 14:261, 1988.

6. Imura N, Zuolo ML: Factors associated with endodonticflare-ups: a prospective study, Int Endod j 28:261, 1995.

7. Kakehashi S, Stanley H, Fitzgerald R: The effect of sur-gical exposure of dental pulps in germ-free and con-ventional laboratory rats, Oral Surg Oral Med Oral Pathol20:340, 1965.

8. Miller AJ, Fabricius L, Dahlen G, et al: Influence onperiapical tissues of indigenous oral bacteria andnecrotic pulp tissue in monkeys, Scand J Dent Res89:475, 1981.

9. Griffee MG, Patterson SS, Miller CH, et al: The rela-tionship of bacteroides melaninogenicus to symptomsassociated with pulpal necrosis, Oral Surg Oral Med OralPatho150:457, 1986.

10. Van Winkelhoff AJ, Carlee AW, Graaff DE: Bacteroides en-dodontalis and other black-pigmented bacteroides speciesin odontogenic abscesses, Infect Immunol 49:494, 1985.

11. Hashioka K, Suzuki K, Yoshida T, et al: Relationshipbetween clinical symptoms and enzyme-producingbacteria isolated from infected root canals, J Endod20:75, 1994.

12. Torabinejad M, Cotti E, Jung T: Concentrations ofleukotriene B, in symptomatic and asymptomatic pe-riapical lesions, JEndod 18:205, 1992.

13. Weyman BJ: Psychological components of pain per-ception, Dent Clin North Am 22:101, 1978.

14. Torabinejad M, Walton RE: Managing endodonticemergencies, J Am Dent Assoc 122:102, 1991.

15. Torabinejad M, Eby WC, Naidorf IJ: Inflammatory andi mmunological aspects of the pathogenesis of humanperiapical lesions, JEndod 11:479, 1985.

16. Torabinejad M: Mediators of acute and chronic peri-radicular lesions, Oral Surg Oral Med Oral Pathol 78:511, 1994.

17. Walton RE: The periodontal ligament injection as aprimary technique, JEndod 16:62, 1990.

18. Nusstein J, Reader A, Nist R, et al: Anesthetic efficacyof the supplemental intraosseous injection of 2% lido-caine with 1:100,000 epinephrine in irreversible pulpi-tis,JEndod 24:487, 1998.

19. Hasselgren G, Reit C: Emergency pulpotomy: pain re-lieving effect with and without the use of sedativedressings, JEndod 15:254, 1989.

20. Oguntebi B, De Schepper E, Taylor T, et al: Postopera-tive pain incidence related to the type of emergencytreatment of symptomatic pulpitis, Oral Surg Oral MedOral Pathol 73:179, 1992.

21. Rosenberg P, Babick P, Schertzer L, Leung A: The effectof occlusal reduction on pain after endodontic instru-mentation,JEndod 24:492, 1998.

22. Moos HL, Bramwell JD, Roahen JO: A comparison ofpulpectomy alone versus pulpectomy with trephina-tion for the relief of pain, JEndod 22:422, 1996.

23. Nist E, Reader A, Beck M: Effect of apical trephinationon postoperative pain and swelling in symptomaticnecrotic teeth, JEndod 27:415, 2001.

COLOR FIGURE 17-1Management of acute apical abscess. Patientdemonstrates extraoral swelling of upper lip (A)and intraoral swelling of vestibule (B). C, Theincisor has a history of trauma with inadequateroot canal treatment. The diagnosis is necroticpulp/acute apical abscess. D, Blocking the ante-rior superior nerve by infiltrating over the infra-orbital foramen aids in anesthesia. Gutta percharemoval (E) and partial debridement (F), resultedi n drainage from the abscess.

continued

COLOR FIGURE 17-1, CONT'DI ncision of the soft tissue swelling (G) released serosanguinous, purulent exudation (H). A self-retentive "ChristmasTree" rubber dam drain is cut (I), rolled and placed with cotton pliers (J), and inserted in the incision (K). The drainmay be removed in 1 to 2 days by the patient or by the dentist. This removal of necrotic debris and drainage ofpurulence usually results in rapid resolution.


309

24. Barnett EM, Jacobsen G, Evans G, et al: Herpes simplex

encephalitis in the temporal cortex and limbic system

after trigeminal nerve inoculation, J Infect Dis 169:

782, 1994.

25. Fouad A, Rivera E, Walton R: Penicillin as a supple-

ment in resolving localized acute apical abscess, Oral


26. Henry M, Reader A, Beck M: Effect of penicillin on

postoperative endodontic pain and swelling in symp-

tomatic necrotic teeth, JEndod 27:117, 2001.

27. Prescription for the future: Responsible use of antibi-

otics in endodontics, Am Assoc Endod Newslett,Spring/Summer, Pl, 1999.

28. Pallasch TJ: Antibiotics: myths and reality, Calif DentAssoc J 14:40, 1986.

29. Peterson L: Principles of management and prevention

of odontogenic infections. In Peterson L, editor: Con-temporary oral and maxillofacial surgery, ed 3, St Louis,

1998, Mosby.

30. Touyz LZG, Marchand S: The influence of postoperative

telephone calls on pain perception: a study of 118 peri-

odontal surgical procedures, J Orofac Pain 12:219, 1998.31. Morse DR: Infection-related mental and inferior alve-

olar nerve paresthesia: literature review and presenta-

tion of two cases, JEndod 23:457,1997.32. Barnett F, Tronstad L: The incidence of flare-ups fol-

lowing endodontic treatment, J Dent Res 68 (specialissue):1253, 1989.

33. Trope M: Flare-up rate of single-visit endodontics, Int

Endodj 24:24, 1991.

34. Mara E, Koren LZ, Morse DR, Sinai IH: Prophylactic

use of penicillin V in teeth with necrotic pulps and

asymptomatic periapical radiolucencies, Oral Surg Oral


35. Kvist T, Reit C: Postoperative discomfort associated

with surgical and nonsurgical endodontic retreat-

ment, Endod Dent Traumatol 16:71, 2000.

36. Torabinejad M, Cymberman JJ, Frankson M, et al: The

effectiveness of various medications on postoperative

pain following complete instrumentation, J Endod20:345, 1994.

37. Walton RE, Chiappenelli J: Prophylactic penicillin: ef-

fect on posttreatment symptoms following root canal

treatment of asymptomatic periapical pathosis, J

Endod 19:466, 1993.

38. Pickenpaugh L, Reader A, Beck M, et al: Effect of pro-

phylactic amoxicillin on endodontic flare-up in

asymptomatic, necrotic teeth, JEndod 27:53, 2001.

39. Calderon A: Prevention of apical periodontal ligament

pain: a preliminary report of 100 vital pulp cases, JEndod 19:247, 1993.

40. Liesinger A, Marshall JF, Marshall GJ: Effect of variable

doses of dexamethasone on postoperative endodontic

pain, J Endod 19:35, 1993.

41. Nobuhara WK, Carries DL, Gilles JA: Anti-inflammatory

effects of dexamethasone on periapical tissues following

endodontic overinstrumentation,JEndod 19:501, 1993.

42. Marshall G, Walton RE: The effect of intramuscular

injection of steroid on posttreatment endodontic

pain, J Endod 10:584, 1984.

43. Krasner P, Jackson E: Management of posttreatment

endodontic pain with oral dexamethasone: a double-

blind study, Oral SurgOral Med Oral Pathol62:187, 1986.44. Trope M: Relationship of intracanal medicaments to

endodontic flare-ups, Endod Dent Traumatol 6:226,1990.

45. Seltzer S: Pain. In Endodontology: biologic considerations inendodontic procedures, ed 2, Philadelphia, 1988, Lea &

Febiger.

46. Harrison JW, Baumgartner JC, Svec TA: Incidence of

pain associated with clinical factors during and after

root canal therapy. Part 2. Postobturation pain, J

Endod 9:434, 1983.

47. Torabinejad M, Dorn SO, Eleazer PD, et al: The effec-

tiveness of various medications on postoperative pain

following root canal obturation, J Endod 20:427, 1994.


LEARNING OBJECTIVES


1 / Recognize procedural accidents and describe the cause(s), prevention, and treatment of the following:

a. Pulp chamber perforation

b. Ledging

c. Separated instrument

d. Coronal or radicular perforation

e. Obturation short of prepared working length

f. Obturation materials expressed beyond apex

g. Incomplete obturation

h. Vertical root fracture

i.

Post space preparation mishaps

j.

Dental materials or dentin shavings obstructing the canal

310

Perforations During Access Preparation

Causes

Prevention

Recognition and Treatment

Prognosis

Accidents During Cleaning and Shaping

Ledge Formation

Creating an Artificial Canal

Root Perforations

Separated Instruments

Other Accidents

Accidents During Obturation

Underfilling

Overfilling

Vertical Root Fracture

Accidents During Post Space Preparation

I ndicators

Treatment and Prognosis

18 / Procedural Accidents

31 1

i ke other complex disciplines ofdentistry, an operator may encounterunwanted or unforeseen circumstances

during root canal therapy that can affect theprognosis. These mishaps are collectively termedprocedural accidents. However, fear of proceduralaccident should not deter a practitioner from per-forming endodontic therapy if proper case selec-tion and competency issues are observed.

Knowledge of the etiologic factors involved inprocedural accidents is essential for their preven-tion. In addition, methods of recognition andtreatment as well as the effects of such accidentson prognosis must be learned. Most problems canbe avoided by adhering to the basic principles ofdiagnosis, case selection, treatment planning, ac-cess preparation, cleaning and shaping, obtura-tion, and postpreparation.

Examples of procedural accidents includeswallowed or aspirated endodontic instruments,crown or root perforation, ledge formation, sepa-rated instruments, underfilled or overfilledcanals, and vertically fractured roots. A good prac-titioner uses his or her knowledge, dexterity, intu-ition, patience, and awareness of his or her ownlimitations to minimize these accidents. When anaccident occurs during root canal treatment, thepatient should be informed about (1) the inci-dent, (2) procedures necessary for correction, (3)alternative treatment modalities, and (4) the ef-fect of this accident on prognosis. Proper medical-legal documentation is mandatory. A successfuloperator learns from past experiences and appliesthem to future challenges. In addition, the practi-tioner who knows his or her limitations will rec-ognize potentially difficult cases and will refer thepatient to an endodontist. The beneficiary will bethe patient, who will receive the best care.

This chapter will discuss the causes, preven-tion, and treatment of various types of proce-dural accidents that may occur at differentphases of root canal treatment. The effect ofthese accidents on short-and long-term progno-sis will be also described.

Perforations During AccessPreparationThe prime objective of an access cavity is to pro-vide an unobstructed or straight-line pathway tothe apical foramen. Accidents such as excess re-moval of tooth structure or perforation may occurduring attempts to locate canals. Failure to achievestraight-line access is often the main etiologic fac-tor for other types of intracanal accidents.

312


CAUSES

Despite anatomic variations in the configurationof various teeth, the pulp chamber, in most cases,is located in the center of the anatomic crown.The pulp system is located in the long axis of thetooth. Lack of attention to the degree of axial in-clination of a tooth in relation to adjacent teethand to alveolar bone may result in either gougingor perforation of the crown or the root at variouslevels (Figure 18-1). Failure to direct the bur parallelto the long axis of a tooth will cause gouging or perfora-tion (see Chapter 12). This problem often occurswhen the dentist must use the reflected imagefrom an intraoral mirror to make the accesspreparation. In these situations, the natural ten-dency is to direct the bur away from the long axisof the root to improve vision through the mirror.Failure to check the orientation of the accessopening during preparation may result in a per-foration. The dentist should stop periodically toreview the bur-tooth relationship. Aids for evalu-

ating progress include transillumination, magni-fication, and radiographs.

Searching for the pulp chamber or orifices ofcanals through an underprepared access cavitymay also result in accidents (Figure 18-2). Failingto recognize when the bur passes through a smallor flattened (disklike) pulp chamber in a multi-rooted tooth may also result in gouging or perfo-ration of the furcation (Figure 18-3).

A cast crown often is not aligned in the longaxis of the tooth; directing the bur along the mis-aligned casting may result in a coronal or radicu-lar perforation.

PREVENTION

Clinical Examination

Thorough knowledge of tooth morphology, in-cluding both surface anatomy and internalanatomy and their relationships, is mandatory toprevent pulp chamber perforations. Next, loca-

FIGURE 18-1A misdirected bur created severe gouging and near-perforationduring an otherwise routine access cavity preparation.

FIGURE 18-2I nadequate access cavities not only result in compromisedpreparation and obturation but also may cause proceduralaccidents such as chamber perforation, canal ledging, androot perforation.


31 3

tion and angulation of the tooth must be relatedto adjacent teeth and alveolar bone to avoid a mis-aligned access preparation. In addition, radio-graphs of teeth from different angles provide in-formation about the size and extent of the pulpchamber and the presence of internal changessuch as calcification or resorption. The radiograpb isa two-dimensional projection of a three-dimensional ob-ject; varying the horizontal exposure angle willprovide at least a distorted view of the third di-mension and may be helpful in supplying addi-tional anatomic information.

Operative Procedures

Use of a rubber dam during root canal treat-ment is usually indicated.' However, in situa-tions in which problems are anticipated in lo-cating pulp chambers (e.g., tilted teeth,misoriented castings, or calcified chambers),initiating access without a rubber dam is pre-

ferred2 because it allows better crown-root align-ment (see Chapter 12). However, when access ismade without rubber dam placement, no intra-canal instruments such as files, reamers, orbroaches should be used unless they are securedby a piece of floss' and a throat pack is placed.Constricted chambers or canals must be sought

patiently, with small amounts of dentin re-moved at a time.

Another useful method of providing isolationand also visualizing the crown-root alignment isthe use of a "split" dam (Figure 18-4). This damcan be applied in the anterior region without arubber dam clamp (see Chapter 8) or in posteriorregions by quadrant isolation if a distal tooth canbe clamped. Also, elimination of the metal clampfrom the field of operation allows radiographicorientation of coronal access preparation.

To orient the access, a bur may be placed in thepreparation hole (secured with cotton pellets) andthen radiographed (Figure 18-5). This provides in-formation about depth of access in relation tocanal location. Remember, a single canal is lo-cated in the center of the root. A direct facialradiograph will show the mesiodistal relation-ship; a mesial or distal angled film will show thefaciolingual location. This procedure is helpfulfor locating small canals.

Use of a fiberoptic light during access prepa-ration may assist in locating canals. This stronglight illuminates the cavity when the beam is di-rected through the access opening (reflectedlight) and illuminates the pulp chamber floor(transmitted light). In the latter case, a canal ori-fice appears as a dark spot. Using magnifyingglasses or ar. operative microscope will also aidin locating a small orifice. Magnification loops(2.5 or greater) are useful especially when com-bined with transillumination. But the ultimateaid in canal location is the operating micro-scope. patients with problems requiring signifi-cant magnification for canal location should bereferred to an endodontist who has this special-ized equipment.

FIGURE 18-aFailure to recognize when the bur passes through the roof ofthe pulp chamber if the chamber is calcified may result in goug-ing or perforation of the furcation. The use of apex locators andangled radiographs is necessary for early perforation detection.Early detection reduces damage and improves repair.

FIGURE 18-4A rubber dam can be applied in the anterior region withoutplacing the clamp on the tooth that is undergoing root canaltherapy or in posterior regions by quadrant isolation if a dis-tal tooth can be clamped.

31 4


FIGURE 18-5

A small bur is placed during access preparation when orien-tation is a problem. This provides information about data suchas angulation and depth of bur penetration. Continuation ofthe search without a radiograph to check position wouldprobably have resulted in a perforation into the furcation.

RECOGNITION AND TREATMENT

Perforation into the periodontal ligament or boneusually (but not always) results in immediate andcontinuous hemorrhage. The canal or chamber isdifficult to dry; placement of a paper point or cot-ton pellet may increase or renew the bleeding.Bone is relatively avascular compared with softtissue; mechanical perforation may occasionallyinitially produce only hemorrhage equal to that ofpulp tissue.

Perforations must be recognized early to avoidsubsequent damage to the periodontal tissueswith intracanal instruments and irrigants. Earlysigns of perforation may include one or more ofthe following: (1) sudden pain during the workinglength determination when local anesthesia wasadequate during access preparation; (2) suddenappearance of hemorrhage; (3) burning pain or abad taste during irrigation with sodium hypochlo-rite; (4) other signs, including a radiographicallymalpositioned file (see Figure 18-3) or a periodon-tal ligament reading from an apex locator that isfar short of the working length on an initial fileentry.

Unusually severe postoperative pain may resultfrom cleaning and shaping procedures performedthrough an undetected perforation. At a subse-quent appointment, the perforation site will behemorrhagic due to the inflammation of the sur-rounding tissues. The overall prognosis of thetooth must be evaluated with respect to thestrategic value of the tooth, the location and sizeof the defect, and the potential for repair.

Perforation into the periodontal ligament atany location will have a negative effect on long-term prognosis. The dentist must inform the pa-tient of the questionable prognosis' and closelymonitor the long-term periodontal response toany treatment. In addition, the patient mustknow what signs or symptoms indicate failureand, if failure occurs, what the subsequent treat-ment will be.

Perforations during access cavity preparationpresent a variety of problems. When a perforationoccurs or is strongly suspected, the patient shouldbe considered for referral to an endodontist. Ingeneral, a specialist is better equipped to managethese patients. Also, after long-term evaluation,other procedures such as surgery may be neces-sary if future failure occurs (Figure 18-6).

Lateral Root Perforation

The location and size of the perforation duringaccess are important factors in a lateral perfora-tion. If the defect is located at or above the heightof crestal bone, the prognosis for perforation re-pair is favorable.3,4 These defects can be easily "ex-teriorized" and repaired with standard restorativematerial such as amalgam, glass ionomer, or com-posite. Periodontal curettage or a flap procedureis occasionally required to place, remove, orsmooth excess repair material. In some cases, thebest repair is placement of a full crown with themargin extended apically to cover the defect.

Teeth with perforations below the crestal bonein the coronal third of the root generally have thepoorest prognosis. Attachment often recedes anda periodontal pocket forms, with attachment lossextending apically to at least the depth of the de-fect. The treatment goal is to position the apicalportion of the defect above crestal bone. Ortho-dontic root extrusion is generally the procedure ofchoice for teeth in the aesthetic zone.5,6 Crownlengthening may be considered when the aes-thetic result will not be compromised or when ap-proximal teeth require surgical periodontal ther-apy. Internal repair of these perforations bymineral trioxide aggregate (MTA) has been shownto provide an excellent seal as compared to othermaterials.'

Furcation Perforation

A perforation of the furcation is generally one oftwo types: the "direct" or the "stripping" type;each is created and managed differently and theprognoses vary. The direct perforation usually oc-curs during a search for a canal orifice. It is moreof a "punched-out" defect into the furcation with


315

FIGURE 18-6A, A search for the mesiobuccal canal in a partially calci-fied chamber resulted in a furcation perforation and ex-trusion of filling materials into the periapical tissues. Anapex locator reading or an angled radiograph would havedetected this type of error. B, The initial treatment was re-done and the perforation was sealed with MTA. C, Aradiograph 3 years later shows no evidence of pathosis in

the repaired area. (Courtesy Dr. George Bogen.)

a bur; therefore, it is usually accessible and may besmall and have walls. This type of perforationshould be immediately (if possible) repaired withMTA (Figure 18-7), or, if proper conditions exist(dryness), glass ionomer or composite, in an at-tempt to seal the defect. Prognosis is usually goodif the defect is sealed immediately.

A stripping perforation involving the furcationside of the coronal root surface results from ex-cessive flaring with files or drills. Whereas direct

perforations are usually accessible and thereforecan be repaired nonsurgically, stripping perfora-tions are generally inaccessible, requiring moreelaborate approaches. The usual sequelae of strip-ping perforations are inflammation followed bydevelopment of a periodontal pocket. Long-termfailure results from leakage of the repair material,which produces periodontal breakdown with at-tachment loss. Skillful use of MTA has signifi-cantly improved the prognosis of nonsurgical

316


FIGURE 78-7Immediate repair of perforation in furcation of a dog premo-lar with MTA results in formation of cementum (arrow) adja-cent to the material.

repair of stripping perforations compared toother repair materials (Figure 18-8).

Nonsurgical Treatment

If feasible, nonsurgical repair of furcation perfo-rations is preferred to surgical alteration of thetooth' (Figure 18-9). Traditionally, materials suchas amalgam, gutta-percha, zinc oxide-eugenol,Cavit, calcium hydroxide, freeze-dried bone, andindium foil have been used clinically and experi-mentally to seal these defects."' Repair is difficultbecause of potential problems with visibility, hem-orrhage control, and management and sealingability of the repair materials. In general, perfora-tions occurring during access preparation shouldbe sealed immediately, but the patency of the

FIGURE 18-8A, A stripping perforation (arrow) is evident in themesiobuccal root. B, The mesial roots were filledwith MTA and the distal root with gutta-percha androot canal sealer. C, A radiograph made 1 year latershows no periradicular pathosis.


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canals must be protected. Immediate repair of theperforations with MTA offers the best results forperforation repair."

Surgical Treatment

Surgery requires more complex restorative proce-dures and more demanding oral hygiene fromthe patient.' Surgical alternatives are hemisec-tion, bicuspidization, root amputation, and in-tentional replantation. Teeth with divergentroots and bone levels that allow preparation ofadequate crown margins are suitable for either

hemisection or bicuspidization. Intentional re-plantation is indicated when the defect is inac-cessible or when multiple problems exist, such asa perforation combined with a separated instru-ment, or when the prognosis with other surgicalprocedures is poor (Figure 18-10). Dentist andpatient must recognize that the prognosis fortreatment of surgically altered teeth is guardedbecause of the increased technical difficulty asso-ciated with restorative procedures and demand-ing oral hygiene requirements. The remainingroots are prone to caries, periodontal disease, andvertical root fracture.

FIGURE 18-9A, Furcation perforation is evident in the first molar.

B, The root canal was retreated and the perforation wasrepaired with MTA. C, A radiograph made 26 months later

shows no evidence of furcal pathosis.

31 8


FIGURE 18-10A, A postoperative radiograph 6 years after endodontictreatment. The tooth is percussion sensitive, and periapi-cal lesions are present. A 5-mm probing defect exists onthe distolingual root. A fracture is suspected and extract-replant was performed for diagnostic reasons. The toothwas extracted, and no fracture was seen. B, The tooth isreplanted after a root-end filling with MTA. The cause offailure was probably leakage. C, A radiograph 1 year latershowed osseous repair. The probing defect healed.

PROGNOSIS

Factors affecting the long-term prognosis of teethafter perforation repair include the location of thedefect in relation to crestal bone, the length of theroot trunk, the accessibility for repair, the size of

the defect, the presence or absence of a periodon-tal communication to the defect, the time lapsebetween perforation and repair, the sealing abilityof restorative material, and subjective factors suchas the technical competence of the dentist and the

1 8 I Procedural Accidents

31 9

attitude and oral hygiene of the patient.' Earlyrecognition and repair will improve the prognosisby minimizing damage to the periodontal tissuesby bacteria, files, and irrigants. Additionally, asmall perforation (less than 1 mm) causes less tis-sue destruction and is more amenable to repairthan a larger perforation. Electronic apex locatorsor angled radiographs with files in place aid inearly detection.

An unrecognized or untreated perforation inthe furcation usually results in a periodontal defectthat communicates through the gingival sulcuswithin weeks or sometimes days. A preexistingperiodontal communication caused by perforationworsens the prognosis; therefore, the time betweenperforation and repair should be as short as possi-ble.18,19 Immediate sealing of the defect reduces theincidence of periodontal breakdown. To best deter-mine the long-term prognosis, the dentist mustmonitor the patient's symptoms, radiographicchanges, and, most importantly, periodontal sta-tus. Radiographs and periodontal probing duringrecall examination are the best measures of successor failure of the repair procedure.

Accidents During Cleaningand ShapingThe most common procedural accidents duringcleaning and shaping of the root canal system areledge formation, artificial canal creation, root per-foration, instrument separation, and extrusion ofirrigating solution periapically. Correction ofthese accidents is usually difficult and the patientshould be referred to an endodontist.

LEDGE FORMATION

By definition, a ledge has been created when theworking length can no longer be negotiated andthe original patency of the canal is lost. The majorcauses of ledge formation include (1) inadequatestraight-line access into the canal (2) inadequateirrigation and/or lubrication, (3) excessive en-largement of a curved canal with files, and (4)packing debris in the apical portion of the canal.

Prevention of a Ledge

Preoperative Evaluation. Prevention of ledgingbegins with examination of the preoperativeradiograph for curvatures, length, and initial size.

Curvatures. Most important is the coronalthird of the root canal. Severe coronal curvaturepredisposes the apical canal to ledging. Straight-line access to the orifice of the canal can be

achieved during access preparation, but accessi-bility to the apical third of the canal is achievedonly with coronal flaring. Severe apical curvaturesrequire a proper sequence of cleaning and shapingprocedures to maintain patency (see Chapter 13).

Length. Longer canals are more prone to ledg-ing than shorter canals. Careful attention to main-taining patency is required to prevent ledging.

I nitial Size. Canals of smaller diameter are moreeasily ledged than larger-diameter canals.

In summary, the canals most prone to ledging aresmall, curved, and long. Radiographs are two-dimen-sional and cannot provide accurate informationabout the actual shape and curvature of the rootcanal system. All root canals have some degree ofcurvature including facial-lingual curves, whichmay not be apparent on straight facial exposures.

Technical Procedures. Determination of workinglength in the cleaning and shaping process is acontinuation of the access preparation. Optimumstraight-line access to the apical third is notachieved until cleaning and shaping have beencompleted. An accurate working length measure-ment is a requirement because cleaning and shap-ing short of the ideal length is a prelude to ledgeformation. Frequent recapitulation and irriga-tion, along with the use of lubricants, are manda-tory! Sodium hypochlorite may be used initiallyfor hemorrhage control and removal of debris.However, this agent alone may not be adequate toprovide maximum lubrication.

Silicone, glycerine, and wax-based lubricants arecommercially available for canal lubrication. Be-cause these materials are viscous, they are carriedinto the apical regions of the canal with the file. En-hanced lubrication permits easier file insertion, re-duces stress to the file, and assists with removal ofdebris. The lubricant is easily removed with so-dium hypochlorite irrigation. Flexible files (nickel-titanium) reduce the chances for ledge formation.

A one-eighth to one-fourth reaming motionwith the files should be used in the apical third. Afiling motion directed away from the furcation isused to form the funnel shape of the canal and re-duce the coronal curvature. Each file must beworked until it is loose before a larger size is used.

Canals with a severe coronal curvature requirea passive step-back cleaning and shaping tech-nique (see Chapter 13). A No. 15 file is used atworking length. With maximum irrigation or lu-brication, the canal is passively and progressivelyflared in a step-back fashion. The No. 15 file is re-capitulated many times to maintain patency. Thispreflaring technique reduces the coronal curva-ture and enlarges the canal. Better control of thefiles is gained for enlarging and cleaning the api-cal third of the canal as the last step (see "Apical

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Clearing" in Chapter 13). Using this technique,the chances of ledge formation are reduced. Ro-tary files with increased taper will blend and jointhe shape into a tapering funnel.

Management of a Ledge

Once created, a ledge is difficult to correct. An ini-tial attempt should be made to bypass the ledgewith a No. 10 steel file to regain working length.The file tip (2 to 3 mm) is sharply curved andworked in the canal in the direction of the canalcurvature. Lubricants are helpful. A "picking" mo-tion is used to attempt to feel the catch of the orig-inal canal space, which is slightly short of the api-cal extent of the ledge. If the original canal islocated, the file is then worked with a reaming mo-tion and occasionally an up-and-down movementto maintain the space and remove debris (Fig-ure 18-11), although this may be only partiallysuccessful. Once a ledge is created, even if it is ini-tially bypassed, instruments and obturating mate-rials tend to be continually directed into the ledge.

If the original canal cannot be located by thismethod, then cleaning and shaping of the exist-ing canal space is completed at the new workinglength. At times, flaring of the canal may allow theledge to be bypassed by providing improved ac-cess to the apical canal. Small, curved files areused in the manner previously described in a finalattempt to bypass the ledge. If this is successful,the apical canal space must be sequentiallycleaned and flared to an appropriate size. Com-plete removal or reduction of the ledge facilitatesobturation.

Prognosis

Failure of root canal treatment associated withledging depends on the amount of debris left inthe uninstrumented and unfilled portion of thecanal. The amount depends on when ledge for-mation occurred during the cleaning and shapingprocess. In general, short and cleaned apicalledges have good prognoses. The patient must beinformed about the prognosis, the importance ofthe recall examination, and what signs indicatefailure. Future appearance of clinical symptomsor radiographic evidence of failure may require re-ferral for apical surgery or rerreatment.

CREATING AN ARTIFICIAL CANALCause and Prevention

Deviation from the original pathway of the rootcanal system and creation of an artificial canalcause an exaggerated ledge; it is initiated by thefactors that cause ledge formation. Therefore, the

recommendations for preventing ledge formationshould be followed to avoid creating artificialcanals. The unfortunate sequence is as follows: Aledge is created and the proper working length islost. The operator, eager to regain that length,"bores" apically with each file, thus creating an ar-tificial canal. Used persistently, the file eventuallyperforates the root surface.

Management

Negotiating the original canal that has an exag-gerated ledge is normally very difficult. Rarely canthe original canal be located, renegotiated, andprepared. To obturate, the dentist should deter-mine whether a perforation exists. Methods in-clude apex locator readings, hemorrhage on paperpoints while drying, and radiographs with a file inposition. If confirmed, the working length is ad-justed, an apical stop is created at the adjustedlength with larger files, and obturation is begun.If there is no perforation, the canal is obturatedwith a warm or softened gutta-percha techniquein conjunction with a root canal sealer. If there isa perforation, the defect should be repaired inter-nally or surgically (see "Root Perforations" below).

Prognosis

Prognosis depends on the ability of the operator torenegotiate the original canal and the remainingamount of uninstrumented and unfilled portionof the main canal. Unless a perforation exists, teethin which the original canal can be renegotiated andobturated have a prognosis similar to those with-out procedure complications. In contrast, when alarge portion of the main canal is uninstrumentedand unobturated, a poorer prognosis exists, andthe tooth must be examined periodically. Failureusually means surgery will be required to resect theuninstrumented and unobturated root canal.

ROOT PERFORATIONS

Roots may be perforated at different levels duringcleaning and shaping. Location (apical, middle, orcervical) of the perforation as well as the stage oftreatment affects prognosis." The periodontal re-sponse to the injury is affected by the level andsize of the perforation. Perforation in the earlystages of cleaning and shaping affects prognosissignificantly.

Apical Perforations

This type of perforation occurs through the apicalforamen (overinstrumentation) or through thebody of the root (perforated new canal).

Evaluation of Success and Failure

LEARNING OBJECTIVES


1 / Describe a successful root canal treatment.

z / Describe an unsuccessful root canal treatment.

a / Describe the most common modalities used to determine success or failure.

4 / State the approximate range of expected outcomes of routine, uncomplicated root canal treatment based

on pretreatment conditions.

s / Describe the factors that influence the outcome of treatment.

6 / Describe how to explain the prognosis to the patient.

7 / Evaluate and estimate prognosis before, during, and after treatment.

s / Describe the importance of recall appointments.

s / Recognize signs of unsuccessful root canal treatment.

10 / Identify causes, both endodontic and nonendodontic, that may lead to failure of treatment.

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19 1 Evaluation of Success and Failure

What Is Success?

Prognosis

Success Rates

When to Prognosticate

How to Prognosticate

Variability of Treatment Results

Factors Influencing Success and Failure

When to Evaluate

Methods of Evaluation


Radiographic Findings

Histologic Examination

Causes of Endodontic Failures

Preoperative Causes

Operative Causes

Postoperative Factors

Retreatment of Failures

What is Success?

With a vital pulp, success means that the rootcanal treatment prevents bacteria from enteringthe canal system; thereby, the treatment preventsa periradicular lesion from forming. With anecrotic pulp, the treatment is considered suc-cessful if it eliminates or significantly reduces bac-teria in the root canal system so that an associatedperiradicular lesion heals.

Unfortunately, not all root canal treatmentsare successful. Recognition, acceptance, and man-agement of treatments that do not resolve andheal can be difficult and often involve a complexset of factors. Historically the popular belief hasbeen that the success rate for root canal treatmentis between SO% and 95%. However general per-centages should be taken with caution; rather,each case should be individually assessed to determine thepercentage probability of success. Several variables af-fect the outcome of a root canal treatment,' manyof which will be discussed later in this chapter.Importantly, the clinician should attempt to pre-dict the outcome of each treatment based on theexisting situation and current knowledge andthen inform the patient about the expected out-come. The status and prediction should be as-sessed before and immediately after the treat-ment, and then at reasonable intervals. Theimportance of communication, both dentist topatient and patient to dentist, is discussed inmore detail in Chapter 6.

Prognosis

Prognosis is a key word. This refers to the predic-tion of whether an endodontic treatment will pre-vent the development of apical periodontitis orheal it if present. But how are success and failuredefined? Interpretation of success varies with theindividual practitioner. One dentist's criterion forsuccess may be if the treatment lasts long enoughfor the patient to pay the bill! And the criterionfor failure may be that the patient contacts thedentist complaining of severe symptoms. At theother extreme may be the unreasonably rigorousrequirement that no inflammatory cells are pres-ent in the periradicular tissues subsequent totreatment. Realistic criteria are somewhere be-tween these two and obviously more toward thelatter than the former. It is important to remem-ber that apical periodontitis, which is often aprinciple indication of a failing endodontic treat-ment, is frequently asymptomatic; the radiographis the only way to demonstrate the lesion.'

SUCCESS RATES

What is the anticipated outcome of root canaltreatment? Studies vary, with reported successrates ranging from a high of 95% to a low of53%.''3' ' There are some known factors that ac-count for at least some of these differences.

Studies on prognosis have analyzed the ef-fects of various factors in relation to success andfailure.5-8 These numerous variables can makeinterpretation and comparison of prognosisstudy results difficult. These difficulties includeobserver bias (with varying criteria for success),bias in interpreting radiographs, varying levelsof patient compliance (recall) subjectivity ofpatient response, host variability in respondingto treatment, relative validity and reproducibil-ity of the method of evaluation, degree of con-trol of variables such as sample size, and differ-ences in observation periods. However some ofthose studies have clearly shown a significant ef-fect of some factors on the ultimate outcome oftreatment.

Clearly a very significant factor is the presenceof a periradicular lesion associated with thetooth before treatment"' The significance ofbacteria in causing and maintaining a periradic-ular lesion was shown in a classic study by Kake-hashi et al.9 They demonstrated that only rootcanal systems infected with bacteria would de-velop periradicular lesions. If there is a periradic-ular lesion before treatment the prognosis forsuccess is reduced by 10% to 20%.'"" Elimina-tion or at a least significant reduction in thenumber of bacteria seems to produce resultssimilar to those expected when noninfectedcanals are treated."

At least two other factors are important in theultimate outcome of the treatment. Those fac-tors are the technical quality of the root canalfilling itself and, more importantly, the effective-ness of the coronal seal. ' 3 With a poor coronalseal most treatments probably will eventuallyfail irrespective of the periradicular status of thetooth before treatment or the quality of debride-ment and obturation.

The advantages of understanding the progno-sis for root canal treatment procedures includedevelopment of more rational treatment meth-ods, avoidance of factors that result in a higher in-cidence of failure, and a better understanding ofthe healing process. To reemphasize and to re-peat: generalizations in predicting success andfailure are inappropriate when assessing an indi-vidual situation; prognosis for each clinical casemust be based on the findings and treatment fac-tors relevant to that case.

19 1 Evaluation of Success and Failure

333

WHEN TO PROGNOSTICATE

Determining or attempting to predict outcomeshould be done at three times: before, during, andafter treatment. The prognosis often changes atthese intervals, depending on what occurs or whatis discovered during or after treatment. Thus,what may have been a favorable prognosis at thebeginning may change to a poorer or less favor-able prognosis at the conclusion of the procedure.

HOW TO PROGNOSTICATE

Patients must always be informed about the pos-sibility of failure. The outcome prediction(whether made before, during, or after treatment)may be explained in one of two ways. One ap-proach is to generalize about whether the antici-pated outcome is favorable, questionable, or unfa-vorable. A second approach is to make aprediction using percentages; patients usuallyeasily understand this. However, predicting usingpercentages is somewhat difficult for the dentist,because there are several variables that can affectthe ultimate outcome, especially when prognosti-cating is done before the treatment. By using per-centage estimation (particularly if the prognosisis not excellent) patients might have better graspof the status of their tooth and then participate inthe decision about whether to proceed. They needto understand that there is always a possibility ofcomplications during or after treatment. Also, pa-tients can better accept failure if they were in-formed of that possibility before treatment.

Variability of Treatment Results

Explaining the marked differences in the successrates seen in different prognosis studies is not dif-ficult. There are many variables, alone or in combi-nation, that affect the outcome of treatment; someof these variables are easily identified and othersare probably unknown. Thus, no single study hasall the answers, and all studies considered as agroup are, at best, only overall indicators.'

Factors Influencing Successand Failure

An early "classic" comprehensive study performedby Strindberg' related treatment outcomes to bio-logic and therapeutic factors. With time, othervariables have been related to success and failure.Few of these variables have been proven to have aclear effect on the final outcome of the root canal

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19 / Evaluation of Success and Failure

treatment. Others are generalities, and their fulleffects are unknown because of the nature andcomplexity of the problems. Some of the factorsthat consistently impact prognosis are (1) apicalpathosis, (2) bacterial status of the canal, (3) ex-tent and quality of the obturation, and (4) qualityof the coronal restoration.

The presence of bacteria in the canal before ob-turation predicts a poorer prognosis." In relationto extension of the obturation, healing is less pre-dictable if the filling is too short (more than 2 mmfrom the radiographic apex) or too long (exitingthe apex) 6,14,15 More voids or less density of theobturating materials is also related to lower suc-cess rates.' And again and importantly, the qual-i ty of the coronal restoration is more critically re-lated to the final outcome than the quality of theobturation.13

Other variables such as tooth type, age and sexof the patient, technique of obturation, observa-tion period, and type of intracanal medicationhave been shown to have a slight effect (but usu-ally none) on the results.17 Medical (health) statusor age of the patient has no significant bearing onsuccess or failure. 18 No specific systemic disease orcondition has been related to delayed or impairedhealing or seems to precipitate failure. Obviously,a patient who is debilitated or whose condition isseverely compromised medically may be a poorcandidate for root canal treatment.

When to Evaluate

The length of time necessary for adequate post-operative follow-up has been studied. Suggestedfollow-up periods range from 6 months to 4 years;6 months is a reasonable interval for a recall eval-uation for most patients. However, the importantquestion is,. at what point is it unlikely that atreatment outcome will change? In other words,when can it be determined that treatment is suc-cessful or has failed and the outcome is unlikelyto change so that no further recall is necessary?There is good evidence that a radiographic lesionthat is unchanged or has increased in size after1 year is unlikely to ever resolve; therefore, thetreatment is deemed unsuccessful. If at 6 monthsthe lesion is still present but smaller in size, thereis an indication that it might heal but additionalrecall is needed. The larger the per1radicular le-sion before the root canal treatment, the longerthe healing period. Unfortunately, apparent suc-cess may revert to failure at a later time (often as aresult of coronal leakage), so clinical and radio-graphic examination of teeth treated with rootcanals is indicated as a part of routine full-statusevaluation of all dental patients.

Methods of Evaluation

The most accurate determinations of healing ornonhealing are based on signs and symptoms andradiographic and histologic examinations. Obvi-ously, at present only clinical findings and radio-graphic criteria can be readily evaluated by thedentist, current technology precludes histologicexamination without surgical intervention.

CLINICAL EXAMINATION

Signs and/or symptoms, if marked and persistent,are probably indications of disease and of failure.Importantly, absence of pain or other symptomsdoes not confirm success. This is because peri-radicular pathosis without significant symptomsis usually present in teeth before as well as afterroot canal treatment.2 There is little correlationbetween the presence of pathosis and correspond-ing symptoms; yet when signs and/or symptomsare evident there is a strong likelihood that thereis a pathosis.19

Persistence of adverse significant signs (e.g.,swelling or sinus tract) or symptoms (e.g., sponta-neous pain, dull persistent ache, or masticationsensitivity) indicates failure.

RADIOGRAPHIC FINDINGS

According to the findings, the outcome of eachtreatment could be classified as a success, a fail-ure, or a questionable status. To be able to accu-rately compare radiographs made at differenttimes, it is important that they are taken in a re-producible fashion and with minimal distortion.The best way to ensure reproducibility is with par-alleling radiographic devices (see Chapter 9).

Success is the absence of an apical radiolucentlesion. This means that a resorptive lesion presentat the time of treatment has resolved or if therewas no lesion present at the time of treatment,none has developed. Thus, success is evident bythe elimination or nondevelopment of an area ofrarefaction for a minimum of 1 year after treat-ment (Figure 19-1).

Failure is the persistence or development of ra-diographically evident pathosis. Specifically, thisis a radiolucent lesion that has remained thesame, has enlarged, or has developed since treat-ment (Figure 19-2).


335

FIGURE 19-1Success. A, Diagnosis of 20: irreversible pulpitis, normalperiapex. Pretreatment prognosis: favorable. B, Obtura-tion 1 month later. As occasionally occurs, periradicularpathosis has developed during the treatment interval,which involved three appointments in the 1-month pe-riod. Posttreatment prognosis: questionable. C, Six-monthrecall shows resolution and a classification of success. Be-cause the periradicular irritation was neither severe norpersistent and because the primary obturating materialwas contained and condensed within the canal, the slightamount of sealer extruded (arrow) neither resorbed norprevented healing.

FIGURE 79-2

Failure. A, Apparently adequate root canal treatment. Tooth was restored later with a post and core and crown.B, Two-year recall. The patient reports persistent discomfort. Periradicular radiolucency indicates failure, probablydue to coronal leakage at a defective margin (arrow). Surgery was required (root end resection and filling) be-cause of restoration.

336

19 I Evaluation of Success and Failure

FIGURE 19-3Questionable. A, Inadequate canal preparation, poor obturation, and coronal leakage all contributed to failure.The tooth is suitable for conventional retreatment and restoration. B, Twelve-month recall after retreatment. Asinus tract has disappeared, and the patient reports absence of symptoms. The radiolucent lesion is decreasing insize but has not resolved. Because outcome is still questionable, additional recall evaluation is necessary.

Questionable status indicates a state of uncer-tainty. The situation (radiolucent lesion) has nei-ther become larger nor significantly decreased insize. A questionable status is considered to benonhealing if there is no resolution after morethan 1 year (Figure 19-3).

Complete radiographic regeneration of peri-radicular structures does not always occur. Varia-tions in radiographic appearance that are definedas healed are occasionally seen. Large periradicularlesions present before treatment might not com-pletely regenerate normal bony architecture butrather persist as a slightly larger than normal api-cal periodontal ligament space. There may also bean unusual trabecular pattern or lack of completereplacement of the cortical plate adjacent to thetooth, giving the appearance of a persistent lesion.

Fallibilities of radiographic interpretation areadditional complications. Because radiographs areusually the primary evaluative tools, techniques andinterpretation are critical; guidelines must be fol-

lowed carefully. Consistency in film type, exposuretime, cone angulations, film development, and sim-ilar radiograph viewing conditions are important.Inconsistency with follow-up radiographs may leadto false assessments of either success or nonhealing.There could be false-positive or false-negative inter-pretations. For example, an anatomic landmarksuch as a radiolucent or radiopaque structure maybe "pushed" over the apex by a change in cone an-gulation and may then be misinterpreted as a devel-oping lesion. Also, opacity may obscure a develop-ing lesion. Because of these variations, the validityof evaluating treatment outcome solely with radio-graphs is unacceptable; other signs and symptomsare considered as well." Periradicular lesions havebeen "healed" simply by changing radiographictechniques or cone angles. (Figure 19-4).

Personal bias may influence radiographic inter-pretation.'"' Each radiograph must be inter-preted objectively and honestly to determine thedegree of healing.

1 9 / Evaluation of Success and Failure

33 7

FIGURE 19-4A, Panoramic radiograph revealed an apical radiolucency on the premolar. B, Periradicular film taken 1 week latershows no apparent radiolucency associated with the apex. The tooth responded within normal limits. The likelyexplanation of the radiolucency on the panoramic film is superimposition of the mental foramen.

HISTOLOGIC EXAMINATION

Routine histologic evaluation of periradiculartissues after root canal treatment is impracticaland not possible without surgery. 13 If a treatedtooth were to be evaluated histologically, success-ful treatment would be indicated by reconstitu-tion of periradicular structures and an absence ofinflammation.

There is uncertainty about the degree of corre-lation between histologic findings and radio-graphic appearance because of the lack of well-controlled, prospective histologic studies. Twohistologic investigations of teeth treated withroot canals in cadavers reached very different con-clusions . 24,2 s Brynolf4 concluded that almost alltreated teeth showed some periradicular inflam-mation despite the appearance of successful treat-ment on radiographs. In contrast, Green et al . 2 5

observed that most treated teeth that showed anormal periapex radiographically were indeed freeof inflammation histologically. Thus, with cur-

rent technology, clinical findings (signs, symp-toms, and radiographic evaluation) are the onlypractical means of assessing degree of healingafter root canal treatment.

Causes of Endodontic Failures

Most nonhealing (failures) of root canal treat-ments is directly or indirectly caused by bacteriasomewhere in the root canal system. In general,the most common causes of failure are (1) errorsin diagnosis and treatment planning, (2) coronalleakage, (3) lack of knowledge of pulp anatomy, (4)inadequate debridement and/or disinfection ofthe root canal system, (5) inadequate restorativeprotection, (6) operative errors, (7) obturation de-ficiencies or errors, and (8) vertical root fracture.

The various procedures associated with rootcanal treatment can be divided into three phases:preoperative, operative, and postoperative.

338


FIGURE 19-5A, The patient complained of pain in right maxillary teeth when drinking hot liquids. The sensitivity to heat wasconfirmed to be from tooth 3 by rubber dam isolation and then bathing it with hot water. B, The tooth was care-fully accessed without anesthesia; vital tissue was located in the mesiolingual canal (arrow). The tooth was thenanesthetized, and the canal was instrumented and obturated.

PREOPERATIVE CAUSES

Failure of root canal treatment is often traced tomisdiagnosis, errors in treatment planning, poorcase selection (dentists attempting treatment be-yond their skill levels), or treatment of a toothwith a poor prognosis. All of these are preopera-tive considerations.

Before any invasive dental procedure, includ-ing root canal treatment, the dentist should makea "tentative" pulpal and periradicular diagnosis.That diagnosis is based on all available informa-tion: history of signs and symptoms, current signsand symptoms, radiographic evaluation, and vi-tality tests (see Chapter 4). Without evaluating allthese factors and forming a diagnosis, there is arisk of inappropriate treatment and/or the wrongtooth being treated. Obviously, the problemwould not be resolved.

Not using good radiographic projection, in-cluding different mesiodistal angulation to deter-mine various canal system aberrations (extracanals: for example, the mesiolingual canal in

maxillary molars and second canals in mandibu-lar incisors), often results in failure, even with cor-rect diagnosis (Figure 19-5).

Coronal or root dentin fractures are also oftenmisdiagnosed or escape early detection. Periodon-tal defects with associated bone loss often appearafter the fracture has been on the crown and rootfor long enough for the crack to become infected(Figure 19-6) .z6-Z9 However, if there is an isolated,deep probing defect associated with the suspecttooth, vertical root fracture must be considered(Figure 19-7).

OPERATIVE CAUSES

Many failures result from errors in operative pro-cedures. For predictable success, several stepsneed to be followed. These include chemome-chanical cleaning and shaping of the canal spacefollowed by a dense obturation that is confined tothe root canal system and then by a quality coro-nal restoration.


339

FIGURE 19-6A, Large periradicular lesion around mesial and distal roots of the first molar.The patient denied any history of symptoms. The tooth was unresponsive toCO, snow, but responded normally to percussion and palpation. B, Accesswas attained without anesthesia (test cavity), confirming necrotic pulp. Rootcanal treatment was performed in two appointments using Ca(OH) Z as ani ntra-appointment medicament. C, After 3 months, severe pain was reportedon biting. Extraction revealed a split tooth that was probably present beforethe initial root canal treatment, as there was no restoration or caries, yet thepulp was necrotic.

Mechanical Objectives

An overlooked but important part of successfulroot canal treatment is a straight-line accesspreparation that will facilitate debridement andobturation. The access is even more important,with the use of rotary nickel-titanium file systems.If the access is underextended, several mishapsmay occur that ultimately will lead to failure. A

canal may be missed; the treatment is likely to failalthough the located canals were appropriatelytreated. If the pulp horns are not opened in ante-rior teeth, debris and sealer may remain in thecoronal pulp space. Such remnants often result indiscoloration and therefore treatment failure. Inaddition, with a too small access, instrument ma-neuverability is limited, resulting in insufficient

340


cleaning and aberrant shaping, or even instru-ment breakage.

Overextended access cavities, prepared at theexpense of dentin, are also a problem. Excessiveloss of dentin weakens the tooth, possibly allowingfractures, and increases the risk of perforation .29,30

A common error of instrumentation is failure tomaintain canal curvature because files cut to theoutside of the curve ("transportation" of the canaland/or apex). This alters canal morphology andleaves potentially infected debris in the canal system.Marked deviation or overzealous flaring or over-preparation in the "danger" zone or in the apical '/3may result in perforation (Figure 19-8). These perfo-rations are possible to repair but are difficult to sealnonsurgically3l Leakage and/or mechanical irrita-tion may result, and a lesion may develop .12

The outcome of a separated instrument (brokenendodontic file) in a root canal system depends

FIGURE 19-7A, Root canal treatment on the first molar was completed2 months previously. Discomfort persisted with occasionalswelling and drainage into the sulcus in the mesiofacialaspect of the treated tooth. A deep probing defect on themesiofacial aspect indicated the possibility of a verticalroot fracture. However, further testing showed that thesecond premolar was sensitive to percussion and unre-sponsive to CO, snow and test cavity. B, Treatment was

i nitiated on the premolar. C, One year after root canaltreatment, there is partial periradicular healing aroundboth apexes. Results of periodontal probing were within

normal limits. (Courtesy Dr. G. Shuping.)

on the stage of canal preparation and the pretreat-ment pulp status (vital versus necrotic) (see Fig-ure 19-7).33,34 The outcome may be unaffected if theinstrument can be removed or bypassed.

Confining operative procedures and materialsto the canal space enhances repair."' Overinstru-mentation causes some tissue damage, periradic-ular hemorrhage, and transitory inflammation.Continuous overinstrumentation provokes a per-sistent inflammatory response capable of resorb-ing dental and osseous tissues." Overinstrumen-tation may also transfer microorganisms from thecanal into the periapex, possibly compromisingthe outcome. 37

Likewise, overextended obturation may lead totreatment failure. In many cases it is probably notthe material that causes the periradicular lesion;gutta-percha is relatively inert. Rather, the combi-nation of an inadequate seal probably preceded by

1 8 / Procedural Accidents

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FIGURE 78-11A, Preoperative radiograph. B, Ledges have been formed in the mesial and distal canals with stainless steel files.Ledges can be bypassed only with small, curved stainless steel files. C, Ledges are bypassed, and proper lengthi s established. D, Final radiograph. Nickel-titanium files can be used only after ledges are removed.

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Etiology and Indicators. Instrumentation of thecanal beyond the apical constriction results in per-foration. Incorrect working length or inability tomaintain proper working length causes "zipping"Zor "blowing out" of the apical foramen. Appear-ance of fresh hemorrhage in the canal or on in-struments, pain during canal preparation in a pre-viously asymptomatic tooth, and sudden loss ofthe apical stop are indicators of foramen perfora-tion. Extension of the largest (final) file beyond theradiographic apex is also a sign. An electronic apexlocator may also confirm this procedural accident.

Prevention. To prevent apical perforation,proper working lengths must be established andmaintained throughout the procedure. In curvedcanals, the flexibility of files with respect to sizemust be considered. Step-back and flaring proce-dures straighten the canal somewhat and effec-tively decrease the working length by as much as1 to 2 mm, requiring compensation.

Treatment. Treatment includes establishing anew working length, creating an apical seat(taper), and obturating the canal to its newlength. Depending on the size and location of theapical foramen, a new working length 1 to 2 mmshort of the point of perforation should be estab-lished. The canal is then cleaned, shaped, and ob-turated to the new working length. The mastercone must have a positive apical stop at the work-ing length before obturation. Placement of MTAas an apical barrier can prevent extrusion of obtu-ration materials.

Prognosis. Success of treatment depends pri-marily on the size and shape of the defect. Anopen apex or reverse funnel is difficult to seal andalso allows extrusion of the filling materials. Inaddition, the feasibility of repairing the perfora-tion surgically may influence the final outcome.

Lateral (Midroot) Perforations

Etiology and Indicators. As discussed earlier, in-ability to maintain canal curvature is the majorcause of ledge formation. Negotiation of ledgedcanals is not always possible; misdirected pressureand force applied to a file may result in formationof an artificial canal and eventually in an apical ormidroot perforation. To avoid these perforations,the same factors mentioned earlier for preventionof ledge formation should be considered: (1) de-gree of canal curvature and size and (2) inflexibil-ity of the larger files, especially stainless steel files.

Indicators of lateral perforation are similar tothose of apical perforation, i.e., fresh hemorrhagein the root canal or sudden pain and deviation ofinstruments from their original course. Penetra-tion of the instrument out of the root radio-

graphically (or, as indicated by an apex locator) isthe ultimate indicator.

Treatment. The optimal goal is to clean,shape, and obturate the entire root canal systemof the affected tooth. After the perforation isconfirmed, the steps discussed previously forbypassing of ledged canals are followed. If at-tempts to negotiate the apical portion of thecanal are unsuccessful, the operator should con-centrate on cleaning, shaping, and obturatingthe coronal segment of the canal. A new work-ing length confined to the root is established;the canal is then cleaned, shaped, and obturatedto the new working length. A low concentration(O.S%) of sodium hypochlorite or saline shouldbe used for irrigation in a perforated canal. Ex-trusion of concentrated irrigant into the sur-rounding periodontal tissues would produce se-vere inflammation.

Prognosis. Success depends partially on the re-maining amount of undebrided and unobturatedcanal. Obturation is difficult because of lack of astop (matrix); gutta-percha tends to be extrudedduring condensation. Teeth with perforationsclose to the apex after complete or partial debride-ment of the canal have a better prognosis thanthose with perforations that occur earlier. In ad-dition to the length of uncleaned and unfilledportions of the canal, size and surgical accessibil-ity of perforations are important. In general,small perforations are easier to seal than largeones. Because of surgical accessibility, perfora-tions toward the facial aspect are more easily re-paired and therefore these teeth have a betterprognosis than those with perforations in otherareas.

On recall, both radiographic and periodontalexaminations for signs and symptoms are per-formed; failure generally requires surgery or otherapproaches. These approaches depend on theseverity of perforation, the strategic importanceof the tooth, and the location and accessibility ofthe perforation. Corrective techniques include re-pair of the perforation site, root resection to thelevel of the perforation, root amputation, hemi-section, replantation, and extraction.

Coronal Root Perforations

Etiology and Indicators. Coronal root perfora-tions occur during access preparation while theoperator attempts to locate canal orifices or dur-ing flaring procedures with files, Gates-Gliddendrills, or Peeso reamers. Perforations during ac-cess preparation can be minimized by using themethods described earlier in this chapter. Re-moval of restorations when possible, use of


32 3

fiberoptic lights for illumination, magnification,and cautious exploration for calcified canals canprevent most problems during access prepara-tion. Careful flaring (step-back) and conservativeuse of flaring instruments are required duringcleaning and shaping procedures.

Treatment and Prognosis. Repair of a strippingperforation in the coronal third of the root has thepoorest long-term prognosis of any type of perfo-ration.4 The defect is usually inaccessible for ade-quate repair. An attempt should be made to sealthe defect internally, even though the prognosis isguarded. Patency of the canal system must bemaintained during the repair process. Referral ofthe patient to a specialist is recommended.

SEPARATED INSTRUMENTSEtiology

Limited flexibility and strength of intracanal in-struments combined with improper use may re-sult in an intracanal instrument separation. Anyinstrument may break-steel, nickel-titanium,hand, or rotary. Overuse or excessive force appliedto files is the main cause of separation. Manufac-turing defects in files are rare.

Recognition

Removal of a shortened file with a blunt tip froma canal and subsequent loss of patency to the orig-inal length are the main clues for the presence of aseparated instrument. A radiograph is essential forconfirmation. It is imperative that the patient be in-formed of the accident and its effect on progno-sis.1 As with other procedural accidents, detaileddocumentation is also necessary for medical-legalconsiderations.

Prevention

Recognition of the physical properties and stresslimitations of files is critical. Continual lubrica-tion with either irrigating solution or lubricantsis required. Each instrument is examined beforeuse. If an unwound or twisted file is rotated andviewed, reflections from the chairside light willmagnify fluting distortions (Figure 18-12).Small files must be replaced often. To minimizebinding, each file size is worked in the canaluntil it is very loose before the next file size isused.20 Nickel-titanium files usually do not showvisual signs of fatigue similar to the "untwist-ing" of steel files. Many factors may affect the fa-tiguing of nickel-titanium files, and they shouldbe discarded before visual signs of untwisting areseen.

FIGURE 18-12Each steel file should be inspected for fluting distortion be-fore use in the canal. Only untwisted files will show a shinyspot (arrow). This file must be discarded. Nickel-titanium filesusually will not show this distortion and must be discardedafter three to six uses.

Treatment

There are basically three approaches: (1) attemptto remove the instrument, (2) attempt to bypassit, and (3) prepare and obturate to the segment.Initial treatment is similar to that discussed ear-lier for a ledge. Using a small file and followingthe guidelines described for negotiating a ledge,the operator should attempt to bypass the sepa-rated instrument. If this is successful, broaches orHedstrom files are used to try to grasp and re-move the segment, this usually does not work.Then the canal is cleaned, shaped, and obturatedto its new working length (Figure 18-13). If the in-strument cannot be bypassed, preparation andobturation should be performed to the coronallevel of the fragment.

Prognosis

Prognosis depends on how much undebrided andunobturated canal apical to and including the in-strument remains. The prognosis is best whenseparation of a large instrument occurs in the

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FIGURE 78-73A, A file is separated in the buccal canal (arrow) of thesecond maxillary premolar. B, The separated instrument isbypassed. C, Both canals are cleaned, shaped, and obtu-rated. Prognosis is good.

later stages of preparation close to the workinglength. Prognosis is poorer for teeth withundebrided canals in which a small instrument isseparated short of the apex or beyond the apicalforamen early in preparation. For medical-legalreasons, the patient must be informed (with doc-umentation in the record) of an instrument sepa-ration. Despite the concern of both patient anddentist,21 clinical studies indicate that the prog-nosis in most procedures involving broken instru-ments that are managed properly is favorable.22

If the patient remains symptomatic or there isa subsequent failure, the tooth can be treated sur-gically. Accessible roots are resected with place-ment of a root-end filling material (Figure 18-14).Accessibility of the root apex for surgical inter-vention is critical to the final outcome.

OTHER ACCIDENTS

Aspiration or Ingestion

Aspiration or ingestion of instruments is a seriousevent but is easily avoided with proper precau-tions. Use of the rubber dam is the standard of care toprevent such ingestion or aspiration and subsequentl awsuits.'

The disappearance of an instrument that hasslipped from the dentist's fingers, followed by vi-olent coughing or gagging by the patient and ra-diographic confirmation of a file in the alimen-tary tract or airway, is the chief sign. Thesepatients require immediate referral to a medicalservice for appropriate diagnosis and treatment.According to a survey by Grossman," 87% ofthese instruments are swallowed and the rest areaspirated. Surgical removal is required for some

swallowed (Figure 18-15) and nearly all aspiratedinstruments.

Extrusion of Irrigant

Wedging of a needle in the canal (or particularlyout of a perforation) with forceful expression ofirrigant (usually sodium hypochlorite) causespenetration of irrigants into the periradicular tis-sues and inflammation and discomfort for pa-tients. Loose placement of irrigation needles andcareful irrigation with light pressure or use of aperforated needle24 precludes forcing of the irri-gating solution into the periradicular tissues.Sudden prolonged and sharp pain during irriga-tion followed by rapid diffuse swelling (the"sodium hypochlorite accident") usually indicates


32 5

FIGURE 18-14A, A Nickel titanium file was broken inside the mesiobuc-cal canal. B, Because of patient discomfort, the root seg-ment was removed surgically and MTA was used as root-end filling material. C, A periapical radiograph 1 year later

shows excellent healing.

FIGURE 18-15A swallowed broach lodged in a patent's appendix, resultingi n the removal of the appendix and a subsequent lawsuitagainst a dentist who did not use rubber dam during rootcanal therapy.

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FIGURE 78-76A, Sodium hypochlorite was inadvertently expressed through an apical perforation in a maxillary canine duringi rrigation. Hemorrhagic reaction was rapid and diffuse. B, No treatment was necessary; the swelling andhematoma disappeared within a few weeks. (Courtesy Dr. James Stick.)

penetration of solution into the periradicular tis-sues. The acute episode will subside sponta-neously with time (Figure 18-16).

Initially there is no reason to prescribe antibi-otics or attempt surgical drainage. Treatment ispalliative. Analgesics are prescribed, and the pa-tient is reassured. Because the outcome is so dra-matic, evaluation is performed frequently to fol-low progress.

Accidents During Obturation

Appropriate cleaning and shaping are the keys topreventing obturation problems because these ac-cidents usually result from improper canal prepa-ration. In general, adequately prepared canals areobturated without mishap. The quality of obturationreflects canal preparation. However, problems dooccur.

UNDERFILLINGEtiology

Some causes of underfilling include a natural bar-rier in the canal, a ledge created during prepara-tion, insufficient flaring, a poorly adapted mastercone, and inadequate condensation pressure. By-passing (if possible) of any natural or artificial bar-rier to create a smooth funnel is one key to avoid-ing an underfill. The advent of nickel-titaniumrotary files of increased taper has greatly improvedthe predictability of proper funnel and taper.


Removal of underfilled gutta-percha and retreat-ment is preferred. Forcing gutta-percha apicallyby increased spreader or plugger pressure canfracture the root. If lateral condensation is themethod of obturation, the master cone should bemarked to indicate the working length. If dis-


327

FIGURE 18-17A, Lack of proper length measurements resulted in overpreparation and then overfill of the distal root and un-derfill of the mesial root. The tooth remained percussion sensitive. B, Surgical curettage, apical root resection, androot-end filling with MTA were necessary to correct the technical deficiencies.

placement of the master cone during condensa-tion is suspected, a radiograph is made before ex-cess gutta-percha is removed. Removal can thenbe accomplished by pulling the cones in the re-verse order of placement. Removal of gutta-percha in canals obturated with lateral condensa-tion is easier than removal with other obturationtechniques. However, warm gutta-percha tech-niques allow better obturation of irregularitieswithin the canal.

OVERFILLING

Extruded obturation material causes tissue dam-age and inflammation. Postoperative discomfort(mastication sensitivity) usually lasts for a fewdays.

condensation forces extrusion of materials (Fig-ure 18-17). Other causes include inflammatoryresorption and incomplete development of theroot.

Prevention

To avoid overfilling, guidelines for preventing api-cal foramen perforation should be followed. Ta-pered preparation with an apical "matrix" usuallyprevents overfill. The largest file and master coneat working length should have a positive stop. Acustomized master cone may be fabricated bybriefly applying solvent on the tip. If overfilling issuspected, a radiograph should be made beforeexcess gutta-percha is removed. As with underfill-ing, the gutta-percha mass may be removed if thesealer has not set.

Etiology

Overfilling is usually the sequela of overinstru-mentation through the apical constriction orlack of proper taper in prepared canals. When theapex is open naturally or its constriction is re-moved during cleaning and shaping, there is nomatrix against which to condense; uncontrolled


When signs or symptoms of endodontic failureappear, apical surgery may be required to removethe material from apical tissues and place root-end filling material. Long-term prognosis is dic-tated by the quality of the apical seal, the amount

328

18 1 Procedural Accidents

FIGURE 18-18I ndicators of vertical root fracture. A, A "tear-drop" lateral radiolucency is noted along the root. B, Narrow prob-i ng defect extends to the apex.

and biocompatibility of extruded material, hostresponse, and toxicity and sealability of the root-end filling material.

VERTICAL ROOT FRACTURE

Complete vertical root fracture causes untreatablefailure. Aspects of vertical root fracture are de-scribed in more detail in Chapter 28.

Etiology

Causative factors include root canal treatmentprocedures and associated factors such as postplacement. The main cause of vertical root frac-ture is post cementation; second in importanceis overzealous application of condensationforces to obturate an under- or overpreparedcanal . 2s

Prevention

As related to root canal treatment procedures, thebest means of preventing vertical root fracturesare appropriate canal preparation and use of bal-anced pressure during obturation. A major reasonfor flaring canals is to provide space for conden-sation instruments. Finger spreaders produce lessstress and distortion of the root than their handcounterparts. 26-Z$

Indicators

Long-standing vertical root fractures are often as-sociated with a narrow periodontal pocket orsinus tract stoma as well as with a lateral radiolu-cency extending to the apical portion of the verti-cal fracture 29 (Figure 18-18). To confirm the diag-

nosis, a vertical fracture must be visualized. Ex-ploratory surgery or removal or the restoration isusually necessary to visualize this mishap.

Prognosis and Treatment

Complete vertical root fracture predicts the poor-est prognosis of any procedural accident. Treat-ment is removal of the involved root in multi-rooted teeth and extraction of single-rooted teeth.

Accidents During Post SpacePreparation

To prevent root perforation, gutta-percha may beremoved to the desired level with heated pluggersor softened with chloroform and removed by files.This "pilot" post space provides a path of least re-sistance for sizing drills. When a canal is preparedto receive a post, drills should be used sequen-tially, starting with a size that fits passively to thedesired level. Miscalculation and incorrect prepa-ration may result in perforation at any level.Knowledge of root anatomy is necessary for deter-mining the size and depth of posts.

I NDICATORS

The indicators of perforations and vertical rootfractures are somewhat similar. Appearance offresh blood during post space preparation is anindication for the presence of a root perforation.The presence of a sinus tract stoma or probing de-fects extending to the base of a post is often a signof root fracture or perforation. Radiographs oftenshow a lateral radiolucency along the root or per-foration site.


329

TREATMENT AND PROGNOSIS

Prognosis for teeth with vertical root fractures re-sulting from post space preparation and postin-sertion is similar to that for teeth with fracturesdeveloping during obturation; the involved root(or tooth) is hopeless and must be removed. Asoutlined earlier, the prognosis of teeth with rootperforation during post space preparation de-

pends on the root size, location relative to epithe-lial attachment, and accessibility for repair. Man-agement of the post perforation generally is sur-gical if the post cannot be removed. If the post canbe removed, nonsurgical repair is preferred (Fig-ure 18-19). Teeth with small root perforationsthat are located in the apical region and are acces-sible for surgical repair have a better prognosis

FIGURE 18-19A, A lateral root perforation is evident. The patient pre-sented with swelling and percussion sensitivity. B, Afterremoval of the post and retreatment of previous therapy,the perforation was repaired with MTA. C, A clinical ex-amination and radiograph of the patient 4 years latershowed absence of symptoms and absence of periradicu-l ar pathosis. (Courtesy Dr. D. McKendry.)

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than those with large perforations, close to thegingival sulcus, or inaccessible. Because of thecomplexity in diagnosis, surgical techniques, andfollow-up evaluation, patients with post perfora-tions should be referred to an endodontist.

REFERENCES

1. Cohen S, Schwartz S: Endodontic complications andthe law, J Endod 13:191, 1987.

2. Weine FS: Access cavity preparation and initiatingtreatment. In Weine F, editor, Endodontic therapy, ed 5,

221, St Louis, 1996, Mosby.3. Lemon RR: Furcation perforation management:

classic and new concepts. In Hardin JF, editor:Clark's clinical dentistry, vol 1, Philadelphia, 1990, JBLippincott.

4. Lemon RR: Nonsurgical repair of perforation defects: in-ternal matrix concept, Dent Clan North Am 36:448, 1992.

5. Simon J, Kelly WH, Gordon DG, Ericksen GW: Extru-sion of endodontically treated teeth, J Am Dent Assoc97:17, 1978.

6. Lemon RR: Simplified esthetic root extrusion tech-niques, Oral Surg Oral Med Oral Pathol 54:93, 1982.

7. Lee SJ, Monsef M, Torabinejad M: Sealing ability of amineral trioxide aggregate for repair of lateral root per-foration,JEndod 19:541, 1993.

8. Nicholls E: Treatment of traumatic perforations of thepulp cavity, Oral Surg 15:603, 1962.

9. Stromberg T, Hasselgran G, Bergstedt H: Endodontictreatment of traumatic root perforation in man: aclinical and roentgenological follow up study, Sven

Tandlakidskr 64:487, 1972.

10. Harris W: A simplified method of treatment for en-dodontic perforations, JEndod 2:126, 1976.

11. Benenati FW, Roane JB, Biggs JT, Simon JH: Recallevaluation of iatrogenic root perforations repairedwith amalgam and gutta percha, J Endod 12:161, 1986.

12. Sinai J: Endodontic perforations: their prognosis andtreatment,J Am Dent Assoc 95:90, 1977.

13. Hartwell G, England M: Healing of furcation perfora-tions in primate teeth after repair with decalcified freeze-dried bone: a longitudinal study,JEndod 19:357, 1993.

14. Aguirre R, El Deeb ME, El Deeb ME: Evaluation of therepair of mechanical furcation perforations using amal-gam, gutta percha, or indium foil, JEndod 12:249,1986.

15. Oswald RJ: Procedural accidents and their repair, Dent

Clin North Am 23:593, 1979.

16. Pitt Ford TR, Torabinejad M, et al: The sealing abilityof a mineral trioxide aggregate for repair of furcal per-forations, Oral Surg 79:756, 1995.

17. Hong CU, McKendry DJ, Pitt Ford TR, Torabinejad M:Healing of furcal lesions repaired by amalgam or min-eral trioxide aggregate, JEndod 20:197, 1994.

18. Bhaskar S, Rappaport H: Histologic evaluation of en-dodontic procedures in dogs, Oral Surg Oral Med Oral

Pathol 32:26 35, 1971.

19. Selzer S, Sinai I, August D: Periodontal effects of rootperforations before and during endodontic proce-dures, J Dent Res 49:332, 1970.

20. Grossman LI: Guidelines for the prevention of fractureof root canal instruments, Oral Surg Oral Med Oral

Pathol28:746, 1969.

21. Frank AL: The dilemma of the fractured instrument, J

Endod 9:515, 1983.

22. Crump MC, Natkin E: Relationship of broken rootcanal instruments to endodontic case prognosis: aclinical investigation, JAm Dent Assoc 80:1341, 1970.

23. Grossman LI: Prevention in endodontic practice,JAmDentAssoc 82:395, 1971.

24. Goldman M, Kronman JH, Goldman LB, et a1: Newmethod of irrigation during endodontic treatment, JEndod 2:257, 1976.

25. Obermayr G, Walton RE, Leary JM, et al: Vertical rootfracture and relative deformation during obturationand post cementation, JProsthetDent 66:181, 1991.

26. Murgel CA, Walton RE: Vertical root fracture anddentin deformation in curved roots: the influence ofspreader design, Endodont Dent Traumatol 6:273,1990.

27. Dang D, Walton R: Vertical root fracture and root dis-tortion: effect of spreader design, JEndod 15:294, 1989.

28. Leutchirakarn V, Palamara J, Messer H: Load andstrain during lateral condensation and vertical rootfracture, J Endod 25:99, 1999.

29. Walton RE, Michelich RJ, Smith NG: The histopatho-genesis of vertical root fractures, J Endod 10:48, 1984.


341

FIGURE 19-5A, History of recent root canal treatment with sensitivityto mastication. The diagnostic radiograph reveals a zip-ping perforation of one canal and a separated instrumenti n the other. The lesion is associated with the zip (arrow).Root-end surgery was the approach. B, immediately aftersurgery and root-end filling with SuperEBA. C, One-yearrecall; the tooth is asymptomatic, and bony regenerationi s seen around the apex.

overinstrumentation causes the failure. Thegutta-percha cone slips through the apex becausethere was inadequate taper or shelf, resulting ininadequate matrix to confine and condense andseal with the gutta-percha. In addition, sealers areirritating or toxic to the periradicular tissue.23,38,39

Errors in obturation result from poor canalshaping or selecting an inappropriate obturatingtechnique. A poorly condensed obturation (eitherunderfilled or containing voids) is related to api-cal and/or coronal percolation .3,23,40 Either under-obturation or overfilling is likely to result in fail-

ure, particularly in the presence of pulp necrosisand an apical lesion . 41

Biologic Objectives

Ideally, after preparation the root canal would befree of bacteria .42 With a vital pulp this means pre-vention of contamination and with a necrotic pulp,to achieve disinfection. However, as shown experi-mentally, complete debridement of the canal is vir-tually impossible .43,44 Therefore, bacterial countsare minimized by careful instrumentation, with

342


copious NaOCI irrigation.45 The intracanal medi-cament, calcium hydroxide, will reduce the numberof bacteria,46 enhance the speed of healing, and re-duce inflammation."" However, there is uncer-tainty whether use of this medicament ultimatelyresults in a better prognosis.49

POSTOPERATIVE FACTORS

Lack of a coronal seal is probably the most com-mon, but best controllable, problem. Coronalrestoration protects and seals the tooth, pre-venting diffusion of saliva and bacteria apically(Figure 19-9), which results in failed treat-ment." , ' "' There is a definite correlation be-tween poorly restored crowns of endodonticallytreated teeth and leakage of dye or bacteria orendotoxin through the canals and a poorerprognosis. 13,50-53

Restoration should occur soon after obtura-tion, using the same disinfection barriers asthose used during the root canal treatment, i.e.,rubber dam isolation in a saliva-free environ-ment.There should be no space between thecoronal filling and the obturation in the cervicalarea; there is a risk for bacterial contaminationthrough exposed cervical root dentin. Restora-tive errors also may compromise success. For ex-ample, excessive dentin removal for posts weak-ens the root and increases susceptibility tofracture (Figure 19-10).29

Retreatment of FailuresFIGURE 19-9Coronal leakage. Crown (left) has open margins. Saliva, bac-teria, and other irritants have access to canal space. The irri-tants will percolate through gutta-percha and out of the apex.The same thing may occur with an improperly sealed com-posite on an anterior tooth (righ). (Courtesy Dr. K. Barrieshi.)

Interestingly, if a failure is retreated by conven-tional means, the success rate is equivalent to thatof initial conventional treatment if the cause of fail-ure is identified and corrected. 54 Specific details of re-treatment are included in Chapter 20.

FIGURE 79-70Hopeless prognosis. A, Overenlargement has weakened the root. B, Then, placement of oversized post com-bined with earlier condensation forces resulted in a vertical fracture and apical-lateral pathosis. The tooth mustbe extracted.

19 I Evaluation of Success and Failure

343

1. Eriksen H: Endodontology epidemiologic considera-tions, Endod Dent Traumatol 7:189, 1991.

2. Lin LM, Pascon EA, Skribner J, et al: Clinical, radio-graphic, and histologic study of endodontic treatmentfailures, Oral Surg Oral Med Oral Pathol 71:603, 1991.

3. Pekruhn RB: The incidence of failure following single-visit endodontic therapy, J Endod 12:68, 1986.

4. Jokinen MA, Kotilainen R, Pockkeus P, et al: Clinicaland radiographic study of pulpectomy and root canaltherapy, ScandJ Dent Res 86:366, 1978.

5. Strindberg LZ: The dependence of the results of pulptherapy on certain factors: An analytic study based onradiographic and clinical follow-up examination, ActaOdontol Scand 14(Suppl21):1956.

6. Seltzer S, Bender IB, Turkenkopf S: Factors affectingsuccessful repair after root canal therapy, J Am DentAssoc 67:651 1963.

7. Grahnen J, Hansson L: The prognosis of pulp and rootcanal therapy, Odontol Rev 12:146, 1961.

8. Sjogren U, Hagglund B, Sundqvist G, Wing K: Factorsaffecting the long term results of endodontic treat-

ment,J Endod 16:498, 1990.

9. Kakehashi S, Stanely HR, Fitzgerald RJ: The effects ofsurgical exposures of dental pulps in germ-free andconventional laboratory rats, Oral Surg Oral Med Oral

Pathol 20:340, 1965.10. Molven O, Halse A: Success rate for gutta-percha and

Kloroperka N-O root filling made by undergraduatestudents; radiographic findings after 10-17 years, IntEndod J 21:243, 1988.

11. Sjogren U, Figdor D, Persson S, Sundqvist G: Influenceof infection at the time of root filling on the outcomeof endodontic treatment of teeth with apical peri-

odontitis,Int Endod J 30:297, 1997.

12. Sundqvist G, Figdor D, Persson S, Sjbgren U: Microbi-ologic analysis of teeth with failed endodontic treat-ment and the outcome of conservative retreatment,Oral Surg Oral Med Oral Pathol 85:86, 1998.

13. Ray HA, Trope M: Periapical status of endodonticallytreated teeth in relation to the technical quality of theroot filling and the coronal restoration, Int Endod J28:12, 1995.

14. Bergenholtz G, Lekholm U, Milthon R, Engstrom B:Influence of apical overinstrumentation and overfill-ing on re-treated root canals, JEndod 5:310, 1979.

I5. Orstavik D, Horsted-Bindslev P: A comparsion of en-dodontic treatment results at two dental schools, Int

Endod j 26:348, 1993.

16. De Moor RJG, Hommez GMG, De Boever JG, et al: Peri-apical health related to the quality of root canal treat-ment in a Belgian population, Int Endod j 33:113, 2000.

17. Stabholz A: Success rate in endodontics, Alpha Omegan

83:20, 1990.

18. Storms JL: Factors that influence the success of en-dodontic treatment, J Can Dent Assoc 35:83, 1969.

19. Bender 113, Selzer S, Soltanoff W: Endodontic success:a reappraisal of criteria. I and 11, Oral Surg Oral Med Oral

Pathol 22:780, 1966.

20. Swartz DB, Skidmore AE, Griffin JA: Twenty years ofendodontic success and failure, JEndod 9:198, 1983.

21. Goldman M, Pearson AH, Darzenta N: Endodonticsuccess: who's reading the radiograph? Oral Surg Oral


22. Zakariasen KL, Scott DA, Jensen JR: Endodontic recallradiographs: how reliable is our interpretation of en-dodontic success or failure and what factors affect ourreliability? Oral Surg Oral Med Oral Pathol 57:343, 1984.

23. Ricucci D, Langeland K: Apical limits of root canal in-strumentation and obturation, Int Endod j31:384, 1998.

24. Brynolf I: A histological and roentgenological study ofthe periapical region of human upper incisors, OdontolRev 18(Suppl 11), 1967.

25. Green TL, Walton RE, Taylor JK, Merrell P: Radio-graphic and histologic periapical findings of rootcanal treated teeth in cadavers, Oral Surg Oral Med Oral

Pathol 83:707, 1997.

26. Ehrmann E, Tyas M: Cracked tooth syndrome: diag-nosis, treatment and correlation between symptomsand post-extraction findings, Aust DentJ 35:105, 1990.

27. Schweitzer J, Gutmann J, Bliss R: Odontoiatrogenictooth fracture, Int Endod J 22:64, 1989.

28. Yang SF, Rivera EM, Walton RE: Vertical root fracture innonendodontically treated teeth, JEndod 21:337, 1995.

29. Trope M, Maltz DO, Tronstad L: Resistance to fractureof restored endodontically treated teeth, Endodont Dent


30. Sails S, et al: Patterns of indirect fracture in intact andrestored human premolar teeth, Endodont Dent Trau-

matol 3:10, 1987.

31. Hartwell G, England M: Healing of furcation perfora-tions in primate teeth after repair with decalcified freeze-dried bone: a longitudinal study, JEndod 19:357, 1993.

32. Seltzer S, Sinai I, August D: Periodontal effects of rootperforations prior to and during endodontic proce-dures, J Dent Res 49:332, 1970.

33. Fors UG, Berg JO: Endodontic treatment of root canalsobstructed by foreign objects, Int Endod J 19:2, 1986.

34. Grossman LL editor: Transactions. First International

Conference on Endodontics, Philadelphia, 1953, Univer-sity of Pennsylvania Press.

35. Wu MK, Wesselink PR, Walton RE: Apical terminus lo-cation of root canal treatment procedures, Oral Surg

Oral Med Oral Pathol 89:99, 2000.36. Seltzer S, Bender I, Soltanoff I: Biological aspects of en-

dodontics. III. Periapical reactions to root canal instru-mentation, Oral Surg Oral Med Oral Pathol 26:534, 1968.

37. Seltzer S: Endodontology, ed 2, Philadelphia, 1988, Lea &Febiger.

38. Morse DR, Wilcko J, Pullon P, et al: A comparative tis-sue toxicity evaluation of the liquid components ofgutta-percha root canal sealers, JEndod 7:545, 1981.

39. Seltzer S: Long-term radiographic and histological ob-servation of endodontically treated teeth, J Endod

25:12, 1999.

40. Wu M, DeGee A, Wesselink P, Moorer W: Fluid trans-port and bacterial penetration along root canal fill-i ngs, Int Endod J 26:1, 1993.

41. Smith C, Setchell D, Harty F: Factors influencing suc-cess of conventional root canal therapy: a five-year ret-rospective study, Int Endod J 26:321, 1993.

42. Grossman LI: Endodontic failures, Dent Clin North Am

16:59, 1972.

REFERENCES

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43. Mandel E, Machtou P, Friedman S: Scanning electronmicroscope observation of canal cleanliness, J Endod16:279, 1990.

44. Dalton BC, Orstavik D, Phillips C, et al: Bacterial re-duction with nickel-titanium rotary instrumentation,JEndod 24:763, 1998.

45. Bystrom A, Sundqvist G: Bacteriologic evaluation of theeffect of 0.5 percent sodium hypochlorite in endodontictherapy, Oral Surg Oral Med Oral Pathol 55:35, 1983.

46. Sjogren U, Figdor D, Spangberg L, Sundqvist G: Theantimicrobial effect of calcium hydroxide as a short-term intracanal dressing, Int Endod j 24:119, 1991.

47. Katebzadeh N, Sigurdsson A, Trope M: Radiographicevaluation of periapical healing after obturation ofinfected root canals: an in vivo study, Int Endod J33:60, 2000.

48. Katebzadeh N, Hupp J, Trope M: Histological periapi-cal repair after obturation of infected root canals indogs, J Endod 25:364, 1999.

49. Weiger R, Rosendahl R, Lost C: Influence of calciumhydroxide intracanal dressings on the prognosis ofteeth with endodontically induced periapical lesions,Int Endod J 33:219, 2000.

50. Swanson K, Madison S: An evaluation of coronalmicroleakage in endodontically treated teeth. Time

periods,J Endod 13:56, 1987.51. Magura ME, Kafrawy A, Brown C, Newton C: Human

saliva coronal microleakage in obturated root canals.An in vitro study, JEndod 17:324, 1991.

52. Khayat A, Lee S-J, Torabinejad M: Human saliva pene-tration of coronally unsealed obturated root canals,JEndod 19:458, 1993.

53. Alves J, Walton R, Drake D: Coronal leakage: endo-toxin penetration from mixed bacterial communitiesthrough obturated post-prepared root canals, JEndod24:587, 1998.

54. Bergenholtz G, Lekholm U, et al: Retreatment of en-dodontic fillings, Scand J Dent Res 87:217, 1979.

Orthograde Retreatment

LEARNING OBJECTIVES


Describe differences from initial treatment.

t / State rationale and indications.

a / Discuss considerations for case selection.

4 / Identify restrictive clinical conditions.

s / Identify patients with difficult problems who should be referred.

6 / Describe a basic armamentarium and techniques.

7 / Communicate benefits and risks, alternative treatments, and reasons for referral.

345

346

20 / Orthograde Retreatment

Unique Considerations

Case Selection

Diagnosis

Selection of Treatment

Treatment of Existing Disease

Prevention of Disease

Retreatment Techniques

Access-Crowns

Access-Post and Core

Canal Obstructions

Completion of Retreatment

Degree of Difficulty

Short-Term and Long-Term Treatment

Outcome

Communication and Referral

ross-sectional studies of popula-tions in various countries, includingthe United States, indicate that, overall,

treatment failure, characterized by endodontic dis-ease (apical periodontitis), is seen in more than30% of root canal treated teeth.' Most patientscan relate to the concept of disease-treatment-healing, whereas failure, apart from being a nega-tive and relative term, does not imply the necessityto pursue treatment. Therefore, use of the term"disease" will minimize ambiguity and facilitatecommunication between the clinician and the pa-tient. In this chapter, post-treatment disease is usedrather than treatment failure, although the latterterm appears in this textbook's other chapters.

Post-treatment disease (apical periodontitis as-sociated with root canal-treated teeth) is primarilycaused by infection of the root canal system.' ,' Mi-croorganisms may either have survived the previ-ous treatment or invaded the filled canal spaceafter treatment, mainly because of coronal leak-age.'` Less often, specific microorganisms (Actino-myces species in particular) may have become es-tablished in the periradicular tissue.6

The affected teeth can be treated either by re-treatment (orthograde) or by apical surgery (retro-grade). These two approaches differ significantly inrationale-retreatment is an attempt to eliminateroot canal microorganisms, whereas surgery is anattempt to confine the microorganisms within thecanal. The main benefit of retreatment, therefore, isbetter curtailment of the root canal infection.Being limited in this regard, surgery is a compro-mise unless microorganisms are assumed to beharbored periapically, retreatment is unfeasible orrestricted, or a retreatment attempt has failed.'

Retreatment is distinguished from initial rootcanal treatment by unique considerations andtechniques." Because of the complexity, retreat-ment is often performed by the endodontist.However, the general dentist must understand re-treatment in order to support diagnosis, case se-lection, and treatment or referral as appropriateand to communicate with the patient and en-dodontist. The objective of this chapter is to pro-vide an understanding of retreatment.

Unique ConsiderationsRetreatment and initial root canal treatment sharesimilar biologic principles and objectives. How-ever, the following are unique to retreatment:$

1. An extensive restoration may have to be sac-rificed and remade.

2. Retreatment may be performed to preventpotential disease.7-9

3. Morphologic alterations resulting from theprevious treatment may present unusualtechnical and therapeutic challenges.10

4. Root filling and possibly restorative mate-rials must be removed from the canals.

5. The healing rate is generally slower than thatafter initial treatment, because of greater dif-ficulty in eliminating the infection.'

G. Patients may be more apprehensive thanwith the "routine" initial treatment; effec-tive communication is required.

These considerations distinguish retreatmentfrom initial root canal treatment and make patientselection complicated.' As a result, clinicians facedwith post-treatment disease frequently hesitate tointervene despite the presence of pathosis. 11-14

To foster confidence and appropriate manage-ment, definitive criteria are required to select casesfor tooth extraction, retreatment, and apical surgery.

Case SelectionRetreatment is usually performed to treat exist-ing disease, presenting with definitive signs andsymptoms. However, even in the absence of dis-ease, retreatment may be indicated to prevent fu-ture emergence of disease.', '

DIAGNOSIS

The presence or absence of periradicular disease isdetermined according to clinical and radiographicfindings, as discussed in Chapter 19. Differential di-agnosis of nonendodontic disease is also consid-ered.15 In this regard, the case history is reviewed byexamining previous radiographs when available andby noting past symptoms, time elapsed since previ-ous treatment (to avoid premature diagnosis ofpost-treatment disease), and previous attempts toretreat or to perform apical surgery (may suggestvertical fracture).

SELECTION OF TREATMENT

After diagnosis, the most appropriate treatmentmodality is selected based on the criteria outlinedbelow. In the past, the clinician selected and thenperformed the treatment. Currently, however, thepatient ultimately selects the treatment, based on in-formation communicated by the clinician. Thefollowing section is consistent with this concept.

TREATMENT OF EXISTING DISEASE

Post-treatment disease definitely requires inter-vention, even when symptoms are absent.' When


347

treatment is preferred over extraction, both re-treatment and apical surgery should be consid-ered. Comparing the two modalities, retreatmentoffers a greater benefit-a better ability to elim-inate the disease's etiology (root canal infec-tion) with minimal invasion-and a smaller risk-significantly less postoperative discomfort and alesser chance of injuring nerves, sinuses, or otherstructures. 16 Therefore, retreatment is generallyconsidered the treatment of choice; however, it isnot always feasible.

At times, retreatment can be more time con-suming and costly than surgery, particularlywhen an extensive restoration must be replaced.Also, the ability to attain the goals of retreat-ment may be restricted.' Furthermore, clini-cians' capabilities to perform retreatment andsurgery may vary considerably. In summary, re-treatment is generally selected because of itsgreater benefit and smaller risk compared withapical surgery. Therefore, case selection is basedon considerations that either preclude retreat-ment or restrict its feasibility in a way that de-creases the potential benefits and increases thepotential risks; the modified benefit-risk bal-ance may not outweigh that of apical surgery.

Patient Considerations

Patients' (and clinicians') attitudes toward dentaldisease and the necessity to treat it differ signifi-cantly." Moreover, the motivation to retain everytooth and pursue the best long-term treatmentoutcome may vary, as do the motivation and abil-ity to allocate time and finances. Because thesegeneral attitudes influence the patient's prefer-ences of treatment, they are primary considera-tions in the process of case selection (Box 20-1).

Motivation to retain the tooth. The considerableeffort associated with both retreatment andsurgery is justifiable by the potential to retainthe tooth. For the unmotivated patient, extrac-tion is selected.

Motivation to pursue the best long-term outcome.For the patient who is receptive to a compromisedlong-term outcome, apical surgery is selectedwhen retreatment is expected to be very involved.

Time. For the time-restricted patient who is re-ceptive to a compromise to minimize time com-mitment, the quicker apical surgery procedure isselected. However, the associated postoperativediscomfort and recovery can cause loss of worktime and income."

Finances. For the financially restricted patientwho is willing to compromise in order to min-imize cost, apical surgery is selected when thecombined cost of retreatment and restoration is

348

20 I Orthograde Retreatment

higher. Again, the potential loss of income associ-ated with postoperative recovery is considered."

Tooth Considerations

When the patient indicates a preference for re-treatment, the tooth and surrounding tissues arescrutinized to identify clinical conditions thatmight adversely affect the prognosis, either by de-creasing the benefits or by increasing the risks ofretreatment. In selected situations, the modifiedbenefit-risk balance no longer justifies the prefer-ence of retreatment over surgery.

Site of infection. Root canal infection is besteliminated by retreatment.' Periapical (extraradic-ular) infection independent of the root canal florais best eliminated by apical surgery." In contrast,when a vertical root fracture is present, infectioncannot be eliminated with either procedure."Therefore, differential diagnosis is required to es-tablish the likely site of infection. This difficulttask is facilitated by recognizing the typical man-ifestation of extraradicular infection (one or moresinus tracts), and that of vertical crack/fracture(isolated, narrow defect along the root), and bycomparing older and recent radiographs (seeChapter 28). 6 ' 9

Root canal obstacles. For retreatment to elimi-nate canal infection, the canal must be renegoti-ated throughout. Therefore, obstacles to totalrenegotiation reduce the potential benefit of re-treatment, while attempts to overcome the obsta-cles increase the risk of procedural complica-tions. The principal obstacles are (Figure 20-1):calcification, complex morphology of the root canalsystem, suspected ledge, and separated instrument.The feasibility of overcoming these obstaclesmust be assessed; again, the benefit-risk balancemay change in favor of surgery.

A post may obstruct the canal. Because postscan usually be removed (see discussion later inthis chapter), they do not influence the benefit-risk balance as described above.

Perforation. Perforation of the pulp chamber orroot can be a pathway of infection to worsen theprognosis.' Therefore, retreatment in conjunctionwith internal repair of the perforation is usuallywarranted (Figure 20-2). Nevertheless, when heal-ing is not expected or does not occur, surgery maybe required. The surgical procedure includes ex-ternal repair of the perforation (see Chapter 18).

Restorative, periodontal, and esthetic factors. Teethconsidered to have a hopeless prognosis for eitherrestoration or periodontal healing should be ex-tracted. With compromised periodontal support,surgery may result in an unfavorable crown-rootratio; therefore, retreatment is selected. With an ex-traoral sinus tract, surgery may be an adjunct to re-treatment to minimize scarring associated with thehealing of the sinus.

Clinician Considerations

Clinicians vary in capability as well as availabilityof armamentarium and time that can be spent oninvolved treatment of one tooth; their confidencelevels regarding specific treatment proceduresvary accordingly. When the patient's treatmentpreference conflicts with that of the clinician, thepatient should be referred to another dentist whocan perform the preferred procedure. When refer-ral is unfeasible, however, it is appropriate to se-lect the treatment with which the clinician is mostconfident.

Capability. Capability is a combination of train-ing, skill, and experience. Endodontists usuallyare more capable of treating post-treatment dis-ease than general dentists. Occasionally, however,an endodontist may not be equally adept at bothretreatment and apical surgery. When referral isnot an option, the procedure is selected that canbe performed best by the endodontist.$

Armamentarium. Use of special instruments canoptimize the benefit-risk balance of both retreat-ment and apical surgery. Without the option ofreferral, if the instruments required to perform


349

FIGURE 20-1Root canal obstacles that may compromise retreatment. A, Calcific metamorphosis. B, Complex morphology.C, Suspected ledges. D, Separated instrument (arrow). These obstacles restrict renegotiation of the canal andi ncrease the risk of perforation.

350


FIGURE 20-2Retreatment in conjunction with an internal perforation repair. A, Distal root perforation into the furcation; therei s post-treatment disease. B, Distal access through the crown without disturbing the mesial root. C, Completedretreatment and perforation seal with mineral trioxide aggregate (MTA). D, Progressive healing at 4 months.


351

only one procedure are available to the attendingendodontist, that procedure is usually selected.8

Time availability. In specific circumstances (geo-graphically remote areas, community clinics), anexcessive practice load may prevent the clinicianfrom undertaking an elaborate retreatment ofone tooth with a complex problem. In these cir-cumstances only and without an option for refer-ral, surgery is selected.

Previous Treatment Attempts

If a previous retreatment or apical surgery pro-cedure did not result in healing, the quality ofthat procedure should be evaluated. If the initialcase selection was appropriate and the quality canbe significantly improved, the same procedure isrepeated. Otherwise, the alternative is selected,which may better address the site of the infection(Figure 20-3).

PREVENTION OF DISEASE

Root canal-treated teeth may appear to be disease-free, yet harbor microorganisms in the canal . 3 Theapparent absence of disease suggests a balance be-tween the intracanal microorganisms, their envi-ronment, and the host; a change in this balancecan result in infection and disease. Another possi-bility is coronal leakage. The microorganisms in-vade the filled canal and cause infection withinweeks or months, even if the root canal is wellfilled.5

The factors that may affect emergence of post-treatment disease are the following:

1. Coronal restoration: If the endodontic sys-tem (pulp chamber, canals) has beenexposed to coronal leakage or secondarycaries, replacing the restoration may mod-ify the canal environment. This modifica-tion may result in availability of oxygenand substrate to favor pathogenic micro-bial strains, which may then establish in-fection (Figure 20-4).

2. Post restoration: There is a risk of canal con-tamination during post space preparationor post cementation.

3. Compromised host resistance: Theoretically,weakened host resistance can modify thebalance and prompt infection. This factor,however, has not been thoroughly investi-gated and its incidence is unknown.

Considerations controlling prevention of post-treatment disease include the following: (1) ade-quacy of the root filling; (2) adequacy of the coro-

nal seal; and (3) need for a new restoration (postand crown/bridge restorations represent a partic-ular concern, because they will restrict the optionof retreatment should disease emerge). The likeli-hood of emergence of post-treatment disease ap-pears to be highest when both the root filling andthe coronal seal are suspect and a new restorationis needed. In these cases retreatment is indicated,because it offers the benefit of preventing post-treatment disease. However, when a new restora-tion is not needed and only the root filling is sus-pect, emergence of post-treatment disease is lesslikely, and the benefit of retreatment is smaller.For these patients only follow-up is indicated;retreatment (and possible complications) can beavoided.7,8

Retreatment TechniquesTo perform retreatment, obstructions must beovercome to fully renegotiate the canal. These in-clude the coronal restoration, post and core, androot filling materials. Other occasional obstruc-tions, such as separated instruments, may alsohave to be dealt with.

ACCESS-CROWNS

Many retreatments require removal of a crown.On the other hand, a crown may be retained if sat-isfactory." In these cases, retreatment can be per-formed through the crown; rubber dam isolationand temporization are facilitated, function andesthetics are maintained, and additional cost ofreplacement is avoided. However, visibility may beobscured of key factors such as perforations, coro-nal extension of silver points, small canal orifices,and vertical cracks. Also, with the crown in place,the risk of irreparable errors during access is in-creased." If crown margins are poorly adapted,leakage and microbial contamination may occurduring retreatment and between appointments(Figure 20-5).

To avoid complications, crowns are removed forretreatment when marginal leakage or a crackedtooth is suspected or when future remake of thecrown is planned. However, to facilitate func-tion, esthetics, and isolation in selected teeth, thecrown may be retained temporarily with appro-priate steps to prevent complications.

Satisfactory crowns should be retained. Usu-ally, a wider-than-usual access is prepared throughthe crown and repaired later (see Figure 20-2). Forselected teeth, the crown may be removed intact

35 2


FIGURE 20-3Persistent disease after retreatment. A, Post-treatment disease in lateral incisor. B, Completed retreatment.C, Disease persists at 1 year; because healing is unlikely after another retreatment, root-end surgery is indicated.D, Complete healing at 6 months after surgery.


353

FIGURE 20-4Delayed emergence of post-treatment disease. A, Absence of disease 10 years after inadequate initial treatmenti n mandibular first molar. Restoration is required. B, Post-treatment disease at 6 months after restoration was per-formed. Retreatment was not performed and is now indicated, necessitating access through new crown.

and reused later (Figure 20-6). Removal of perma-nently cemented crowns may cause fracture oftooth structure; special devices must be used cau-tiously during this procedure. Crown removal isavoided when the type of cement and amount ofsupporting tooth structure are unknown.

ACCESS-POST AND CORE

Many retreatments require removal of a post andcore. Long and large posts are often strongly re-tained; attempts to remove them must precluderisks of root fracture or post breakage.22 A tech-nique for post removal with minimal risk is out-lined below.

Retention

Post retention must first be weakened (Fig-ure 20-7, A and B) . 2° The core is drilled away(cast core is reduced), leaving just the post ex-tending from the canal. The cement is then bro-ken up with piezoelectric ultrasonic vibration onthe post for 10 to 20 minutes. 23 Pointed tips areused to ultrasonically trough around the post.24

Extraction of Post

If the post has not been loosened and removedby vibration, it must be extracted with special

FIGURE 20-5Recurrent caries at the margins of the existing crown willallow leakage and microbial contamination during retreat-ment and between appointments. The crown must be re-moved before retreatment.

354


FIGURE 20-6Crown removed before retreatment and then reused after retreatment. A, Crown removal is required to examinethe possibility of vertical root fracture or pin perforation with post-treatment disease. B, Crown was removed withno fracture or perforation. Note the previously untreated distal canal. C, Original crown is recemented afterretreatment. D, Complete healing at 1 year. A defect is now visible at the distal crown margin; the crown shouldbe replaced.


355

FIGURE 20-7Extraction of a cast post and core. A, Rubber dam is applied. B, To weaken retention, core diameter is reduced toestimated post size, followed by ultrasonic vibration. C, Post diameter is standardized with a trepan bur (shown),then tapped with the extractor. D, Tapped post ready for extraction.

Continued

356


FIGURE 20-7, cont'dE, Extractor with washers fastened to the post.F, Pliers applied to the extractor. The washers reducepressure on the tooth. Pulling force is gradually in-creased. G, Extracted post.

instruments (Figure 20-7, C through G) . 22,24,25

The post is bored with a trepan and then tappedand firmly engaged with the matching size ex-tractor. Special pliers are applied to the extrac-tor. The tooth is used as the fulcrum, while rub-ber (and possibly steel) washers are placed as acushion to reduce pressure. This technique is ef-fective and relatively safe (Figure 20-8).26 In se-

lected situations, posts can be removed throughan in-crown access (Figure 20-9).

Avoiding Post Removal

In a multirooted tooth, retreatment may be indi-cated specifically in canal(s) other than the one re-taining the post. If post removal is considered


357

risky, access can be established through the coreonly to the retreated canal(s), without disturbingthe post (Figures 20-10 and 20-2).20

CANAL OBSTRUCTIONS

Canal patency is regained by eliminating the rootfilling and occasionally separated instruments. Tobe successful, this procedure requires a nonre-strictive straight-line access.27 Previous access isevaluated; often it must be extended before elimi-nation of canal obstructions is attempted.

The basic techniques for removing most ob-structions are outlined in the following sectionsfor general understanding, further details areavailable in reference articles.

Gutta-Percha

Gutta-percha is eliminated with rotary instru-ments and hand files. Solvent is used selectively. A"crown-down" sequence (progressing from largerto smaller instruments, coronal to apical) ispreferable.28

Rotary instruments. A variety of instrumentscan effectively remove gutta-percha, when ro-tated at 350 to 1000 rpm (exceeds the safetylimits of nickel titanium) . 29 °3° In the coronal por-tion of the canal, wide-taper rotary instrumentssuch as Gates-Glidden burs are used with mini-mal apical pressure. This expedites the proce-dure, forms a receptacle for solvent, and improves access (Figure 20-11).24,28,29 Use of heatedinstruments creates only a limited space withoutimproving access . 24

Further apically, nickel titanium rotary filescan be used .24,29,30 Caution is required to avoidseparation; pressure is very light, and drillingmust cease when gutta-percha debris stopssurfacing.

Solvent. Solvent softens gutta-percha andhelps prevent canal transportation. Therefore, itis used specifically for dense root fillings andcurved canal S.27 However, because of toxicity,solvent must not be extruded periapically. 31

Gutta-percha and sealers are soluble to a vary-ing degree in chloroform, carbon disulfide, ben-zene, xylene, essential oils, methyl chloroform,halothane, and white rectified turpentine ......Being highly volatile, chloroform is the most ef-fective. 33 It is safe for use in dentistry; however, inhigh concentrations its vapor is potentially haz-ardous . 3 5 -37 Therefore, chloroform is dripped di-rectly into the canal orifice, avoiding excessiveflooding of the chamber. The operating teamwears protective masks, and the patient's nose iscovered with the rubber dam.

FIGURE 20-sRetreatment in tooth with a well-retained post. A, Long castpost and crown in maxillary canine with post-treatment dis-ease. B, Proximal view of the post and extractor. Note theparallel design of this strongly retained post. C, Completedretreatment. D, Complete healing at 6 months.

Hand files. These are used mainly in the apicalportion of the canal.'"' When gutta-percha conesare poorly condensed or overextended, solvent isavoided. A reamer or file is used first to negotiatea pathway along the root filling. A larger file is

358


FIGURE 20-9Retreatment and post removal through crown. A, Three prefabricated posts in molar with post-treatment disease.B, Access for retreatment of mesial canals is through the crown and core. C, Completed retreatment. D, Progres-sive healing at 6 months.


35 9

FIGURE 20-1oRetreatment avoiding post removal in a multirooted tooth. A, Post-treatment disease associated with the mesialroot of the mandibular first molar. Removal of oversized post from the distal root is risky, with minimal benefitfrom retreatment of the distal canal. B, Access is through the crown and core with retreatment of mesial canals.C, Completed retreatment. D, Complete healing at 6 months.

360


FIGURE 20-11I nitial removal of gutta-percha. A, Poorly condensed root fillings. B, Coronal portion of gutta-percha is removedwith a Gates-Glidden bur. Access is improved, and a receptacle for solvent is formed.

then carefully "screwed" into the filling mass andpulled back, often retrieving all the gutta-perchacones27 With overextended cones, the file mayhave to be extended periapically to avoid sep-aration of the cone at the apical foramen(Figure 20-12).2 ' Overextended cones may sepa-rate at the apex and cannot be retrieved.

Pastes and Cements

Pastes and cements of varying hardness are usedas the principal root filling materials in certain re-gions of the world. To assess its hardness, the ma-terial must be evaluated clinically." Some fillingpastes are very hard and insoluble.

Soft-setting pastes. Canals filled with soft-settingpastes may be penetrated with files 2' A "crown-down" sequence is used to gradually eliminate thepaste from the entire canal . 2 $

Hard-setting cements. Resin-type cements shouldbe exposed to solvents such as tetrachlorethylene,xylene, eucalyptol, or eugenol.24 If softened, thecement is managed like soft-setting pastes . 2° Ifnot, the cement is broken down with moderateultrasonic vibration, using special pointed tips(Figure 20-13) under light apical pressure . 24,2' Toprevent perforation, the procedure is frequently

monitored with radiographs or an operating micro-scope?' This procedure is time consuming.38

As a last resort, the cement is drilled out withlong-shank, small round burs (Mueller burs areuseful) . 2 7 This is a very exacting procedure; fre-quent radiographic or microscopic control isimperative to prevent perforation .2' The cementis intermittently probed with a sharp endodonticexplorer to identify spaces that would permitrenegotiating the canal with instruments .2'

Metallic Objects-Silver Pointsand Separated Instruments

Metallic objects may often be retrieved or by-passed27 These procedures depend on accessibil-ity and canal anatomy.20 Accessibility is graduallymore restricted from the orifice level apically,particularly in curved canals.39 Bypass is most fea-sible in oval canals. 39

Retrieval from the chamber. Extension of thesilver point into the chamber is key to retrieval.27Ultrasonic vibration is carefully applied to reduceretention and free the point from the surround-ing core cement.24 After being loosened, the pointis grasped and retrieved with small pliers or spe-cial extractors .2'


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FIGURE 20- 12Removal of overextended gutta-percha. A, Root filling extends beyond the apices; there is post-treatment disease.B, After initial use of burs (see Figure 20-11), the gutta-percha cones were engaged with files and retrieved. Sol-vent was avoided. C, Completed retreatment. D, Progressive healing at 6 months.

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FIGURE 20-13Ultrasonic tips for breaking up hard-setting cements and loosening separated instru-ments under the operating microscope.

An amalgam core is separated from the sur-rounding dentin with ultrasonic tips or bursand dislodged as a whole.20 If the silver pointsare embedded in the core, they may be retrieved(Figure 20-14).

Bypass. The canal is first flared with Gates-Glidden burs. Hand files are then used with sol-vent to prepare a pathway around the metallicobject and possibly retrieve it."" Ultrasonic filesor pointed tips (see Figure 20-13) can be usedto vibrate the object, which may dislodge (Fig-ure 20-15) or shatter .24,39 If the object is bypassedbut not retrieved, it will be enclosed in the rootfilling.39 This procedure can be very time con-suming and possibly complicated by additionalfile separation, perforation, or apical displace-ment of the object.39 Visualization is optimizedwith the operating microscope."

Extraction from the canal. As a last resort, objectscan be extracted with special devices.20 Most avail-able devices include end-cutting trepans and ex-tracting tubes, with or without a locking mecha-nism (Figure 20-16).22,24,27 A trough is cut aroundthe object with ultrasonic tips or the trepans. Amatching extracting tube is applied, locked, ul-trasonically vibrated, and withdrawn. This is anexacting procedure; frequent radiographic or mi-croscopic control is imperative to prevent perfora-tion (Figure 20-17).

Because the extraction procedure requires con-siderable sacrifice of root dentin, it is safe only inlarge, straight roots.27 It is also time consuming,

particularly in posterior teeth .27,39 For these rea-sons, extraction is not the first choice for retrievalof metallic objects. 39

If the object is not bypassed or retrieved, by ne-cessity, only the accessible canal portion is re-treated. Prognosis is better when there is no rootcanal infection and periradicular disease.'

COMPLETION OF RETREATMENT

After renegotiating the canal, treatment is com-pleted using routine procedures. However, elimi-nation of root canal infection in retreatment ismore challenging than in initial treatment, pri-marily because there may be therapy-resistant mi-croorganisms, such as Enterococcus faecalis.1-3 Also,microorganisms may persist under residual rootfilling "patches," which usually remain during re-treatment.'""' Finally, canal wall surfaces mayremain untouched during retreatment."

The following are important for managementof post-treatment disease:

1. A wide, direct access is needed for betterinstrumentation.

2. The canal is enlarged somewhat beyond itsprevious size (see examples in figures) to re-duce residue of root filling materials.

3. Calcium hydroxide is used for canal disin-fection; therefore, two or more visits arerequired.

When retreatment is performed to preventpost-treatment disease, the canal enlargement is


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FIGURE 20- 14Retrieval of silver points extending into the pulp chamber. A, Silver points in molar with post-treatment disease.The points may be embedded in the amalgam partial core. B, The amalgam core was dislodged with one pointembedded. The underlying cement was dispersed ultrasonically, and the second point was retrieved with smallpliers. C, Completed retreatment, with sealer extruded. D, Complete healing at 6 months.

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FIGURE 20-15Retrieval of Thermafil carriers. A, Poorly adapted Thermafil root fillings; there is extensive post-treatment disease.B, Mesial carrier is removed with ultrasonic vibration. Distal carrier is bypassed. C, Completed retreatment afterthe distal carrier was retrieved. D, Incomplete healing at 1 year.


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FIGURE 20-16Hollow tubes to extract separated silver points and instruments from root canals. Cyano-acrylate glue is used in lieu of a locking mechanism.

moderate and use of intracanal medication is lesscritical. Therefore, retreatment can be completedi n one visit, when feasible.

As a final step, the canal is obturated and thetooth is restored. Outcome assessment is similarto that for initial root canal treatment, as outlinedin Chapter 19.

DEGREE OF DIFFICULTY

Clinical conditions that require particular exper-tise are listed below, with indication of the de-gree of difficulty (e = extreme; m = moderate).To avoid complications, these conditions shouldbe managed by endodontists.

Crown: Removal of the crown intact (e); re-treatment through an in-crown access (m).

Post: Cast post (e); oversized prefabricatedpost (e); retreatment avoiding post removal(e); regular-sized prefabricated post (m).

Root filling: Overextended gutta-percha (e);well-compacted gutta-percha (m); gutta-percha in a curved or ledged canal (m); hard-setting cement (e); silver point with coronalextension (m); silver point with restrictedaccessibility (e); separated instrument (e).

erative discomfort, including pain and swelling. '6

This is an additional reason why retreatment forexistent disease should not be completed in onevisit."

The long-term outcome of retreatment de-pends largely on regaining canal patency. Thehealing rate after retreatment for existent dis-ease is 74%, which is lower than after initialtreatment.1,2 The probability of healing is higherwhen factors facilitating infection (untreated orpoorly treated canal) are identified and can beaddressed satisfactorily during retreatment.9The healing rate after retreatment for preven-tion of disease is higher, comparable to initialtreatment.'

Short-Term and Long-TermTreatment OutcomeIn the short term, retreatment with existent post-treatment disease may be associated with postop-

Communication and ReferralRetreatment is more frequently associated withprocedural complications than is initial treat-ment." Effective communication requires thatthe patient be informed of potential problems be-fore retreatment is initiated to avoid frustration, dis-content, and possible litigation. This communica-tion includes explanation of the benefits, risks,potential restrictive factors as well as the short-and long-term outcome. Both retreatment andsubsequent restorative procedures are then au-thorized by the patient.43

Even when the patient is referred to the en-dodontist, explanation by the generalist is stillessential; it allows the patient to consider theoption of referral and consultation with the

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FIGURE 20-17Extraction of separated files. A, Both canals are blocked by separated files. B, Trepan bur is used to cut a trougharound each separated file. The trepan bur must remain centered to avoid perforation. C, Completed retreatmentafter both files were extracted. Note the sacrifice of root dentin. D, Complete healing at 1 year.


367

endodontist. Furthermore, the patient will haverealistic expectations.

The referral should be in writing and include allpertinent information: case history, previous radio-graphs, and an outline of the restorative/prosthetictreatment plan, particularly for the tooth to be re-treated. Emergency procedures performed by thereferring dentist are also mentioned. Midtreat-ment referrals (aborted retreatment attempt by thegeneralist), frequently associated with complica-tions, are to be avoided.'

REFERENCES

1. Friedman S: Treatment outcome and prognosis of en-dodontic therapy. In Orstavik D, Pitt Ford TR, editors,Essential endodontology: prevention and treatment of apicalperiodontitis, Oxford, 1998, Blackwell Science.

2. Sundqvist G, Figdor D, Persson S, Sjogren U: Microbi-ologic analysis of teeth with failed endodontic treat-ment and the outcome of conservative retreatment,Oral Surg Oral Med Oral Pathol 85:86, 1998.

3. Molander A, Reit C, Dahlen G, Kvist T: Microbiologi-cal status of root filled teeth with apical periodontitis,In[ Endod J 31:1, 1998.

4. Sjogren U, Figdor D, Persson S, Sundgvist G: Influenceof infection at the time of root filling on the outcomeof endodontic treatment of teeth with apical peri-odontitis, Int Endod j 30:297, 1997.

5. Friedman S, Komorowski R, Maillet W, et al: Resis-tance of coronally induced bacterial ingress by an ex-perimental glass ionomer cement root canal sealer invivo, JEndod 26:1, 2000.

6. Sakellariou PL: Periapical actinomycosis: report of acase and review of the literature, Endod Dent Traumatoi12:151, 1996.

7. Taintor JF, Ingle JI, Fahid A: Retreatment versus fur-ther treatment, Clin Prep Dent 5:8, 1983.

8. Friedman S, Stabholz A: Endodontic retreatment: caseselection and technique. Part 1: Criteria for case selec-

tion,J Endod 12:28, 1986.9. Bergenholtz G, Lekholm U, Milthon R, et al: Retreat-

ment of endodontic fillings, Scand J Dent Res 87:217,1979.

10. Lewis RD, Block RM: Management of endodontic fail-ures, Oral Surg Oral Med Oral Pathol 66:711, 1988.

11. Rein C, Grondahl H-G: Endodontic retreatment deci-sion making among a group of general practitioners,Scand J Dent Res 96:112, 1988.

12. Htilsmann M: Retreatment decision-making by agroup of general dental practitioners in Germany, IntEndod J 27:125, 1994.

13. Petersson K, et al: Follow-up study of endodontic sta-tus in an adult Swedish population, Endod Dent Trau-matol7:221, 1991.

14. Friedman S, Lustmann J, Shaharabany V: Treatmentresults of apical surgery in premolar and molar teeth, JEndod 17:30, 1991.

15. Crump M: Differential diagnosis in endodontic fail-ure, Dent Clin North Am 23:617, 1979.

16. Kvist T, Reit C: Postoperative discomfort associatedwith surgical and nonsurgical endodontic retreat-ment, Endod Dent Traumatol 16:71, 2000.

17. Reit C, Kvist T: Endodontic retreatment behavior: theinfluence of disease concepts and personal values, IntEndod j 31:358, 1998.

18. Tronstad L, Kreshtool D, Barnett F: Microbiologicalmonitoring and results of treatment of extraradicularendodontic infection, Endod Dent Traumatol 6:129,1990.

19. Pitts DL, Natkin E: Diagnosis and treatment of verti-cal root fracture, J Endod 9:338, 1983.

20. Stabholz A, Friedman S: Endodontic retreatment: caseselection and technique. Part 2: treatment planningfor retreatment,J Endod 14:607, 1988.

21. Metzger Z, Shperling I: Iatrogenic perforation of theroots ofrestoration-covered teeth,JEndod7:232, 1981.

22. Goon WWY: Managing the obstructed root canalspace: rationale and techniques, CalifDentAssocj 19:51,1991.

23. Johnson WT, Leary JM, Boyer DB: Effect of ultrasonicvibration on post removal in extracted human pre-molar teeth, j Endod 22:487, 1996.

24. Machtou P, Friedman S: Advances in endodontic re-treatment, Alpha Omegan 90:47, 1997.

25. Machtou P, Sarfati P, Cohen AG: Post removal prior toretreatment, J Endod 15:552, 1989.

26. Altshul JH, Marshall G, Morgan LA, Baumgartner JC:Comparison of dentinal crack incidence and of postremoval time resulting from post removal by ultra-sonic or mechanical force,J Endod 23:683, 1997.

27. Friedman S, Stabholz A, Tamse A: Endodontic re-treatment: case selection and technique. Part 3: re-treatment techniques, J Endod 16:543, 1990.

28. Mandel E, Friedman S: Endodontic retreatment: a ra-tional approach to root canal reinstrumentation, JEndod 18:565, 1992.

29. Hulsmann M, Stotz S: Efficacy, cleaning ability andsafety of different devices for gutta-percha removal inroot canal retreatment, Int Endod J 30:227, 1997.

30. Sae-Lira V, Rajamanickam 1, Lim BK, Lee HL: Effec-tiveness of Profile . 04 taper rotary instruments in en-dodontic retreatment,J Endod 26:100, 2000.

31. Barbosa SV, Burkard DH, Spangberg LW: Cytotoxic ef-fects of gutta-percha solvents,J Endod 20:6, 1994.

32. Wennberg A, Orstavik D: Evaluation of alternativesto chloroform in endodontic practice, Endod DentTraumatol5:234, 1989.

33. Wourms DJ, Campbell AD, Hicks ML, Pelleu GB: Al-ternative solvents to chloroform for gutta-percha re-moval, JEndod 16:539, 1990.

34. Whitworth JM, Boursin EM: Dissolution of root canalsealer cements in volatile solvents, Int Endod J 33:19,2000.

35. McDonald MN, Vire DE: Chloroform in the endodon-tic operatory, J Endod 18:301, 1992.

36. Margelos J, Verdelis K, Eliades G: Chloroform uptakeby gutta-percha and assessment of its concentration inair during the chloroform-dip technique, J Endod22:547, 1996.

37. Chutich MJ, Kaminski EJ, Miller DA, LautenschlagerEP: Risk assessment of the toxicity of solvents of gutta-

percha used in endodontic retreatment, J Endod 24:213, 1998.

38. Jeng HW, ElDeeb ME: Removal of the hard paste fill-ings from the root canal by ultrasonic instrumenta-

tion,J Endod 13:295, 1987.39. Nagai O, Yani N, Kayaba Y, et al: Ultrasonic removal of

broken instruments in root canals, Int Endod J 19:298,1986.

40. Wilcox LR, Swift ML: Endodontic retreatment in smalland large curved canals, J Endod 17:313, 1991.

41. Baldassari-Cruz LA, Wilcox LR. Effectiveness of gutta-percha removal with and without the microscope,

J Endod 25:627, 1999.42. Trope M: Flare-up rate of single-visit endodontics, Int

Endod J 24:24, 1991.43. Selbst AG: Understanding informed consent and its

relationship to the incidence of adverse treatmentevents in conventional endodontic therapy, J Endod16:387, 1990.

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Preventive Endodontics:Protecting the Pulp

LEARNING OBJECTIVES


i / Describe anatomic and functional relationships between dentin and pulp.

t / Understand unique physiologic and structural characteristics of the pulp and how these affect pulpresponse to injury.

3 / Discuss the effects of vasoconstrictor-containing local anesthetics on pulpal hemodynamics.

4 / Discuss the formation and role of tertiary dentin in pulp protection.

s / Comprehend the sensory function of the pulp.

6 / Recognize reparative potential of the pulp.

7 / Describe permeability of dentin and under what conditions permeability can be modified.

s / Identify and determine etiologic factors responsible for pulp pathosis.

9 / Recognize effects of chemical components of various restorative materials on the pulp.

10 / Appreciate the significance of microleakage and the smear layer on pulp responses.

11 / Discuss how bacterial growth beneath restorations can affect the pulp.

12 / Provide a rationale for cavity varnishes, liners, bases, and hybridization of dentin.

13 / Understand "thermal shock" and its significance.

14 / Be aware of potentially injurious effects of polishing of restorations, removal of metallic restorations, andplacement of pins.

9s / Understand the relationship between postrestorative pain and injury to the pulp.

16 / Discuss the possible effects of orthodontic tooth movement on the pulp.

17 / Discuss the management of deep carious lesions without pulp exposure.

18 / Discuss management of carious as well as accidental pulp exposure.

19 / Discuss the potential for periapical repair after treatment of deep carious lesions.

20 / Summarize preventive measures that should be observed during dental restorative procedures.

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370

21 / Preventive Endodontics: Protecting the Pulp

Pulp-Dentin Complex

Unique Characteristics of the Pulp

Reduced Blood Flow Associated with Local

Anesthetics

Tertiary (Reparative) Dentin

Sensory Function of the Pulp

Repair Potential of the Pulp

Dentin Permeability

Pulp Pathosis

Effects of Restorative Procedures

Cavity and Crown Preparation Factors

Effects of Restorative Materials

Role of Bacteria

Microleakage

Exothermic Materials

Hygroscopic Materials

Toxicity of Materials

Biologic Properties of Specific Materials

Protectants

Additional Factors

Postrestorative Hypersensitivity

Summary of Protective Measures

Orthodontic Procedures

Management of the Vital Pulp

Effect of Natural Causes of Pathoses

Maintenance of a Vital Pulp

I ndirect Pulp Capping

Direct Pulp Capping

Pulpotomy

Periapical Repair after Treatment of Deep

Carious Lesions

he goal Of this chapter is to con-sider preventive measures to protectthe dentin and pulp from injury. Why

should the dentist be concerned about pulpalprotection? What is so important about thisminuscule tissue?

In addition to its primary responsibility fordentin formation, the pulp serves as a sensoryorgan. Certain stimuli cause sensory receptors inthe pulp to trigger protective reflexes (such as jawopening) that serve to protect the tooth from frac-ture. If it becomes necessary to remove the pulp,the impact of endodontic treatment on toothstrength should be considered. To perform pulp-ectomy, the access cavity that must be preparedresults in the removal of mineralized tooth struc-ture. If removal is excessive, the cusps are weak-ened and prone to fracture. Root canal treatmentmay also compromise an existing restoration,thus necessitating its replacement. Involved thenare both the cost of root canal treatment and thepotential discomfort and inconvenience to the pa-tient. Maintaining the pulp and dentin intact(and healthy) is obviously a desirable objective.Vital pulp therapy as an alternative to pulpectomydeserves serious consideration.

Pulp-Dentin ComplexThe dental pulp is an ectomesenchymal-differen-tiated tissue that produces the dentin componentof mammalian teeth. The term dentin pulp complexemphasizes the intimate anatomic and physio-logic relationships between dentin and pulp. Theodontoblast processes and nerves that residewithin the dentinal tubules make dentin a livingtissue. Consequently, when performing clinicalprocedures, the clinician must view vital dentinthe same as other living tissues.

Unique Characteristicsof the PulpThe pulp is a loose, fibrous connective tissue re-sembling other connective tissues. However, thepulp is unique in that it lacks a collateral circula-tion because its blood supply is limited to the fewarterioles entering the apical foramen. In addition,the pulp is rigidly encased in hard tissue, thus plac-ing it in a low compliance environment similar tobrain, bone marrow, and nail beds. These tissues re-spond somewhat differently to noxious stimulithan do other tissues such as skin. In most tissuesthe cardinal signs of inflammation include redness,heat, swelling, pain, and loss of function.

Swelling results from reactive hyperemia andincreased vascular permeability; these vascular re-actions lead to the accumulation of edema fluidwithin the tissue. As tissue pressure increases, thetissue swells, which tends to ease the tissue pres-sure. Being encased in dentin, the pulp is unableto swell. Elevated tissue pressure is a major factorin pain associated with acute inflammatory reac-tions. For this reason, pain is generally more se-vere in tissues in a tow-compliance (unyielding)environment. Thus, pulpal edema or abscess for-mation is more likely to be painful than compara-ble lesions in a more compliant tissue, such asgingiva and oral mucosa.

When the pulp is subjected to injury, a signifi-cant increase in intrapulpal pressure occurs.'Blood pressure is greatest in arterial vessels andprogressively falls in magnitude in arterioles, cap-illaries, postcapillary venules, and venules, in thatorder. Because of the rigidity of dentin, the pulpdoes not expand; a sharp rise in intrapulpal pres-sure could result in compression of venules, thusi ncreasing vascular hindrance (resistance to bloodflow). This "strangulation" hypothesis holds thatspace for additional blood and tissue fluid is pro-vided by compression of venules, since pressurein the venules is lower than in the arterioles andcapillaries. According to this hypothesis, com-pression of venules would produce increased vas-cular resistance and passive congestion, which inturn would result in hypoxia; pulp tissue wouldeventually become necrotic because of a lack ofoxygen.

Marked compression of venules is unlikely,since the pulp is rich in proteoglycans. These mol-ecules have the ability to bind water, thus makingthe pulp a resilient tissue. Consequently, pulpalvenules are in a relatively compliant environment,which should protect them from abrupt pressurechanges. It has been demonstrated that pressurechanges in one part of the pulp do not necessarilyproduce pressure changes in other parts .

By applying Starling's Law, when interstitialtissue pressure exceeds intravascular pressure,fluid is forced back into the venules. Additionally,lymphatics are capable of removing excess fluid.This removal of fluid seems to be efficient, be-cause increased tissue pressure in the pulp mayactually begin to decrease while blood flow is stillincreasing. These phenomena have been eluci-dated by Heyeraas and Kvinnsland,3 a "must-read" publication.

If the strangulation hypothesis were valid, in-flamed pulps would undergo infarction. An in-farct is an area of ischemic necrosis produced byeither occlusion of the arterial supply or its ve-nous drainage. Pulpal infarcts are uncommon and


371

are usually due to trauma to the vessels entering the pulprather than to intrapulpal inflammation.

How then do pulps die? Much depends on thecause of the injury, the most common being bac-terial infection. Often infection involves the pres-ence of pyogenic bacteria, in which case pulpaldeath is associated with suppuration (liquefactivenecrosis). Bacteria that do not evoke suppurativei nflammation can damage tissues in other ways.For example, endotoxin, even in low concentra-tions, adversely affects the function and meta-bolic processes of cells.' The cell types particularlyinfluenced by endotoxin are fibroblasts, phago-cytes, platelets, and B-lymphocytes. In high con-centration, endotoxin will kill cells.

Activation of the immune system by antigenicbacterial products usually has deleterious effectson cells. For example, macrophages that are acti-vated by the immune system are important in me-diation of tissue destruction by secreting a widevariety of biologically active products, includingtoxic oxygen metabolites, nitric oxide, and pro-teases. The immune system can also stimulatefibroblasts, macrophages, and synovial cells to se-crete metalloproteinases, which can act on a varietyof extracellular components, including proteogly-cans, laminin, fibronectin, and amorphous colla-gens. Activation of the immune system can alsotrigger the proliferation of fibroblasts and produc-tion of collagen fibers. Ultimately, this results inpulpal fibrosis with the replacement of normalconstituents of the pulp and diffuse calcification.

Reduced Blood Flow Associatedwith Local AnestheticsVasoconstrictors added to local anesthetics mayhave a profound effect on pulpal blood flow, de-pending upon where the solution is injected. Aperiodontal ligament (PDL) injection of an anes-thetic such as 2% lidocaine with epinephrine1:100,000 significantly reduces pulpal blood flow(Figure 21-1).5,6 Fortunately, the rate of oxygenconsumption in the pulp is relatively low; if nec-essary, pulp cells can anaerobically produce en-ergy through the pentose phosphate pathway ofcarbohydrate metabolism.' Therefore, a healthypulp may survive episodes of ischemia lasting for1 hour or more. An ischemic pulp subjected to se-vere injury may hemorrhage when subjected totrauma, such as that associated with full crownpreparation without the use of an adequatecoolant. However, under experimental conditions,deep cavity preparation after PDL injection with2% lidocaine and epinephrine failed to evoke pul-pal hemorrhage or other evidence of damage .

FIGURE 21-1Effects of infiltration anesthesia (2% lidocaine with 1:100,000epinephrine) on pulpal blood flow in the maxillary canine teethof dogs. The arrow indicates the time of injection. The bar de-picts SD. (From Kim S, Edwall L, Trowbridge H, Chien S: l Dent

Res 63:650,1984.)

Tertiary (Reparative) DentinTertiary dentin formation is a fundamental de-fense mechanism. This is nature's way to seal offcut or diseased dentinal tubules at the pulpsurface, thereby diminishing the effects of attri-tion, dental caries, and other forms of trauma(Figure 21-2). Primary (developmental) dentinis formed during tooth development whereasphysiologic (regular) secondary dentin is de-posited circumpulpally throughout the life of avital tooth, thus causing the pulp chamber tobecome progressively smaller with age. Tertiary(reparative) dentin forms at the pulpal end ofthose tubules that are in communication withirritants such as attrition of tooth structure anddental caries.

Does tertiary dentin protect the pulp? Yes, inmost cases. There is usually no continuity be-tween the tubules in primary dentin and those intertiary dentin.9 Furthermore, the walls of thetubules along the junction between primary andtertiary dentin are thickened and often oc-cluded.10 Consequently, this junctional zone lim-its the diffusion of irritants into the pulp. Poor-quality tertiary dentin does not afford thisprotection. When the pulp becomes inflamed as aresult of irritation, the tertiary dentin that isformed often contains voids where soft tissue hasbeen entrapped, thus giving the dentin the ap-pearance of Swiss cheese (Figure 21-3). High-speed cutting techniques using water-spray as acoolant decrease tertiary formation by minimiz-ing trauma to the pulp.11

FIGURE 21-2Tertiary dentin (arrow) deposited beneath caries. (FromTrowbridge H0: J Endod 7:52, 1981.)

There is a misconception that calcium hy-droxide stimulates tertiary formation when ap-plied as a cavity liner or base. However, evidencewould suggest that this notion has no validity. ' 2There is no significant difference in the amountor thickness of tertiary dentin under silicate,amalgam, calcium hydroxide, zinc oxide-eugenol(ZnOE), or composites when placed in cavities ofcomparable depth." Tertiary dentin probablyforms in response to the trauma inflicted bycavity preparation rather than to the restorativematerial. As an agent used to cap mechanicalexposures, calcium hydroxide does provide aconsistent, yet transient antimicrobial environ-ment for dentin "bridge" formation. However,the long-term sealing efficacy of calcium hy-droxide is very poor; continual microleakage re-sults in recurrent caries, bacterial penetrationthrough the "bridge," pulp infection, and even-tual necrosis.", '5

372



373

FIGURE 21-3Poor quality tertiary dentin containing voids (arrow). Thisform of dentin is often referred to as "Swiss cheese" dentin.Note the presence of inflammatory cells in the pulp.

Sensory Function of the Pulp

Beyond 150 pin into the dentin from the pulpthe vital tubule complex is essentially devoid ofnerve fibers, yet the dentinoenamel junction(DEJ) is a sensitive area. Dentinal tubules con-tain odontoblast processes and fluid derivedfrom pulpal blood vessels. Stimuli are con-ducted from the outer surface of the tooth tonerve fibers in the underlying pulp via the fluidwithin the dentinal tubules. According to thehydrodynamic theory of dentin sensitivity, ex-posure of the tooth surface to cold or heatcauses contraction or expansion of fluid in thetubules, thus creating hydraulic forces. '6 Appli-cation of a hypertonic solution, air blasts, or aprobe to freshly exposed dentin causes a rapidoutward flow of fluid in the dentinal tubules(Figure 21-4). This rapid fluid movement servesas a transducer mechanism by deforming mech-anoreceptive sensory nerve endings located inthe tubules and underlying pulp, thus elicitingpain signals.

FIGURE 21-4Hydrodynamics. Fluid movement (arrows) in dentinal tubulesresulting from drying of exposed dentin. The movement offluid may stimulate the receptors at the base of the tubules,causing pain.

Repair Potential of the PulpTheoretically, the pulp is as well equipped to copewith injury as any other organ of the body. It iswell vascularized and has an ample supply of con-nective tissue cells capable of initiating repair. Inaddition, the pulp may produce tertiary dentinand thus withdraw from irritation. However,teeth are subjected to various forms of trauma,which may limit the pulp's ability to respond toi njury. In periodontally involved teeth, for exam-ple, the pulp may have fewer fibroblasts, bloodvessels, more collagen fibers, and dystrophic calci-fications than normal pulp (Figure 21-5). Connec-tive tissue repair may be compromised in a pulpthus affected. However, whether these pulps areless resistant to injury has yet to be determined.

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FIGURE 21- 5Pulp of periodontally involved tooth. Note fewer than normalcells and blood vessels and the presence of collagen fibersand dystrophic calcifications.

Other factors may also limit permeability. Forexample, hours after cavity preparation, the per-meability of dentin may decrease considerably."This dramatic reduction appears to result fromaccumulation of plasma proteins in the tubules.18The precise mechanism responsible for the in-gress of proteins into the tubules is unknown. Ap-parently, trauma associated with cavity prepara-tion results in inflammation and an increase invascular permeability. This allows plasma pro-teins to pass out of small blood vessels and diffuseinto the dentinal tubules. The clinical significanceof this interesting phenomenon requires furtherresearch.

Pulp Pathosis

Dentin PermeabilityDentin is permeable because of the dentinaltubules. Solutes can move through dentin ineither direction, that is, toward the pulp or to-ward the oral cavity. When bacteria invade toothstructure as a result of caries or restorative proce-dures, substances they release diffuse throughthe tubules toward the pulp along a concentra-tion gradient; when these bacterial productsreach the pulp, they evoke inflammation. Poten-tially irritating substances of bacterial origin in-clude enzymes, byproducts of cell respiration,proteases, endotoxin, fragments of cell walls, andammonia. Most of these substances are also anti-gens and elicit an immunologic response. Thus,the permeability of dentin influences the degreeto which the pulp is subjected to inflammatoryand immunologic stimuli.

With caries, dentinal tubules beneath the cari-ous lesion will often become partially occluded bymineral deposits, a condition known as dentinalsclerosis. Other causes of dentinal sclerosis in-clude attrition, erosion, and fracture of toothstructure. This sclerosis reduces the permeabilityof dentin.

Dentin permeability is of particular interestwhen the effects of restorative procedures on thepulp are considered. Restorations that do notprovide an impervious seal permit leakage tooccur between the restoration and tooth struc-ture, thus allowing bacteria to colonize the cavity.Without adequate precautions, toxic bacterialproducts may diffuse from cavity to pulp andevoke inflammation. For this reason, cavity var-nishes and liners were developed to attempt toblock the openings of the dentinal tubules andprevent the ingress of irritating substances.

Specific causes of pulp disease include bacterial in-fection and injury resulting from impact trauma,dentin fracture, attrition, abrasion, erosion, anddental treatment. Bacterial infection most com-monly results from caries, but pulps may also be-come infected as a result of tooth fracture, res-torative procedures, and very severe periodontaldisease (Figure 21-6). Diagnosis and treatment ofperiodontal disease are important if the pulp is tobe maintained in a healthy condition.

In this chapter attention is focused on dentaltreatment procedures as a cause of pulp diseaseand how pulpal injury can be minimized orprevented.

Effects of Restorative ProceduresAmong the various forms of dental treatment,restorative procedures are the greatest cause ofpulpal injury. Trauma to the pulp cannot alwaysbe avoided, particularly with excavation of a deepcarious lesion or preparation of teeth for fullcrowns. However, the astute clinician, by beingaware of the dangers involved in each step of therestorative process, can minimize or avoid injury,as outlined in the following discussion.

CAVITY AND CROWNPREPARATION FACTORS

Depth of Cavity

Dentin permeability increases exponentially withincreasing cavity depth, as both diameter and den-sity of dentinal tubules increase as the cavitydeepens (Figure 21-7). Thus, the deeper the cavity,the greater the tubular surface area into whichpotentially toxic substances can penetrate anddiffuse to the pulp. The length of the dentinal

FIGURE 21-6Severe periodontal disease. Apical migration of pocket ep-i thelium (arrow) has resulted in exposure of the apical fora-men of this tooth; this will often result in severe damage tothe pulp. The space between the tooth and pocket epitheliumi s a fixation artifact.

tubules beneath the cavity is also of importance.The farther substances have to diffuse, the morethey will be diluted and buffered by the dentinalfluid. A remaining dentin thickness of 2 mm isusually sufficient to shield the pulp from mostforms of irritation. However, there is always thethreat of microleakage; it is wise to seal vitaldentin regardless of the thickness of remainingdentin.

As stated earlier, cavity depth determines theextent to which amputation of odontoblastprocesses results in injury to the cell body. Ifprocesses are severed close to the odontoblast cellbody, the cell is likely to suffer irreversible injury.In general, the deeper the cavity preparation, themore damage and death of ontoblasts.1 2,19

Frictional Heat

Frictional heat is produced whenever a revolvingbur or stone is brought into contact with tooth


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FIGURE 21- 7Difference in size and number of tubules in the dentinal floorof a shallow (A) and a deep (8) cavity preparation. (From

Trowbridge H0: Dentistry82:22, 1982.)

structure. Until the 1950s the method of enameland dentin preparation involved heavy torque,low rotational speeds, and steel burs that were notcooled with water. Consequently, vital dentin wasoften scorched, and pulps were injured as a resultof noxious heat.

Dentin is an effective insulator; for this reasonjudicious cutting is not likely to damage the pulpunless the thickness of dentin between prepara-tion and pulp is less than 1.0 mm. Even then, theresponse should be mild. Perhaps the greatestamount of frictional heat is generated with a largediamond stone when teeth are prepared for a fullcrown. The heat generated may also have a desic-cating effect by "boiling" away dentinal tubulefluid at the dentin surface.

"Blushing" of dentin during cavity or crownpreparation is thought to be due to frictional heatresulting in vascular injury (hemorrhage) in thepulp. The dentin takes on an underlying pinkishhue soon after the operative procedure. Crownpreparation performed without the use of acoolant leads to a marked reduction in pulpalblood flow, presumably because of vascular stasisand thrombosis.20

In the absence of infection or other complicat-ing factors, damaged pulps usually undergo re-pair." However, a pulp that has already been com-promised by caries or is ischemic after a PDLinjection of a vasoconstrictor-containing localanesthetic may be more vulnerable to thermal in-jury than an otherwise healthy pulp.

The amount of heat produced during cuttingis determined by sharpness of the bur, theamount of pressure exerted on the bur or stone,and the length of time the cutting instrument

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contacts tooth structure. The safest way to pre-pare tooth structure is to use ultra-high speeds ofrotation (100,000 to 250,000 rpm), an efficientwater cooling system, light pressure, and inter-mittent cutting. During cutting at high speeds,the revolving bur creates an area of turbulencethat tends to deflect a stream of water. Therefore,an air-water spray with sufficient volume andpressure must be used if the coolant is to over-come the rotary turbulence. The bur-dentin inter-face should be constantly wet.

Cavity preparation with a low-speed hand-piece, sharp bur, and light, intermittent pressureis only slightly more injurious than cutting athigh speeds. Hand instruments and low-speedcutting are relatively safe ways to finish a cavitypreparation, rather than using a high-speed hand-piece with the water coolant shut off.

Injury to Odontoblasts

Odontoblasts are vulnerable and, unfortunately,may be subjected to many insults. In addition todesiccation, heat, and vibration, they may beexposed to bacterial toxins, acids, caustic steriliz-ing agents, and other chemical irritants. Even incarefully prepared cavities, intracellular changeswithin odontoblasts located beneath the cavitymay occur, including disruption of mitochondriaand rough endoplasmic reticulum." When cellu-lar injury is reversible, the organelles return tonormal within a few days.

Drying of Dentin

A prolonged blast of compressed air to freshlyexposed vital dentin will cause a rapid outwardmovement of fluid in patent dentinal tubules.Tubule diameter is extraordinarily small; midwaybetween the pulp and the DEJ the mean diameterof the tubules is only 1.5 mm.23 The smaller thebore of a capillary tube, the greater the capillarypressure. Therefore, removal of fluid from thetubules by a blast of air activates strong capil-lary forces. These in turn lead to a rapid outwardflow of dentinal fluid. Fluid removed from thetubules at the dentin surface is replaced by fluidfrom the pulp.

As discussed above, rapid outward flow of fluidin the dentinal tubules stimulates mechanorecep-tors in the subjacent pulp, thus producing pain.Rapid outward fluid movement may also resultin odontoblast displacement; odontoblasts are dis-lodged from the odontoblast layer and pulledoutward into the tubules (Figure 21-8). Within ashort time the displaced cells undergo autolysisand disappear. Providing the pulp has not been

FIGURE 21-8Nuclei of odontoblasts (small arrows) that have been dis-placed into dentinal tubules. Note intact capillary (largearrow). Had desiccation produced trauma to the subodonto-blast zone, the capillary would have been disrupted.

severely injured, either by caries or other factors,displaced odontoblasts are replaced by new cellsthat are derived from odontoprogenitor cells inthe underlying cell-rich zone of the pulp.24 In thisway the odontoblast layer is reconstituted by "re-placement" odontoblasts capable of producingtertiary dentin (Figure 21-9). However, vigorousdrying of dentin alone does not result in severe in-jury to the underlying pulp.25 Loss of odonto-blasts is often followed by the formation of ter-tiary dentin (Figure 21-10).

Recently, drying agents containing lipid sol-vents such as acetone and ether have appeared onthe market. Because of their rapid rate of evapora-tion, application of such substances (includingalcohol) to exposed dentin produces strong hy-drodynamic forces in the tubules, often causingodontoblast displacement.26 Therefore, cavitiesshould be dried with cotton pellets and shortblasts of air rather than harsh chemicals. Pro-longed air-drying should be avoided.

Cavity Cleansing

The traditional method of cleansing cavity wallsof saliva and cutting debris is to flush the cavitywith a stream of water. However, flushing withwater is ineffective in removing the smear layer,


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FIGURE 21-9Layer of replacement odontoblasts. (From Trowbridge H0: J Endod 7:52, 1981.)

which consists of fragments of microscopic min-eral crystals and organic matrix produced whentooth structure is cut with a bur or chisels. Thislayer may interfere with the adherence of adhesiverestorative materials such as dentin bondingagents, although some newer bonding agents re-portedly bond to the smear layer. Acidic cavitycleansing products and chelating agents havebeen used to remove the smear layer.

Complete dissolution of the smear layer opensthe dentinal tubules, significantly increasing thepermeability of dentin. if the dentin is left un-sealed, diffusion of irritants to the pulp may in-tensify and prolong the severity of pulp reac-tions.27,28 However, the smear layer does havesome desirable properties. By blocking the orificesof dentinal tubules, the smear plugs greatly de-crease the permeability of dentin, thus limitingthe diffusion of substances to the pulp.26 Whilethe smear layer is impervious to bacteria, thus pre-venting microorganisms from gaining access tothe dentinal tubules, it is not a barrier to bacterialproducts, the primary cause of pulpal irritation.29

Acid Etching

Organic and inorganic acids are often used toetch the enamel and dentin to enhance the reten-tion of adhesive resin systems. Even with the de-velopment of acidic gels for enamel etching, acidmay flow onto dentin. Acid etching of dentingreatly increases dentin permeability. Thus, if mi-croleakage develops in a cavity in which the wallshave been acid etched and poorly sealed, irritants

FIGURE 21-10Formation of tertiary dentin (TD) resulting from loss of pri-mary odontoblasts during a restorative procedure. The ter-tiary dentin is being formed by replacement odontoblasts.

are likely to reach the pulp. However, in the ab-sence of microleakage, acid etching of dentin initself does not appear to produce injury to thepulp.30,31 The reason is that when dentin is dem-ineralized by acid, calcium and phosphate ionsare released, thus producing a buffering action.Data show that even when placed in deep cavities,acid etchants produce only a small increase in hy-drogen ion concentration in the pulp.32

Cavity Disinfection

Until the 1950s, potent antimicrobial agents suchas phenol, thymol, beechwood creosote, and silver

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nitrate were routinely used for cavity disinfection.These caustic substances are not recommended;agents that destroy bacteria also injure the pulp.Although milder germicides such as benzalko-nium chloride and 9-aminoacridine are probablywell tolerated by the pulp, their clinical effective-ness is untested .

33,34

Making of Impressions

Rubber base and hydrocolloid materials do not in-jure the pulp when they are used for impressionsof cavity and crown preparations. However, heatedmodeling compound may be damaging; the com-bination of heat and pressure can be deleterious.35Devastating temperatures of up to 52'C have beenrecorded in the pulp during impressions withmodeling compound in copper bands . 36

FIGURE 21-11Pulpal abscess that has developed as a result of severe mi-croleakage around a restoration.

Fabrication of ProvisionalResinous Crowns

Heat generated during the exothermic polymer-ization of autopolymerizing resinous materialsmay injure the pulp. 37 The use of cooling proce-dures is strongly recommended when provisionalcrowns are directly fabricated. Before cementingprovisional crowns, the crown preparation shouldbe carefully lined with temporary cement to min-imize microleakage. It is important to have the ce-ment in place for a short period of time; tempo-rary cements are not stable and will eventuallywash out.

Cementation of Castings

During cementation of crowns, inlays, and bridges,strong hydraulic forces may be exerted on the pulpas cement compresses the fluid in the dentinaltubules. In deep preparations this can result in aseparation of the odontoblast layer from the pre-dentin, which is a mild injury. To reduce this pres-sure, vents in the casting will allow cement to es-cape. This also facilitates seating of the casting andrelieves pressure on the pulp.

Occasionally pain occurs during or after ce-mentation of castings. Pain may occur wheneither zinc phosphate or glass ionomer cementsare used, but generally the discomfort does notlast very long.38

Effects of Restorative MaterialsWith regard to the biologic impact of restorativematerials on the pulp, the physical properties areconsiderably more important than the chemical

components. For many years it was thought thatcertain restorative materials were more irritatingthan others. However, the cause of irritation re-mained speculative. Presumably, restorative mate-rials contain toxic chemicals that leach from therestoration and diffuse through the dentinaltubules to injure the pulp. Until recently this ex-planation was universally accepted, but more so-phisticated investigative techniques and better in-terpretation of research results have provided newi nsights into the cause of pulpal injury.

ROLE OF BACTERIA

There is strong evidence that microleakage result-ing in bacterial colonization of cavity walls is themajor cause of pulpal injury. Histobacterial stainshave been used to relate the response of pulps torestorative materials. A high correlation was foundbetween the presence of bacteria beneath res-torations and inflammation in the underlyingpulp.21,39 Development of an abscess is not uncom-mon when microleakage is severe (Figure 21-11).

Germ-free animal studies also implicated bac-teria as a factor in pulpal injury resulting fromrestorative procedures. When acidic cements wereapplied to exposed pulps in molars of germ-freeand conventional rats, there was no pulpal in-flammation in the germ-free group. 4 0 In the pulpsof conventional animals, bacteria were observedin association with inflammation and necrosis.

Another means of studying the role of bacteriais "surface-sealing" of restorations. Surface seal-ing involves the removal of the outer part of arestoration and replacement with ZnOE. Thismaterial prevents bacteria from penetrating thegap between the restoration and the walls ofthe cavity. Such surface-sealing experiments have


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FIGURE 21-12Specimen from a surface-sealing experiment showing pulp7 days after placement of amalgam (A) against exposedpulp tissue. Note absence of pulpal inflammation. (FromCox CF, Keall CL, Keall HJ, Ostro E: J Prosthet Dent 57:1,1 987.)

shown that potentially irritating restorative mate-rials such as amalgam, composite resins, silicatecement, and zinc phosphate cement produce onlya thin zone of contact necrosis with no significantinflammation when placed on exposed humanand primate pulps (Figures 21-12 and 21-13). 41Cox et al . 31 usually observed dentin bridge forma-tion when composite resins, silicate cement, andzinc phosphate cement were placed in contactwith the pulp.

Some bacteria may remain in the smear layerafter the tooth has been restored.42 However,microorganisms require nutrients to maintaintheir viability; if denied substrate they eventu-ally die . 43 Evidence suggests that bacteria willgrow beneath a restoration only in the presenceof microleakage.44

MICROLEAKAGE

Microleakage is a major problem in restorativedentistry. Until the advent of more advanced

FIGURE 21-13Surface-sealing experiment demonstrating 14-day responseof the pulp to silicate cement (SC), which was occupying thespace. In the absence of bacterial leakage new dentin matrixhas been deposited adjacent to remaining dentin walls aswell as to the silicate interface. (From Cox CF, Keall CL, KeallHJ, Ostro E: J Prosthet Dent 57:1, 1987.)

dentin bonding adhesive systems, most materialsdid not adapt to tooth structure well enough toprovide a leak-proof marginal seal. Or, if there wasgood adaptation at the time of insertion, shrink-age resulting from physical or chemical changeswithin the material commonly caused gaps toopen, resulting in microleakage .2' This is exem-plified by shrinkage of certain acrylic resins dur-ing polymerization. If a restorative material hasa higher coefficient of thermal expansion thantooth structure, a decrease in temperature willcause contraction gaps to develop.

Another cause of microleakage is elastic de-formation of tooth structure produced by mas-ticatory forces. 45 In other words, the enameland dentin surrounding the rigid restorationflex and move, resulting in gaps (an "unzipping"from occlusal to cervical). This is particularly

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apt to increase leakage in deep MOD restora-tions.46 Masticatory forces may have a markedeffect on leakage in class V cavities restored withcomposite. In one primate study, leakage wasgreater in teeth in functional occlusion than inadjacent teeth without antagonists.47

Skill of the operator also influences microleak-age. The quality of the preparation and the waythe material is inserted can greatly influence adap-tation. In the case of amalgam alloy, the methodof insertion and plasticity of the mix are the mostimportant factors in determining the extent ofmicroleakage." In this respect, computer-drivenamalgamators provide better amalgam tritura-tion than the older mechanical units.

Moisture control is also important becausecertain restorative materials may develop mar-ginal leakage if they are contaminated with saliva,blood, or water during placement.

None of the older permanent resin-based, es-thetic restorative materials mentioned previouslyconsistently provided a long-term marginal seal.Recently developed dentin bonding and adhesiveagents have been shown to couple (hybridize*)within vital dentin." These new materials showpromise in preventing microleakage. Without along-term seal of the remaining dentin or dentinbridges, microleakage will occur, leading to bacte-rial colonization and eventual pulpal inflamma-tion (Figure 21-14). It is for this reason that adhe-sive systems such as 4-meta are recommended.

EXOTHERMIC MATERIALS

Some luting cements generate heat during setting;it has been suggested that this might cause pulpalinjury. The most exothermic luting material iszinc phosphate (ZnOP) cement." However, duringsetting an intrapulpal temperature increase ofonly 2'C was recorded. Heat of this magnitude isnot sufficient to injure the pulp.

HYGROSCOPIC MATERIALS

FIGURE 21-14Eight-week response after restoring with a composite resin.I nflammatory reaction adjacent to tertiary dentin indicatingcontinued irritation. (From Heys RJ, Heys DR, Fitzgerald M: IntEndod J 18:260, 1985.)

much less than that removed from dentin duringcavity drying, a procedure that produces an in-significant amount of pulpal inflammation.25

TOXICITY OF MATERIALS

Certain restorative materials are composed ofchemicals that have the potential to irritate thepulp. However, when placed in a cavity, the inter-vening dentin usually neutralizes or preventsleachable ingredients from reaching the pulp in ahigh enough concentration to cause injury. Forexample, eugenol in ZnOE is potentially irritat-ing, but very little can diffuse to the pulp.51 Phos-phoric acid is a component of silicate and zincphosphate cements. For decades it was thoughtthat injury was due to the high concentration ofhydrogen ions reaching the pulp. However, thebuffering capacity of dentin greatly limits theability of hydrogen ions to reach the pulp.52

Some hygroscopic materials may potentially causeinjury by withdrawing fluid from dentin. However,little relationship exists between the hydrophilicproperties of materials and their effect on thepulp." Moisture absorbed by materials is probably

*Hybridization is the mechanical penetration of adhesivepolymers with both collagen and carbonate dentin sub-strate. Specifically, the polymers infiltrate the intertubular,peritubular, and dentinal tubule complex to provide a sealagainst microleakage. In addition, the hybrid layer pro-vides a bonding substrate in preparation for placement ofthe definitive restoration.

BIOLOGIC PROPERTIESOF SPECIFIC MATERIALS

Zinc Oxide-Eugenol

Zinc oxide-eugenol (ZnOE) has many uses indentistry, having had a long history as a tempo-rary filling material, cavity liner, cement base, andluting agent for provisional cementation of cast-ings. Before the introduction of calcium hydrox-ide, ZnOE was the material of choice for directpulp capping.

Eugenol, biologically the most active ingredi-ent in ZnOE, is a phenol derivative and is toxic

FIGURE 21-15Positive bacterial staining reaction showing bacteria on cavitywall beneath composite resin restoration. These bacteria pro-duce by-products that may diffuse through tubules to causepulpal inflammation. (From Heys R1, Heys DR, Fitzgerald M:Int Endod J 18:260,1985.)

when placed in direct contact with tissue. It alsopossesses antibacterial properties. Eugenol's use-fulness in pain control is attributed to its abilityto block the transmission of nerve impulses.53 Re-searchers have found that a thin mix of ZnOE sig-nificantly reduces intradental nerve activity whenplaced in a deep cavity preparation in cats' teeth;however, a dry mix of ZnOE has no effect.54

It is the physical and chemical properties ofZnOE that are beneficial in preventing pulpal in-jury and in reducing postoperative tooth sensi-tivity. Importantly, it provides a good biologicseal; also its antimicrobial properties enable itto suppress bacterial growth, thus reducing for-mation of toxic metabolites that might result inpulpal inflammation. Of the restorative materialstested, only ZnOE consistently inhibited bacterialgrowth beneath restorations . 44

Zinc Phosphate Cement

Zinc phosphate is a popular luting and basingagent. It has a high modulus of elasticity and there-fore is commonly used as a base beneath amalgamrestorations. The phosphoric acid liquid phase wasformerly thought to injure the pulp. However, re-cent studies have shown that this is not the case .31Cementation of castings with ZnOP is well toler-ated by the pulp.55 Researchers reported that ZnOPis more likely to produce pulpal sensitivity at thetime of cementation and 2 weeks after cementationthan glass ionomer.38 However, 3 months after ce-mentation there was no difference in sensitivity.


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Polycarboxylate Cement

When placed in cavities or used as a luting ce-ment, zinc polycarboxylate does not irritate thepulp.56 In cementing well-fitting crowns and in-lays, neither polycarboxylate nor ZnOP cementscontract enough to permit the ingress of bacteria.Consequently, it is unnecessary to apply a varnishor liner to cavity walls; doing so only reduces ce-ment adhesion.

Restorative Resins

Early adhesive bonding and resin composite sys-tems contracted during polymerization, resultingin gross microleakage and bacterial contamina-tion of the cavity. Bacteria on cavity walls andwithin axial dentin are associated with moderatepulpal inflammation (Figure 21-15).5' Over a pe-riod of time, some composites absorb water andexpand; this tends to compensate for initial con-traction. To limit microleakage and improve re-tention, the enamel margins are beveled and acidetched to facilitate mechanical bonding. Whencompared with unfilled resins, the newer resincomposites present a coefficient of thermal ex-pansion similar to that of tooth structure. Withrecently developed hydrophilic adhesive bondingcomposite systems, the problem of marginal leak-age appears to have been diminished. 58

Glass lonomer Cements

Glass ionomer cement originally was used asan esthetic restorative material. Biocompatibilitystudies'"' show that these cements generallyhave no effect on the pulp. However, when usedas a bulk filling material, glass ionomer leaks; acavity liner is strongly suggested with this typeof cement.61

Through the use of finely ground powders andlight-curing technology, glass ionomer luting ce-ments have evolved to rival the use of other lutingagents. The results of a microleakage study showedthat glass ionomer cements provide a good mar-ginal seal when used to cement castings in vitro .6z

Although many reports of pulpal sensitivity havebeen associated with the use of glass ionomer ce-ments, there appear to be no sensitivity differencesbetween glass ionomer and ZnOP cements. En-dodontic problems are infrequent.38

Amalgam

Amalgam alloy is the most widely used dentalmaterial for restoring posterior teeth. A problemwith older, lathe-cut amalgams was shrinkageduring setting, which resulted in microleakage.

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Over time, this initial microleakage decreases ascorrosion products accumulate between restora-tion and cavity walls.63 Newer high-copper spheri-cal amalgam alloys show slight to moderate put-pal inflammation that diminishes with time, alsoprobably because of progressive corrosion (whichis slower than lathe-cut amalgams) and reductionin microleakage."

PROTECTANTSCavity Varnishes, Liners, and Bases

An attempt has been made to minimize the effectsof microleakage through the use of cavity var-nishes and liners. Varnishes are solutions of or-ganic solvent and resin. Liners are a suspension ofmaterials such as calcium hydroxide, polystyrene,and ZnOE in a volatile organic liquid or aqueoussolution. When the solvent evaporates, a thinfilm of residue forms a coating on the dentin tohopefully seal tubule openings. Thicker cements(bases) may also be used to line the cavity; in shal-low cavities thick bases take up too much space,interfere with retention, weaken the restoration,and provide no protection.65

Varnishes provide a partial short-term barrierto irritants that might injure the pulp. 66,67 Whenapplied to dentin, they neither bond nor form animpervious coating. Application of two or threecoats is necessary to minimize the voids. Al-though the varnish layers eventually disintegrate,they compensate for the initial contraction ofamalgam and thus reduce microleakage until cor-rosion products fill the contraction gaps. Pashleyet a1 .68 determined that varnishes, liners, andbases all reduced dentin permeability-varnishesthe least and bases the most.

"Insulating" Effect of Bases

A common misconception is the necessity of plac-ing an insulator beneath metallic restorations toprotect the pulp from thermal shock (hypersensi-tivity). Dentin is an excellent insulator; additionalthermal insulation is rarely if ever needed. In fact,thick cement bases are no more effective than justa thin layer of varnish in preventing thermal sen-sitivity, indicating that postrestorative sensitivityis at least partly due to microleakage.69

According to the hydrodynamic theory ofdentin sensitivity, rapid heating or cooling of thetooth causes fluid in the dentinal tubules to ex-pand or contract, resulting in rapid movement offluid in the dentinal tubules.16-70 Presumably thisfluid movement produces pressure changes thatactivate mechanosensitive nerve endings locatedin the underlying pulp, thus producing pain.

When a tooth is restored with amalgam, gapsopen around the restoration as the material sets,and fluid accumulates in these gaps. Unlessdentin is sealed, fluid in the contraction gapscommunicates directly with fluid in the underly-ing tubules. When the restoration is subjected toice-cold foods or liquids, fluid in the contractiongaps and dentinal tubules contracts, resulting inhydrodynamic activation of sensory nerve fibersand sharp pain. Newer adhesive dentin bondingsystems minimize microleakage; therefore, fluidin the marginal gap is separated from the fluid inthe dentinal tubules, thus reducing the volume offluid affected by temperature change.58

Inflammation may also relate to postoperativehypersensitivity. Traumatic cavity preparationoften produces an acute inflammatory reaction inthe pulp. This results in an elevation in intrapul-pal pressure and activation of inflammatory me-diators such as bradykinin and prostaglandin E 2,which may produce a state of hyperalgesia. Untilthe inflammation resolves, the pulp may respondto stimuli that would not normally evoke painsignals.71 Hyperalgesia is more profound in low-compliance tissues such as the pulp and nail bed.

ADDITIONAL FACTORSHeat of Polishing

Enough frictional heat may be generated duringpolishing of a restoration to seriously injure thepulp. Continuous polishing of amalgam restora-tions with rubber cups at high speeds causes adamaging temperature increase of up to 20°C inthe pulp; heat of this magnitude may produce tis-sue necrosis. For safety, polishing with rubberwheels or rubber cups should be at low speedsusing intermittent pressure and a coolant.72.73

Removal of Metallic Restorations

The use of burs to remove metallic restorationsmay also produce very high levels of frictionalheat, exposing the pulp to injury. A coolant suchas water spray or a combination of water and airavoids a burn lesion in the pulp. It is also advisableto use intermittent grinding using light pressure.

Pins

Pins to retain amalgam or other material requirecaution; pulp damage may result from pinholepreparation or pin placement. Coolants do notreach the depth of the pin preparation. Duringpinhole preparation there is always the risk ofpulp exposure. Furthermore, friction-locked pinsoften produce microfractures that may extend


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through dentin to the pulp, subjecting it to irrita-tion and the effects of microleakage.74

POSTRESTORATIVEHYPERSENSITIVITY

Many patients complain of hypersensitivity after arestorative procedure .75 Pain may be a warning sig-nal that the pulp has been injured. Often (but notalways) a relationship exists between tooth sensi-tivity and pulpal inflammation.66 Discomfort isusually of short duration; if pain is persistent orspontaneous, the injury probably resulted in irre-versible pulpitis. Many patients receiving resto-rative treatment experience some degree of post-operative discomfort. Hypersensitivity to cold iscommon; sensitivity to heat is less so.

Pain evoked by biting pressure indicates injuryto the periodontal ligament resulting from hyper-occlusion. Hyperocclusion is not injurious to thepulp but may cause a transient hypersensitivity,which usually resolves with occlusal adjustment.

SUMMARY OFPROTECTIVE MEASURES

Most injuries to the pulp from restorative proce-dures are avoided with certain precautions.

Heat produced during cavity preparation isminimized using light, intermittent cutting, anefficient water-cooling system, and a handpiecewith high speeds rather than high torque. Prepa-rations should be finished using hand instru-ments or with low speed and sharp burs.

Desiccation of dentin is avoided by drying thepreparation with cotton pellets and short airblasts from an air syringe; prolonged air blasts aredamaging. Newer hydrophilic primers bond andhybridize vital dentin while some surface mois-ture is still present.

Chemicals on freshly exposed dentin may dif-fuse to the pulp and produce injury. Therefore,caustic drying, cleansing, and sterilizing agentssuch as alcohol, acetone, phenol, and silver nitrateshould be avoided and are ineffective anyway.

Physical as well as chemical properties should beconsidered when a restorative material is selected.These include aspects such as coefficient of ther-mal expansion, modulus of elasticity, contractionduring polymerization, and adaptation to toothstructure.

Unstable, soluble liners and bases (most containcalcium hydroxide) should not be used on thefloor of a deep cavity. Within a few years recurrentcaries may develop beneath such liners and bases.

Microleakage must be minimized; it is a muchgreater threat than the toxic ingredients of mate-

rials per se. Because gaps form around restora-tions, a bonded hybridized adhesive, varnish, orliner should be used in conjunction with mostrestorative materials to prevent microleakage."

Polishing of metallic restorations is a potentialsource of noxious heat. Intermittent polishingwith an adequate air-water coolant will reducethe risk of pulpal injury.

Long-term assessment is critical whenever there isdoubt as to the pulp response to previous patho-sis or to the restorative procedure.

Orthodontic ProceduresFortunately, tooth movement is not a commoncause of pulp pathosis, although pulp necrosis isan occasional complication." Forces involved intooth movement may produce changes in pulpalblood flow.78 Also, oxygen utilization by pulpcells is depressed after application of orthodonticforces.7 9 Subsequent to arch wire activation, teethoften are hypersensitive to cold for a few days,suggesting that sensory structures are transientlyaffected.80 At times, orthodontically treated teethwith vital pulps do not respond to the electricpulp test.81 This condition may result from al-tered blood flow or injury to the sensory nervefibers entering the apex.

Management of the Vital PulpEFFECT OF NATURAL CAUSESOF PATHOSESCaries

Caries is a localized, progressive destruction oftooth structure and the most common cause ofpulp disease. It is now generally accepted that forcaries to develop, specific bacteria must becomeestablished on the tooth surface. Products of bac-terial metabolism, notably organic acids and pro-teolytic enzymes, cause the destruction of enameland dentin. Bacterial metabolites diffusing fromthe lesion to the pulp are capable of elicitingan immune response and inflammatory reaction.Eventually, extensive dentin involvement resultsin bacterial infection of the pulp, particularlyafter carious exposure.

Removal of gross caries and preparation forrestoration are generally accomplished with ro-tary instruments. Hand instruments are avoidednear the pulpal wall to prevent accidental me-chanical pulp exposure. Final removal of cariousdentin is generally accomplished with a large,sharp round bur at slow speed to remove the lastlaver of softened and discolored dentin.

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21 / Preventive Encloclontics: Protecting the Pulp

Erosion, Abrasion, and Attrition

With increasing frequency, our senior citizens areretaining their natural teeth. Consequently, den-tists are dealing with an increasing incidence ofage-related dental problems. In addition to rootcaries, older teeth exhibit the typical signs of wearand tear. Erosion results from the effects of oral orgastric acids on enamel and dentin from the con-stant "sipping" of acidic drinks. Abrasion lesionsgenerally occur from improper oral habits such asthe use of toothpicks, pins, or other hard objectsor from overaggressive tooth brushing with abra-sive toothpastes, often in an attempt to whitenthe teeth. The result of this is the creation of facialcervical defects. Attrition lesions appear in thoseteeth with malocclusions or with certain oralhabits of individuals, resulting in the grindingaway of enamel and vital dentin. Previously, theselesions were restored with unsightly materialssuch as gold foil, amalgam, silicate, or resin com-posite systems. However, with recent improve-ments in composite systems, permanent resto-rations that are functionally and aestheticallyacceptable are now available.

Maintenance of a Vital Pulp

Maintaining an intact healthy pulp is preferableto root canal treatment or other endodontic pro-cedures that are complex, expensive, and timeconsuming. When dealing with a deep cariouslesion, some authors advocate indirect pulp cap-ping, a procedure that avoids pulp exposure dur-ing the removal of carious dentin. Another ap-proach is to remove all carious dentin, even if itmeans producing a carious exposure and thencovering the exposed pulp tissue with a biocom-patible liner (direct pulp capping). Others advo-cate a procedure involving surgical removal of in-flamed pulp tissue (pulpotomy); the remainingtissue is then covered with dressing that hopefullyallows healing. The success rate of these proce-dures is variable and depends upon proper diag-nosis and clinical judgment, but primarily on thestatus of the pulp before the procedure.

I NDIRECT PULP CAPPING

This procedure is used in the management ofdeep carious lesions where removal of all cariousdentin would probably result in pulp exposure.Proponents believe that accidental mechanical ex-posure is to be avoided so the pulp is not sub-jected to additional injury. Indirect pulp cappingis considered only if there is no history of pulpal-gia or signs of irreversible pulpitis. After all of the

softened, mushy dentin is removed, either ZnOEor calcium hydroxide is placed on the remainingcarious dentin to suppress bacteria. 82.83 It is feltthat indirect pulp capping causes less damagethan exposure and allows pulpal inflammation toundergo resolution. After several weeks, the tem-porary filling and ZnOE or calcium hydroxideliner may be removed and replaced with a defini-tive restoration.

Indirect pulp capping remains a matter of con-siderable controversy. Some dentists feel that thisform of treatment is not warranted under any cir-cumstances, arguing that it is not possible to per-form a diagnosis of the pulp unless all cariousdentin is removed. If caries has exposed pulp, al-lowing a large number of bacteria to invade, ir-reversible pulpitis has already developed. Othersreason that the biologic principles of restorativedentistry dictate that all carious dentin must be re-moved, even if it means exposing the pulp. Stillothers believe that if irreversible pulpitis has not al-ready developed, indirect pulp capping is likely tobe successful."' Evidence supports the latter view.

DIRECT PULP CAPPING

There are two considerations for direct pulp cap-ping: accidental mechanical pulp exposure and ex-posure caused by caries. Accidental exposure maybe caused by injudicious cavity or crown prepara-tion, placement of pins or retention points. Thesetwo types of exposure differ in that the conditionof the pulp is normal in the case of accidental me-chanical exposure whereas it is likely to be in-flamed beneath a deep carious lesion.

The long-term success rate of direct pulp cap-ping is approximately 80%. 84,853 The degree of bleed-ing indicates the prognosis. 86 The application of10% sodium hypochlorite for "chemical surgery"of the exposed pulp tissue has been advocated."Control of bleeding is a must! Once bleedinghas stopped, a pulp-capping agent can be appliedto the exposure site, followed by placement of apermanent restoration. With the advent of adhe-sive systems, investigators have found that, underexperimental conditions, mechanically exposedpulps can be successfully capped with adhesiveresins.88 Long-term success of capping of cariousexposures is lower. Failure tends to increase withlonger observation periods.89

Until recently, calcium hydroxide has remainedthe standard for treatment of mechanical expo-sures. This material was thought to stimulate dif-ferentiation of new odontoblast-like cells, whichwould then form tertiary dentin. However, studieshave shown that neither the calcium ion nor thehydroxyl ion is necessary for "dentin bridge" forma-

tion.12 However, calcium hydroxide is an effectivematerial when placed in direct contact with vitalpulp tissue. It provides a short-term antimicrobialeffect, and certain commercial calcium hydroxideliners provide a hard-set interface upon which fi-broblasts are able to proliferate and differentiateinto cells capable of elaborating dentin matrix.

PULPOTOMY

Pulpotomy is an alternative to direct pulp cap-ping or root canal treatment when carious pulpexposures occur in young permanent incisors.Pulpotomy involves the removal of all cariousdentin and then ablation of pulp tissue to thelevel of the radicular pulp.90.91 The vital pulpstump is capped with a calcium hydroxide linerand the tooth is temporarily restored with in-termediate restorative material (IRM). Severalmonths later the liner and IRM are replaced by ahybridized adhesive seal bonded into the remain-ing enamel and dentin and the cavity is filled witha permanent restorative material. This procedurehas been shown to be successful providing there isno bacterial microleakage.92,93

Partial pulpotomy has been used to success-fully treat cariously exposed pulps in permanentmolars.91.94 This procedure involves the removal ofcoronal pulp tissue to the level of healthy tissue,which may at times be difficult to determine.Bleeding should be within normal limits and eas-ily controlled.

There are two potential problems with pulpo-tomy as a permanent endodontic treatment. It isnot possible to determine whether all diseased tis-sue has been removed, as inflammation or necrosismay extend into one or more of the root canals andcause the pulpotomy to fail. However, the apparentclinical success of total and partial pulpotomymakes them a viable alternative to pulpotomy.

PERIAPICAL REPAIR AFTERTREATMENT OF DEEPCARIOUS LESIONS

Endodontic treatment is usually indicated wheredeep carious lesions have resulted in periapicalbone resorption. It is likely that these small apicalradiolucencies represent bone resorption in re-sponse to chemical mediators diffusing from aninflamed coronal pulp. There have been reports ofresolution of periapical pathosis and preservationof pulp vitality after pulpotomy or direct or indi-rect pulp capping. 9S,96 Careful case selection iscritical to success. Jordan and Suzuki82 found thatonly young patients benefited from this proce-dure. There are no reports of success in patients


385

older than age 24. The tooth to be treated must bevital on pulp testing and lack a history of sponta-neous pain. Presumably the pulps of young teethare better able to respond favorably to pulp cap-ping procedures because of a richer blood supplyand greater degree of cellularity.

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44. Bergenholtz G, Cox CF, Loesche WJ, Syed SA: Bacterialleakage around dental restorations: its effect on thepulp, J Oral Pathol 11:439, 1982.

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47. Qvist V: The effect of mastication on marginal adapta-tion of composite restorations in vivo, J Dent Res62:904, 1983.

48. Mahler DB, Nelson LW: Factors affecting the marginalleakage of amalgam, J Am Dent Assoc 108:51, 1984.

49. Nakabayashi N, Ashizawa M, Nakamura M: Identifi-cation of a resin-dentin hybrid layer in vital humandentin created in vivo: durable bonding to vitaldentin, Quintessence Int 23:135, 1992.

50. Plant CG, Jones DW: The damaging effects of restora-tive materials. Part 1. Physical and chemical proper-ties, Br DentJ 140:373, 1976.

51. Hume WR: An analysis of the release and the diffusionthrough dentin of eugenol from zinc oxide-eugenolmixtures, JDent Res 63:881, 1984.

52. Silver D, Trowbridge H, Greco M, Yankell S: In vitro as-sessment of permeability of dentin to acid, J Dent Res67(special issue):276, 1988.

53. Kozam G: The effect of eugenol on nerve transmission,Oral Surg Oral Med Oral Pathol 44:799, 1977.

54. Trowbridge H, Edwall L, Panopoulos P: Effect of zincoxide-eugenol and calcium hydroxide on intradentalnerve activity, JEndod 8:403, 1982.

55. Brannstrbm M, Nyborg H: Pulpal reaction to polycar-boxylate and zinc phosphate cements used with inlaysin deep cavity preparations, J Am Dent Assoc 94:308,1977.

56. Jendresen M, Trowbridge H: Biologic and physicalproperties of a zinc polycarboxylate cement J ProsthetDent 28:264, 1972.

57. Heys RJ, Heys DR, Fitzgerald M: Histological evalua-tion of microfilled and conventional composite resinson monkey dental pulps, IntEndodJ 18:260, 1985.


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59. Nordenvall K -J, Brannstram M, Torstensson B: Pulpreactions and microorganisms under ASPA and con-cise composite restorations, JDent Child 46:449, 1979.

60. Kawahara H, Imanishi Y, Oshima H: Biological evalu-ation on glass ionomer cement, J Dent Res 58:1080,1979.

61. Alperstein KS, Graver HT, Herold RCB: Marginal leak-age of glass-ionomer cement restorations, J ProsthetDent 50:803, 1983.

62. Graver HT, Alperstein K, Trowbridge H: Microleakageof castings cemented with glass ionomer cements,Oper Dent 15:2, 1990.

63. Phillips RW, Gilmore HW, Swartz ML, Schenker SI:Adaptation of restorations in vivo as assessed by Ca",JAm DentAssoc 62:9,1961.

64. Heys DR, Cox CF, Heys RJ, et al: Histopathologic andbacterial evaluation of conventional and new copperamalgams, J Oral Pathol 8:65, 1979.

65. Cox CF, Suzuki S: Re-evaluation of pulp protection:calcium hydroxide liners vs. cohesive hybridization,JAm Dent Assoc 125:823, 1994.

66. Edwards DJ: The response of the human dental pulpto the use of a cavity varnish beneath amalgam fillings,Br DentJ145:39, 1978.

67. Yates JL, Murray GA, Hembree JH: Cavity varnishes ap-plied over insulating bases: effect on microleakage,OperDent 5:43, 1980.

68. Pashley DH, O'Meara JA, Williams EC, Kepler EE:Dentin permeability: effects of cavity varnishes andbases, JProsthetDent 53:511, 1985.

69. Piperno S, Barouch E, Hirsch SM, Kaim JM: Thermaldiscomfort of teeth related to presence or absence ofcement bases under amalgam restorations, Oper Dent7:92, 1982.

70. Trowbridge HO: Intradental sensory units: physiolog-ical and clinical aspects,JEndod 11:489, 1985.

71. Johnson RH, Dachi SF, Haley, JV: Pulpal hyperemia-acorrelation of clinical and histologic data from 706teeth, JAm Dent Assoc 81:108, 1970.

72. Grajower R, Kaufman E, Rajstein J: Temperature in thepulp chamber during polishing of amalgam restora-tions,JDentRes 53:1189, 1974.

73. Hatton J, Holtzmann D, Ferrillo P, et al: Effect ofhandpiece pressure and speed on intrapulpal tempera-ture rise, AmJDent7:108, 1994.

74. Felton DA, Webb EL, Kanoy BE, Cox CF: Pulpal re-sponse to threaded pin and retentive slot techniques: apilot investigation, J Prosthet Dent 66:597, 1991.

75. Silvestri AR Jr, Cohen SN, Wetz JH: Character and fre-quency of discomfort immediately following restora-tive procedures, J Am Dent Assoc 95:85, 1977.

76. Subay R, Cox C, Kaya H, et al: Human pulp reactionsto dentine bonded amalgam restorations: a histologicstudy, JDent 28:327, 2000.

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78. Brodin P, Linge L, Aars H: Instant assessment of pul-pal blood flow after orthodontic force application,JOrofac Orthop 57:306, 1996.

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84. Horsted P, Sondergaard B, Thylstrup A, et al: A retro-spective study of pulp capping with calcium hydroxidecompounds, Endod Dent Traumatol 1:29, 1985.

85. Fuks AB, Bielak S, Chosak A: Clinical and radiologicassessments of direct pulp capping and pulpotomy inyoung permanent teeth, Pediatr Dent 24:244, 1982.

86. Matsuo T, Nakanishi T, Shimizu H, Ebisu S: A clini-cal study of direct pulp capping applied to carious-exposed pulps, JEndod 22:551, 1996.

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96. Caliskan MK: Pulpotomy of carious vital teeth withperiapical involvement, Int Endod J 28:172, 1995.

Management of IncompletelyFormed Roots

LEARNING OBJECTIVES


1 / Describe and differentiate between the open and closed apices.

z / Discuss methods of diagnosis and selection of appropriate treatment.

3 / Identify situations in which a tooth with an open apex requires vital pulp therapy or root-end closure and

root canal therapy.

a / Explain why nonsurgical root canal treatment and periapical surgery are technically difficult and

i nappropriate in a tooth with an open apex.

s / Describe the prognosis for vital pulp therapy and root-end closure.

6 / Describe how to perform vital pulp therapy by pulpotomy.

7 / Describe how to perform root-end closure.

8 / Recognize the success or failure of treatment of an open apex.

Select appropriate treatment when failure has occurred.

10 / Recognize when a patient should be considered for referral.

388

Definition of Terms

Open Apex

Vital Pulp Therapy

Root-End Closure

Diagnosis and Treatment Planning

Subjective Examination

Objective Examination

Treatment Planning

Case Selection and Referrals

I ndications and Contraindications

Vital Pulp Therapy

Root-End Closure

Treatment Techniques

Vital Pulp Therapy

Root-End Closure

Coronal Restoration

Root-End Closure with MTA

Follow-Up

Successful Treatment

Failed Treatment

22 / Management of Incompletely Formed Roots

389

n immature tooth that developspulpal disease presents special prob-lems. When the apex is not closed but

is wide open, routine root canal treatment proce-dures cannot be performed and results are un-predictable. This chapter discusses the endodon-tic management of teeth with open apices andwith pulp and/or periradicular pathoses. Thediagnosis and treatment planning, case selec-tion, techniques of management, and outcomesof treatment are also discussed. Included arethose situations and reasons why patients need-ing open apex treatment should be consideredfor referral.

Definition of Terms

OPEN APEX

An open apex is found in the developing roots ofimmature teeth and, in the absence of pulp orperiradicular disease, is normal. Apical closure oc-curs approximately 3 years after eruption. How-ever, when the pulp undergoes necrosis beforeroot growth is complete, dentin formation ceases,and root growth is arrested. Therefore, the canaland the apex remain wide (Figures 22-1 and 22-2);

the root may also be shorter. An open apex maydevelop also as a result of extensive resorption ofa mature apex after orthodontic treatment, orfrom periradicular inflammation (Figure 22-3), oras part of healing after trauma. The normal ma-ture permanent tooth often has an apical con-striction of the canal approximately 0.5 to 1.0 mmfrom the anatomic apex.' An immature root hasan apical opening that is comparatively very large.The walls of the canal in an immature root withan open apex are thinner than those of a matureroot. They may diverge (see Figure 22-1), be paral-lel (see Figure 22-2), or converge slightly, depend-ing on the stage of root formation.

VITAL PULP THERAPY

Vital pulp therapy, previously called apexogenesis,

is defined as treatment of a vital pulp in an im-mature tooth to permit continued dentin forma-tion and apical closure. The current, more generalterminology refers to maintenance of pulp vitalityto allow continued development of the entire rootand not just the apex. The objective is to maintainthe vitality of the radicular pulp.

A vital pulp of an immature tooth may presentwith a small coronal exposure after trauma; nor-mal formation of root dentin will continue bymeans of a shallow pulpotomy. Most immatureteeth with crown fractures and exposed pulps

390


FIGURE 22-1A, Incisor (history of luxation injury) with an open apex (divergent walls), necrotic pulp, and apical pathosis. Root-end closure is indicated. B, Apical region of an immature central incisor extracted from a 7-year-old. Besides beingwide open, the apical dentin walls are egg-shell thin. These teeth are difficult to treat; long-term prognosis wouldbe questionable. (Courtesy Dr. L. Baldassari-Cruz.)

have vital pulps in which inflammation is limitedto the pulp surface.' Treatment that allows theroot to continue developing may also be indicatedin immature teeth with a small carious pulpal ex-posure; success is dependent on the extent of pul-pal damage and on the restorability of the tooth.A large carious or traumatic exposure may requirea pulpotomy at the level of the cervical constric-tion to retain radicular pulp viability.

ROOT-END CLOSURE

Root-end closure, previously referred to as apexifi-cation, is defined as the process of creating an en-vironment within the root canal and periapicaltissues after pulp death that allows a calcified bar-rier to form across the open apex. This barrier hasbeen characterized as dentin, cementum, bone,and osteodentin (Figure 22-4). The usual result isblunting of the end of the root and very little, ifany, increase in root length.

Creation of the proper environment for for-mation of the calcified barrier involves clean-ing and removal of debris and bacteria, as wellas the placement of a material to induce api-cal closure. Different materials have been usedsuccessfully to induce root-end closure. Mostfavored has been a paste of calcium hydroxideand water. The addition of other medicamentsto calcium hydroxide has been suggested, butwith no beneficial effect on root-end closure.3Calcium hydroxide has been used as a tempo-rary obturating material; it is bactericidal withan alkaline pH that may be responsible for stim-ulating apical calcification.' Complete debride-ment to remove bacteria and necrotic tissuefrom the root canal system is an essential factorresponsible for apical closure.5 Recently, place-ment of an apical plug of mineral trioxide ag-gregate (MTA) has been shown to be more effec-tive and convenient than the use of calciumhydroxide.


391

FIGURE 22-2I ncisor with a necrotic pulp, but with substantial dentin for-mation and an open apex (parallel walls). An access openinghas been made into the pulp chamber. Root-end closure is in-dicated. Long-term prognosis is good.

Diagnosis andTreatment Planning

The essentials of diagnosis and treatment plan-ning are reviewed here; details of diagnosis andtreatment planning are discussed in Chapter 4.Before treatment of an incompletely formedroot is started, tests are essential. A commoncause of pulp damage is trauma, but damagemay also result from caries, mechanical expo-sure, or a developmental anomaly (e.g., dens in-vaginatus). Depending on the diagnosis andfindings, vital pulp therapy, root-end closureand obturation, nonsurgical root canal treat-ment, or possibly periapical surgery may beappropriate.


History

There is often a history (usually much earlier) of atraumatic injury (blow) that may or may not in-

FIGURE 22-3Resorbed apex (now open) caused by periapical inflamma-tion resulting from pulpal necrosis.

volve a crown fracture. If fractured, the tooth mayhave been restored with composite resin retainedby etched enamel; however, the tooth may sincehave become discolored or may show symptomsindicating pulp necrosis.

Symptoms

The symptoms most helpful in diagnosis re-late primarily to duration of pain. Durationmay vary, but if pain is spontaneous or persistsafter stimulus in a tooth with a vital pulp, irre-versible pulpitis is likely. Of course, both irre-versible pulpitis and necrosis are often asymp-tomatic. If the pain has a throbbing characterand the tooth is tender to touch, either api-cal periodontitis or a symptomatic abscesswith a necrotic pulp is likely. Confirmation ofthese findings by performing objective tests isnecessary.

OBJECTIVE EXAMINATION

Visual Examination

Both hard and soft tissues are examined. If painis due to irreversible pulpitis, there should bean etiologic factor to explain it, such as a deeprestoration, history of trauma, tooth fracture, orcaries. The crown may be discolored. Apical red-ness, tenderness, or swelling may indicate thepresence of a symptomatic periradicular ab-scess, whereas a sinus tract indicates an asymp-tomatic periradicular abscess (suppurative api-cal periodontitis).

392


FIGURE 22-4Histology of apical barrier after root-end closure of an open-apex tooth treated with MTA. Osteodentin deposi-tion is shown as an irregular cellular calcified tissue unlike dentin or bone. Note the numerous spaces (sponge-li ke) that contain tissue remnants.

Percussion

Pain on pressure is diagnostic only when a sig-nificant painful response is elicited from theaffected tooth. Digital pressure is preferred; tap-ping with a mirror handle to elicit pain is unre-liable and unpleasant for the patient.

Thermal Testing

Thermal testing is widely used with open apicesbut may be complicated by a lack of neuraldevelopment or by an exaggerated responsecaused by apprehension in a young patient. Noresponse to repeated thermal testing, as com-pared to a positive response in the contralat-eral control tooth, may indicate the presenceof a necrotic pulp; this can be confirmed by

other tests. A problem (with an open or closedapex) after a luxation injury is that nerves maybe damaged while the blood supply remainsintact, and, therefore, the pulp is healthy butunresponsive.

Electric Pulp Testing

Electric pulp testing is unreliable in trauma-tized young teeth with wide open apices becauseof the injury and because sensory nerves maynot yet have developed fully. Results must there-fore be interpreted with caution; lack of re-sponse does not necessarily indicate pulpalnecrosis. The presence of a response may alsobe inaccurate because the child may overreactor be unreliable.


393

FIGURE 22-5A, The apex appears to be near parallel as seen from the facial aspect. B, From the proximal aspect, the apicalwalls diverge.


It is normal for a radiolucent area with a corti-cated margin to surround the developing openapex of an immature tooth with a healthy pulp. Itis sometimes difficult to differentiate this fromthe pathologic radiolucency (usually there is not acorticated bony margin) resulting from a necroticpulp. Comparison with the periapex of the con-tralateral tooth is helpful, especially in conjunc-tion with the results of other diagnostic tests.When a sinus tract is present, a radiograph with agutta-percha point in the tract may indicate thesource.

A radiograph provides only a two-dimensionalimage and does not reveal the third dimension,which is important in teeth with an open apex.Only the mesiodistal aspect is seen in a routine ra-diograph. Although the apical opening appearsalmost closed, it is more open when seen from theproximal aspect (Figure 22-5). Thus, conventionalradiographs may result in selection of inappropri-ate routine root canal treatment when vital pulptherapy or root-end closure is indicated instead.

If there is doubt about the apical anatomy, anangled radiograph is helpful (see Chapter 9).

TREATMENT PLANNING

Pulpal status and degree of root developmentare the major factors in treatment planning (Fig-ure 22-6). If the pulpal diagnosis is reversiblepulpitis, the treatment of choice is vital pulptherapy, regardless of the degree of root develop-ment. Depending on the extent of pulpal dam-age, pulp capping or shallow or conventionalpulpotomy may be indicated.

If the diagnosis is irreversible pulpitis or pulpnecrosis, the amount of root development willdetermine the proper treatment. If the apex isclosed, root canal therapy can be performed.However, in a tooth with incomplete root devel-opment, root-end closure must be performed be-fore the obturation. A number of other factorsmust also be considered. The patient may becomeimpatient or disinterested, especially when manyvisits are required. The risk of root fracture is high

FIGURE 22-6Case selection decision tree.

in immature teeth, especially in thin-walled roots;other treatment options require consideration.'Alternative treatments include (1) apical plug,(2) root canal treatment, (3) periapical surgery,and (4) extraction.

Vital Pulp Therapy

A patient with a tooth suitable for vital pulp ther-apy after trauma should be seen immediately orpreferably not more than a few days later, al-though teeth with long exposure times have beensuccessfully treated .z As with any traumatic in-jury, a thorough general, facial, and oral examina-tion should be carried out; these aspects are dis-cussed in detail in Chapter 25. Normally, thecrown fracture involves the pulp, which is vitaland can be seen directly. Radiographs do not usu-ally show apical pathosis.

Another possible indication for vital pulp ther-apy is a tooth with an open apex that has a cariousexposure.

Root-End Closure

The patient may or may not be having pain andmay have suffered previous trauma. The pulp isnecrotic, usually accompanied by periradicularinflammation.

Apical Plug

The advantage of placing an apical plug is elimi-nation of repeated placement of calcium hydrox-ide. It is often difficult to recall some of thesepatients because of relocation. It would be ad-vantageous to be able to complete the treatmentin two appointments so that the risk of contam-ination caused by loss of the temporary sealwould be reduced and the outcome would bemore predictable .6,8

Root Canal Treatment

The presence of an open apex is a major problemin routine root canal treatment. Obtaining a well-condensed obturation to the desired level is verydifficult. The likely result is extrusion of excessmaterial periapically as well as large voids withinthe material.

Surgery

Surgical intervention is possible but is bestavoided in children. If surgery is necessary, itshould be performed by an endodontist. Theprocedure is complicated by the short root andthin fragile walls at the root end, which compro-mise the strength of the tooth. If surgery is indi-cated, MTA is the preferred root-end filling mate-ria1. 9 Root-end resection should be minimized oravoided because it reduces the length of an al-ready short root.

Extraction

If the tooth has a very poor prognosis, extractionmust be considered, together with the orthodon-tic implications. The space may be allowed toclose or may be maintained with a prosthesis; amultidisciplinary assessment is required. A re-movable provisional partial denture is often theimmediate replacement. For the longer term, anadhesive or conventional bridge or an implant is apossibility. Remember that adjacent teeth will alsorequire assessment as suitable abutments becausethey may also have suffered from trauma.

CASE SELECTION AND REFERRALS

The need to refer patients requiring vital pulptherapy is not great. Generally, after traumatic ex-posure, treatment (shallow pulpotomy) is straight-forward and predictable. In contrast, general den-tists should be selective about treating teethneeding root-end closure; treatment is time con-suming and unpredictable. There may be compli-cations such as displacement (leakage) of the tem-porary restoration or root fracture. In addition,the average practitioner has limited experiencewith such situations. When treatment is techni-cally difficult, such as in patients with very imma-ture or badly fractured teeth that cannot be prop-erly isolated, the dentist should consider referral.

Expense is another factor; the patient (or par-ent) must be aware that these procedures requiremuch more time and more appointments thanconventional root canal treatment. The specialistwho has more experience can manage these prob-lems more efficiently.

394


Indications andContraindicationsVITAL PULP THERAPYIndications

Vital pulp therapy (Figure 22-7) is indicated for animmature tooth with incomplete root formationand with damage to the coronal pulp but whoseradicular pulp is presumed to be healthy. Thecrown must be fairly intact and restorable.


395

FIGURE 22-7A, Second molar with carious exposure, an open apex,and a vital pulp; vital pulp therapy is indicated. B, Thecoronal pulp is amputated (pulpotomy); hard-set calciumhydroxide is placed, followed by zinc oxide and eugenolbase, and then occlusal amalgam. C, Three-year recallevaluation. The tooth is asymptomatic and root dentinformation is evident. Root canal treatment is not indi-cated. (Courtesy Dr. T. Erickson.)

Contraindications

Contradictions include the following:1. Avulsed and replanted or severely luxated

tooth2. Severe crown-root fracture that requires

intraradicular retention for restoration3. Tooth with an unfavorable horizontal root

fracture (i.e., close to the gingival margin)4. Carious tooth that is unrestorable5. Necrotic pulp

396

22 I Management of Incompletely Formed Roots

Prognosis

The prognosis is good when pulp capping or shal-low pulpotomy (Cvek technique 2) is done cor-rectly after a traumatic exposure. A completelyformed root is then produced that can support anappropriate restoration. Subsequent root canaltreatment is unlikely to be necessary. Conven-tional pulpotomy is slightly less successful, par-ticularly in anterior teeth because of tissue dam-age when the coronal pulp is severed.

Complications

Complications should be few. Microbial contami-nation through a leaking or lost temporary orpermanent restoration may cause pulpal necro-sis and periradicular pathosis. If this occurs be-fore complete root development, root-end closurewould be necessary; if contamination occurs afterroot formation, root canal treatment is required.

ROOT-END CLOSURE

Indications

Root-end closure is required for a restorable im-mature tooth with pulp necrosis.

Contraindications

Contraindications include the following:1. All vertical and most horizontal root

fractures2. Replacement resorption (ankylosis)3. Very short roots4. Marginal periodontal breakdown5. Vital pulps

Prognosis

Generally, root-end closure procedures have agood success rate. 10-12 However, very immatureteeth (thin dentin walls) are at high risk for rootfracture either during or after treatment; the inci-dence of fracture depends on the stage of root de-velopment. Also, barrier formation occurs morerapidly when the apical opening is less wide. 1 2

Treatment TechniquesVITAL PULP THERAPY

Either pulp capping, shallow pulpotomy, or con-ventional pulpotomy (Figure 22-8) is indicatedfor crown fracture of an anterior tooth involvingexposure of the pulp and an open apex." Conven-tional pulpotomy is difficult to perform in an im-mature incisor, which has a large pulp in the cer-

FIGURE 22-sConventional pulpotomy. Pulp is amputated at the cervicallevel and covered with calcium hydroxide and then a sealinglayer of fortified zinc oxide-eugenol (ZnOE) cement and glassionomer cement. The incisal is restored with composite resin.

vital region. Pulp capping or shallow or conven-tional pulpotomy is suitable in posterior teeth.

Techniques

Pulp capping. After anesthesia is obtained and arubber dam is applied, the exposed pulp is rinsedwith 2.5% sodium hypochlorite (NaOCI). Heavybleeding from the exposure site can be controlledwith a cotton pellet moistened with NaOCI. MTApowder is mixed with sterile water and placed inthe access cavity with a large plastic amalgam car-rier and then patted against the exposures site(s)with a moist cotton pellet. A moist cotton pellet isplaced on the MTA, and then a temporary fillingis placed. In compliant patients, the cavity is filledwith MTA, and then a wet piece of gauze is placedbetween the treated and opposing teeth for 3 to4 hours. Because MTA cannot be used as a perma-nent filling material, the coronal 3 to 4 mm ofMTA is removed after setting and the cavity is re-stored permanently.8 Pulp status is evaluated clin-ically and radiographically every 3 to 6 months.

Shallow pulpotomy. Shallow pulpotomy was de-veloped in Scandinavia.2,14 In crown-fracturedteeth, the pulp is vital and often inflamed on theexposed surface; the pulp may become hyperplas-tic with time. Because the inflammation is super-

ficial (2 to 3 mm deep), only the inflamed tissue isremoved, leaving a small wound surface. The pro-cedure is outlined in Chapter 25.

There is a high success rate when the techniqueis carefully performed and the essential overlyingseal is produced and maintained .2 This is a per-manent procedure; normally, root canal treat-ment is not required subsequently. The techniquehas also been used for managing carious expo-sures; however, success depends on careful caseselection and treatment.15 In the pulp capping orshallow pulpotomy technique, MTA has been rec-ommended instead of calcium hydroxide." 6

Pulpotomy with calcium hydroxide. The technique(see Figure 22-8) involves the following steps:

1. After local anesthesia, rubber dam isolation,and surface disinfection, a conventional ac-cess cavity is made with a high-speed burusing copious water spray coolant. Waterspray and gradual reduction minimize em-bedding of dentinal debris in the pulp.-'

2. Strands of pulp and debris are removedcoronal to the amputation site. Amputationof the coronal pulp at the cervical level isperformed with a sharp spoon excavator ora large sterile round metal or diamond bur.Creation of a clean wound without damag-ing the underlying pulp is difficult with anexcavator. Low-speed burs may cause con-tusion and tearing of the remaining pulp,leading to calcific metamorphosis.

3. Bleeding of the cut pulp stump is controlledwith local anesthetic, sodium hypochlorite,or saline on a cotton pellet applied with gen-tle pressure. Caustic chemicals or medica-ments should not be used so that the healthof the radicular pulp is maintained.

4. Calcium hydroxide powder is mixed withsterile water, saline, or anesthetic solutionto a thick consistency. The paste is carefullyplaced on the pulp stump surface 1 to 2 mmthick.' 6

5. A layer of zinc oxide-eugenol cement mustbe placed over the calcium hydroxide fortwo reasons: first, to protect against leakageof bacteria from saliva around the finalrestoration, and second, to provide a rigidbase against which a final restoration canbe placed.

G. A permanent well-sealing restoration is es-sential. Temporary restorations invariablydeteriorate and leak over a period of time,resulting in bacterial contamination andsubsequent pulp necrosis. Acid-etched com-posite resin is recommended for anteriorteeth and amalgam for posterior teeth. Thecomposite resin should be placed below the


397

cement-enamel junction to reduce the inci-dence of subsequent tooth fracture."

Pulp capping or pulpotomy with mineral trioxide

aggregate. The technique involves the followingsteps:

1. After local anesthesia and rubber dam isola-tion is obtained, access to the pulp chamberis made, and depending on the extent ofpulpal damage, pulp capping or pulpotomyis performed. Control of bleeding is ob-tained as described for pulpotomy with cal-cium hydroxide.

2. The MTA is prepared immediately beforeuse by mixing the powder with sterile wateror saline at a ratio of 3:1 on a glass or paperslab. The mixture is placed on the exposedpulp or pulp stump surface and patted witha moist cotton pellet. The amount of mois-ture in the MTA can be manipulated byadding more water or absorbing excessmoisture with a small dry piece of gauze.'

3. Because MTA sets in the presence of mois-ture over a 3-hour period, a wet cotton pel-let is placed over the material and the rest ofthe cavity is filled with temporary filling ma-terial. Alternatively the entire cavity can befilled with MTA and protected by a wetpiece of gauze for 3 to 4 hours."

4. The coronal 3 to 4 mm of MTA is removed,and a final restoration is placed 1 weeklater.

Recall Schedule

The patient is usually scheduled for recall ap-pointments at 3- to 6-month intervals to monitorpulp vitality and apical growth. The total follow-up time varies, depending on the initial degree ofroot maturation. If the root were in a very earlystage of development, root formation could take2 to 3 years. Recall appointments should then bedone for at least 4 years.

Absence of symptoms does not indicate ab-sence of disease. Monitoring of signs and symp-toms, periodic pulp testing, and radiographs arerequired to determine pulp and periapical status.One advantage of pulp capping or shallow pulpo-tomy over conventional pulpotomy is of the abil-ity to test the pulp.

Possible Outcomes

The ideal result is continued apical growth ofthe root with a normal or nearly normal apex(Figure 22-9). Treatment failure is cessation ofgrowth and apical disease, requiring root-endclosure or root canal treatment.

398


FIGURE 22-9Preoperative (A) and postoperative (B) radiographs demonstrate continued root development after pulpotomyprocedures on both incisors. If these are restored with good sealing restorations, the pulps should remain healthy;

root canal treatment would be unnecessary.

Pulp capping or shallow pulpotomy. After rootformation, vital tissue may be maintained forlong periods of time, usually indefinitely. His-tologic examination of pulps of some crown-fractured teeth after pulp capping or shallowpulpotomy has usually shown normal tissue.18The tissue response to MTA has been excellent(Figure 22-10).16 Histologic evidence does notsupport the use of routine pulp extirpation androot filling after apical closure. Cvek 2 reported avery high clinical success rate.

Conventional pulpotomy. Conventional pulpo-tomy can also be permanent treatment. However,after conventional pulpotomy, the success rate islower and calcific metamorphosis is a commonoccurrence." When there is evidence of this typeof calcification, a case has been made for rootcanal treatment, although this is probably unwar-ranted; calcific metamorphosis is not pathosis.One problem with calcific metamorphosis is thatif the pulp becomes necrotic and root canal treat-ment is necessary, canals may not be negotiable,and surgery may be necessary.

Treatment of Failures

After pulpotomy, teeth must be evaluated period-ically with subjective and objective tests and ra-diographs. If failure occurs after root formation iscomplete, conventional root canal treatment is in-dicated. If failure (pulp necrosis) occurs beforeapical closure, root-end closure is required.

ROOT-END CLOSURE

This is the induction of a calcified barrier (or thecreation of an artificial barrier) across an openapex . 2°-22 The factors most critical to success arethorough debridement of the pulp space and acomplete coronal seal. The material placed in thecanal to allow barrier formation is less impor-tant than has been believed historically, al-though calcium hydroxide has been commonlyused in the mistaken belief that it stimulateshard tissue formation. Calcium hydroxide doesprovide a suitable medium, however, to permitapical closure.


399

FIGURE 22-10A, Premolar with dens evaginatis resulting in pulp expo-sure. B, One-year postoperative radiograph after pulpo-tomy with MIA demonstrating evidence of a dentin bar-rier. C, Histologic section of the MTA-pulp interface. Acontinuous layer of hard tissue bridge is interposed be-tween the MIA and underlying healthy pulp.

Technique

The technique of creating this environment is di-vided into three general phases: access, instru-mentation, and placement of calcium hydroxideor MTA. The steps for root-end closure with cal-cium hydroxide are the following:

1. After isolation, a large access is made toallow removal of all necrotic tissue.

2. Necrotic pulp or a large part of it (unlessliquefied) is removed by inserting, rotating,and withdrawing a large barbed broach ora large Hedstrom file.

3. Working length is determined slightly shortof the radiographic apex.

4. Instrumentation is performed with a gentlecircumferential filing motion, beginningwith a relatively large file and progressing upthrough the file sizes. The use of Hedstromfiles is not advocated because their sharpflutes may perforate the thin fragile walls ofdentin. The aim is to maximize cleansing,aided by copious irrigation with sodiumhypochlorite and to minimize dentin re-moval. Instrumentation beyond the apex isavoided because of damage to the tissue thatwill ultimately form the barrier.

5. Large sterile paper points or cotton rolledon a broach are used to dry the canal.

400


FIGURE 22-11Placement of calcium hydroxide in the canal with amalgam carrier and pluggers. A, The plugger is prefitted 2 to3 mm short of the apex, and the depth is marked with a rubber stop (arrow). B, A 3- to 4-mm section of a cal-cium hydroxide pellet is placed with an amalgam carrier. C, The material is pushed apically with the plugger andverified radiographically. D, Successive increments are placed and condensed. (Modified from Webber R: Dent Clin

North Am 28:688,1984.)

6. Calcium hydroxide powder with barium sul-fate added for radiopacity (9:1 ratio) is mixedwith saline (or local anesthetic or glycerine)to form a stiff paste. This or a manufacturedpaste of calcium hydroxide is introducedwith either an amalgam carrier or the manu-facturer's syringe in the canal at the workinglength (Figure 22-11). An alternative mate-rial, particularly in larger canals, is dry pow-der; pellets of packed powder are made bypacking calcium hydroxide into an amalgamcarrier .23 Displacing too much material peri-apically should be avoided. Subsequent in-crements should fill the canal without voids.

7. A radiograph verifies that the canal space isfilled (Figure 22-12). If voids exist, calciumhydroxide is recondensed before temporiza-tion. Although extrusion of calcium hy-droxide apically should be minimized, thereare no apparent long-term adverse effects.

Coronal Seal

An effective temporary seal between visits is criti-cal.5 Fortified zinc oxide-eugenol cement (IRM) is

preferred. In selected instances it may be coveredby composite resin to restore the missing toothstructure.

Recall Schedule

The patient is recalled in 4 to 6 weeks. Inflamedperiapical tissue fluids may have dissolved the cal-

cium hydroxide; if so, the material will not appeardense radiographically. In such cases the tooth isreopened, the calcium hydroxide is washed outand repacked, and a temporary filling is placed. Ifat recall, the calcium hydroxide appears dense andthere are no clinical signs or symptoms of disease,it need not be replaced. Recall is then scheduledfor 3 and 6 months; the calcium hydroxide ischanged only if radiographic density significantlydecreases.

If healing (bony resolution) has progressedwell after 1 year, the calcium hydroxide is re-moved. A hard tissue barrier is often not visibleradiographically but is detected tactically.'° Thehard tissue barrier is probed with a medium-sizedfile or observed by an operating microscope. If asmall file does not pass through an opening, suf-ficient closure has occurred, permitting successfulobturation. If the apex is still open, the canal isirrigated thoroughly, the calcium hydroxide re-placed, and the patient recalled in 3 months.

Obturation

The canal is cleaned and irrigated copiously andthen dried. A modified lateral condensationtechnique is often necessary. When the canal islarge, even large standardized gutta-perchacones will not fit snugly. A large cone of gutta-percha is warmed and softened slightly over aflame or in hot water, introduced into the canal,and adapted to the shape of the apical canal andbarrier.24 Then accessory points are laterally con-

FIGURE 22-12Root-end closure. A, Calcium hydroxide adequately fills thecanal space. A zinc oxide-eugenol cement temporary fillingseals the access. B, Incisor after 12 months and successful

root-end closure. Apical barrier formation is complete, allow-i ng dense, laterally condensed gutta-percha obturation.

densed using an appropriate sealer. A warmedspreader may improve condensation.

A master cone may be customized by warmingseveral cones and rolling and fusing them be-tween two glass slabs.3 Then they are introducedand condensed into the canal as just described.Another method of softening gutta-percha is todip the master gutta-percha cone briefly in chlo-roform or other suitable solvent. Alternatively, thecanal may be filled with warm gutta-percha deliv-


401

FIGURE 22-13Unusual root-end closure. A barrier has formed, leaving awide, divergent canal space. Obturation was accomplishedwith thermoplasticized gutta-percha. Access was restoredwith glass ionomer.

ered by an appropriate system (Figure 22-13).After obturation recall appointments should bescheduled annually up to 4 years.

CORONAL RESTORATION

After obturation, the pulp chamber should bepartially filled with composite resin to strengthenthe tooth and reduce the risk of fracture."

ROOT-END CLOSURE WITH MTA25

The steps for root-end closure with MTA are thefollowing:

1. After local anesthesia is obtained and a rub-ber dam is applied, a large access is made toallow debridement of the canal(s) with intra-canal instruments and sodium hypochlorite.

2. Calcium hydroxide paste is placed in thecanal for a period of 1 week to disinfect theroot canal system.

3. After the calcium hydroxide is rinsed fromthe canal at the subsequent appointment,a mixture of MTA powder with sterilewater is carried into the canal with anamalgam carrier. The mix is condensed to

402


FIGURE 22-14Root-end closure with MTA. A, Preoperative radiograph demonstrating a radiolucent periradicular lesion. B, Inter-operative placement of an apical plug of MTA. C, Radiograph 6 months after obturation demonstrates healing.

the apical extent using pluggers or paperpoints to create a 3- to 4-mm apical plug(see Figure 22-13). 8

4. The MTA placement is radiographically ex-amined. If ideal extension is not accom-plished, the MTA is rinsed out with sterilewater and the procedure is repeated.'

5. To ensure proper setting of MTA, a moistcotton pellet is placed in the canal over thematerial and the tooth is temporized.'

6. The remainder of the canal is obturatedwith gutta-percha and sealer or bondedcomposite resin and the final restoration isplaced in the access cavity (Figure 22-14).'

Follow-upSUCCESSFUL TREATMENT

Vital Pulp Therapy

Successfully treated teeth (Figure 22-15) have thefollowing characteristics:

1. Presence of a vital pulp2. Absence of signs or symptoms of pulp or

periapical disease: no pain, swelling, sinustract, radiolucency, or deep probing defects

3. Continued growth of the root and canalnarrowing, indicating dentin formation

4. A bridge of calcification (may not be visibleradiographically) beneath the filling material

Root-End Closure

Successfully treated teeth are characterized by thefollowing:

1. Absence of signs or symptoms of periradic-ular pathosis

2. Presence of a calcific barrier across the apexas demonstrated by radiographs or, moreoften, by careful tactile probing with a filetypically with a short and blunt root

Root-End Closure with MTA

Successfully treated teeth (see Figure 22-14) arecharacterized by the following:

1. Absence of signs or symptoms of periradic-ular pathosis

2. Presence of a calcific barrier across the rootapex as demonstrated by radiographs

FAILED TREATMENT

During Treatment

Vital pulp therapy for continued root developmentand root-end closure usually fails because of onecommon cause: bacterial contamination. This ismanifested by the absence of apical closure. Gen-erally, the source of bacteria is loss of the coronalseal or inadequate debridement (with root-end clo-sure). One or more of the following are also present:

1. Symptoms (pain, tenderness to pressure)2. Signs (sinus tract, swelling, probing defects,

periapical radiolucency)3. No evidence of root-end closure either ra-

diographically or by tactile examination orresorption of a previously formed apicalbarrier 16

4. Continual loss of calcium hydroxide fromthe canal space, indicating persistent peri-radicular inflammation

5. Down-growth of granulomatous tissue intothe canal, manifested by bleeding when filesare placed short of the apex

After Treatment

After apparently successful treatment, all pa-tients should be recalled at 12-month intervalsfor 4 years for clinical and radiographic evalua-tion. Conventional pulpotomy may show short-term clinical success but long-term failure. Fail-ure usually results from bacterial contaminationthrough microleakage around the restoration

FIGURE 22-75Vital pulp therapy. A, Trauma resulted in fracture and large pulp exposure. Pulp is vital. B, Conventional pulpo-tomy was performed. C, Apical development 11 months later. D, Irreversible pulpitis subsequently developed, re-quiring root canal treatment. (Courtesy Dr. G. Parsons.)

and through the porous bridge at the pulpotomysite. This is likely if the zinc oxide-eugenol basedid not seal and cover the calcium hydroxide.

Some root-end closures that were initially suc-cessful may eventually fail, even though a calcifiedbarrier was present across the apex and a properroot canal filling was placed. Infected necrotic ma-terial trapped in the barrier may contribute tothese failures, particularly if treatment was notperformed under strict aseptic conditions. A fur-


403

ther reason for failure is an undetected vertical orhorizontal root fracture.'°

REFERENCES

1. Kuttler Y: A precision and biologic root canal fillingtechnique, JAm DentAssoc 56:38, 1958.

2. Cvek M: A clinical report on partial pulpotomy andcapping with calcium hydroxide in permanent incisorswith complicated crown fracture, J Endod 4:232, 1978.

404


3. Gutmann JL, Heaton JF: Management of the open (im-mature) apex. 2. Non-vital teeth, Int Endod J 14:173,1981.

4. Binnie WH, Mitchell DF: Induced calcification in thesubdermal tissues of the rat, JDent Res 52:1087, 1973.

5. Torneck C, Smith JS, Grindall P: Biologic effects of en-dodontic procedures on developing incisor teeth. Il.Effect of pulp injury and oral contamination, Oral SurgOral Med Oral Pathol 35:378, 1973.

6. Shabahang S, Torabinejad M, Boyne P, et al: A com-parative study of root-end induction using osteogenicprotein-1, calcium hydroxide, and mineral trioxide ag-gregate in dogs, JEndod 25:1, 1999.

7. Morse DR, O'Larnic J, Yesilsoy C: Apexification: reviewof the literature, Quintessence Int 21:589, 1990.

8. Torabinejad M, Chivian N: Clinical applications ofmineral trioxide aggregate, JEndod 25:197, 1999.

9. Torabinejad M, Pitt Ford T, McKendry D, et al: Histo-logic assessment of mineral trioxide aggregate as aroot-end filling in monkeys, JEndod 23:225, 1997.

L 0. Cvek M: Prognosis of luxated non-vital maxillary in-cisors treated with calcium hydroxide and filled withgutta-percha. A retrospective clinical study, Endod DentTraumatol 8:45, 1992.

l1. Kleier D, Barr E: A study of endodontically apexifiedteeth, Endod Dent Traumatol 7:112, 1991.

L2. Finucane D, Kinirons M: Non-vital immature perma-nent incisor factors that may influence treatment out-come, Endod Dent Traumatol 15:273, 1999.

13. Gutmann JL, Heaton JF: Management of the open(i mmature) apex. 1. Vital teeth, Int Endod J 14:166,1981.

L4. Granath L, Hagman G: Experimental pulpotomy inhuman bicuspids with reference to cutting technique,Acta Odontol Scand 29:155, 1971.

15. Mejare I, Cvek M: Partial pulpotomy in young per-manent teeth with deep carious lesions, Endod DentTraumatol9:238, 1993.

16. Pitt Ford TR, Torabinejad M, Abedi HR, et al: Usingmineral trioxide aggregate as a pulp-capping material,JAmDent Assoc 127:1491, 1996.

17. Katebzadeh N, Dalton BC, Trope M: Strengtheningi mmature teeth during and after apexification, JEndod24:256, 1998.

18. Cvek M, Lundberg M: Histological appearance ofpulps after exposure by a crown fracture, partialpulpotomy, and clinical diagnosis of healing, J Endod9:8, 1983.

19. Hallett GEM, Porteous JR: Fractured incisors treatedby vital pulpotomy, Br DentJ 115:279, 1963.

20. Cvek M: Treatment of non-vital permanent incisorswith calcium hydroxide. I. Follow-up of periapical re-pair and apical closure of immature roots, Odontol Rev23:27, 1972.

21. Frank AL: Therapy for the divergent pulpless tooth bycontinued apical formation, J Am Dent Assoc 72:87,1966.

22. Heithersay GS: Stimulation of root formation in in-completely developed pulpless teeth, Oral Surg OralMed Oral Patbol 29:620, 1970.

23. Krell KV, Madison S: The use of the Messing gun inplacing calcium hydroxide powder, J Endod 11:233,1985.

24. Cvek M: Endodontic management of traumatizedteeth. In Andreasen JO, Andreasen FM, editors, Text-book and color atlas of traumatic injuries to the teeth, ed 3,p 517, Copenhagen, 1993, Munksgaard.

25. Shabahang S, Torabinejad M: Treatment of teeth withopen apices using mineral trioxide aggregate, Pract Pe-riodontics Aesthet Dent 12:315, 2000.

26. Capurro M, Zmener O: Delayed apical healing afterapexification treatment of non-vital immature tooth: acase report, Endod Dent Traumatol 15:244, 1999.

Bleaching Discolored Teeth:I nternal and External

LEARNING OBJECTIVES


1 / I dentify the cause and nature of tooth discoloration.

z / Describe means of preventing coronal discolorations.

s / Differentiate between dentin and enamel discolorations.

4 / Evaluate the prognosis of bleaching treatments.

s / Select the appropriate bleaching agent and technique according to the cause of the discoloration.

6 / Describe, step by step, the internal "walking bleach" technique.

7 / Describe briefly an external bleaching technique for intrinsic developmental discolorations (for example,

tetracycline).

s / Describe, step-by-step, an external bleaching technique for extrinsic developmental discolorations (for

example, fluorosis).

s / Describe briefly a mouthguard vital bleaching technique.

10 / Recognize the potential adverse effects of bleaching and discuss means of prevention.

405

406

23 I Bleaching Discolored Teeth: Internal and External

Causes of Discoloration

"Natural" or Acquired Discolorations

l atrogenic or Inflicted Discolorations

Endodontically Related Discolorations

Obturating Materials

Remnants of Pulpal Tissue

I ntracanal Medicaments

Coronal Restorations

Bleaching Materials

Hydrogen Peroxide

Sodium Perborate

Carbamide Peroxide

Other Oxidizing Agents

I nternal (Nonvital) Bleaching Techniques

Thermocatalytic Technique

Walking Bleach

Final Restoration

When to Bleach

Complications and Safety

External Resorption

Coronal Fracture

Chemical Burns

External (Vital) Bleaching Techniques

I ntrinsic Discolorations

Extrinsic Discolorations

Mouthguard Bleaching

Bleaching Technique


Prognosis

Safety

Laser Bleaching


i scoloration of anterior teeth is acosmetic problem that is often signifi-cant enough to induce patients to seek

corrective measures. Although restorative methodssuch as crowns and veneers are available, discol-oration can often be corrected totally or partially bybleaching. Bleaching procedures are more conserv-ative than restorative methods, relatively simple toperform, and less expensive. Procedures may be in-ternal (within the pulp chamber) or external (on theenamel surface) and involve various approaches (seeColor Figures 23-1 to 23-3 after page 436).

To better understand bleaching techniques, it isimportant to know the causes of discoloration, lo-cation of the discoloring agent, and the treatmentmodalities available.' Also important is the abilityto predict the outcome of treatment; that is, howsuccessfully can various discolorations be treatedand how long will the esthetic result last. In otherwords, before attempting to correct discoloration,a diagnosis must be made (determine the causeand location of the discoloration), treatment plan-ning must be done (internal and/or externalbleaching and technique), and a prognosis arrivedat (anticipated short-term and long-term success).Patients must be informed of these factors beforeundergoing the procedure; they should not antici-pate esthetic results that may not occur. Any dis-coloration treatment must be tempered by the ex-planation that substantial improvement may ormay not occur. However, internal bleaching isworth a try; with proper and careful technique, noirreversible damage to the crown or root occurs.

This chapter reviews discoloration and its cor-rection. Discussed are the causes and managementof discoloration as related to (1) location of dis-coloration, (2) approach used for correction, and(3) anticipated short-term and long-term success ofbleaching. Specially discussed are the following as-pects of discoloration and bleaching procedures:

1. Causes and location of discoloration.2. Commonly used bleaching agents.3. Internal bleaching techniques (usually in con-

junction with or after root canal treatment).4. External bleaching techniques (usually in

teeth with a vital pulp).5. Predictability and permanence of each pro-

cedure.6. Possible complications and safety of the var-

ious procedures.

Causes of Discoloration

Discolorations occur during or after enamel anddentin formation. Some discolorations appear aftertooth eruption, and others are the result of dental

23 / Bleaching Discolored Teeth: Internal and External

407

procedures. The first group, natural (acquired) dis-colorations, may be on the surface or incorporatedinto tooth structure. Sometimes they result fromflaws in enamel or a traumatic injury. The secondgroup, iatrogenic (inflicted) discolorations, whichresult from dental procedures, are usually incorpo-rated into tooth structure and are preventable.

"NATURAL" OR ACQUIRED

DISCOLORATIONS

Pulp Necrosis

Bacterial, mechanical, or chemical irritation of thepulp may result in necrosis. Tissue disintegrationbyproducts are then released; these colored com-pounds may permeate tubules to stain surround-ing dentin. The degree of discoloration is directlyrelated to how long the pulp has been necrotic.The longer the discoloration compounds are pres-ent in the pulp chamber, the greater the discol-oration. This type of discoloration can be bleachedinternally, usually with both short-term and long-term success.

Intrapulpal Hemorrhage

Generally, intrapulpal hemorrhage is associatedwith an impact injury to a tooth, which results indisrupted coronal blood vessels, hemorrhage and

lysis of erythrocytes. It has been theorized thatblood disintegration products, presumably as ironsulfides, permeate tubules to stain surroundingdentin. Discoloration tends to increase with time.

If the pulp becomes necrotic, the discolorationusually remains. If the pulp survives, the discol-oration may resolve, and the tooth reverts to itsoriginal shade. Sometimes, mainly in young indi-viduals, the tooth remains discolored even if thepulp responds to vitality tests.

Internal bleaching of discoloration after intra-pulpal hemorrhage is usually successful bothshort and,long term . 1 ,3

Calcific Metamorphosis

Calcific metamorphosis is extensive formation oftertiary (irregular secondary) dentin in the pulpchamber or on canal walls. This phenomenonusually follows an impact injury that did not re-sult in pulp necrosis. There is temporary disrup-tion of blood supply with partial destruction ofodontoblasts. These are usually replaced by cellsthat rapidly form irregular dentin on the walls ofthe pulp space. As a result, the crowns of theseteeth gradually decrease in translucency and mayacquire a yellowish or yellow-brown discoloration(Figure 23-1). The pulp usually remains vital anddoes not require root canal treatment.¢

FIGURE 23-1Calcific metamorphosis. Impact trauma resulted in reversible pulp damage with (A) extensive tertiary dentin for-mation (arrow) and (B) lost translucency and darkening of the crown. These teeth present difficulties with rootcanal treatment and internal bleaching.

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If the patient desires color correction, externalbleaching should be attempted first. If this isunsuccessful, root canal treatment is performed(sometimes with difficulty), and internal bleach-ing is done. This may be carried out whether thepulp is vital or necrotic. Such teeth are bleachedwith fair esthetic prognosis.

Age

In older patients, color changes in the crown occurphysiologically as a result of extensive dentin ap-position as well as thinning of and optical changesin enamel. Food and beverages also have a cumula-tive discoloring effect because of the inevitablecracking and other changes on the enamel surfaceand in the underlying dentin. In addition, previ-ously applied restorations that degrade over timecause further discoloration. There is an increasingdemand for bleaching among these older patients.

Developmental Defects

Discolorations may result from developmental de-fects or from substances incorporated into enamelor dentin during tooth formation.

Endemic fluorosis. Ingestion of excessive amountsof fluoride during tooth formation produces de-fects in mineralized structures, particularly enamelmatrix, with resultant hypoplasia. The severity anddegree of subsequent staining generally depend onthe degree of hypoplasia, which depends in turnon the amount of fluoride ingested during odon-togenesis.' The teeth are not discolored on eruptionbut may appear chalky. Their surface, however, isporous, and gradually absorbs stains from chemi-cals in the oral cavity.

Because the discoloration is in the porousenamel, such teeth are bleached (or corrected) ex-ternally. Success depends mainly on the degree andduration of the discoloration. Some regression andreoccurrence of discoloration tend to occur but canbe corrected with future rebleaching.

Systemic drugs. Administration or ingestion ofcertain drugs or chemicals (many of which havenot been identified) during tooth formation maycause discoloration, which is occasionally severe.

The most common as well as the most dra-matic discoloration of this type occurs after tet-racycline ingestion, usually in children. Discol-oration is usually bilateral, affecting multipleteeth in both arches. It may range from yellowthrough brownish to dark gray, depending on theamount, frequency, and type of tetracycline andthe patient's age (stage of development) duringadministration. Tetracycline discoloration hasbeen classified into three groups according to

severity.' First-degree discoloration is light yellow,light brown, or light gray and occurs uniformlythroughout the crown without banding. Second-degree discoloration is more intense and is alsowithout banding. Third-degree discoloration isvery intense and the clinical crown exhibits hori-zontal color banding. This type of discolorationusually predominates in the cervical region.

Tetracycline binds to calcium, which then is in-corporated into the hydroxyapatite crystal in bothenamel and dentin. Most of the tetracycline isfound in dentin. Chronic sun exposure of teethwith the incorporated drug may cause formationof a reddish-purple tetracycline oxidation byprod-uct, resulting in further discoloration of perma-nent teeth.

A phenomenon of adult-onset tetracycline dis-coloration is also reported.' This type of discol-oration occurs occasionally in mature teeth in pa-tients receiving long-term tetracycline therapy,usually given for control of cystic acne. The dis-coloration is gradual and generally is not severe.

Two approaches have been used for bleachingtetracycline discoloration. The first, which in-volves bleaching the external enamel surface, is oflimited usefulness and is generally unsuccessfulin the long term.' The second, root canal treat-ment followed by internal bleaching, is a morepredictable procedure and has proved successful,in both the short and long term."° These tech-niques are discussed in more detail later in thischapter.

Defects in tooth formation. Defects in tooth for-mation are confined to the enamel and are eitherhypocalcific or hypoplastic. Enamel hypocalcifica-tion is common, appearing as a distinct brownishor whitish area, often on the facial aspect of acrown. The enamel is well formed and intact onthe surface and feels hard to the explorer. Boththe whitish and the brownish spots are amenableto bleaching with the pumice and acid technique(described later in this chapter) with good results.

Enamel hypoplasia differs from hypocalcifica-tion in that the enamel in the former is defectiveand porous. This condition may be hereditary(amelogenesis imperfecta) or may result fromenvironmental factors. In the hereditary type,both deciduous and permanent dentitions are in-volved. Defects caused by environmental factorsmay involve only one or several teeth. Presumablyduring tooth formation the matrix is altered anddoes not totally or properly mineralize. Theporous enamel readily acquires stains from theoral cavity. Depending on the severity and extentof hypoplasia and the nature of the stain, theseteeth may be bleached (or corrected by the acid-pumice method) from the enamel surface with


409

upon completion of treatment often results indark discoloration. Such discoloration can be pre-vented by removing all obturation materials to alevel just cervical to the gingival margin. Primaryoffenders are sealer remnants, whether of the zincoxide-eugenol type or plastics." The prognosis ofbleaching in such cases depends on the con-stituents of the sealer. Sealers with metallic com-ponents often do not bleach well, and any bleach-ing effect tends to regress with time.

REMNANTS OF PULPAL TISSUE

Pulp fragments remaining in the crown, usuallyin pulp horns, may cause gradual discoloration.Pulp horns must be "opened up" and exposedduring access to ensure removal of pulpal rem-nants and to prevent retention of sealer at a laterstage. Internal bleaching in such cases is usuallysuccessful.

I NTRACANAL MEDICAMENTS

Most medicaments, but not all, have the potentialto cause internal discoloration of the dentin."Phenolic or iodoform-based intracanal medica-tions, sealed in the root canal space, are in directcontact with dentin, sometimes for long periods,allowing for their penetration and oxidization.These compounds have a tendency to discolorthe dentin gradually. Fortunately, most discolo-rations are not marked and they are readily andpermanently corrected by bleaching. Iodoform-induced discolorations tend to be more severe.

CORONAL RESTORATIONS

Restorations are generally of two types, metallicor composite. The reasons for discoloration (andtherefore, the appropriate correction) are quitedifferent.

Metallic Restorations

Amalgam is the worst offender because its dark-colored elements may turn dentin dark gray. Ifused to restore a lingual access preparation, amal-gam often discolors the crown. Such discolo-rations are difficult to bleach and tend to reoccurwith time. However, bleaching them is worth a try.

Discoloration from inappropriately placedmetal pins and prefabricated posts in anteriorteeth may sometimes occur. This is due to metalthat can be seen through the composite or toothstructure. Occasionally, discoloration from amal-gam is also caused by visibility of the restorationthrough translucent tooth structure. In such cases,

some degree of success." The bleaching effectmay not be permanent, and stains may recur withtime. These stains may, however, be recorrected.As stated earlier, it is most important to informthe patient of the likely reoccurrence of discol-oration of these teeth.

Blood dyscrasias and other factors. Various sys-temic conditions may cause massive lysis of eryth-rocytes. If this occurs in the pulp at an early age,blood disintegration products are incorporatedinto and discolor the forming dentin. An exampleof this phenomenon is the severe discoloration ofprimary teeth that usually follows erythroblasto-sis fetalis. This disease in the fetus or newborn re-sults from Rh incompatibility factors, which leadto massive systemic lysis of erythrocytes. Largeamounts of hemosiderin pigment then stain theforming dentin of the primary teeth. This type oflysis is now uncommon because of new preventivemeasures. This discoloration is not correctable bybleaching.

High fever during tooth formation may re-sult in linear defined hypoplasia. This condition,known as chronologic hypoplasia, is a temporarydisruption in enamel formation that results in abanding-type of surface defect that acquires stain.Porphyria, a metabolic disease, may cause decidu-ous and permanent teeth to show a red or brown-ish discoloration. Thalassemia and sickle cell ane-mia may cause intrinsic blue, brown, or greendiscolorations. Amelogenesis imperfecta may re-sult in yellow or brown discolorations. Dentino-genesis imperfecta can cause brownish violet, yel-lowish, or gray discoloration. These conditionsare also not amenable to bleaching and should becorrected restoratively.

Other staining factors related to systemic con-ditions or ingested drugs are rare and may not beidentifiable.

IATROGENIC OR INFLICTEDDISCOLORATIONS

Discolorations caused by various chemicals andmaterials used in dentistry are usually avoidable.Many of these stains are very difficult to correct bybleaching.

Endodontically RelatedDiscolorations

OBTURATING MATERIALS

Obturating materials are the most common andsevere cause of single tooth discoloration. Incom-plete removal of materials from the pulp chamber

41 0


replacement of old metallic restorations with anesthetically pleasing composite will suffice.

Composite Restorations

Microleakage of composites causes discoloration.Open margins may permit chemicals to penetratebetween the restoration and tooth structure tostain the underlying dentin. In addition, compos-ites may become discolored with time and alterthe shade of the crown. These conditions cansometimes be corrected by replacing the old com-posite with a new well-sealed esthetic restoration.In many cases, internal bleaching is carried outfirst with good results.

Bleaching Materials

Bleaching chemicals may act as either oxidizingor reducing agents. Most bleaching agents areoxidizers and many preparations are available.Commonly used agents are solutions of hydro-gen peroxide of different strengths, sodium per-borate, and carbamide peroxide. Sodium per-borate and carbamide peroxide are chemicalscompounds that are gradually degraded to re-lease low levels of hydrogen peroxide. Hydrogenperoxide and carbamide peroxide are mainly in-dicated for external bleaching, whereas sodiumperborate is mostly used for internal bleaching.All have proved effective.

HYDROGEN PEROXIDE

Hydrogen peroxide is a powerful oxidizer that isavailable in various strengths, but 30% to 35% sta-bilized solutions (Superoxol, Perhydrol) are themost common. These high-concentration solu-tions must be handled with care because they areunstable, lose oxygen quickly, and may explodeunless they are refrigerated and kept in a darkcontainer." Also, these are caustic chemicals andwill burn tissue on contact.

SODIUM PERBORATE

This agent is available in powder form or invarious commercial proprietary combinations.When fresh, it contains about 95% perborate,corresponding to 9.9% available oxygen. Sodiumperborate is stable when dry, but in the pres-ence of acid, warm air, or water it decomposes toform sodium metaborate, hydrogen peroxide,and nascent oxygen." Various types of sodiumperborate preparations are available: monohy-drate, trihydrate, and tetrahydrate. They differ in

oxygen content, which determines their bleach-ing efficacy." Commonly used sodium perboratepreparations are alkaline, and their pH dependson the amount of hydrogen peroxide releasedand the residual sodium metaborate. 17

Sodium perborate is more easily controlled andsafer than concentrated hydrogen peroxide solu-tions. Therefore, it should be the material ofchoice for internal bleaching.

CARBAMIDE PEROXIDE

Carbamide peroxide, also known as urea hydro-gen peroxide, is available in concentrations vary-ing between 3% and 15%. Popular commercialpreparations contain about 10% carbamide perox-ide and have an average pH of 5 to G.S. They usu-ally also include glycerin or propylene glycol,sodium stannate, phosphoric or citric acid, andflavor. In some preparations Carbopol, a watersoluble resin, is added to prolong the release of ac-tive peroxide and to improve shelf life. Ten per-cent carbamide peroxide breaks down into urea,ammonia, carbon dioxide, and approximately3.S% hydrogen peroxide.

Carbamide peroxide systems are for externalbleaching and have been associated with varyingdegrees (usually slight) of damage to teeth andsurrounding mucosa." , " They may adversely af-fect the bond strength of composite resins andtheir marginal seal. 11U0,2' Therefore, these materi-als must be used with caution and usually understrict supervision of the dentist.

OTHER OXIDIZING AGENTS

In the past, a preparation of sodium peroxyboratemonohydrate (Amosan R), which releases moreoxygen than does sodium perborate, was recom-mended for internal bleaching.zz Today, its clini-cal use is less common.

Sodium hypochlorite is a common root canalirrigant that is available commercially as a 3% to5.25% household bleach. Although used as ahousehold bleaching agent, it does not releaseenough oxidizer to be effective and is not recom-mended for routine bleaching.

Other nonperoxide bleaching agents were alsosuggested for clinical use; however, these havebeen no more effective than traditional agents . 21,21

I nternal (Nonvital)Bleaching Techniques

The methods most commonly used to bleachteeth in conjunction with root canal treatment


411

are the thermocatalytic technique and the so-calledwalking bleach technique. 15,22 These techniques aresomewhat different, but both produce similar re-sults. 2,3 The walking bleach technique is preferredbecause it requires the least chair time and is morecomfortable and safer for the patient. The walk-ing bleach technique is described in detail later inthis chapter. Whatever technique is used, the ac-tive ingredient is the oxidizer, which is available indifferent chemical forms. The least potent form ispreferred.

Indications for internal bleaching techniqueare (1) discolorations of pulp chamber origin,(2) dentin discolorations, and (3) discolorationsthat are not amenable to external bleaching.Contraindications are (1) superficial enamel dis-colorations, (2) defective enamel formation,(3) severe dentin loss, (4) presence of caries, and(5) discolored composites.

THERMOCATALYTIC TECHNIQUE

The thermocatalytic technique involves placingthe oxidizing agent in the pulp chamber and thenapplying heat. Heat may be supplied by heatlamps, flamed instruments, or electrical heatingdevices, which are manufactured specifically tobleach teeth.

Potential damage from the thermocatalytic ap-proach includes the possibility of external cervicalroot resorption because of irritation to cementumand periodontal ligament, possibly from the oxidiz-ing agent in combination with heat. 25.26 Therefore,the application of heat during bleaching should belimited. The thermocatalytic technique has notproved more effective than other methods and isnot recommended for routine internal bleaching.

A thermocatalytic variation is ultraviolet photo-oxidation. Ultraviolet light is applied to the labialsurface. A 30% to 35% hydrogen peroxide solutionis placed in the chamber on a cotton pellet, fol-lowed by a 2-minute exposure to ultraviolet light.Supposedly, this causes the release of oxygen sim-ilar to that seen in other thermocatalytic bleach-ing techniques .2',28

There has been little clinical experience in theuse of ultraviolet photo-oxidation. Probably, it isno more effective than the walking bleach tech-nique and requires more chair time.

WALKING BLEACH

The walking bleach technique should be used inall situations requiring internal bleaching. Notonly is it as effective as the techniques previouslydescribed, but it also is the safest and requires theleast chair time (Box 23-1).29-32

It is commonly believed that "overbleaching" isdesirable because of future reoccurrence of discol-oration. However, bleaching a tooth to a lightershade than its neighbors should be performedwith caution; the overbleached tooth may not dis-color again .33 A tooth that is too light may be asunesthetic as one too dark.

Repeat treatments are similar. If early bleach-ing does not provide satisfactory results, the fol-lowing additional procedures may be attempted.(1) A thin layer of stained facial dentin is removedwith a small round bur (see step 7). (2) The walk-ing bleach paste is strengthened by mixing thesodium perborate with increasing concentrationsof hydrogen peroxide (3% to 30%) instead ofwater. The more potent oxidizer may enhance thebleaching effect, but with the possibility of subse-quent root resorption.25,26

Recently, 10% carbamide peroxide was sug-gested for internal bleaching.34 This agent, how-ever, is probably not superior to sodium perborate.

Although usually the final results are excellent,occasionally only partial lightening is achieved.Surprisingly, the patient often is very pleased andsatisfied with a modest improvement and doesnot expect perfection . 35 Therefore, internal bleach-ing is worth the attempt.

FINAL RESTORATION

The pulp chamber and access cavity are restoredat the final visit (Figure 23-2, E). Although ithas been proposed that substances (such asacrylic monomer or silicones) be placed in thechamber to fill the dentinal tubules, this isbeneficial. Furthermore, these substances maythemselves lead to discoloration with time.However, it is important to restore the chambercarefully and to seal the lingual access to aug-ment the new shade and prevent leakage. Theideal method for filling the chamber after toothbleaching has not been determined. However, byno means should the chamber be filled totallywith composite, because this causes a loss oftranslucency and an actual darkening of thetooth .36

It is easy and effective to fill the chamber witha light-colored gutta-percha temporary stopping,glass ionomer, or a light shade of zinc phosphatecement and then to restore the lingual accesswith a light-cured acid-etched composite (Fig-ure 23-2, E) . 3' An adequate depth of compositeshould be ensured to seal the cavity and providesome incisal support. Light curing from thelabial, rather than the lingual, surface is recom-mended, because this results in shrinkage of thecomposite resin toward the axial walls, reducing

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41 3

the rate of microleakage.38 Proper restoration isessential for long-term successful bleaching re-sults. Coronal microleakage of lingual accessrestorations is a problem 39, a leaky restorationmay lead to reoccurrence of discoloration.

Residual peroxides of bleaching agents, mainlyhydrogen peroxide and carbamide peroxide, mayaffect the bonding strength of composites to thetooth .21,40 Therefore, it is not recommended thatthe tooth be restored with composite immediately

FIGURE z3-zWalking bleach. A, Internal staining of dentin caused by remnants of obturating materials (OM) in the chamber,as well as by materials and tissue debris in pulp horns (PH). B, Coronal restoration is removed completely, accesspreparation is improved, and gutta-percha is removed to just below the cervical margin. Next, the pulp horns arecleaned with a round bur (shaving a thin layer of dentin from the facial wall is optional and may be attemptedat later appointments if discoloration persists). C, A protective cement base (8) is placed over the gutta-percha,not extending above the cervical margin. After removal of sealer remnants and materials from the chamberwith solvents, a paste (P) composed of sodium perborate and water (mixed to the consistency of wet sand) isplaced. The incisal area is undercut to retain the temporary restoration. D, A thick mix of zinc oxide-eugenol typetemporary filling (Z) seals access. E, At a subsequent appointment, when the desired shade has been reached, apermanent restoration is placed. A suggested method is to fill the chamber with white temporary stopping (TS)or with light polycarboxylate or zinc phosphate base. Acid-etched composite (C) restores lingual access and ex-tends into the pulp horns for retention and to support of the incisal. (From Walton RE: Bleaching procedures forteeth with vital and nonvital pulps. In Levine N, editor: Current treatment in dental practice, Philadelphia, 1986,

WB Saunders.)

41 4


after bleaching but only after an interval of a fewdays. The use of catalase has also been proposedfor fast elimination of residual peroxides from theaccess cavity41 this merits further investigation.

Another suggestion is that packing calcium hy-droxide paste in the chamber for a few weeks be-fore the final restoration is placed would reversethe acidity caused by bleaching agents and pre-vent resorption. This procedure is ineffective andunnecessary.

WHEN TO BLEACH

Internal bleaching may be performed at various in-tervals after root canal treatment (Figures 23-3and 23-4). The appearance of the discolored toothmay be improved soon after treatment. However,the walking bleach technique may be initiated atthe same appointment as the endodontic obtura-tion. In fact, this may motivate the patient toaccept bleaching because the appearance of thediscolored tooth may be improved soon after treat-ment. Bleaching may also be attempted success-fully many years after discoloration has occurred(Figures 23-5 and 23-6). Such teeth show nomarkedly greater tendency toward reoccurrence ofdiscoloration than teeth stained for shorter peri-ods. 33 However, it is probable that a shorter discol-oration period tends to improve the chances forsuccessful bleaching as well as to reduce the likeli-hood of reoccurrence of discoloration .42

FIGURE z3-3

A, Discoloration as a result of a traumatic injury followed by pulp necrosis. B, After root canal treatment, a pasteof sodium perborate and water to a consistency of wet sand was sealed in the chamber. After 21 days of "walk-i ng bleach" the tooth regained its original shade. (Courtesy Dr. A. Claisse.)

Other factors that may influence long-termsuccess have also been evaluated clinically. Thepatient's age and the rate of discoloration haveno major effect on the long-term stability ofbleaching. 33

Complications and Safety

Patient safety is always the major concern in anyprocedure. Some possible adverse effects pro-duced by chemicals and bleaching procedures arelisted in the following section.

EXTERNAL RESORPTION

Clinical reports 43_45 and histologic studies25-26 haveshown that internal bleaching may induce externalroot resorption. The oxidizing agent, particularly30% hydrogen peroxide, may be the culprit. How-ever, the exact mechanism by which periodon-tium or cementum is damaged has not been eluci-dated. Presumably, the irritating chemical diffusesthrough the dentinal tubules46 and reaches the peri-odontium through defects in the cementoenameljunction.47 Chemicals combined with heat are likelyto cause necrosis of the cementum, inflammation ofthe periodontal ligament, and root resorption.25-26The process is liable to be enhanced in the presenceof bacteria.48 Previous traumatic injury and youngage may also act as predisposing factors .43

Therefore, injurious chemicals and proce-dures should be avoided if they are not essen-tial for bleaching. Also, below the cervical mar-gin, oxidizing agents should not be exposed tomore of the pulp space and dentin than is ab-solutely necessary to obtain a satisfactory clini-cal result.

CORONALFRACTURE

Increased brittleness of the coronal tooth struc-ture, particularly when heat is applied, is alsothought to result from bleaching. This may bedue to desiccation of the dentin and enamel. Clin-ical experience suggests that bleached teeth are nomore susceptible to fracture, although this hasnot been proven conclusively.


41 5

CHEMICAL BURNS

As mentioned earlier, sodium perborate is safe,but 30% hydrogen peroxide is caustic and willcause chemical burns and sloughing of gingiva.When this strong chemical is used, the soft tissuesshould be coated with an isolating cream. Animalstudies suggest that catalase applied to oral tis-sues before hydrogen peroxide treatment fullyprevents the associated tissue damage.49

External (Vital)Bleaching Techniques

Results of the so-called vital bleaching technique(application of oxidizer to the enamel surface of atooth with vital pulp) are much less predictable.

FIGURE 23-4A, Discoloration of endodontically treated incisor. B, Fail-ure to remove all remnants of pulpal tissue from the cham-ber and amalgam placed in the access cavity appear to bethe causes of discoloration. C, Removal of amalgam, intra-coronal bleaching, and placement of a new composite re-stored esthetics. (Courtesy Dr. A. Claisse.)

41 6


FIGURE 23-5A, Discoloration as a result of trauma and subsequent treatment. The patient was involved in an accident caus-i ng coronal fracture. Root canal treatment was done, but gutta-percha and sealer were not completely removedfrom the chamber. An additional discoloration factor was the defective leaking restoration. B, Two appointmentsof "walking bleach" and placement of a new well-sealed composite restored esthetics. (Courtesy Dr. M. Israel.)

More variables are present with this techniquethan with internal bleaching. When discolora-tions are in dentin, bleaching agents placed on rel-atively impermeable enamel have less chance ofreaching the stain. If discoloration is on theenamel surface or the enamel is defective andporous, a better result is expected.

Many techniques have been advocated forexternal bleaching of vital teeth. Some condi-tions and types of discoloration are potentiallytreatable by this method, others are not. Criti-cal factors are the location and nature of thediscoloration.

Indications for these bleaching methods usuallyare (1) light enamel discolorations, (2) endemicfluorosis discolorations, and (3) age-related dis-colorations. Contraindications are (1) severe darkdiscolorations, (2) severe enamel loss, (3) closeproximity of pulp horns, (4) presence of caries,(5) hypersensitive teeth, and (6) poor coronalrestorations.

I NTRINSIC DISCOLORATIONS

Intrinsic discolorations are those incorporatedi nto tooth structure during tooth formation."Significantly, most of these discolorations arein dentin and are relatively difficult to treat ex-ternally." A good example is staining due totetracycline, which is incorporated into the min-

eral structure of the developing tooth. The in-corporated tetracycline imparts its color to thedentin.

Tetracycline

Both external and internal bleaching techniqueshave been advocated as means of improving theappearance of tetracycline discolored teeth. Asnoted earlier, the internal technique is more effec-tive. 10.11.51.52 However, the best resolution for tetra-cycline discolorations is prevention.

External bleaching. Techniques advocated forapplying oxidizing agents to enamel surface arelargely based on case reports. Long-term follow-up studies in humans are limited and partial suc-cess has been seen only for light-yellow stainedteeth in young patients. The more prevalentdarker discolorations have generally shown littleresponse to surface bleaching, although at its in-troduction the vital bleaching technique gener-ated considerable optimism.

Animal studies of tetracycline-stained teethdemonstrated that success is minimal.," External

bleaching was done after dogs were given largedoses of discoloring tetracycline. Although a sig-nificantly lighter shade of the enamel surfacecould be obtained, the original dark color soonreappeared.51 Techniques used in these studieswere similar to those proposed for humans.

http://effec-tive.10.11.51.52





417

FIGURE 23-6A, Severely discolored canine. B, Poor root canal

treatment in which material extended intothe chamber caused some of the discoloration.C, After retreatment and three appointments of"walking bleach", esthetics has markedly im-proved. Although some cervical discoloration re-mains, this is largely hidden by the upper lip.(Courtesy Dr. H. Libfeld.)

Technique. Basically the technique involves ap-plication of 30% hydrogen peroxide to the enamelsurface combined with the application of heat( +125 ° F) (commercial instruments are avail-able). Supposedly, higher temperature (+ 142' F)and repeated applications as well as numer-ous treatments are beneficia1. 53 Photobleachingdentin by shortwave ultraviolet light has also beensuggested .28

Results obtained over time must be evaluatedwith clinical photographs. Regression to the orig-inal shade confirms that bleaching has been inef-fective and that repetition of the procedure is notindicated. As stated earlier, success is more com-mon with yellowish or cream discoloration butnot gray discoloration.

Safety. The benefits of these bleaching tech-niques are questionable, and the effect of thebleaching solution or heat on the underlying pulpis a matter of concern. Various studies have shownthat bleaching agents may penetrate the pulpchamber through enamel and dentin and alter the

activity of certain pulpal enzymes.54,55 Althoughlong-term irreversible effects on the pulp wereusually not demonstrated, the procedure must beapproached with caution .56.57

Internal bleaching. Internal bleaching of tetracy-cline-stained teeth has been shown clinically'" ,"

and experimentally52 to lighten severe discolora-tions. Effects persist for long periods, perhapsindefinitely.

The technique involves root canal treatmentfollowed by an internal walking bleach technique,as outlined earlier in this chapter (Figure 23-7). Ifthe procedure is explained to patients, they mayaccept this approach with gratifying results.

Other Intrinsic Discolorations

Other drugs or ingested chemicals are incor-porated into teeth that are forming and causediscoloration; there are no reports of attemptsto bleach these teeth. Presumably attempts tolighten teeth with dentinal discolorations by the

418

23 1 Bleaching Discolored Teeth: Internal and External

FIGURE 23-7

A, Characteristic grayish discoloration and banding of tetracycline discolorations. Cervical regions on maxillaryand mandibular teeth show no discoloration; tetracycline was not administered during those periods of tooth de-velopment. B, Root canal treatments have been completed on the maxillary anterior teeth, with subsequent"walking bleach" procedures. C, After the necessary number of bleaching appointments, the teeth are restoredpermanently. Note the marked contrast with the mandibular incisors, which remain untreated. D, A 4-year follow-up shows no regression and no recurrence of discoloration. (Courtesy Dr. H. Wayne Mohorn.)

external application of bleaching agents wouldbe only marginally effective.

EXTRINSIC DISCOLORATIONS

These discolorations are more superficial and areobviously more amenable to external bleaching.The success of bleaching, however, depends moreon the depth of the stain in the enamel ratherthan on the color of the stain itself.

Superficial Defects

Although a number of conditions may result in hy-poplasia of enamel accompanied by porosity, the

most common and often the most disfiguring is en-demic fluorosis. This hypopatic defect may resultin various degrees and colors of superficial stains.

Mechanism of discoloration. Ingestion of highlevels of fluoride during tooth formation disruptsthe ameloblasts and leads to hypoplasia of theforming enamel.60 After tooth eruption, the porousenamel is gradually discolored. The discolorationmay vary from chalky white through light yellowand brown to almost black, depending on the de-gree of fluorosis (enamel porosity) and the type ofchemical stain.

The appearance of all such discolorations maybe improved with bleaching or other measures,some dramatically. Although a variety of tech-

niques involving different chemicals and proce-dures have been suggested, probably the mosteffective is the "controlled hydrochloric acid-pumice abrasion" technique.11 This is not a truebleaching (oxidizing) technique but decalcifica-tion and removal of a thin layer of stained enamel.This technique has been modified somewhatsince its development in the mid 1980s.11, 6'

Acid-pumice technique. The procedure is as fol-lows (Figure 23- 8):

1. The teeth to be treated are photographed toserve as a permanent record and as a basisfor future comparison.

2. The gingiva is protected, and the teeth arecarefully isolated with an inverted rubberdam and ligatures. The rubber dam is ex-tended over the patient's nostrils.

3. Exposed areas of the patient's face and eyesare covered with a suitable drape or towelfor added safety from acid spatter.

4. A 36% hydrochloric acid solution is mixedwith an equal volume of distilled water tomake an 18% hydrochloric acid solution. Asubstantial amount of fine flour of pumiceis added to form a thick paste. In anotherdappen dish, sodium bicarbonate and waterare mixed to a thick paste, which will be usedlater for acid neutralization. Ready-madecommercial products are also available.


419

FIGURE 23-8Controlled hydrochloric acid-pumice abrasion technique.A, Marked discoloration results from surface hypoplasticdefects. B, Hydrochloric acid 18% is mixed with fine flourof pumice to form a thick paste, which is applied to thesurface with a crushed orangewood stick. The paste isworked into the enamel with a swirling motion for 5 sec-onds; this is followed by a water rinse. Paste is reappliedas necessary. Finally, acid is neutralized with sodium bicar-bonate. C, The desired improvement was obtained in asingle appointment. There was no regression. (CourtesyDr. S. Goepferd.)

5. The hydrochloric acid and pumice paste isapplied to the enamel surface with a piece ofwooden tongue blade or crushed orange-wood stick. Exerting firm pressure, thepaste is worked into the enamel surfacewith a swirling motion for 5 seconds. Theenamel surface is then rinsed for 10 secondswith water.

6. The paste is reapplied until the desiredcolor is achieved.

7. The surface is neutralized with sodium bi-carbonate and water. The rubber dam isremoved, and the teeth are pumiced witha fine prophylactic paste to smooth theabraded surface. Usually the desired shadeis obtained in a single appointment. If not,the stains may be too deep and not amen-able to lightening.

Alternative techniques. Another traditional ap-proach, the McInnes technique,6z is essentiallysimilar to the previous one but uses a solutioncomposed of five parts of 30% hydrogen perox-ide, five parts of 36% hydrochloric acid, and onepart of diethyl ether. The solution is applied di-rectly to the stained areas for 1 to 2 minutes withcotton applicators. While the surface is wet, afine cuttle disc is run over the stained surfacesfor 15 seconds. This process is repeated severaltimes.

420


Additional appointments may be necessary tobleach the tooth to the desired shade. The num-ber of appointments increases with the severity ofthe stain.

Comparison of techniques. The acid-pumicemethod does not actually bleach the stain as inthe McInnes technique, which uses hydrogen per-oxide. The acid-pumice technique is probably themost effective and requires the least amount ofchair time.

Prognosis. The acid-pumice abrasion techniqueis relatively permanent if initial lightening isachieved. Many patients have been followed forlong periods of time with no reoccurrence ofdiscoloration."

Safety. There are two areas in which safety is aconcern: the effects on enamel (excessive decalcifi-cation) and chemical burns of soft tissue.

With care and judicious application of acid ineither of the hydrochloric acid techniques, an in-significant amount of enamel is removed. Chemi-cal burns of the gingiva by either concentratedacid or hydrogen peroxide may be easily preventedby coating the gingiva with isolating materials, in-verting the rubber dam, and ligating the teeth.There are minimal to no pulpal effects, at leastwith the McInnes technique.63 Other studiesusing radioactive labels demonstrated an absenceof penetration of such agents into the pulp cham-ber as well as a decrease in enamel permeability.'

Mouthguard Bleaching

This technique is generally used for mild discol-orations. It has been basically advocated as ahome bleaching technique, and there are widevariations in materials, bleaching agents, and fre-quency and duration of treatment.' Numerousproducts are available for both home and in-officeuse. Most are composed of either 1.5% to 10% hy-drogen peroxide or 10% to 15% carbamide perox-ide, which degrades slowly to release hydrogenperoxide. Higher concentrations of the active in-gredient are also available and may reach up to50%, levels that are very toxic and contraindicated.The carbamide peroxide products are more com-monly used, although carbamide peroxide (20%)and hydrogen peroxide (7.5%) have been shown tobe equally effective and safe.66

BLEACHING TECHNIQUE

Owing to a lack of consensus about treatmenttechniques, step-by-step instructions shown inBox 23-2 should be used only as a generalguideline.

ALTERNATIVE TECHNIQUES

A modification of technique has been suggestedin which the discolored tooth is first treated


421

by enamel microabrasion (acid-pumice) and laterby home bleaching (carbamide peroxide mouth-guard system) . 66 This method enhances theesthetic results of the enamel microabrasiontechnique.

often without professional control. The use ofthese materials should be discouraged.

Laser Bleaching

PROGNOSIS

Long-term esthetic results of mouthguard bleach-ing are still unknown although short-term effec-tiveness is very good. 67.68 Reoccurrence of discol-oration occurs no more often than with the othertechniques.

SAFETY

The techniques, if well controlled, are relativelysafe and have little effect on sound enamel . 69 Ad-verse effects such as unpleasant taste, burningsensation in the oral tissues, and tooth sensitivitymay be associated with these products. Effectsare usually temporary and disappear within sev-eral days. However, accidental ingestion of largeamounts of bleaching gel is of concern. Animalstudies have indicated that ingestion of largeamounts of bleaching gel is toxic and may causeirritation to the gastric and respiratory mucosa. 70Bleaching gels containing carbopol, which re-tards the rate of oxygen release from peroxide, areusually more toxic.

Mouthguard bleaching is contraindicated inpatients with hypersensitive teeth, bruxism, or al-lergic reactions to any of the bleaching productcomponents. Gingival irritation is apparentlyminor." Although peroxide may penetrate thepulp in teeth with esthetic restorations, theamount and effect are probably insignificant.55

Some studies suggest that certain damage tocomposite resins may occur.","," Therefore, pa-tients must be informed that old composites mayrequire replacement after bleaching. It was alsoreported that bleaching agents enhance the liber-ation of mercury from amalgam restorations,thus possibly increasing exposure of patients totoxic byproducts 72.74 Although bleaching gels aremainly applied to anterior teeth, excessive gel mayinadvertently make contact with amalgam resto-rations placed in premolar and molar teeth. Cov-erage of amalgam restorations with a protectivelayer (such as Copalite) before gel application maybe beneficial .'s

To date, few conclusive experimental or clinicalstudies on the safety of prolonged use of thesebleaching agents are available. Therefore, cautionshould be exercised in prescribing and applyingthem. Of major concern are the products mar-keted directly to the public (over the counter),

This relatively new technique uses laser energy forbleaching vital teeth .76,7' The bleaching effect isachieved by a laser-induced chemical oxidationprocess, which rapidly breaks down the hydrogenperoxide to oxygen and water. Two types of lasersare usually used: the argon laser, which emits visi-ble blue light at a wavelength of 480 nm; and theCO2 laser, which emits invisible infrared light at awavelength of 10,600 nm. The argon laser is ab-sorbed by dark colors and therefore can easily re-move yellow-brown discolorations. The CO2 laser,which has no affinity to colors, emits heat and thusenhances the bleaching effect initiated by the argonlaser. These lasers are designed to work in conjunc-tion with patented commercial catalysts that areapplied on the external surfaces of the discoloredteeth. The combination of catalyst and peroxide ispotentially damaging; exposed soft tissues, eyes,and clothing must be carefully protected.

Combined use of argon and CO2 lasers can ef-fectively reduce intrinsic stains in dentin. Theargon laser can remove stain molecules withoutoverheating the pulp but becomes less effective asthe tooth whitens. The CO2 laser interacts directlywith the catalyst-peroxide combination and re-moves the stain regardless of tooth color.

Some laser bleaching techniques involve hy-drogen peroxide formulations at high concentra-tions (up to 50%). Although such techniqueslightened teeth faster, severe postoperative toothsensitivity was a common complication. Also, 50%hydrogen peroxide is a caustic chemical.

Laser bleaching is a relatively new technique.Sufficient controlled long-term studies of safetyand efficacy are currently lacking.


Most bleaching procedures can be performed bygeneral dentists, particularly if the cause of thediscoloration is diagnosed. If the general practi-tioner cannot make this identification, referral toa specialist should be considered.

The practitioner may also wish to refer patientswhose tooth discoloration does not respond toconventional methods of bleaching, either exter-nal or internal. Unidentified factors may be pre-venting the bleaching chemicals from effectivelyreaching the stain. The specialist may be able toidentify and correct these factors.

REFERENCES

1. Walton R: Bleaching procedures for teeth with vitaland nonvital pulps. In Levine N, editor: Current treat-ment in dental practice, Philadelphia, 1986, WB Saun-ders.

2. Rotstein I, Zalkind M, Mor C, et al: In vitro efficacy ofsodium perborate preparations used for intracoronalbleaching of discolored non-vital teeth, Endod Dent

Traumatol 7:177, 1991.3. Rotstein I, Mor C, Friedman S: Prognosis of intracoro-

nal bleaching with sodium perborate preparations invitro: 1 year study,JEndod 19:10, 1993.

4. Jacobsen 1, Kerkes K: Long-term prognosis of trauma-tized permanent anterior teeth showing calcifyingprocesses in the pulp cavity, Scand J Dent Res 85:588,1977.

5. Driscoll W, Herschel S, Meyers R, et al: Prevalence ofdental caries and dental fluorosis in areas with optimaland above-optimal water fluoride concentrations, J AmDent Assoc 107:42, 1983.

6. Jordan R, Boskman L: Conservative vital bleachingtreatment of discolored dentition, Compend ContinEduc Dent 5:803, 1984.

7. Chiappinelli J, Walton R: Tooth discoloration result-ing from long-term tetracycline therapy: a case report,Quintessence Int 23:539, 1992.

8. Corcoran J, Zillich R: Bleaching of vital tetracyclinestained teeth, JMich DentAssoc 56:340, 1974.

9. Walton R, O'Dell N, Lake F: Internal bleaching oftetracycline stained teeth in dogs, JEndod 9:10, 1983.

10. Abou-Rass M: Long-term prognosis of intentionalendodontics and internal bleaching of tetracycline-stained teeth, Compend Contin Educ Dent 19:1034,1998.

11. Croll T: Enamel microabrasion: observations after 10years, JAm Dent Assoc 128:455, 1997.

12. Van der Burgt T, Plasschaert A: Bleaching of tooth dis-coloration caused by endodontic sealers, J Endod 12:231, 1986.

13. Kim S, Abbott P, McGinley P: Effects of Ledermixpaste on discoloration of mature teeth, Int Endod J33:227, 2000.

14. Hardman P, Moor D, Petteway G: Stability of hydro-gen peroxide as a bleaching agent, Gen Dent 33:121,1985.

15. Spasser H: A simple bleaching technique using sodiumperborate, NY State Dent j 27:332, 1961.

16. Weiger R, Kuhn A, and Lost C: In vitro comparison ofvarious types of sodium perborate used for intracoro-nal bleaching, JEndod 20:338, 1994.

17. Rotstein 1, Friedman S: pH variation among materialsused for intracoronal bleaching, JEndod 17:376, 1991.

18. Swift E, Perdigao J: Effects of bleaching on teeth andrestorations, Compend Contin Educ Dent 19:815, 1998.

19. Li Y: Tooth bleaching using peroxide-containingagents: current status of safety issues, Compend ContinEduc Dent 19:783, 1998.

20. Crim GA: Post-operative bleaching: effect on micro-leakage, Am JDent 5:109, 1992.

21. Titley K, Torneck C, Ruse N: The effect of carbamide-peroxide gel on the shear bond strength of a microfilresin to bovine enamel, JDent Res 71:20, 1992.

22. Nutting E, Poe G: Chemical bleaching of discoloredendodontically treated teeth, Dent Clin North Am 15:655, 1970.

23. Marin P, Heithersay G, Bridges T: A quantitative com-parison of traditional and non-peroxide bleachingagents, Endod Dent Traumatol 14:64, 1998.

24. Kaneko J, Inoue S, Kawakami S, Sano H: Bleaching ef-fect of sodium percarbonate on discolored teeth invitro, JEndod 26:25, 2000.

25. Madison S, Walton R: Cervical root resorption follow-ing bleaching of endodontically treated teeth, JEndod16:570, 1990.

26. Rotstein I, Friedman S, Mor C, et al: Histological char-acterization of bleaching-induced external root re-sorption in dogs,JEndod 17:436, 1991.

27. Howell R: Bleaching discolored root-filled teeth, BrDent) 148:159, 1980.

28. Lin L, Pitts D, Burgess L: An investigation into the fea-sibility of photobleaching tetracycline-stained teeth,JEndod 14:293, 1988.

29. Rotstein 1, Zyskind D, Lewinstein 1, Bamberger N: Ef-fect of different protective base materials on hydrogenperoxide leakage during intracoronal bleaching invitro,JEndod 18:114, 1992.

30. Steiner D, West J: A method to determine the locationand shape of an intracoronal bleach barrier, J Endod20:304, 1994.

31. Casey L, Schindler W, Murata S, Burgess J: The use ofdentinal etching with endodontic bleaching proce-dures,JEndod 15:535, 1989.

32. Holmstrup G, Palm A, Lambjerg-Hansen H: Bleachingof discoloured root-filled teeth, Endod Dent Traumatol4:197, 1988.

33. Howell R: The prognosis of bleached root-filled teeth,Int Endod J 14:22, 1981.

34. Vachon C, Vanek P, Friedman S: Internal bleachingwith 10% carbamide peroxide in vitro, Pract PeriodonticsAesthet Dent 10:1145, 1998.

35. Glockner K, Hulla H, Eberleseder K, Stadtler P: Five-year follow-up of internal bleaching, Braz Dent j 10:105, 1999.

36. Freccia W, Peters D, Lorton L: An evaluation of variouspermanent restorative materials' effect on the shade ofbleached teeth, JEndod 8:265, 1982.

37. Rivera E, Vargas M, Ricks-Williamson L: Considera-tions for the aesthetic restoration of endodonticallytreated anterior teeth following intracoronal bleach-ing, PractPeriodontics AesthetDent 9:117, 1997.

38. Lemon R: Bleaching and restoring endodonticallytreated teeth, Curr Opin Dent 1:754, 1991.

39. Wilcox L, Diaz-Arnold A: Coronal microleakage of per-manent lingual access restorations in endodonticallytreated anterior teeth, JEndod 15:584, 1989.

40. Titley K, Torneck C, Ruse N, Krmec D: Adhesion of aresin composite to bleached and unbleached humanenamel, JEndod 19:112, 1993.

41. Rotstein I: Role of catalase in the elimination of resid-ual hydrogen peroxide following tooth bleaching, JEndod 19:567, 1993.

42. Brown G: Factors influencing successful bleaching ofthe discolored root-filled tooth, Oral Surg Oral Med OralPathol 20:238, 1965.

422


23 I Bleaching Discolored Teeth: Internal and External

423

43. Harrington G, Natkin E: External resorption associ-ated with bleaching of pulpless teeth, J Endod 5:344,1979.

44. Friedman S, Rotstein 1, Libfeld H, et al: Incidence ofexternal root resorption and esthetic results in 58bleached pulpless teeth, Endod Dent Traumatol 4:23,1988.

45. Heithersay GS, Dahlstrom SW, Marin PD: Incidence ofinvasive cervical resorption in bleached root-filledteeth, AustDentJ39:82, 1994.

46. Rotstein I, Torek Y, Misgav R: Effect of cementum de-fects on radicular penetration of 30% H20 2 during in-tracoronal bleaching, JEndod 17:230, 1991.

47. Newvald L, Consolaro A: Cementoenamel junction:microscopic analysis and external cervical resorption,JEndod 26:503, 2000.

48. Heling 1, Parson A, Rotstein 1: Effect of bleachingagents on dentin permeability to Streptococcus faecalis,JEndod 21:540, 1995.

49. Rotstein I, Wesselink PR, Bab I: Catalase protectionagainst hydrogen peroxide-induced injury in rat oralmucosa, Oral Surg Oral Med Oral Patbol 75:744, 1993.

50. Skinner H, Nalbandian J: Tetracyclines and mineral-ized tissues: review and perspectives, Yale J Biol Med48:377, 1975.

51. Walton R, O'Dell N, Myers D, et al: External bleachingof tetracycline stained teeth in dogs, J Ended 8:536,1982.

52. Lake F, O'Dell N, Walton R: The effect of internalbleaching on tetracycline in dentin, J Endod 11:415,1985.

53. Seale N, Thrash W: Systematic assessment of color re-moval following vital bleaching of intrinsically stainedteeth, JDent Res 64:457, 1985.

54. Cooper J, Bokmeyer T, Bowers W: Penetration of thepulp chamber by carbamide peroxide bleachingagents, J Ended 18:315, 1992.

55. Gokay O, Yilmaz F, Akin S, et al: Penetration of thepulp chamber by bleaching agents in teeth restoredwith various restorative materials, JEndod 26:92, 2000.

56. Cohen S: Human pulpal response to bleaching proce-dures on vital teeth, JEndod 5:134, 1979.

57. Robertson W, Melfi R: Pulpal response to vital bleach-ing procedures, J Endod 6:645, 1980.

58. Anitua E, Zabalegui B, Gil J, et al: Internal bleaching ofsevere tetracycline discolorations: four-year clinicalevaluation, Quintessence Int 21:783, 1990.

59. Aldecoa E, Mayordomo F: Modified internal bleachingof severe tetracycline discoloration: A 6-year clinicalevaluation, Quintessence Int23:83, 1992.

60. Walton R, Eisenmann D: Ultrastructural examinationof dentine formation following multiple fluoride in-jections, Arcb Oral Biol 20:485, 1975.

61. DeAbranjo F, Zia V, Dutra C: Enamel color change bymicroabrasion and resin-based composite, Am J Dent13:6, 2000.

62. McInnes JW: Removing brown stain from teeth, ArizDentJ 12:13, 1966.

63. Baumgartner JC, Reid DE, Pickett AB: Human pulpalreaction to the modified McInnes bleaching tech-nique,JEndod 9:12, 1983.

64. Griffen R, Grower M, Ayer W: Effects of solutions usedto treat dental fluorosis on permeability of teeth, JEndod 3:139, 1977.

65. Haywood V, Heymann H: Nightguard vital bleaching,Quintessence Int 20:173, 1989.

66. Reinhardt J, Eivins S, Swift E, Denehy G: A clinicalstudy of nightguard vital bleaching, Quintessence Int24:379, 1993.

67. Mokhlis G, Mateo B, Cochren M, Eckert G: A clinicalevaluation of carbamide peroxide and hydrogen perox-ide whitening agents during daytime use, J Am DentAssoc 131:1269, 2000.

68. Blankenau R, Goldstein R, Haywood V: The currentstatus of vital tooth whitening techniques, CompendContin Educ Dent 20:781, 1999.

69. Potocnik 1, Kosec L, Gaspersic D: Effect of 10% car-bamide peroxide bleaching gel on enamel microhard-ness, microstructure, and mineral content, J Endod26:203, 2000.

70. Redmond A, Cherry D, Bowers D Jr: Acute illness andrecovery in adult female rats following ingestion of atooth whitener containing 6% hydrogen peroxide, AmJDent 10:268, 1997.

71. Schultz J, Morrissette D, Gasior E, et al: Clinicalchanges in the gingiva as a result of at home bleaching,Compend Contin Educ Dent 14:1362, 1993.

72. Hummert T, Osborne J, Norling B, Cardenas H: Mer-cury in solution following exposure of various amal-gams to carbamide peroxide, Am JDent 6:305, 1993.

73. Rotstein I, Mor C, Arwaz J: Changes in surface levels ofmercury, silver, tin and copper of dental amalgamtreated with carbamide peroxide and hydrogen perox-ide, Oral Surg Oral Med Oral Patbol 83:506, 1997.

74. Rotstein I, Dogan H, Avron Y, et al: Mercury releasefrom dental amalgam following treatment with 10%carbamide peroxide in vitro, Oral Surg Oral Med OralPatbol 89:216, 2000.

75. Rotstein 1, Dogan H, Avron Y, et al: Protective effect ofCopalite surface coating on mercury release from den-tal amalgam following treatment with carbamide per-oxide, Endod Dent Traumatol 16:107, 2000.

76. Garber D: Dentist-monitored bleaching: a discussionof combination and laser bleaching, J Am Dent Assoc128(suppl.):26S, 1997.

77. Reyto R: Laser tooth whitening, Dent Clin Nortb Am42:755, 1998.

Endodontic Surgery

LEARNING OBJECTIVES


/ Discuss the role of endodontic surgery as compared with nonsurgical root canal therapy.

z / Recognize situations in which surgery is not the treatment of choice.

3 / Define the terms incision for drainage, apical curettage, root-end resection, root-end preparation andfilling, root amputation, hemisection, and bicuspidization.

a / Discuss the indications for each procedure listed in Objective 3.

s / Discuss the prognosis for each procedure listed in Objective 3.

6 / Recognize the medical or dental situations in which endodontic surgery is contraindicated or, if performed,

has a questionable outcome.

7 / State the principles of flap design.

s

Diagram the various flap designs and describe the indications, advantages, and disadvantages of each.

s / Describe, in brief, the step-by-step procedures involved in periradicular surgery, including those for incision

and reflection, access to the apex, apical curettage, root-end resection, root-end preparation and filling, flap

replacement, and suturing.

10 / List the more commonly used root-end filling materials.

11 / Review the basic principles of suturing.

12 / Describe general patterns of soft and hard tissue healing.

93 / Write out postsurgical instructions to be given to the patient concerning bleeding, pain, swelling, diet, and

suture removal.

14 / List and describe conditions that indicate referral to a specialist for evaluation and/or treatment.

424

I ncision for Drainage

I ndications

Contraindications

Procedure


I ndications

Contraindications

Sequence of Procedures

Healing

Soft Tissue

Hard Tissue

Corrective Surgery

I ndications

Techniques

Root Amputation, Hemisection,

and Bicuspidization

Definitions

I ndications and Contraindications

Techniques

Prognosis

Conditions That Indicate Referral

24 / Endodontic Surgery

425

onsurgical root canal therapy is ahighly successful procedure if the diag-nosis is correct and technical aspects

are carefully performed.1.2 There is a common be-lief that if root canal therapy fails, surgery is indi-cated for correction. This is not necessarily true;most failures are best corrected by retreatment.Studies have shown that more than two thirds ofretreatments after original root canal therapy aresuccessful.3.4 However, in some situations surgeryis necessary to retain a tooth that would otherwisebe extracted.'

This chapter describes both the indications andthe procedures used for endodontic surgery. Experi-enced clinicians and specialists should performmost of these procedures. However, general practi-tioners should be skilled in diagnosis and treatmentplanning and should be able to recognize what pro-cedures are appropriate in different situations. Inother words, clinicians must be aware of what pro-cedures are available, in order to present these pro-cedures to patients as treatment options. Includedin this chapter are descriptions of incision fordrainage, periradicular surgery, corrective surgery,root amputation, hemisection, and bicuspidization.

Incision for Drainage

Incision for drainage releases purulent and or hem-orrhagic exudate from a soft tissue swelling. Theobjectives are to evacuate exudate and purulence,which are potent and toxic irritants. Removalspeeds healing and reduces discomfort resultingfrom the irritants and from the buildup of pres-sure. Performance of most intraoral incisions isgenerally within the ability of general practitioners.

INDICATIONS

The best treatment for swelling originating froman acute apical abscess of pulpal origin is to es-tablish drainage through the offending tooth (seeColor Figure 24-1, A, following page 436). Often,adequate drainage cannot be accomplishedthrough the tooth itself, the second choice is toobtain soft tissue drainage. Occasionally drainageis performed through the soft tissue even if it hasalso been obtained through the tooth. The reasonis that there may be two (or more) separate, non-communicating abscesses-one at the apex andanother in a submucosal location or in ananatomic space. So, if necessary and feasible, suchsupplemental drainage is indicated.

Drainage through the soft tissue is accom-plished most effectively when the swelling is fluc-tuant. A fluctuant swelling is a fluid-containing

426


mass in which a wavelike sensation or motion isfelt as pressure is applied (see Color Figure 24-1, B).The feeling is similar to that experienced whenpushing on a water balloon or a small plasticpacket of catsup. Incising a fluctuant swelling re-leases purulence immediately and provides rapidrelief. If the swelling is nonfluctuant or indurated(firm), the outcome is somewhat less predictableand often results in drainage of only blood andserous fluids. Although the results may not be asdramatic or complete as those achieved by incis-ing a fluctuant swelling, incising a nonfluctuantswelling releases pressure and facilitates healingby reducing irritants and increasing circulation inthe area.

CONTRAINDICATIONS

There are relatively few contraindications to theuse of incisions. Diffuse swellings are not usuallyincised. Patients with prolonged bleeding or clot-ting times must be treated cautiously, and hema-tologic screening is often indicated. An abscess inan anatomic space may require more involvedtreatment; the patient should be referred to anoral and maxillofacial surgeon for an extraoral oraggressive intraoral incision.

PROCEDUREAnesthesia

Profound anesthesia is difficult to achieve in thepresence of inflammation, swelling, and exudatebecause of hyperalgesia. Direct subperiosteal infil-tration not only is ineffective but also may be quitepainful. Standard infiltration may not be totally ef-fective either. Therefore, regional block anesthesiatechniques are preferred. Mandibular blocks forposterior areas, bilateral mental blocks for the an-terior mandible, posterior superior alveolar blocksfor the posterior maxilla, and infraorbital blocksfor the premaxilla are preferred choices. These maybe supplemented by regional infiltration.

If regional block anesthesia is not sufficient,one of the following methods may be used. Thefirst technique is infiltration starting peripheralto the swelling. The solution is injected slowlywith limited pressure and depth; this is followedby additional injections in previously anesthe-tized tissue, moving progressively closer to thecenter of the swelling. This procedure results inimproved anesthesia without extreme discomfort.

A second technique is the use of topical ethylchloride . 6 A stream of this agent is directed ontothe swelling from a distance, permitting the liquidto volatilize on the tissue surface. Within seconds,the tissue at the site of volatilization turns white.

The incision is quickly accomplished with contin-ued ethyl chloride spray. This topical anesthesia isa supplement to block anesthesia when a quick in-cision is required. If none of these procedures work,the incision for drainage may be done with intra-venous sedation.

Incision

After anesthesia, the incision is made horizontallyor vertically with a No. 11, 12, or 15 blade. Verti-cal incisions are parallel with the major blood ves-sels and nerves and leave very little scarring. Theincision should be made firmly through perios-teum to bone. If the swelling is fluctuant, pus usu-ally flows immediately, followed by blood. Occa-sionally, there is only a serosanguineous exudate,which is acceptable. If the swelling is nonfluctu-ant, the predominant flow is hemorrhagic.

Drainage

After the initial incision, a small closed hemostatmay be placed in the incision and then opened toenlarge the draining tract.' This procedure is indi-cated with more extensive swellings; the initial in-cision and subsequent enlargement usually pro-vide the needed drainage. If a drain is necessarybecause of limited initial drainage, a self-retentiveI -shaped or "Christmas tree" drain cut from a rub-ber dam or a piece of iodoform gauze is placed(suturing is optional) in the incision (see ColorFigure 24-1, C). The drain should be removedafter 2 to 3 days; if it is not sutured, the patientmay remove the drain at home.


This surgery is commonly performed to remove aportion of the root with undebrided canal spaceor to retroseal the canal when a complete sealcannot be obtained with an orthograde (throughthe crown) approach. Occasionally, periradicularcurettage without root resection is needed.

I NDICATIONS

The main indications for periradicular surgery(PS) are (1) nonsurgical root canal therapy is un-feasible, (2) retreatment of failed root canal ther-apy is impossible or would not produce a betterresult, or (3) biopsy is indicated.

In the following situations, periapical surgerymay be necessary:

Anatomic problemsProcedural accidents requiring surgery


42 7

Irretrievable materials in the root canalPersistent symptomsHorizontal apical fractureBiopsy

Anatomic Problems

A non-negotiable canal, blockage, or severe rootcurvature may prevent adequate cleaning andshaping or obturation. Nonsurgical root canaltherapy or retreatment (if possible) before surgeryimproves the surgical success rate.8.9 However, ifneither is feasible, removal of the uninstrumentedand unfilled portion of the root or apical surgerymay be necessary (Figure 24-1). Anatomic perfo-ration of the root apex through the bone (fenes-tration), although uncommon, may necessitateapical surgery after root canal treatment. Occa-sionally, even after an apparently adequate obtu-ration, inflammation and discomfort continue ifthe root apex protrudes outside the bony corticalplate. This condition is corrected by beveling theroot apex and placing it within the bone.

Occasionally, adequate root canal therapy iscompromised by extensive apical root resorption.It may then be necessary to expose the root, thenremove and repair the resorbed area.


Separated instruments, ledging, perforations, andgross overfills may cause failure of root canal

treatment which will require surgical interven-tion. Slight to moderate overfilling is not in itselfan indication for surgery; if symptoms persist ordevelop or if nonhealing is shown radiographi-cally, surgery is usually necessary.

Irretrievable Materials in the Root Canal

Retreatment is recommended for treatment fail-ures when retreatment is possible. However, irre-trievable posts or dowels or root filling materialssuch as silver cones, amalgam, or nonabsorbablepastes often prevent retreatment, or their removalwould result in further damage to the root struc-ture. The best alternative is a surgical approach,including placement of a root-end filling material(Figure 24-2).

Persistent Symptoms

Most symptoms disappear after complete clean-ing and obturation of root canals. However, ifsymptoms persist after meticulous performanceof these procedures endodontic surgery shouldbe considered to identify the cause(s) for thepersistence of the symptoms. The main causefor persistent pain is the presence of inflam-mation because of the inability of the operatorto completely clean the root canal(s). Explo-ratory surgery may identify undetected verticalroot fractures, additional apical and lateralforamina (possible missed canals), perforations,

FIGURE 24-7A, A non-negotiable ledge in present in the mesiobuccal root of the first maxillary molar. B, Periradicular surgery(root-end resection and filling) corrected this accident and deficiencies in the distobuccal root.

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FIGURE 24-2A, Preoperative radiograph shows failing root canal treat-ments in the canine and lateral incisor. B, The caninepathosis caused an extraoral sinus tract on the cheek ofthe patient. C, Because of the presence of a new bridgeand a large post in the canine, periapical surgery was per-formed; the lateral incisor was retreated. D, The surgicalsite and placement of MTA as root-end filling material.


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FIGURE 24-2, cont'dE, The sinus tract disappeared 6 weeks after the surgery.F, A 5-year recall shows complete resolution of the lesioni n the canine. (Courtesy Dr. C. Hong.)

apical ramifications, overfills, or other causes offailure. Once the cause has been determined aproper treatment plan can be initiated. Sur-gery should be performed only after causes thatare correctable without surgery are ruled out.Examples of such causes are missed canals,cracked teeth, occlusal trauma, referred pain(from another tooth), or inadequate debride-ment or obturation.

lignancy, lip paresthesia, or anesthesia. Theseconditions are indications for biopsy.

CONTRAINDICATIONS

Contraindications are relatively few. There arefour major categories': (1) anatomic factors,(2) medical or systemic complications, (3) indis-criminate use of surgery, and (4) unidentifiedcause of treatment failure.

Horizontal Apical Fracture

Although most traumatic horizontal apical frac-tures usually heal without intervention, occasion-ally the apical canal becomes necrotic and cannotbe treated. In these cases, the apical segment ofthe root must be removed.

Biopsy

Although most pathoses are of pulpal origin,nonpulpal lesions do exist (see Chapter 3). Find-ings include the presence of a vital pulp in atooth with a radicular radiolucency (Figure 24-3),undefined periapical lesions in teeth with vitalpulps in patients with a history of previous ma-

Anatomic Factors

Inaccessibility of the surgical site owing to toothlocation, spaces such as maxillary sinus or nasalfossa, unusual bony configuration, or proximityof neurovascular bundles may be a contraindi-cation or at least require caution or special ap-proaches. For example, a thick external obliqueridge associated with a mandibular molar orapices contiguous with the mandibular canal maycompromise surgical access. These factors arealso related to operator skill. Other situationsthat may contraindicate periradicular surgeryor modify the approaches used include veryshort root length (precluding root-end resection),

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FIGURE 24-3A, Presence of vital pulps in the left anterior teeth and amultilocular large radiolucency indicated the probability ofa lesion of a nonpulpal origin. B, A panoramic radiographshows the extent of this lesion (arrows). A biopsy revealedthe presence of a keratocyst.

severe periodontal disease (hopeless prognosis,even with surgery), or unresrorable teeth.

Medical or Systemic Complications

Serious systemic health problems or extreme ap-prehension makes the patient a poor candidatefor surgery. Surgery may also be contraindicatedin patients with blood disorders, terminal disease,uncontrolled diabetes, or severe heart disease, orfor those who are immunocompromised.

Indiscriminate Use of Surgery

As previously stated, surgery is not indicatedwhen a nonsurgical approach would probably re-sult in successful treatment. The practice of man-aging all accessible periapical parhoses or largeperiradicular lesions surgically is unethical andnot rational. In these situations, root canal treat-ment resolves the problem without subjecting thepatient to additional trauma.

Unidentified Cause of Treatment Failure

Importantly, surgery to correct a treatment failurefor which the cause cannot be identified is un-likely to be successful.

SEQUENCE OF PROCEDURES

The typical sequence of procedures used in peri-radicular surgery (with modifications accordingto the situation) is the following:

1. Flap design2. Incision and reflection3. Apical access4. Periradicular curettage5. Root-end resection6. Root-end cavity preparation7. Root-end filling8. Flap replacement and suturing9. Postoperative care and instructions

10. Suture removal and evaluation

Flap Design

The first stage requires exposure of the surgicalsite by incising and reflecting the overlying softtissues of gingiva, mucosa, and periosteum. Aproperly designed and carefully reflected flapgives good surgical access and results in improvedhealing. The following are general guidelines andprinciples'°":

1. Adequate blood supply to the reflected tis-sue is maintained with a wide flap base.

2. Incisions over bony defects or over the peri-radicular lesion should be avoided; these

FIGURE 24-4A submarginal curved (semilunar) flap is shown in the at-tached gingiva to perform periapical surgery on the rightlateral incisor (X). This design has deficiencies and usually isnot indicated.

might cause postsurgical soft tissue fenes-trations or nonunion of the incision.

3. The flap should be designed for maximumaccess by avoiding limited tissue reflection.The actual bone resorption is larger thanthe size observed radiographically.

4. Acute angles in the flap are avoided. Sharpcorners are difficult to reposition and su-ture and may become ischemic and slough,resulting in delayed healing and possiblyscar formation.

5. Incisions and reflections include periosteumas part of the flap. Any remaining pieces ortags of cellular nonreflected periosteum willhemorrhage, compromising visibility.

6. The interdental papilla must not be split(incised through). The interdental papillashould be either fully included or excludedfrom the flap; dividing may result in slough-ing of the tissue.

7. Vertical incisions must be extended to allowthe retractor to rest on bone and not crushportions of the flap.

8. A minimal flap, which should include atleast one tooth on either side of the in-tended tooth, should be used.

Although there are numerous flap designs, twomeet most periradicular surgery needs: the sub-marginal (curved, triangular, and rectangular)and the full mucoperiosteal (triangular and rec-tangular) flaps.

Submarginal curved flap. Also known as the semi-lunar flap, this flap is a slightly curved, half-moon-shaped, horizontal incision made in oral mucosa,or in the attached gingiva with the convexity near-est the free gingival margin (Figure 24-4). It issimple and easily reflected and provides access tothe apex without impinging on the tissue sur-rounding the crowns. Its disadvantages include re-stricted access with limited visibility, tearing of the


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FIGURE 24-5A scalloped submarginal horizontal incision (Ochsenbein-Luebke) is made in the attached gingiva with two accompa-

nying vertical incisions to perform surgery on the right cen-tral incisor.

incision corners when attempting to improve ac-cess by stretching the tissue, and leaving the inci-sion directly over the lesion if the surgical defect islarger than anticipated. The incision often healswith scarring.5.12 The submarginal curved flap islimited by the presence of the frenum, muscle at-tachments, or canine and other bony eminences.Because of its many problems, this design is gen-erally not indicated.

Submarginal triangular and rectangular flaps. Thetriangular or rectangular flaps are known asmodified submarginal curved flaps. A scallopedhorizontal incision (Ochsenbein-Luebke) is madein the attached gingiva with one or two accom-panying vertical incisions (Figure 24-5). This flapis used most successfully in maxillary ante-rior teeth with crowns. Prerequisites are at least4.0 mm of attached gingiva and good periodon-tal health.

This flap design provides better access and vis-ibility compared with the submarginal curved flapand less risk of incising tissue over a bony defectand no recession of marginal gingiva postsur-gically. Disadvantages are possible scarring andhemorrhaging from the cut margins to the surgi-cal site." It also provides less visibility than thefull mucoperiosteal flap.

Full mucoperiosteal flap. The full mucoperi-osteal (sulcular) flap consists of an incisionat the gingival crest with full elevation of theinterdental papillae, free gingival margin, at-tached gingiva, and alveolar mucosa. It mayhave either a single (triangular) or double (rec-tangular) vertical releasing incision (Figure 24-6and Color Figure 24-1, D). It allows maximal ac-cess and visibility, precludes incising over a bonydefect, and has fewer tendencies for hemor-

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FIGURE 24-6A triangular full mucoperiosteal (sulcular) flap with one ver-

tical incision is made to access the right central incisor.

rhage. This design permits periodontal curet-tage, root planing, and bony reshaping andheals with minimal scar formation. Its disad-vantages include the difficulty of replacement,suturing, and making alterations (height andshape) to the free gingival margin, as well as pos-sible gingival recession postsurgically and ex-posing the crown margins." ."

Incision and Reflection

A firm incision is made with a No. 15 or anothersuitable blade. To prevent tearing during reflec-tion, the incision must be made through perios-teum to bone. The tissue is reflected with a sharpperiosteal elevator beginning in the vertical inci-sion and then raising the horizontal component.Because periosteum is reflected as part of the flap,the elevator must firmly contact bone as the tissueis peeled back, using firm controlled force. Thetissue is reflected to a level that will provide ade-quate access and visibility of the surgical sitewhile allowing a retractor to be placed on soundbone (Figure 24-7).

Access to Apex

In many cases because of the presence of a lesion,bone has been resorbed, and either a soft tissue le-sion is visible, or firm probing with an explorerwill locate the apical lesion. If the opening issmall, the bone can be removed by a sharp roundbur until the apex is visible. If there is limitedbone destruction, after placement of a radiopaqueobject near the apex a radiograph should be takento locate the apex. Removal of bone with a bur isperformed in the presence of copious sterile salineirrigation.

FIGURE 24-7The flap is reflected with a periosteal elevator and held with

a retractor to allow visibility and access to the surgical site.

The retractor must be placed on sound bone.

Periradicular Curettage

Removal of pathologic soft tissue surrounding theapex is necessary because it does the following:

1. Provides access and visibility of the apex2. Removes inflamed tissue3. Provides a biopsy specimen for histologic

examination4. Reduces hemorrhageThe tissue should be carefully peeled out,

ideally in one piece, with a suitably sized sharpcurette (see Color Figure 24-1, E). This processshould leave a clean bony cavity. When the le-sion is very large, portions of tissue can be leftwithout compromising the blood supply to anadjacent tooth. This should not affect periradic-ular healing.

Root-End Resection

Root-end resection involves beveling of the apicalportion of the root. This step is often an integralpart of periradicular surgery and serves the fol-lowing two purposes:

1. It removes the untreated apical portion ofthe root and enables the operator to deter-mine the cause of failure.

2. It provides a flat surface to prepare a rootend cavity and pack it with a root-end fillingmaterial.

Apical sectioning is done with a tapered fissurebur in a high-speed handpiece and copious sterilesaline irrigation (Figure 24-8). The bevel shouldbe made at approximately 45 degrees in a facial-lingual direction, with the least amount of bevelto give maximum visibility to the root apex." ," In

FIGURE 24-8Root-end resection (apicoectomy). A, A fissure bur is used to remove the apical portion of the root. B, The entireresected portion should be visible.

general, the amount of root removed depends onthe reason for performing the root-end resection.However, resection must be sufficient to do thefollowing:

1. Provide access to the palatal-lingual rootsurface

2. Place the canal in the center of the sectionedroot

3. Expose additional canals or fractures

Root-End Cavity Preparation and Filling

Root-end cavity preparation and filling are indi-cated when the apical seal appears to be inade-quate. A class I type preparation is made with ul-trasonic tips to a minimum depth of 3 mm intothe canal 10.11.13.16.17 (Figure 24-9). More compli-cated apical root anatomy may require other typesof preparation." The ultrasonic instrument offersadvantages of control and ease of use and permitsless apical root beveling and uniform depth ofpreparation. 16.17 In addition, the ultrasonic tipsfollow the direction of the canals and clean thecanal surfaces better than burs."

A root-end filling material is then inserted intothe prepared cavity (Figure 24-10). These materi-als should have the following characteristics

1. Well sealing2. Well tolerated by the periradicular tissue3. Nonresorbable4. Easily inserted


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5. Unaffected by moisture6. Radiographic visibility7. Ability to allow regeneration of periradicu-

lar tissuesMany materials have been used as root-end

filling materials. 19-24 Amalgam, SuperEBA, IRM,mineral trioxide aggregate (MTA) and ProRootMTA, are acceptable and the most commonlyused materials.

Flap Replacement and Suturing

After a root-end filling material is placed and a ra-diograph is made, the flap should be placed intoits original position and held it in place for 5 min-utes using moderate digital pressure with moist-ened gauze. This allows expression of hemorrhagefrom under the flap, initial adaptation, and easiersuturing and produces less postoperative swellingand bleeding.

Suturing is commonly done with silk, al-though other materials are acceptable . 25,26 Thereare many suturing techniques, including inter-rupted, continuous mattress, and sling sutures."Interrupted sutures are commonly used (Fig-ure 24-11, A). In these, the needle passes firstthrough reflected and then through attachedtissue. The sutures are tied with a simple sur-geon's knot. The knot should not be placed overthe incision line because it collects debris andbacteria, which will promote inflammation and

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FIGURE 24-9Root-end cavity preparation. An ultrasonic unit using specialized tips (A) is used to create a class I preparation inthe apical portion of the root canal (B). (Courtesy Dr. R. Rubinstein.)

FIGURE 24-10Root-end filling placement. MIA (3 mm) is placed in the root-end cavity preparation to provide a fluid-tight apical seal.(Courtesy Dr. R. Rubinstein.)

infection. The sutures are usually removed 3 to7 days after surgery (Figure 24-11, B); shortertimes are preferred.

Postoperative Care and Instructions

Both oral and written postoperative instructionsshould be given to the patient. Instructionsshould be written in simple, straightforward lan-guage. They should minimize patient anxiety aris-

ing from normal postoperative sequelae by de-scribing how to promote healing and comfort.

The following instructions are for patients.The items in parentheses identified as "Note" areintended for the practitioner, not the patient.

1. Some swelling and discoloration are com-mon. Use an ice pack with moderate pres-sure on the outside of your face (20 min-utes on, 5 minutes off) until you go to bedtonight. (Note: Ice and pressure [primar-ily] decrease bleeding and swelling andprovide an analgesic effect.)

2. Some oozing of blood is normal. If bleed-ing increases, place a moistened gauze pador facial tissues over the area and applyfinger pressure for IS minutes. If bleedingcontinues, call our office.

3. Do not lift up your lip or cheek to look atthe area. The stitches are tied and you maytear them out.

4. Starting tomorrow, dissolve 1 teaspoon ofsalt in a glass of warm water and gentlyrinse your mouth three or four times daily.Rising with a mouthwash can promotehealing. Careful brushing is important,but vigorous brushing may damage thearea. Tonight you should brush and flossall areas except the surgery site. Tomorrownight carefully brush the surgery site.

5. Eat a diet of soft food and chew on the op-posite side of your mouth. Drink lots offluids and eat foods such as cottage cheeseand yogurt, eggs, and ice cream. (Note:Proper diet and fluid intake are essential

FIGURE 24- 11A, Interrupted sutures are commonly used to hold the soft tissue flap in its original location. B, Sutures are re-moved 3 to 7 days after surgery.

after surgery. Patients often lose their ap-petite after the procedure, so they need tobe encouraged to drink fluids and to eat.)

6. Some discomfort is normal. If pain med-ication was prescribed, follow the instruc-tions. If no medication was prescribed,take your preferred nonprescription painremedy if needed. If this is not sufficient,call our office. (Note: Surprisingly, pain isusually minimal after endodontic surgery,and strong analgesics are not required.)

7. Do not smoke for the first 3 days afterthe procedure. (Note: Smoking has beenshown to adversely affect healing; this is anopportunity to counsel a patient to quitpermanently.)

8. If you experience excessive swelling orpain or if you have a fever, call our officeimmediately. (Note: Excessive swelling,pain, or fever may indicate the presenceof an infection [very rare] that requiresantibiotic or other therapy. The patientmust be evaluated.)

9. Keep your appointment to have the stitchesremoved. (Note: Sutures are removed 3 to7 days after surgery.)

10. Call our office if you have any concerns orquestions.

Suture Removal and Evaluation

Sutures are carefully removed by cutting withsmall scissors. The sutures are removed only if theflap margins are in contact and are adhering to

the underlying tissues. Usually, anesthesia is un-necessary for this procedure.

HealingSurgery involves the manipulation of soft andhard tissues. Handling of both soft tissues (pe-riosteum, gingiva, periodontal ligament, and alve-olar mucosa) and hard tissues (dentin, cementum,and bone) is accomplished by incision, dissection,and excision.

SOFT TISSUE

Healing involves clotting, inflammation, epithe-lialization, connective tissue healing, and matura-tion and remodeling of both connective tissueand bone.27 Clotting and inflammation consist ofboth chemical and cellular phases. The clottingmechanism is important because it is based onthe conversion of fibrinogen to fibrin; under pres-sure, the clot should be a thin layer. Failure of aclot to form results in leakage of blood into thewound site. The inflammatory components ofhealing are a complex network of both extrinsicand intrinsic elements.27

Initial epithelial healing consists of the forma-tion of the epithelial barrier, made up of layers ofepithelial cells that depend on the underlying con-nective tissue for nutrients. This epithelial layermigrates along the fibrin surface until it makescontact with epithelial cells from the opposite bor-der of the wound, forming an epithelial bridge.


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The connective tissue component comes fromfibroblasts, which are differentiated from ecto-mesenchymal cells and are attracted to the woundsite by cellular and humoral mediators. Adjacentblood vessels provide nutrients for the fibroblastsand their precursors, which elaborate collagen,initially type III, followed by type 1. Macrophagesare an important part of these processes. As heal-ing matures, there is a decrease in the amount ofinflammation and numbers of fibroblasts, accom-panied by deaggregation and reaggregation of col-lagen with formation of collagen fibers into amore organized pattern.27-30

HARD TISSUE

As with soft tissue, the hard tissue response isbased on the fibroblast, which results in synthesisof ground substance, cementum, and bone matrixformation . 3 ' New cementum deposition from ce-mentoblasts begins about 12 days after surgery;eventually a thin layer of cementum may cover re-sected dentin and even certain root end filling ma-terials (see Color Figure 24-1, F). The exposeddentin acts as an inductive force with new cemen-tum forming from the periphery to the center.

Osseous healing begins by the proliferation ofendosteal cells into the coagulum of the woundsite. At 12 to 14 days, woven trabeculae and osteo-cytes appear, leading to early maturation of thecollagen matrix at about 30 days. This process oc-curs from inside to outside, ending in the forma-tion of mature lamellar bone ,32-35 which is visibleradiographically (Figure 24-12).

Corrective SurgeryThese procedures are especially designed to cor-rect pathologic or iatrogenic entities (procedureerrors) that have damaged the root and are notcorrectable via the pulp space (internally).

INDICATIONSProcedural Errors

Correction of root perforations often presents amore difficult challenge than procedures thatmerely involve periradicular surgery. Typicallythese accidents occur during access, canal prepa-ration, or restorative procedures (usually postplacement). They require restorative as well as en-dodontic management (Figure 24-13). See Chap-ter 18 for more detail. The location of the perfo-ration is often the factor that determines the

success of treatment. If the defect is on the proxi-mal root surfaces in close proximity to adjacentteeth, repair is a problem; access to the site is dif-ficult without damaging adjacent teeth. This isparticularly true of the lingual surface of man-dibular teeth. However, defects on the facial sur-face are easier to treat.

Resorptive Perforations

Resorptive root perforations typically occur as se-quela to trauma or internal bleaching procedures.The defects may be localized to the root surface orcommunicate with the canal.

TECHNIQUES

Repair of these defects poses unique problems.Often a defect on the root surface wraps onto thepalatal or lingual surface, compromising accessand hemostasis. Repair can be accomplished withvarious materials. If the field can be kept dry, glassionomer, dentin-bonding agent with compositeresin, or MTA (white ProRoot MTA) can be used.Esthetically pleasing materials are preferred forfacial repairs because dark materials such as amal-gam or gray ProRoot MTA may stain the teeth. Ifa post perforates the root, it must be shortened sothat it is well within the root structure. Then thedefect is repaired with ProRoot MTA.

Repairs in the cervical portion of the root areoften difficult to manage and maintain becausecommunication with the gingival sulcus leadsto periodontal breakdown. This often meansthat periodontal treatment (such as crown length-ening), orthodontic extrusion, or a combina-tion thereof is necessary in conjunction with therepair.

Root Amputation, Hemisection,and BicuspidizationThe three categories described previously, incisionfor drainage, periradicular surgery and correctivesurgery, involve cutting bone, soft tissue, androot. This last category involves resecting theroot(s) and/or crown .36

DEFINITIONS

Root amputation is the removal of one or moreroots of a multirooted tooth. The involved root(s)is (are) separated at the junction of and into thecrown (Figure 24-14). In general, this procedure is

COLOR FIGURE 23-1I nternal bleaching. A, Pulp necrosis resulting from a traumatic injury caused severe dentin discoloration. B, Afteri nternal bleaching with a "walking bleach" paste the tooth regained its original shade. (Refer to Figure 23-3.)

COLOR FIGURE 23-2I nternal bleaching. A, Tetracycline discoloration caused a marked esthetic problem. B, Root canal treatment fol-lowed by "walking bleach" results in a permanent, pleasing shade change. (Refer to Figure 23-7, A and C)

COLOR FIGURE 23-3External bleaching. A, Enamel hypoplasia resulted in surface stains. B, An acid-pumice burnishing of the enamelsurface removes much of the discoloration (Refer to Figure 23-8, A and C)

COLOR FIGURE 24-1A, Establishment of drainage through an offending tooth. B, A fluctuant swelling is the result of an abscess fromthe lateral incisor. C, An incision for drainage is made horizontally into the swelling. A rubber drain is sutured inplace to prevent closure of the incision. D, A rectangular flap with a sulcular and two vertical incisions is createdto perform periapical surgery on the left central incisor. E, Apical curettage. Removal of diseased tissue at the apexenhances visualization of the apex and surrounding bone. This tissue may be submitted for histologic evaluation.F, Complete periapical healing and formation of cellular cementum (arrows) adjacent to mineral trioxide aggre-gate when it is used as a root-end filling material in monkeys.


437

FIGURE 24-12A, Failed root canal treatment requiring surgery. B, Theroot end is resected, and a cavity is prepared and is filledwith MTA. C, One-year recall shows complete healing.(Courtesy Dr. R. Rubinstein.)

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FIGURE 24-13

Perforation repair. A, An off-centered post has perforatedthe root, causing a bony lesion. (B) Internal and external

perforation repairs with MIA resulted in complete repair(C) of the bony lesion in 3 years. (Courtesy Dr. N. Chivian.)

performed in maxillary molars, but it can be per-formed in mandibular molars.

Hemisection is the surgical division of a multi-rooted tooth. In mandibular molars the tooth isdivided buccolingually through the bifurcation(Figure 24-15). In maxillary molars the cut ismade mesiodistally, also through the furcation.The defective or periodontally involved root andits coronal crown are then removed . 37

Bicuspidization is a surgical division (as in hemi-section, usually a mandibular molar), but thecrown and root of both halves are retained. If se-vere bone loss or destruction of tooth structure isconfined primarily to the furcation area, hemisec-tion and furcal curettage may allow retention ofboth halves (Figure 24-16). Each half may be re-stored to approximate a bicuspid, hence the termbicuspidization.


439

FIGURE 24-14Root amputation. A, Internal resorption with severebone loss around the distobuccal root. Amputation ofthe distobuccal root was planned. B, Root canal treat-ment was followed by an amalgam core extending4 mm into the distobuccal canal. C, The root was am-putated and a crown was subsequently placed.

INDICATIONS ANDCONTRAINDICATIONS

Indications for Root Amputationor Hemisection

Indications include the following:The presence of severe bone loss in a non-surgical treatable periodontally involvedrnnr nr fnrcarion

Roots that are untreatable because ofbroken instruments, perforations, caries,resorption, vertical fractures, or calcifiedcanalsStrategically important root(s) and accom-panvin2 crown

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FIGURE 24-15Hemisection. A, Furcation caries and bone loss have compromised the distal root. B, After root canal treatment,the crown was divided through the furcation (C). D, Twenty-month recall, after posts and core and a crown wereplaced. The extraction socket has healed and the tooth is stable.

Contraindications for Root Amputationor Hemisection

Contraindications include the following:Insufficient bony support for the remainingroot(s)Root fusion or proximity such that rootseparation is not possibleStrong abutment teeth available (the in-volved tooth should be extracted and a pros-thesis fabricated)

Inability to complete root canal treatmenton the remaining root(s)

Indications for Bicuspidization

Indications include the following:Furcation perforationFurcation pathosis from periodontal diseaseBuccolingual cervical caries or fracture intofurcation

FIGURE 24-16Bicuspidization. A, Caries in the furcation and furcal bone loss are evident, but there is adequate support for bothroots. B, Root canal treatment and bur separation through furcation and crown. C, Restoration with a porcelainfused to metal crown splinting the two roots. D, Good home care and a good gingival response at 30-month re-

call with no probing defects. Note that the furcation is open to facilitate special oral hygiene procedures. (Cour-

tesy of Dr. R. Walton.)

Contraindications for Bicuspidization

Contraindications include the following:Deep furcation (thick floor of pulp chamber)Unrestorable halfPeriodontal disease (each half must be peri-odontally sound)


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Inability to complete root canal treatmenton either halfRoot fusionSevere periodontal disease

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TECHNIQUES

Root amputation is performed by making an angledcut from the furcation to the proximal aspect toseparate the root from the crown. The crown re-mains intact, and the root is removed. Therefore,the crown is cantilevered over the extracted rootsegment and remains in contact with the approx-imating tooth. A second approach is to use an an-gled vertical cut in which the crown above theroot to be amputated is recontoured, decreasingthe occlusal forces and making the procedure eas-ier. As the crown is shaped, the bur is graduallyangled into the root, resulting in good anatomiccontour.

Hemisection involves making a vertical cutthrough the crown into the furcation. This re-sults in complete separation of the hemisectedsection (crown and root) from the tooth seg-ment that is retained. The defective half of thetooth is extracted.

Bicuspidization is performed after a verticalcut is made through the crown into the furca-tion with a fissure bur. This procedure resultsin complete separation of the roots and creationof two separate crowns. After healing of tissuesthe teeth can be restored to form two separatepremolars.

(These techniques may or may not require flapreflection. Often, if the root is periodontally in-volved, it is removed without a flap. If bony re-contouring is indicated, a flap is necessary beforeroot resection is carried out. A sulcular flap designis often possible without a vertical releasing inci-sion. However, when in doubt, a flap should beraised; doing so will always help.)

PROGNOSIS

Each case is unique and has a different prognosisaccording to the situation. Varying results havebeen reported for root removal."' Success is de-fined by tooth retention with absence of pathosis.Success depends on the following factors:

Case selectionCutting and preparing the tooth withoutcreating additional damageRestorationGood oral hygieneDevelopment of caries (most common causeof failure)Root fracturesExcessive occlusal forcesPoor restorative proceduresUntreatable endodontic problemsPeriodontal disease (second most commoncause of failure)

The major factor affecting success is the pa-tient's oral hygiene, even if these procedures areperformed correctly, and the tooth is restoredproperly. The patient must be willing and able toperform extra procedures to prevent plaque accu-mulation, particularly in the area adjacent towhat was once the furcation. Failure to do socould possibly result in untreatable caries or peri-odontal disease. The dentist must work carefullywith the patient to render this area plaque-free. Aprocedure that appears to be a success at 5 yearsmay fail later. Thus the judgment of success orfailure should be guarded and should extend overmany years.

Conditions That Indicate Referral

Although the procedures described in this chap-ter may appear straightforward, endodontic sur-gery requires advanced training, experience, andconsiderable surgical skill. There is concern aboutstandard of care and litigation. This, coupled withthe availability of experienced specialists, meansthat general dentists must carefully examine theirown expertise and accurately assess the difficultyof the situation before they attempt a surgicalprocedure. These procedures are often the lasthope for retaining the tooth and require the high-est level of skill and expertise and use of opticalaids, special instruments and materials to en-hance success. Lack of training may result notonly in the loss of the tooth but also in damage toadjacent structures, paresthesia from nerve injury,sinus perforations, soft tissue fenestrations, andpostoperative complications such as hemorrhageand infection.

In many situations, access to the surgical site islimited and potentially hazardous. Long-standinglarge lesions may impinge on adjacent structures,requiring special techniques for resolution (Fig-ure 24-17). The neurovascular bundle near theapexes of mandibular molars, premolars, andmaxillary palatal roots predisposes the patient topostsurgical paresthesia or excessive hemorrhage.The treatment of endodontic problems in theseareas requires careful preoperative assessmentand considerable surgical skill. The presence ofthick cortical bone and bony eminences through-out the mandible and in the palate, frenum, andmuscle attachments, fenestrations of the corticalbone, and the various sinus cavities all requireconsiderable surgical skill and experience in gain-ing access to most teeth.

Most important is the need for appropri-ate diagnosis, treatment planning, case assess-

ment, prognostication, and follow-up evalua-tion. The general dentist should have knowledgein these areas but may prefer to refer the patientto or request input from an endodontist. Thespecialist is better able to accomplish thesegoals as well as to assess the short- and long-term outcome. 39


443

FIGURE 24-17Decompression. Some cases require special procedures.A, A very large cyst fails to heal after root canal treatment.B, After surgical exposure and root-end surgery, a poly-ethylene tube is placed for several weeks to allow com-munication between the cyst cavity and the oral cavity.This allows collapse of the cyst wall. C, The lesion has re-solved 1 year later, showing regeneration of bone. (Cour-tesy Dr. S. Gish.)

REFERENCES

1. Hession RW: Long term evaluation of endodontictreatment, Int Endod J 14:179, 1981.

2. Morse DR, Esposito JV, Pike C, Furst ML: A ra-diographic evaluation of the periapical status ofteeth treated by gutta-percha-eucapercha endodontic

444


method. Part III. A one-year follow-up study of 458root canals, Oral Surg Oral Med Oral Pathol 56:190, 1983.

3. Van Nieuwenhuysen JP, et al: Re-treatment or radio-graphic monitoring in endodontics, Int Endod J 27:75,1975.

4. Sundqvist G, Figdor D, Persson S, Sjogren U: Microbi-ologic analysis of teeth with failed endodontic treat-ment and the outcome of conservative re-treatment,Oral Surg Oral Med Oral Pathol Radiol Endod 85:86, 1998.

5. Chivian N: Surgical endodontics: a conservative ap-proach, JNJDent Soc 40:1, 1969.

6. Siskin M: Surgical techniques applicable to endodon-tics, Dent Clin North Am 11:745, 1967.

7. Bellizzi R, Loushine R: Clinical atlas of endodontic surgery,Chicago, 1991, Quintessence Publishing.

8. Molven O, Halse A, Gruning B: Surgical managementof endodontic failures: Indications and treatment re-sults, IntDentJ 46:33, 1994.

9. Friedman S: Retrograde approaches in endodonticsurgery, Endod Dent Traumatol 7:97, 1991.

10. Gutmann JL, Harrison JW: Surgical endodontics, Boston,1991, Blackwell Scientific.

11. Arens DE, Torabinejad M, Chivian N, Rubenstein R:Practical lessons in endodontic surgery, Chicago, 1998,Quintessence Publishing.

12. Kramper BJ, Kaminski EJ, Osetek EM, Heuer MA: Acomparative study of the wound healing of three typesof flap design used in periapical surgery, JEndod 10:17,1984.

13. Gilheany PA, Figdor D, Tyas MJ: Apical dentin perme-ability and microleakage associated with root end re-section and retrograde filling, JEndod 20:22, 1994.

14. Grung B: Healing of gingival mucoperiosteal flapsafter marginal incision in apicoectomy procedures, IntJ Oral Surg 2:20, 1973.

15. Fister J, Gross BD: A histologic evaluation of bone re-sponse to bur cutting with and without water coolant,Oral Surg Oral Med Oral Pathol 49:105, 1980.

16. Morgan LA, Marshall JG: A scanning electron micro-scopic study of in vivo ultrasonic root-end prepara-tions,JEndod 25:567, 1999.

17. Pileggi R, McDonald NJ: A qualitative scanning elec-tron microscopic evaluation of ultrasonically cutretropreparations, J Dent Res 73:383, 1994.

18. Wuchenich G, Meadows D, Torabinejad M: A compar-ison between two root-end preparation techniques inhuman cadavers, J Endod 20:279, 1994.

19. Pantschev A, Carlsson A-P, Andersson L: Retrograderoot filling with EBA cement or amalgam, a compara-tive clinical study, Oral Surg Oral Med Oral Pathol78:101,1994.

20. Marcotte LR, Dowson J, Rowe NH: Apical healing withretrofilling materials amalgam and gutta-percha, JEndod 2:63, 1975.

21. Flanders DH, James GA, Burch B, Dockum N: Com-parative histopathologic study of zinc-free amalgam

and Cavit in connective tissue of the rat, JEndod 1:56,1975.

22. Witherspoon DE, Gutmann JL: Analysis of the healingresponse to gutta-percha and Diaket when used asroot-end filling materials in periradicular surgery, IntEndod J 33:37, 2000.

23. Torabinejad M, Hong CU, Lee SJ, et al: Investigation ofmineral trioxide aggregate for root-end filling in dogs,JEndod 21:603, 1995

24. Torabinejad M, Pitt Ford TR, McKendry DJ, et al: His-tologic assessment of mineral trioxide aggregate asroot-end filling in monkeys, JEndod 23:225, 1997.

25. Racey GL, Wallace WR, Cavalaris CJ, Marquard JV:Comparison of a polyglycolic acid suture to black silkand plain catgut in human oral tissues, J Oral Surg36:766, 1978.

26. Lilly GE, Salem JE, Armstrong JH, Cutcher JL: Reac-tion of oral tissues to suture materials, Oral Surg OralMed Oral Pathol 28:433, 1969.

27. Harrison JW, Jurosky KA Wound healing in the tissuesof the periodontium following periradicular surgery. I.The incisional wound, JEndod 17:425, 1991.

28. Robbins SL, Kumar V: Inflammation and repair. InRobbins SL, Kumar V, editors: Basic pathology, ed 4,pp 28-61, Philadelphia, 1987, WB Sounders.

29. Hunt TK, Knighton DR, Thakral KK, et al: Studies oninflammation and wound healing: angiogenesis andcollagen synthesis stimulated in vivo by resident andactivated wound macrophages, Surgery 96:46, 1984.

30. Melcher AH, Chan J: Phagocytosis and digestion ofcollagen by gingival fibroblasts in vivo: a study of ser-ial sections, J Ultrastruct Res 77:1, 1981.

31. Ross R: The fibroblast and wound repair, Biol Rev43:51, 1968.

32. Harrison JW, Jurosky KA: Wound healing in the tissuesof the periodontium following periradicular surgery.111. The osseous incisional wound, JEndod 18:76,1992.

33. Ighaut J, Aukhill I, Simpson DM, et al: Progenitor cellkinetics during guided tissue regeneration in experi-mental periodontal wounds, J Periodontal Res 23:10,1988.

34. Davis WL: Oral histology: cell structure and function,Philadelphia, 1986, WB Sounders.

35. Melcher AH, Irving JT: The healing mechanism in arti-ficially created circumscribed defects in the femora ofalbino rats, JBone Joint Surg 44:928, 1962.

36. American Association of Endodontists: An annotatedglossary of terms used in endodontics, ed 6, Chicago, 1998,American Association of Endodontists.

37. Bergenholtz A: Radectomy of multirooted teeth, J AmDent Assoc 85:870, 1972.

38. Langer B, Stein JD, Wagenberg B: An evaluation ofroot resections, JPeriodontol 52:719, 1981.

39. Zuolo ML, Ferreira MOF, Gutmann JL. Prognosis inperiradicular surgery: a clinical prospective study, IntEndod J 33:91, 2000.

Management ofTraumatized Teeth

LEARNING OBJECTIVES


1 / Describe the clinical and radiographic features of the following: enamel fractures, crown fracture without

pulp exposure, crown fracture with pulp exposure, crown-root fracture, root fracture, tooth luxation

(concussion, subluxation, lateral luxation, extrusive luxation, intrusive luxation), avulsion, and alveolar

fracture.

z / Describe possible short- and long-term responses of pulp, periradicular tissues, and hard tissues to the

i njuries listed above.

3 / List pertinent information needed when examining patients with dental injuries (from health history, nature

of injury, and symptoms).

4 / Describe the diagnostic tests and procedures used in examination of patients with dental injuries and

i nterpret the findings.

s / Describe appropriate treatment strategies (both at the time of injury and at follow-up) for various types of

traumatic injuries.

6 / Identify the criteria for success or failure of various treatment modalities.

7 / Define pulp canal obliteration (calcific metamorphosis) and factors determining the appropriate treatment

strategy.

s / Differentiate between surface, inflammatory, and replacement resorption (ankylosis) and their respective

treatment strategies.

s / Describe the differences in treatment strategies for traumatic dental injuries in primary and permanent

dentitions.

445

446

25 / Management of Traumatized Teeth

Examination and Diagnosis

History


Specific Injuries

Enamel Fractures

Crown Fractures without Pulp Exposure

Crown Fractures with Pulp Exposure

Crown-Root Fractures

Root Fractures

Luxation Injuries

Avulsions

Alveolar Fractures

rauma to teeth involves the dentalpulp either directly or indirectly; conse-quently, endodontic considerations are

important in evaluating and treating dental in-juries. The purpose of this chapter is to describeexamination procedures, emergency care, treat-ment options, and possible sequelae in trauma-tized teeth. Because injuries occur to primaryteeth also, some of the topics discussed under"Specific Injuries" will include recommendationsfor these teeth.

Age is a significant factor in trauma to teeth.Injuries occur most often in the 7- to 12-yearage group.' The significance of age is a "goodnews/bad news" situation. The good news is thatpulps of teeth in children have a better bloodsupply than those in adults and better repairpotential. The bad news is that growth may be in-terrupted in immature roots in teeth with dam-aged pulps, leaving the roots thin and weak (Fig-ure 25-1). Spontaneous cervical fractures oftenoccur because of thin dentin walls. Thereforewhen dental injuries occur in children, every ef-fort is made to preserve pulp vitality.

Classification of traumatic injuries promotesbetter communication and dissemination of in-formation. The system used in this chapter isbased on Andreasen's modification of the WorldHealth Organization's classification1.2 (Box 25-1).It is preferable to other classification systems be-cause it is internationally accepted and has a de-scriptive format based on anatomic and therapeu-tic considerations.


Examination of a patient with dental injuriesshould include the following: chief complaint,history of present illness, pertinent medical his-tory, and clinical examination. The emphasis inthis chapter is on those aspects of the examina-tion that specifically relate to dental trauma . 3

HISTORY

Pertinent information regarding traumatic in-juries should be obtained expeditiously by follow-ing a system.

Chief Complaint

The chief complaint is simply a statement in thepatient's (or parent's) own words of the currentproblem, for example, "I broke my tooth," or "Mytooth feels loose." It may also be unstated, as in apatient with obvious injuries.

FIGURE 25-1Trauma to an immature incisor resulted in pulp necrosis withi nterruption of tooth development, leaving the root with thin,weak walls (arrow). Root canal treatment can be performed,

but the tooth will be weak and prone to fracture.

History of Present Illness

To obtain the history of the present illness (in-jury), the dentist asks a few specific questions,such as the following:

When and bow did the injury occur? The date andtime of the accident are recorded. Therecord should include how it took place: caraccident, playground, or other. Such infor-mation is useful in the search for avulsedteeth and embedded tooth fragments, as-sessment of possible contamination, deter-mination of time factor with respect tochoice of treatment and healing potential,and filling out accident reports.

Have you had any other injuries to your mouth orteeth in the past? Individuals may have re-peated traumatic injuries if they are acci-dent prone or participate in contact sports. 4Crown or root fractures may have occurredas a result of an earlier injury but are ob-served at a later time.

What problems are you now having with your toothor teeth? Pain, mobility, and occlusal inter-


447

ference are common symptoms. The pa-tient's description of symptoms will help indiagnosis.

Medical History

The patient's medical history is often significant.For example, the patient may have an allergy toprescribed medication, may be taking medica-tions that interact with proposed new medica-tions, or may have a medical condition that af-fects treatment. Tetanus immunization statusshould be recorded; a booster may be indicatedwhen there are contaminating injuries such asavulsions, intrusions, and penetrating lip and softtissue lesions.-'

CLINICAL EXAMINATION

The lips and oral soft tissues and facial skeletonshould be examined as well as the teeth and sup-porting structures.

Soft Tissues

The purpose of the soft tissue evaluation is to de-termine the extent of tissue damage and to iden-tify and remove foreign objects from wounds. In

448


crown fractures with adjacent soft tissue lacera-tions, wounds are examined visually and radio-graphically for tooth fragments. Lips are likelyareas for a foreign body impaction. Also, severelacerations require suturing.

Facial Skeleton

The facial skeleton is evaluated for possible frac-tures of the jaw or alveolar process. Such frac-tures, when they involve tooth sockets, may pro-duce pulpal necrosis in teeth associated withfracture lines . 6,7 Alveolar fractures are suspectedwhen several teeth are displaced or move as a unit,when tooth displacement is extensive, or when oc-clusal misalignment is present.

Teeth and Supporting Tissues

Examination of teeth and supporting tissuesshould provide information about damage thatmay have occurred to dental hard tissues, pulps,periodontal ligaments, and bony sockets. The fol-lowing guidelines provide a method of collectinginformation systematically.

Mobility. Teeth are examined (gently) for mo-bility, noting whether adjacent teeth also movewhen one tooth is moved (indicating alveolarfracture). The degree of horizontal mobility isrecorded: 0 for no mobility; 1 for slight (<1 mm)mobility, 2 for marked (1 to 3 mm) mobility, and3 for severe (>3 mm) mobility, both horizontallyand vertically. If there is no mobility, the teeth arepercussed for sounds of ankylosis (metallicsound). Absence of mobility may indicate normalstatus or "locking" of the tooth in bone, such aswith intrusion.

Displacement. A displaced tooth has been movedfrom its normal position. If this occurs as a result oftraumatic injury, it is referred to as "luxation." Seethe "Luxation Injuries" later in this chapter for de-scriptions of the various types of displacement.

Periradicular damage. Injury to the supportingstructures of teeth may result in swelling andbleeding involving the periodontal ligament.Such teeth are sensitive to percussion, even lighttapping. Apical displacement with injury to ves-sels entering the apical foramen may lead to pulpnecrosis if the blood supply is compromised.'

Percussion identifies periradicular injury. Per-cussion must be done gently because traumatizedteeth are often exquisitely painful to even lighttapping. When examination or testing proceduresare begun, uninjured teeth are examined first.This enhances the patient's confidence and un-derstanding of the procedures. Importantly, inaddition to testing the tooth or teeth involved

in the patient's complaint, several adjacent andopposing teeth are included also. This permitsrecognition of other dental injuries of which thepatient may not be aware and that may not be ob-vious clinically. If later complications develop in-volving one of these adjacent or opposing teeth,early information will help in diagnosis.

Pulpal injury. Pulpal health is a very importantconsideration. Trauma may lead to resorption ofdentin (internal) or calcific metamorphosis (ra-diographic obliteration) with tooth discoloration(yellowing effect). The trauma may induce pulpnecrosis, which could result in external inflamma-tory root resorption.9

Pulpal status may be determined by symp-toms, history, and clinical tests (see Chapter 4).Two clinical tests, however, deserve considerationhere because of their applicability to traumatizedteeth-the electrical pulp test (EPT) and carbondioxide ice. These tests are generally reliable inevaluating and monitoring pulpal status except inteeth with incomplete root development. 8 A pro-tocol for EPT and carbon dioxide ice is discussedlater under "Luxation Injuries."

Radiographic examination. Radiographs are ex-amined for fractures of bone or teeth and stage ofdevelopment (Fig. 25-1). Horizontal root frac-tures and lateral luxations are often overlookedbecause the conventional angulation may miss ir-regularities that are not parallel with the x-raybeam. Therefore increased vertical occlusal ex-posure is a useful adjunct. Multiple exposuresshould be routine for examination of trauma toteeth to ensure complete disclosure and diagnosisof the injury.'°

The film size should be such that it can accom-modate two incisors without bending or distort-ing the image. It is also important to use a filmholder to achieve standardized radiographic im-ages, especially for subsequent comparisons.

A thorough examination combined with accu-rate records forms the basis of an appropriatetreatment plan. The information gathered alsoprovides information for accident reports thatmay be requested either immediately or later forlegal or insurance purposes.

Specific InjuriesENAMEL FRACTURES

Chips and cracks confined to enamel do not inthemselves constitute a hazard to the pulp. Theprognosis is good; however, the injury that pro-duced the fracture may also have displaced (lux-ated) the tooth and damaged the blood vesselssupplying the pulp. If the tooth is sensitive to

25 / Management of Traumatized Teeth 449

FIGURE 25-2Crown fracture without pulp exposure. A, The injury results in loss of enamel and dentin without direct exposureto the pulp. B, Often a pink spot can be seen (arrow), but if there is no direct exposure of pulp, the fracture is saidto be "without pulp involvement."

percussion or if there are other signs of injury,the recommendations given under "Luxation In-juries" are followed. Grinding and smoothing therough edges or restoring lost tooth structure maybe all that is necessary.

CROWN FRACTURES WITHOUT

PULP EXPOSURE

Description

These crown fractures involve enamel and dentinwithout pulp exposure (Figure 25-2). Such in-juries are usually not associated with severe painand generally do not require urgent care. Theprognosis is good unless there is an accompany-ing Luxation injury to periodontal ligament orto the apical vasculature supplying the pulp, inwhich case the tooth will be sensitive to percus-sion.8 If so, the recommendations are followed asoutlined under "Luxation Injuries" (as well asmanaging the crown fracture).

Treatment

Since the advent of the acid-etch technique,conservative restoration with composite resin ofcrown-fractured incisors has become possible with-out endangering the pulp (Figure 25-3). More con-servative yet is reattachment of the separatedenamel-dentin fragment (Figure 25-4). This re-quires a dentin bonding agent after acid-etching toimprove fracture strength of the restored incisor.Clinical experiments as well as bonding studieshave indicated that reattachment of dentin-enamelcrown fragments is an acceptable restorative proce-dure and does not threaten pulp vitality." Gener-ally speaking, fracture bonding represents an ad-

FIGURE 25-3Restored crown fracture that does not involve the pulp di-rectly. Exposed dentin is covered with a hard-setting liner fol-lowed by restoration of the missing tooth structure usingacid-etched bonded resin.

vance in the treatment of anterior fractures. Dentalanatomy is restored perfectly with normal toothstructure that abrades at a rate identical to that ofthe adjacent noninjured teeth. Also, pulpal statusmay be reliably monitored.

Chair time for the restorative procedure is min-imal. The use of indirect veneering techniques at alater date to reinforce bonding or to restore thefractured incisor is a conservative approach to im-proving esthetics and function."

Primary Teeth

Crown fractures are less common in primary thanin permanent teeth. Ideally, treatment for primaryteeth is the same as that for permanent teeth;however, patient cooperation may dictate the

450


FIGURE 25-4A, An 8-year-old patient with a fractured incisor without pulp exposure. B, Immature tooth with open apex(arrow). C, After the fractured segment was bonded into its original position. D, One-year evaluation showingcontinued root maturation and closing of apex (black arrow). Note the line where the fractured segment wasbonded to the remaining tooth (white arrow). (From Bakland LK, Milledge T, Nation W: Calif Dent Assoc J 24:45,1996.)

management approach. It is not as important torestore a primary crown fracture; thus the fracturesite may be smoothed without restoring.

CROWN FRACTURES

WITH PULP EXPOSURE

Description

This type of fracture involves enamel, dentin, andpulp (Figure 25-5). The pulp is exposed, andtherefore the fracture becomes "complicated," aterm often used for these types of injuries.' Theextent of fracture, the stage of root development,and the length of time since injury are noted.

Extent of fracture helps to determine pulpaltreatment as well as restorative needs; a small frac-ture may undergo vital pulp therapy and can berestored by an acid-etched composite restoration.An extensive fracture may require root canal treat-ment with a post and core-supported crown de-pending on the age of the patient.

The stage of root maturation is an importantfactor in choosing between pulpotomy and pulp-ectomy. Immature teeth have thin-walled roots(see Figure 25-1); an effort should be made to pre-serve the pulp to allow continued root develop-ment. That is best accomplished with a shallowpulpotomy, to be described in the next section. Vitalpulp therapy followed by an acid-etched compositerestoration or rebonding of the fractured segmentis often feasible in mature teeth also. However, ifthe extent of tooth loss dictates restoration with acrown, root canal treatment is recommended.

The amount of time elapsed between injury andexamination may directly affect pulpal health. `zGenerally, the sooner a tooth is treated, the betterthe prognosis for preserving the pulp. However, asa rule, pulps that have been exposed for less than aweek can be treated by pulpotomy, if that is thetreatment of choice. Successful pulpotomy proce-dures after pulp exposure of several weeks' durationhave been reported," but the prognosis becomespoorer the longer the pulp is exposed. 'z

Treatment of Crown Fractures

Teeth with crown fractures and exposed pulps canbe treated either by pulpotomy or by root canaltherapy before restoration of lost tooth structure. Ifvital pulp therapy is planned, it is important to per-form treatment as soon after the injury as possible.

Pulpotomy. The main reason for recommend-ing vital pulp therapy in a tooth with an exposedfracture is to preserve pulp tissue. This is particu-larly important in immature teeth in which con-tinued root formation will result in a strongertooth that is more resistant to fractures than onewith thin root walls.


451

In the past, pulpotomy meant removal of pulptissue to, or below, the cervical level. Loss of pulptissue in that area means there is no additionaldentin formation; this will result in a weakenedtooth that is more prone to fracture. In recentyears a more conservative and shallow pulpotomyhas been popularized by Cvek and has sometimesbeen referred to as the Cvek technique. '3 This shal-low pulpotomy preserves all the radicular andmost of the coronal pulp tissue, allowing morehard tissue to develop in the root.

The pulp may need to be removed to or belowthe cervical level when the entire crown of an im-mature tooth fractures. Pulpotomy then is per-formed to encourage enough additional root de-velopment to allow subsequent post and coreconstruction to support a crown. These situationsare relatively uncommon. Recently a modificationin the Cvek technique has been developed, usingmineral trioxide aggregate (MTA), ProRoot MTA(Tulsa Dental Products, Tulsa, OK)."'s

Case selection. Both immature and matureteeth that can subsequently be restored with acid-etched composite are acceptable for shallow pulp-otomies (Figure 25-6). Generally, immature teethare more likely to be involved for the reasonsstated previously.

Technique. The pulpotomy procedure (Fig-ure 25-7) starts with anesthesia and rubber damisolation. Exposed dentin is washed with salineor sodium hypochlorite solution. Extruding gran-ulation tissue is removed with a spoon excavatorfrom the pulp wound site. This provides an op-portunity to determine more accurately the sizeand location of the exposure. Next, pulp tissue isremoved to a depth of about 2 mm below the ex-posure. This relatively small amount of pulp re-moval is the reason for calling this procedure ashallow or partial pulpotomy.

FIGURE 25-5Crown fracture that results in exposure of the pulp. Granula-tion tissue (arrow) forms at the pulp wound within 24 hoursand may actually proliferate and protrude with time.

452


FIGURE 25-6Shallow pulpotomy. A, A mesial-incisal-lingual chisel fracture occurred 3 days previously, exposing the pulp(arrow). B, Radiographic view. C, Preparation at exposure site is capped with calcium hydroxide liner and thensealed with ZnOE base (arrow). D, Fracture is immediately repaired with acid-etched composite resin. (CourtesyDr. C. Noblett.)


453

FIGURE 25-7Shallow pulpotomy. A, Preparation of the pulp wound areawith a round diamond stone cooled by a constant waterspray. B, Protective dressing (arrow) of hard-setting calciumhydroxide covered with sealing cement (zinc oxide-eugenol,zinc phosphate, or glass ionomer). C, Missing tooth structurerestored with acid-etched composite resin bonded to enamel.

Pulpotomy is accomplished with a water-cooled small round diamond (about the size of aNo. 4 round bur) in the high-speed handpiece.Gently and gradually the surface layers of pulptissue are wiped away, beginning at the exposuresite and extending into the pulp to a depth ofabout 2 mm below the exposure site.

After the pulp is amputated to the desiredlevel, a dentin shelf is created surrounding thepulp wound. The wound is gently washed withsterile saline and hemostasis is awaited. Then thewound is washed again to remove the clot (impor-tant!) and dressed with a hard-setting calcium hy-droxide liner. Now the remainder of the cavity iscarefully sealed with a hard-setting cement, suchas IRM, or glass ionomer. When the cement hasset, the tooth may be restored with acid-etchedcomposite.

Considering the disintegration of calcium hy-droxide liners with time, whenever possible thetooth is reentered after a period of 6 to 12 monthsto remove the initial calcium hydroxide layer andreplace it with a dentin bonding material. This willprevent microleakage at the site where the initialcalcium hydroxide has deteriorated and produceda space between the new dentin bridge and the cov-ering restoration.

If MTA is used in place of calcium hydroxide, itis not necessary to wait for bleeding to stop com-pletely. The material requires moisture for curingand can be placed directly onto the pulp tissue.Care should be followed to reduce the risk offorcing the material into the pulp proper; gently

dab small increments of the material onto thepulp using a moist cotton pellet. The pulpotomyspace is filled with MTA so that it is completelyflush with the fractured dentin surface. The mate-rial is then allowed to cure, which may take 6 to12 hours. During the curing time, it is not neces-sary to protect the material with a restoration, butthe patient must avoid using the tooth. After cur-ing, the tooth may be restored, either with a com-posite resin or by bonding the fractured crownsegment back onto the tooth." It is not necessaryto reenter the tooth after several months; MTAis stable.

Treatment evaluation. Treatment is evaluatedafter 6 months and then yearly. Successful shal-low pulpotomy procedures (Box 2S-2) may beconsidered definitive treatment13 and have avery good long-term success rate. '3.16

Root canal therapy. Teeth with mature rootsmay undergo either pulpotomy or root canal ther-apy; root canal therapy is usually necessary to ac-commodate prosthetic requirements. For exam-ple, if the crown has fractured in the gingivalmargin region, root canal treatment will allowpost and core and crown placement.

Primary Teeth

Crown fractures with pulp exposures occur in pri-mary teeth, although less often than in perma-nent teeth.' Treatment includes pulpotomy, rootcanal therapy, or extraction, depending on patientage and cooperation. If the root is more than halfresorbed apically, the tooth is extracted. If rootcanal therapy is chosen, the canal is filled with aresorbable zinc oxide-eugenol based paste. Frac-tured crowns may be restored with acid-etchedcomposite.

454


CROWN-ROOT FRACTURES

Description

These fractures are usually oblique and involveboth crown and root. Anterior teeth show the so-called chisel-type fracture, which splits the crowndiagonally and extends subgingivally to a rootsurface (Figure 25-8). They resemble a crown frac-ture but are more extensive and more serious be-cause they include the root. Another variation isthe fracture that shatters the crown (Figure 25-9).

The pieces are held in place only by the part of thefractured segment still attached to the periodon-tal ligament or gingival tissues. In all of these frac-tures, the pulp is usually exposed.

In contrast to other traumatic injuries inwhich posterior teeth are rarely involved, crown-

root fractures often include the molars and pre-molars. Cusp fractures that extend subgingivallyare common (Figure 25-10). Diagnostically theymay, however, be difficult to identify in the earlystages of development. Similarly, vertical frac-tures in the long axis of roots are difficult to de-tect and diagnose. Such crown-root fractures arediscussed in more detail in Chapter 28.

Crown-root fractures in posterior teeth can-not always be associated with a single traumaticincident, although bicycle or automobile acci-dents at times may produce these results. Therisk is increased with a sharp blow to the chincausing the jaws to slam together; skin abrasionsunder the chin may be a sign of such an impact.Also, all posterior teeth should be examinedusing a sharp explorer to detect movement ofloose fragments.'

FIGURE 25-8Crown-root fracture. Anterior teeth may develop "chisel-type" fractures, which extend below the cementoenameljunction. Because of the nature and location of these frac-tures, they are difficult to manage.

Examination

Crown-root fractures are complex injuries thatare difficult both to evaluate and to treat. Untilrecently, it was recommended that all loose frag-ments had to be removed to evaluate the extentof injury. This may still be necessary in some in-stances, but with the availability of bondingagents it is now possible to bond loose fragmentsat least temporarily. The current recommenda-tion is to attempt to bond loose fragments to-gether, particularly if the tooth is immature andstill developing. Clinical judgment must be usedto decide when to follow one course of action oranother.

It is not unusual, in a tooth in which the crownhas broken into several pieces, to find that thesame shattering effect has extended to the root aswell. Additional radiographs at different angles

FIGURE 25-9Crown-root fracture resulting in a shattered crown with sub-gingival extension.

FIGURE 25-70Pulp exposure may or may not be present with a crown-rootfracture of a posterior tooth.


455

Treatment Planning

Crown-root fractures are often complicated bypulp exposures and extensive loss of tooth struc-ture. In developing a treatment plan, many ques-tions must be considered: Which is better forthis tooth, pulpotomy or pulpectomy? After allloose fragments have been removed, will therebe enough tooth structure to support a restora-tion? Is the subgingival fracture below a level atwhich a restorative margin can be placed, thusnecessitating root extrusion or gingivoplasty oralveoplasty? Should the tooth be extracted andreplaced with a bridge or implant? Or if extrac-tion is chosen, can the space be closed ortho-dontically? These are but a few of the manyquestions. Because of such complexity, a teamapproach involving specialists in the areas of

FIGURE 25-11Urgent care of crown-root fracture. A, The mesialsegments are mobile and must be removed. B, Afterremoval of all loose fragments, the exposed pulp ismanaged by shallow pulpotomy. C, The crown cannow be restored with acid-etched resin.

(as will be described under "Root Fractures") mayhelp to identify radicular fracture lines.

Emergency Care

Teeth with crown-root fractures are often pain-ful; such injuries often require urgent care. Thismay consist only of removing loose tooth frag-ments but often also includes pulp therapy (Fig-ure 25-11). If the root is immature, pulpotomy(see "Crown Fractures with Pulp Exposure" inthis chapter and also "Vital Pulp Therapy" inChapter 22) is preferable to pulpectomy, whereaspulpectomy is the treatment of choice in patientswith fully developed teeth. Definitive treatmentshould be postponed until an overall endodonticand restorative treatment plan is developed.

456


endodontics, periodontics, orthodontics, and pros-thodontics is beneficial in developing the treat-ment plan.

Primary Teeth

A crown-root fracture in primary teeth usuallydictates extraction. Occasionally, sufficient re-maining tooth structure may be available forrestoration or recontouring.

ROOT FRACTURES

Description

Fractures of roots (Figure 25-12) have been calledintraalveolar root fractures, horizontal root frac-tures, and transverse root fractures. They do notoccur often and may be difficult to detect. 17-21

Radiographically, a root fracture is visualizedif the x-ray beam passes through the fracture line.Because these fractures often are transverse-to-oblique (involving pulp, dentin, and cementum),they may be missed if the central beam's di-rection is not parallel or close to parallel to the

FIGURE 25-12Horizontal root fractures. Central incisors are the teeth mostoften involved. Unless the coronal segments are displaced ormobile, no splinting or other treatment is necessary.

fracture line. For this reason, a steep vertical an-gulation is included in addition to the normalparallel angulation whenever a root fracture issuspected. This additional angulation, i.e., fore-shortened view (approximately 45 degrees), willdetect many fractures, particularly in the apicalregions (Figure 25-13). 120,21

Clinically, root fractures may present as mobileor displaced teeth, with pain on biting. Symptomsare generally mild. If mobility and displacementof the coronal segment are absent or slight, thepatient may have no chief complaint and may notseek treatment. 2 0 Generally, the more cervical thefracture, the more mobility and displacement ofthe coronal segment and a greater likelihood ofpulp necrosis of this segment. Treatment (splint-ing) for root fractures is indicated if the coronalsegment is mobile. Thus root fractures in the api-cal and middle thirds usually require no immedi-ate treatment but must be observed long term .20

Emergency Care

If a root fracture is identified, initial treatmentincludes repositioning of the coronal segment (ifdisplaced) and stabilization by splinting. Reposi-tioning of the coronal segment may be as easy asapplying finger pressure to the crown to alignthe segment, or it may be more complicated, re-quiring orthodontic approaches. When the coro-nal segment has been repositioned, it must be

FIGURE 25-13Radiographic technique used for suspected root fractures. Atl east two angulations are made: the conventional (90 de-gree) view and a steep vertical (45 degree) view. Additionalangulations help to detect suspected root fractures by direct-i ng the x-ray beam through a diagonal fracture.


457

stabilized to allow repair of the periodontium(Figure 25-14).

Stabilization may be accomplished by the useof orthodontic wire and acid-etched resin. Splint-ing time must be sufficient to allow calcificationto take place, probably both internally in the pul-pal space and possibly externally across the frac-ture lines." Up to 12 weeks' stabilization has beenrecommended .z0 if repair takes place with no evi-dence of pulp necrosis, root-fractured teeth donot require root canal treatment."

Sequelae of Root Fractures

Root fractures are often characterized by devel-opment of calcific metamorphosis (radiographicobliteration) in one (usually coronal) or both seg-ments; therefore EPT readings may be very highor absent. Lack of response to EPT by itself, how-ever, in the absence of other evidence of pulpnecrosis (bony lesions apically or laterally, adversesymptoms, and so on), does not indicate a needfor root canal treatment. The majority of rootfractures heal either spontaneously or followingsplint therapy."


Root canal treatment is indicated when pathosisis evident, usually owing to development of pulpnecrosis in the coronal portion, which subse-quently leads to inflammatory lesions adjacentto the fracture lines (Figure 25-15). 19 The endo-dontic procedure, when necessary, usually is com-plex; referral to a specialist should be considered.The various treatment approaches are listed inBox 25-3. The current recommendation is to treatonly the coronal segment canal (Figure 25-16).The pulp in the apical segment usually remainsvital.

Primary Teeth

Root fractures are not common in primary teeth.'Those that occur with marked coronal displace-ment should be treated by removing the coronalsegment and leaving the root apex in situ. Any at-tempt to remove the root apex may damage thesubjacent permanent tooth bud. As in permanentteeth, root fractures not accompanied by mobilityusually require no treatment unless problems de-velop subsequently.

FIGURE 25-74Stabilization of root fractures with a mobile coronal segment. A, Orthodontic wire is adapted to labial surfacesof anterior teeth and attached using the acid-etched resin technique. If possible, all six anterior teeth are includedfor better stabilization. B, At future evaluation, root formation has responded to treatment (stabilization). Inter-nal calcification adjacent to the fracture (arrows) indicates repair.

458


FIGURE 25-15Two different long-term sequelae of horizontal root fractures.The incisor on the /eftshows bony interposition between thefractured segments, with bone growth into the coronal pulpspace and formation of a lamina dura and periodontal liga-ment space (arrow). The incisor on the right has undergonepulp necrosis of both segments; because of the location ofthe fracture and resulting damage, removal of both segmentsi s indicated. (Courtesy Dr. M. Gomez.)

"This procedure is the most common current recommendation andprovides the most consistent results.

FIGURE 25-16

Successful treatment of pulp necrosis in a root-fractured incisor with root canal filling of coronal fragment.A, Condition after the injury. B, Segment is repositioned, stabilized, and treated. C, Five months after obturation;the segment is stable.


459

LUXATION INJURIES

Description

Luxation injuries (Figure 2S-17) cause trauma tothe supporting structures of teeth and often affectthe neural and vascular supply to the pulp. Thecause is usually a sudden impact, such as a blow orstriking a hard object during a fall. 1,22 Generally,the more severe the luxation (involving more dis-placement), the greater the damage to the peri-odontium and to the dental pulp. Table 2S-1 pro-vides a summary of the typical clinical andradiographic findings associated with differenttypes of luxation injuries.'

Concussion. The tooth is sensitive to percussiononly. There is no increase in mobility, and thetooth has not been displaced. The pulp may re-spond normally to testing, and no radiographicchanges are found.

Subluxation. Subluxation injuries include teeththat are sensitive to percussion and also have in-

creased mobility. Often sulcular bleeding is pres-ent, indicating vessel damage and tearing of theperiodontal ligament. No displacement is found,and the pulp may respond normally to testing.Radiographic findings are unremarkable.

Extrusive luxation. These teeth have been par-tially displaced from the socket along the longaxis. Such extruded teeth have greatly increasedmobility, and radiographs show displacement.The pulp usually does not respond to testing.

Lateral luxation. Trauma has displaced the toothlingually, buccally, mesially, or distally, that is,out of its normal position away from its longaxis. If the apex has been translocated duringthe displacement, the tooth may be quite firm.Percussion sensitivity may or may not be presentwith a metallic sound if the tooth is firm, indi-cating that the root has been forced into thealveolar bone.

I ntrusive luxation. Teeth are forced into theirsockets in an axial (apical) direction, at times to

FIGURE 25-17Luxation injuries. A, Subluxation: the tooth is loosened but not displaced. B, Extrusive luxation: the tooth is par-tially extruded from its socket. Occasionally this is accompanied by an alveolar fracture. C, Lateral luxation: thecrown is displaced palatally and the root apex labially. D, Intrusive luxation: the tooth is displaced apically.

TABLE 25-1

460


the point of being buried and not visible. Theyhave decreased mobility and resemble ankylosis.


The clinical descriptions of the five types of luxa-tion injuries should be sufficient to make the ini-tial diagnosis. Pulpal status must be continuallymonitored until a definitive diagnosis can bemade, which in some cases may require severalmonths or years. Carbon dioxide ice and the EPTare used in monitoring pulpal status . 7

Concussion injuries generally respond to pulptesting. Because the injury is less severe, pulpalblood supply is more likely to return to normal.Teeth in the subluxation injury group also tend toretain or recover pulpal responsiveness but lesspredictably than teeth with concussion injuries.In both cases, an immature tooth with an openapex has a better prognosis. Extrusive, lateral, andintrusive injuries involve more displacementand therefore more damage to apical vessels andnerves. Therefore pulp responses in teeth with ex-trusive, lateral, and intrusive luxations are oftenabsent. These pulps often do not recover respon-siveness even if the pulp is vital (has bloodsupply), because sensory nerves are permanentlydamaged. Exceptions are immature teeth withwide-open apices; these teeth often regain or re-tain pulp vitality (responsiveness) even after se-vere injuries . 1°13

Monitoring pulp status requires a schedule ofpulp testing and radiographic evaluation for along enough time to permit determination ofthe outcome with some degree of certainty. Thatmay require 2 or more years. Pulp status is bestmonitored with pulp testing, radiographs, devel-oping symptoms, and observation for crown colorchanges . 7,8,23

Pulp testing. Carbon dioxide ice or the EPT isused to test teeth that have been injured; severaladjacent and opposing teeth are included in thetest. An initial lack of response is neither unusual,nor is a high reading on the pulp tester. Retestingis done in 4 to 6 weeks; the results are recordedand compared with the initial responses. If thepulp responds in both instances, the prognosisfor pulp survival is good. A pulp response that isabsent initially and present at the second visit in-dicates a probable recovery of vitality, althoughcases of subsequent reversals have been noted.' Ifthe pulp fails to respond both times, the progno-sis is questionable and the pulp status uncertain.In the absence of other findings indicating pulpnecrosis, the tooth is retested in 3 to 4 months.Continued lack of response may indicate pulpnecrosis by infarct, but lack of response may not

be enough evidence to make a diagnosis of pulpnecrosis. That is, the pulp may permanently losesensory nerve supply but retain its blood supply.After a period of time, the pulp often responds totesting if it recovers.

Radiographic evaluation. The initial radiographmade after the injury will not disclose the pulpcondition. However, it is very important for evalu-ation of the general injury to the tooth and alveo-lus and serves as a basis for comparison of subse-quent radiographs. These radiographs are takenat the same intervals used for pulp testing. Evi-dence of resorption, both internal and external,and periradicular bony changes is sought. Resorp-tive changes, particularly external changes, mayoccur soon after injury; if no attempt is made toarrest the destructive process, much of the rootmay be rapidly lost. Inflammatory resorption canbe intercepted by timely endodontic intervention.

Pulp space calcification or obliteration is acommon finding after luxation injuries." Alsocalled calcific metamorphosis, this canal obliterationmay be partial or nearly complete (after severalyears) and does not require root canal treatment,except when other signs and symptoms indicatepulp necrosis.

Crown color changes. Pulp injury may causediscoloration, even after only a few days. Initialchanges tend to be pink. Subsequently, if the pulpdoes not recover and becomes necrotic, theremay be a grayish darkening of the crown, oftenaccompanied by a loss in translucency. Also, colorchanges may take place owing to increased calcificmetamorphosis. Such color changes are likelyto be yellow to brown and do not indicate pulppathosis. Other signs, findings, or symptoms arenecessary to diagnose pulp necrosis.

Finally, discoloration may be reversed. Thisusually happens relatively soon after the injuryand indicates that the pulp is vital. Because of un-predictable changes associated with traumatizedteeth, long-term evaluation is recommended.

Treatment of Luxation Injuries

Luxation injuries, regardless of type, often presentdiagnostic and treatment complexities that requireconsultation with specialists. For concussion injuries,no immediate treatment is necessary. The patientshould allow the tooth to "rest" (avoid biting) untilsensitivity has subsided. Pulp status is monitoredas described. Subluxations may likewise require notreatment unless mobility is moderate; if mobility isgraded 2, stabilization may be necessary.'

Extrusive and lateral luxation injuries requirerepositioning and splinting (see Figure 25-14). Thelength of time needed for splinting varies with the


461

severity of injury. Extrusions may need only 2 to3 weeks, whereas luxations that involve bony frac-tures need up to 8 weeks.' Root canal treatment isindicated for teeth with a diagnosis of irreversiblepulpitis or pulp necrosis. Such a diagnosis oftenrequires a combination of signs and symptomssuch as discoloration of the crown, lack of pulpresponse to the EPT, and a periradicular lesionseen radiographically.' Severe pulp damage is morelikely with greater degrees of displacement.

Treatment of intrusive luxation injuries dependson root maturity.25 If the tooth is incompletelyformed with an open apex, it may re-erupt. If it isfully developed, active extrusion will be necessarysoon after the injury, usually by an orthodonticappliance. In extreme cases of intrusion, in whichthe tooth has been totally embedded into the al-veolus, surgical repositioning may be necessary.Surgical repositioning should, however, be onlypartial and should be supplemented with ortho-dontic extrusion to reduce the risk of marginalbone loss and ankylosis. Root canal treatment isindicated for intruded teeth with the exception ofthose with immature roots, in which case the pulpmay revascularize. 23

A tooth with any luxation injury and also signsor symptoms of irreversible pulpitis requires rootcanal treatment; the procedure is conventionaland may be completed in one appointment. If thepulp is necrotic, treatment may be accomplishedin one or two visits with calcium hydroxide placedin the prepared canal for 1 to 2 weeks before ob-turation. If there is also evidence of external re-sorption in addition to pulp necrosis, calcium hy-droxide should be left in the canal until evidenceof root surface repair, such as reestablishment ofperiodontal ligament space, is evident.

Primary Teeth

Concussion and subluxation injuries require notreatment. Pulpal evaluation is limited to radio-graphic and clinical observation. Persistent crowndiscoloration usually indicates pulp necrosis, ne-cessitating either root canal treatment or extrac-tion. 26,2' Discolored primary teeth may return tonormal color, probably indicating recovery of thepulp.9 Calcitic metamorphosis is common afterluxation injuries. This changes the primary crownto a darker yellow color, which is not pathosis andso requires no treatment.

Teeth with lateral and extrusive luxations maybe left untreated, or the tooth may be extracted,depending on the severity of injury. Teeth withintrusive luxations should be carefully evaluatedto determine the direction of intrusion. Radio-graphs provide valuable information. If the in-

truded tooth appears foreshortened on the film,the apex is oriented toward the x-ray cone. There-fore these teeth should present no danger to thepermanent successor and may be left to re-erupt.If the tooth appears elongated, the apex is ori-ented toward the permanent successor and maypose a risk to the permanent tooth bud. Thetooth should be carefully extracted if it impingeson the permanent successor. Also evaluated is thesymmetry of the permanent tooth buds.'

AVULSIONS

Description

An avulsed tooth is one that has been totally dis-placed out of its alveolar socket. If the tooth is re-planted soon after avulsion (immediate replanta-tion), the periodontal ligament has a good chanceof healing. Time out of socket and the storagemedia used are the most critical factors in suc-cessful replantation. It is important to preservethe periodontal ligament cells and the fibers at-tached to the root surface by keeping the toothmoist and minimizing handling of the root.1.28

Treatment

Three situations involving avulsions may occur:(1) someone may telephone for advice about anavulsed tooth, presenting an opportunity for im-mediate replantation (within minutes); (2) the pa-tient may be brought to the office with a tooththat has been out of the alveolus for less than1 hour or kept in a suitable storage medium; or(3) the tooth has been out for more than 1 hourand not kept in a storage medium.

I mmediate replantation. The prognosis is im-proved by replantation immediately after avul-sion." Many individuals-parents, athletic instruc-tors, and others-are aware of this emergencyprocedure and can replant on site. Some may askfor advice by phone. The procedure used for im-mediate replantation is presented in Box 25-4.

462

25 I Management of Traumatized Teeth

When a patient who has had a tooth replantedat the accident site comes to the dental office, thereplantation should be examined both clinicallyand radiographically. The dentist looks for addi-tional injuries to adjacent or opposing teeth andevaluates the replanted tooth for stability andalignment. The procedure outlined in the nextsection (with the exception of the replantationstep) is followed.

Replantation within 1 hour of avulsion. If immedi-ate replantation is not feasible, the injured personshould be brought to the dental office and thetooth transported in such a way as to keep itmoist.29 The best transport medium is a commer-cially available storage-transport medium or phys-iologic saline (usually neither is available); milkis an excellent alternative.28-30 Saliva is acceptable,whereas water is not good for maintaining root-surface cell vitality.'

When the patient arrives:1. The tooth is placed in a cup of physiologic

saline.2. The area of injury is radiographed, looking

for evidence of alveolar fracture.3. The avulsion site is examined carefully for

any loose bone fragments that may be re-moved. if the alveolus is collapsed, it isspread open gently with an instrument.

4. The socket is gently irrigated with saline toremove contaminated coagulum.

5. In the cup of saline, the tooth is graspedwith extraction forceps by the crown toavoid handling the root.

6. The tooth is examined for debris, which, ifpresent, is gently removed with gauzemoistened with saline.

7. The tooth is replaced into the socket; afterpartial insertion using the forceps, gentlefinger pressure is used or the patient biteson gauze until the tooth is seated.

8. Proper alignment is checked, and hyperoc-clusion is corrected. Soft tissue lacerationsare tightly sutured, particularly cervically.

9. The tooth is stabilized for 1 to 2 weekswith a splint (see Figure 25-14).

10. It has been suggested that antibiotics beprescribed in the same dosage as that usedfor mild to moderate oral infections . 31 Atetanus booster injection is recommendedif the last one was administered more than5 years previously. 4

11. Supportive care is given; a soft diet andmild analgesics are suggested as needed.

Root canal treatment is indicated for matureteeth and should be done optimally after 1 weekand before the splint is removed (the splint stabi-lizes the tooth during the procedure). The excep-

tion to routine root canal therapy is immatureteeth with wide-open apices; they may revascular-ize but must be evaluated at regular intervals of2, 6, and 12 months after replantation. If subse-quent evaluations indicate pulp necrosis, rootcanal treatment, probably including apexifica-tion, is indicated . 32

Replantation more than 1 hour after avulsion. If atooth has been out of the alveolar socket for morethan 1 hour (and not kept moist in a suitablemedium), periodontal ligament cells and fiberswill not survive regardless of the stage of root de-velopment. Replacement resorption (ankylosis)will probably be the eventual sequela after replan-tation. Therefore treatment efforts before replan-tation include treating the root surface with fluo-ride to reduce (slow) the resorptive process.'

When the patient arrives:1. The area of tooth avulsion is examined and

radiographs are examined for evidence ofalveolar fractures.

2. Debris and pieces of soft tissue adhering tothe root surface are removed.

3. The tooth is soaked in a 2.4% solution ofsodium fluoride (acidulated to pH 5.5) for5 to 20 minutes.

FIGURE 25-18Replanted tooth with inflammatory resorption characterizedby resorption of tooth structure (curved arrow) and a peri-odontal lesion in the periradicular bone (open arrows). Al-

though the inflammatory resorption appears internal, it is infact superimposed and is external.

4. The pulp is extirpated, and the canal iscleaned, shaped, and filled while the tooth isheld in a fluoride-soaked piece of gauze. Oftenthe procedure can be accomplished from anapical direction if the root is immature.

5. The alveolar socket is carefully suctioned toremove the blood clot. The socket is irri-gated with saline.33 Anesthesia may be nec-essary first.

6. The tooth is gently replanted into thesocket, checking for proper alignment andocclusal contact.

7. The tooth is splinted for 3 to 6 weeks (seeFigure 25-14).

Sequelae to Replantation

Generally external resorption occurs. Three typeshave been identified: surface, inflammatory, andreplacement.'

Surface resorption. Microscopic examination ofreplanted teeth reveals lacunae of resorption inthe cementum. These are not usually visible on ra-diographs. They are repaired by deposition of newcementum, which represents healing.

Inflammatory resorption. Inflammatory resorp-tion occurs as a response to the presence of in-fected necrotic pulp in conjunction with injury tothe periodontal ligament. It occurs with replanted


463

teeth (Figure 25-18) as well as with other types ofluxation injuries. It is characterized by loss oftooth structure and adjacent alveolar bone. Re-sorption usually subsides after removal of thenecrotic pulp, so the prognosis is good. Rootcanal treatment is therefore recommended rou-tinely for replanted teeth with closed apexes.

Replacement resorption. In replacement resorp-tion the tooth structure is resorbed and replacedby bone (Figure 25-19). This is the result of anky-losis; bone fuses directly to the root surface. Thecharacteristics of ankylosis are lack of physio-logic mobility, failure of the tooth to erupt alongwith adjacent teeth (leading to infraocclusion inyoung individuals), and a "solid" metallic soundwhen percussed. Currently, no known treatmentis available for replacement resorption, whichtends to be continuous until the root is replacedby bone. In teeth that have had long extraalveolardry periods, the resorptive process is apparentlyslowed (but not halted) by immersing the toothin fluoride before replantation.'

Primary Teeth

Replantation of avulsed primary teeth is not rec-ommended because of the risk of damage to thepermanent successor. Premature loss of a primaryincisor is generally not serious.

FIGURE 25-79Replacement resorption (ankylosis). A, The root of this replanted root canal treated tooth has been almost totallyresorbed and has been replaced by bone that fuses to the tooth structure, resulting in ankylosis and resorption.B, Tooth is in infraocclusion owing to ankylosis, which prevents normal eruption, as evidenced by continuouseruption of the adjacent teeth.

464

25 1 Management of Traumatized Teeth


Mature avulsed teeth, when replanted, cannot beexpected to reestablish pulpal blood supply.32

Revascularization may occur in immature teethwith wide open apexes, but it is unpredictable.These teeth must be monitored radiographicallyover a period of time to watch for evidence of pulpnecrosis.

In the mature replanted tooth, root canaltreatment is definitely indicated and should bedone about 1 to 2 weeks after replantation. Thesplint may remain during treatment for stability.The use of calcium hydroxide as an antimicrobiali ntracanal interappointment medicament may behelpful34; it is particularly beneficial if the rootcanal is infected, a condition that would be likelyto occur when root canal treatment is delayedmore than a few weeks after replantation.

The procedure consists of cleaning and shap-ing, followed by calcium hydroxide placement fora minimum of 1 to 2 weeks .28 Obturation is thenaccomplished with gutta-percha and sealer. Long-term evaluation is necessary, complex problemsmay develop in the future.

Restoration, both temporary and permanent,is the key to success. Sealing of the access is criti-cal between appointments and after obturation.

FIGURE 25-20Alveolar fracture (arrows). Teeth involved in an alveolar frac-ture should have careful short- and long-term monitoring forpulp responsiveness or other signs of pathosis.

For long-term stability, a dentin bonding agentwith acid-etched composite is indicated.28

ALVEOLAR FRACTURES

Pulp necrosis is often associated with alveolar frac-tures, which may in turn be associated with othermajor facial injuries.' The initial, urgent need ismanagement of the fracture, which is splinting ofthe segment to the adjacent teeth and often is per-formed by oral and maxillofacial surgeons. Whenthe patient is able to have the teeth examined,those in the line of fracture as well as adjacentteeth are evaluated. Lack of response to an EPT, ifnot reversed within 3 to 6 months, often, but notalways, indicates pulp necrosis. Therefore the pres-ence of other indicators (apical radiolucency orsymptoms) is necessary before further treatment isgiven (Figure 25-20). Root canal treatment is indi-cated when pulp necrosis is diagnosed.35

REFERENCES

1. Andreasen JO, Andreasen FM: Textbook and color atlas oftraumatic injuries to the teeth, ed 3, St Louis, 1994, Mosby.

2. World Health Organization: Application of the interna-tional classification of diseases to dentistry and stomatology,ed 3, Geneva, 1993, ICD-DA.

3. Bakland LK, Andreasen JO: Examination of the den-tally traumatized patient, Calif Dent Assoc J 24:35,1996.

4. Glendor U, Koucheki B, Halling A: Risk evaluation andtype of treatment of multiple dental trauma episodesto permanent teeth, Endod Dent Traumatol 16:205,2000.

5. Arnon SS: Tetanus. In Behrman RE, Kleigman R,Arvin AM, editors: Nelson's textbook of pediatrics, ed 15,Philadelphia, 1995, WB Saunders.

6. Kamboozia AH, Punnia-Moorthy A: The fate of teethin mandibular fracture lines. A clinical and radio-graphic follow-up study, IntJOral Maxillofac Surg 22:97,1993.

7. Oikarinen K, Lahti J, Raustia AM: Prognosis of perma-nent teeth in the line of mandibular fractures, EndodDent Traumato16:177, 1990.

8. Andreasen FM, Andreasen JO: Diagnosis of luxationinjuries: the importance of standardized clinical, ra-diographic and photographic techniques in clinical in-vestigations, Endod Dent Traumatol 1:160, 1985.

9. Andreasen FM, Vestergaard Pedersen B: Prognosis ofl uxated permanent teeth the development of pulpnecrosis, Endod Dent Traumatol 1:207, 1985.

10. Andreasen FM, Andreasen JO: Treatment of traumaticinjuries: shift in strategy, IntJTechnol Assess Health Care6:588,1990.

11. Andreasen FM, Flugge E, Daugaard-Jensen J,Munksgaard EC: Treatment of crown fractured in-cisors with laminate veneer restorations. An experi-mental study, Endod Dent Traumatol 8:30, 1992.

12. Heide S: Pulp reactions to exposure for 4, 48, or 168hours, JDent Res 59:1910, 1980 (abstract).

13. Cvek M: A clinical report on partial pulpotomy andcapping with calcium hydroxide in permanent incisorswith complicated crown fracture, J Endod 4:232, 1978.

14. Pitt Ford TR, Torabinejad M, Abedi HR, et al: Usingmineral trioxide aggregate as a pulp-capping material,JAmDent Assoc 127:1491, 1996.

15. Bakland LK: Management of traumatically injuredpulps in immature teeth using MTA, Calif Dent Assoc J28:855, 2000.

16. Fuks A, Chosack S: Long-term follow-up of trauma-tized incisors treated by partial pulpotomy, PediatrDent 15:334, 1993.

17. Herweijer JA, Torabinejad M, Bakland LK: Healing ofhorizontal root fractures, JEndod 18:118, 1992.

18. Zachrisson BV, Jacobsen I: Long-term prognosis of66 permanent anterior teeth with root fracture, ScandJDentRes 83:345, 1975.

19. Andreasen JO, Hjorting-Hansen E: Intraalveolar rootfractures: radiographic and histologic study of 50cases, j Oral Surg 25:414, 1967.

20. Andreasen FM, Andreasen JO, Bayer T: Prognosis ofroot-fractured permanent incisors: prediction of heal-ing modalities, Endod Dent Traumatol 5:11, 1989.

21. Bender IB, Freedland JB: Clinical considerations in thediagnosis and treatment of intra-alveolar root frac-tures,JAmDentAssoc 107:595, 1983.

22. Crona-Larson G, Noren JG: Luxation injuries to per-manent teeth-a retrospective study of etiological fac-tors, Endod Dent Traumatol 5:176, 1989.

23. Andreasen FM: Pulpal healing after luxation injuriesand root fractures in the permanent dentition, EndodDent Traumatol 5:111, 1989.

24. Andreasen FM, Zhijie Y, Thomsen BL, Andersen PK:Occurrence of pulp canal obliteration after luxation

25 1 Management of Traumatized Teeth

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injuries in the permanent dentition, Endod Dent Trau-mato13:103, 1987.

25. Jacobsen I: Long term evaluation, prognosis and sub-sequent management of traumatic tooth injuries. InProceedings of the international Conference on Oral Trauma,Chicago, 1986, American Association of Endodontists.

26. Holan G, Topf J, Fuks A: Effect of root canal infectionand treatment of traumatized primary incisors on per-manent successors, Endod Dent Traumatol 8:12, 1992.

27. Soxman JA, Nazif MM, Bouquot J: Pulpal pathology inrelation to discoloration of primary anterior teeth,J Dent Child 51:282, 1984.

28. American Association of Endodontists: Treating theavulsed permanent tooth, Endodontics: Colleagues forExcellence, Winter/Spring, 1994.

29. Trope M: Protocol for treating the avulsed tooth, CalifDent AssocJ24:43, 1996.

30. Krasner P, Person P: Preserving avulsed teeth for re-plantation, J Am Dent Assoc 123:80, 1992.

31. Hammarstrom L, Blomlof L, Feiglin B, et al: Replanta-tion of teeth and antibiotic treatment, Endod DentTraumatol2:51, 1986.

32. Kling M, Cvek M, Mejare I: Rate and predictability ofpulp revascularization in therapeutically reimplantedpermanent teeth, Endod Dent Traumatol 2:83, 1986.

33. Matsson L, Klinge B, Hallstrom H: Effect on peri-odontal healing of saline irrigation of the tooth socketbefore replantation, Endod Dent Traumatol 3:64, 1987.

34. Trope M, Yesilsoy C, Koren L, et al: Effect of differentendodontic treatment protocols on periodontal repairand root resorption of replanted dog teeth, J Endod18:492, 1992.

35. Andreasen JO: Fractures of the alveolar process of thejaw. A clinical and radiographic follow-up study, ScandJDentRes 78:263, 1970.

Periodontal-EndodonticConsiderations

LEARNING OBJECTIVES


1 / State the anatomic pathways of communication between the dental pulp and the gingival sulcus or

periodontal ligament.

z / Describe the effects of pulpal disease and endodontic procedures on the periodontium.

3 / Describe the effects of periodontal disease and procedures on the pulp.

4 / Identify which clinical diagnostic procedures and findings are of importance in differentiating between

those defects in the integrity of the gingival sulcus that will respond to root canal treatment and those that

will require periodontal therapy for resolution.

s / Establish treatment requirements and sequencing according to diagnostic findings.

6 / Identify which patients with complex problems should be considered for referral.

466

Pathways of Communication between the

Dental Pulp and the Periodontium

Dentinal Tubules

Lateral or Accessory Canals

Apical Foramen

Effects of Pulpal Disease and Endodontic

Procedures on the Periodontium

Pulpal Disease

Endodontic Procedures

Effects of Endodontically Involved Teeth on

Periodontal Health and Healing

Effects of Periodontal Disease and

Procedures on the Pulp

Periodontal Disease

Periodontal Procedures

Clinical Diagnostic Procedures


Pulp Testing Procedures

Periodontal Probing

Definition of a Perio-Endo Lesion*

Clinical Situations That Can Be Identified*

Acute or "Blow-Out" Lesions

Typical Periodontal Lesions

Radiolucent Lesions in Which the Gingival

Sulcus Is Intact

Lesions with Narrow Sinus Tract Type Probing

I ndependent Periodontal and Periapical or

Lateral Lesions That Do Not Communicate

True Combined Perio-Endo Lesions

Basis for Patient Referral

*Adapted with permission from Harrington GW:The perio-endo question: differential diagnosis, DentClin North Am 23(4):673-690, 1979 and from NatkinE: An introduction to endodontic diagnosis and treatment,Seattle, 1989, University of Washington.

26 / Periodontal-Endodontic Considerations

467

ne of the more difficult dilemmas fora clinician is interpretation of the causeof a defect in the integrity of the gingival

sulcus. Such a defect is identified by carefullyprobing all the way around a tooth with a peri-odontal probe. Either the gingival sulcus is intactor it is not. If the gingival sulcus is not intact(probing depth is greater than 2 to 3 mm), it is crit-ical for the patient that the clinician choose ap-propriate treatment for resolution of the defect.The purpose of this chapter is to identify thoseclinical situations that will respond favorably toroot canal treatment and those that will not.

Pathways of CommunicationBetween the Dental Pulpand the PeriodontiumDirect communication between the dental pulpand the periodontium may be through (1) patentdentinal tubules where the cementum is develop-mentally missing on the root surface or has beenremoved by periodontal root planing, (2) lateraland/or accessory canals, and (3) the apical fora-men or foramina.

DENTINAL TUBULES

An understanding of the anatomy of patentdentinal tubules and changes brought about byage or periodontal treatment is essential to ourunderstanding of the permeability of root dentinand dentin hypersensitivity. In the root, dentinaltubules extend from the intermediate dentin justinside the cementum-dentin junction to the pulp-predentin junction. Dentinal tubules in the rootrun a relatively straight course between the pe-riphery and the pulp in contrast to the typicalS-shaped contours of the tubules in the crown.Tubules range in size from about 1 to 3 um in di-ameter.' They are approximately 1 um in diameternear the cementum-dentin junction and approxi-mately 2.5 um near the pulp-predentin junction . 2The diameter of tubules decreases with age by thelaying down of highly mineralized peritubulardentin. It is possible for tubules to become com-pletely calcified, particularly in the root. When thedentinal tubules in a section of root dentin be-come completely calcified, dentin is referred to assclerotic or translucent.

The number of dentinal tubules per squaremillimeter varies from 8000 to 57,000.' At the pe-riphery of the root at the cemento-enamel junc-tion, the number has been estimated to be ap-proximately 15,000/mm 2 . The density, or number

468


of tubules per square millimeter, increases fromthe cementum-dentin junction to the dentin-predentin junction. In periodontal disease theroot surface becomes exposed to the oral cavity.Cementum acts as a protective barrier, but directcommunication may be established between thecontents of patent dentinal tubules and the oralenvironment if the cementum is congenitallymissing at the cementum-dentin junction' or thecementum layer is removed by root planing.Therefore direct communication between the oralenvironment and the dental pulp may be estab-lished through patent dentinal tubules.

LATERAL OR ACCESSORY CANALS

Considerable speculation exists about the role lat-eral or accessory canals may play in the spread ofinflammation from a periodontal pocket into thedental pulp or from the dental pulp into the peri-odontal ligament. Although there is little doubtthat the spread of inflammation can and doesoccur in both directions, the clinical significanceis open to question.

A lateral or accessory canal may be present any-where on a root surface. The majority are found inthe apical third of the root. The occurrence of lat-eral canals in the coronal third of the root is rare.The percentage of roots that may have a lateralcanal or canals increases as the apex of the root isapproached. Overall it is estimated that 30% to40% of teeth have lateral or accessory canals.DeDeus4 suggests that 1.6% of teeth have lateralcanals in the coronal third of the root, 8.8% in themiddle third, and 17% in the apical third. Obvi-ously, the farther periodontal disease extendsdown the root surface, the greater the possibilitythat a lateral canal may become exposed by peri-odontal disease. In a study of 100 human teethwith extensive periodontal disease, however, only2% had lateral canals located in an involved peri-odontal pocket.5

The incidence of lateral canals in the furcationregion of molars is stated to be approximately30% to 50%.6.7 The clinical significance of lateralcanals in the furcation, therefore, has been a sub-ject of much speculation.

Clinical identification of the presence of a lat-eral canal is very difficult or impossible in mostinstances. An overall incidence of 30.6% has beenidentified when two-view radiographs of extractedteeth were examined.8 In interpretation of stan-dard intraoral radiographs, however, an incidenceof only 7.6% was identified.8 This disparity clearlydemonstrates the difficulty encountered in theclinical identification of lateral canals. Moreover,the investigators were unable to identify any lat-

eral canals in the furcation area of molar teeth.Therefore in the usual situations encountered inclinical practice, accurate positive identificationof lateral canals on the basis of radiographic in-terpretation can be accomplished only in a verysmall percentage of cases.

Clinically, positive identification of the pres-ence of a lateral canal can usually be made onlywhen a discrete lateral lesion associated with anecrotic pulp can be identified radiographically orwhen some of the root canal filling material isforced into a lateral canal during the condensa-tion procedure (Figure 26-1). In addition, the ra-diographic identification of a notch on the lateralroot surface suggests the presence of an orificeinto a lateral canal.

The clinical significance of the incidence of lat-eral canals at various levels on the root surface liesin the fact that the farther apical the lateral carnal,the more extensive the periodontal destructionmust be to involve the tissue in the lateral canal inthe inflammatory process. If the incidence of lat-eral canals in the coronal third of the root is rare(with the exception of furcations), the incidencein the middle third is 12% or less,8 and the pre-ponderance of lateral canals occur in the apicalthird, then in most instances periodontal patho-sis would have to be extensive for the inflamma-tory process to extend through a lateral canal toinvolve the dental pulp. In such instances, theoverall prognosis for a tooth will then depend onthe periodontal prognosis, i.e., how extensive theperiodontal destruction is and the likelihood ofresolving such periodontal pathosis with peri-odontal therapy.

If the dental pulp is necrotic and a patent lat-eral canal is exposed, periodontal reattachment tothe root surface can be inhibited if definitive peri-odontal therapy is undertaken before root canaltreatment. Therefore if the pulp is necrotic and the pe-riodontal prognosis is favorable, root canal treatmentshould always precede periodontal therapy.

If the dental pulp is vital but there has been ex-tension of the inflammatory process from a peri-odontal lesion into the tissue in a lateral canal, itis open to question whether or not the amount oftissue irritants present in the lateral canal wouldimpede periodontal reattachment. Because it is notpossible to determine the exact bistologic status of the den-tal pulp by the clinical testing procedures currently avail-able and in most instances impossible to positively iden-tify the presence or absence ofa lateral canal, periodontaltherapy alone should be undertaken to resolve a peri-odontal lesion if the tooth responds within normal limitsto pulp testing procedures and there is no other evidenceto indicate that the clinician should question the validityof the pulp test responses.

COLOR FIGURE 26- 1(Refer to Figure 26-5.) A, Typical swelling in a "blow out" type of lesion. B, A periodontal probe in the lesion atthe time of initial examination. C, Probing is reduced to a narrow sinus tract type of probing after starting rootcanal treatment. D, Resolution of the lesion after completion of root canal treatment. (From Harrington GW:Dent Clin North Am 23:673, 1979.)

COLOR FIGURE 26-2(Refer to Figure 26-8.) Clinical presentation of a narrow sinus tract type of probing. (From Harrington GW: DentClin North Am 23:673, 1979.)

COLOR FIGURE 26- 3(Refer to Figure 26-6.) A to E, Typical probing of a lesion caused by periodontal disease. (From Harrington GIN:Dent Clin North Am 23:673, 1979.)

APICAL FORAMEN

The major pathway of communication betweenthe dental pulp and the periodontal ligament inall teeth is through the apical foramen or foram-ina. The effect of extensive pulp inflammation ornecrosis is extension of the inflammatory processinto the periodontal ligament contiguous withthe pulp at the apical foramen.


469

FIGURE 26-1Lateral canals may be identified (A) when a dis-crete lateral lesion (arrow) is present, as on themesial of this central incisor or (B) radiopaque ma-terials are extruded during obturation. C, A notchon the lateral root surface (arrow) suggests thepresence of a lateral canal. (A and C courtesyDr. E. Natkin.)

Effects of Pulpal Diseaseand Endodontic Procedureson the PeriodontiumPULPAL DISEASE

Pulp inflammation or necrosis may lead to an in-flammatory response in the periodontal ligamentat the apical foramen or foramina or at the site of

470


a lateral or accessory canal. The resulting inflam-matory lesion can range in extent from a minimalinflammatory process confined to the periodontalligament to extensive destruction of the peri-odontal ligament, tooth socket, and surroundingbone. Such a lesion may result in a localized ordiffuse swelling that occasionally may involve thegingival attachment. A lesion related to pulpalnecrosis may also result in a draining sinus tractthat drains through the alveolar mucosa orattached gingiva, but may occasionally drainthrough the gingival sulcus of the involved toothor through the gingival sulcus of an adjacenttooth. After adequate root canal treatment, le-sions resulting from pulpal necrosis resolve an ex-ceptionally high percentage of the time.' The in-tegrity of the periodontium will be reestablishedif root canal treatment is done well. If a drainingsinus tract through the periodontal ligament ispresent before root canal treatment, resolution ofthe defect that can be probed is expected.

ENDODONTIC PROCEDURES

Technical procedures involved in root canal treat-ment, irrigants, medicaments, dressings, sealers,and filling materials have the potential to causean inflammatory response in the periodontium.An inflammatory response resulting from com-monly used root canal treatment methods andmaterials, however, is usually transient in natureand resolves quickly if filling materials are con-fined within the canal space.

In young patients there is evidence that a caus-tic agent such as 30% hydrogen peroxide maymove through large patent dentinal tubules fromthe pulp chamber and canal to cause an inflam-matory response in the periodontal ligament.'o - ' 2

As a tooth matures, however, and the diameter ofdentinal tubules is reduced significantly, there islittle clinical evidence that any of the materialsused in root canal treatment cause an inflamma-tory response in periodontal tissues other thanthrough a lateral canal or the apical foramen.

Procedural errors during root canal treatmentcan, and often do, cause major destructive inflam-matory processes in the periodontium. Break-down of the attachment resulting in a periodon-tal defect that can be probed may occur afterprocedural errors such as access perforations inthe floor of a pulp chamber or on the root surfaceapical to the gingival attachment, strip perfora-tions or root perforations related to cleaning andshaping procedures, and vertical root fractures.Reattachment after a periodontal defect has beenestablished because of a procedural error is usu-ally difficult to attain.

Effects of EndodonticallyI nvolved Teeth on PeriodontalHealth and HealingCurrent literature suggests that a pulpless toothmay be one of several site characteristics that mayinfluence treatment outcomes for periodontal le-sions." In this chapter, a pulpless tooth is definedas a tooth without a vital pulp; i.e., a tooth with anecrotic pulp or a tooth that has previously hadroot canal treatment. Recent retrospective statisti-cal studies suggest that pulpless teeth with peri-apical lesions promote the initiation of periodon-tal pocket formation, promote the progression ofperiodontal disease, and interfere with healingof periodontal lesions after periodontal treat-ment." -18 The presumed pathways include patentdentinal tubules as well as accessory or lateralcanals. 14 The extrapolated difference in periodon-tal pocket depth related to teeth with no periapi-cal lesions compared with teeth with periapicallesions, however, is stated to be 0.5 to 1.0 mm. Ona clinical basis detection of small changes in prob-ing depth with any degree of accuracy is difficult.The standard deviations in clinical probing re-sults are stated to be 0.5 to 1.3 mm."

The reported statistical differences betweenteeth with and without periapical lesions are alsosomewhat inconsistent with differing periodontalresponses to different treatment modalities. Thedata suggest that periodontally involved teethmanaged by periodontal surgery and osteoplastyare not influenced by pulp pathosis." In addition,nonsurgical treatment of vertical marginal defectsshowed no correlation between periapical pathosisand mean pocket depth reduction." In summary,the data presented by these studies are equivocal atbest, appear to present trifling distinctions, andappear to have little clinical significance.

In an attempt to relate disease etiology andprogression with the assignment of prognosis,McGuire and Nunn10-2s found that some com-monly accepted clinical parameters did not accu-rately predict a tooth's survival. Their statisticalmode 12' had predicted that endodontic involve-ment would be associated with the probabilitythat the prognosis for such a tooth would worsenover time. In their clinical stud y,22 however, the ac-tual outcome was that none of the 131 teeth lostout of a total 2509 teeth had endodontic involve-ment. Initial endodontic involvement was deter-mined not to be a significant clinical factor asso-ciated with tooth loss.

Because the alternative to maintenance of apulpless tooth is extraction, long-term prognosisstudies are significant. A recent retrospective clin-


471

ical study of patients with advanced periodontaldisease 5 to 14 years after completion of active pe-riodontal and endodontic treatment showed thatthe risk of endodontic failure is very low and thatthere is little risk of tooth loss for periodontal rea-sons. 24 Of 911 periodontally involved teeth, over-all tooth loss was 2%. Of the 571 teeth that didnot have root canal treatment before the recall pe-riod, only one tooth needed root canal treatmentover the 5- to 14-year follow-up period. None ofthe teeth were lost for endodontic reasons, andthe overall failure rate of the 340 endodonticallytreated teeth was 1.2%.

The prognosis is quite good even for molarswith extensive periodontal disease that requiresroot amputation .25.26 It has been suggested thatsurvival rates of teeth with root resections are notsubstantially different from those for osseointe-grated implants .2' In fact, a current periodonticstextbook suggests that substituting an osseointe-grated implant for a tooth with furcation involve-ment should be considered with extreme cautionand only if the implant will improve the success ofthe overall treatment plan .28 In the benchmark re-search study on prognosis for osseointegrated im-plants, Adell et al . 29 reported an overall successrate of 91% for mandibular implants and 81%for maxillary implants for a follow-up period of5 years or more.

In summary, although it has been suggested that apulpless tooth may represent an etiologic risk factor re-lated to periodontal disease, the comparative risk must beconsidered negligible based on clinical outcomes.

Effects of Periodontal Diseaseand Procedures on the PulpPERIODONTAL DISEASE

Over the years there has been considerable specu-lation on the effect of periodontal disease on thehealth of the pulp. The accumulated evidencesuggests that there is little or no effect on humanpulps ...... In some of these studies, the pulpsof intact, caries-free, periodontally involved teethwere all histologically within normal limits re-gardless of the severity of periodontal disease.32-35Indeed, there is some evidence that periodontaldisease must extend all the way to the apical fora-men before the accumulation of plaque can causesignificant pulp involvement. 36

PERIODONTAL PROCEDURES

Periodontal root planing removes cementumand dentin from the root surface, exposing

patent dentinal tubules to the oral environ-ment. Dentin hypersensitivity often results, butit can usually be managed by desensitizationprocedures.

The pulp response to cementum and dentinremoval and exposure of patent dentinal tubulesby periodontal root planing will vary with theremaining dentin thickness. Unless dentin re-moval is excessive, pulp response will be negligi-ble. Although the pulp is exposed to a bacterialchallenge through patent dentinal tubules, it isquite capable of repair and healing. Productionof reparative dentin and reduced canal diametermay result, but pulp tissue remains relativelyunaffected.

In a study of patients with maxillary molarfurcation involvement in which a high percent-age of the teeth had lost at least 50% percent ormore bone support around one root before peri-odontal treatment, only 4% required root canaltreatment from 5 to 24 years after completion ofperiodontal treatment . 32 In no case was the causefor root canal treatment ascribed to the effects ofperiodontal disease or periodontal treatment. Ina 4- to 13-year recall study of nonabutment teethwith advanced periodontal disease in which thecrestal bone level of over half of the teeth was inthe apical two-thirds of the root, only 3% devel-oped pulp necrosis.35 With the exception of sev-eral teeth that subsequently had progression ofperiodontal disease to involve the root apices,neither the cumulative effects of periodontaltreatment nor periodontal disease itself were rea-sons cited for pulp necrosis.

If periodontal treatment is to be consideredfor managing periodontal disease that extendsaround the apical foramen, curetting the peri-odontal lesion as part of the treatment will severthe blood supply to the pulp and will require pro-phylactic endodontic treatment. Root canal treat-ment should be completed before periodontaltreatment because the necrotic pulp will preventhealing of the periodontal tissues.

In summary, unless periodontal disease has pro-gressed to involve the tooth apex, the effect ofperiodontaldisease on the pulp appears to be negligible. Prognosis fora tooth involved with periodontal disease is determinedby the outcome expected from periodontal therapy.

Clinical Diagnostic Procedures

Appropriate diagnosis is critical. The clinicianmust be able to identify the clinical characteristicsof a lesion, determine whether or not root canaltreatment has the potential to resolve the lesion,and establish a reasoned prognosis.

47 2



Interpretation of radiographs of good quality isa very important part of diagnosis. Identifica-tion of the proximal crestal bone and its positionin relation to the cementum-enamel junctionand the coronal level of superimposition of thetrabecular pattern over the root of a tooth re-quires careful examination. Crestal bone levelcan be identified by the clear-cut image of theroot itself and clarity of the canal space con-trasted with superimposition of the trabecularpattern over the root (Figure 26-2). If there iscrestal bone loss, the more apical margin of thesuperimposed trabecular pattern identifies thelevel of bone loss on one side of the tooth. Insome cases the superimposition of the trabecularpattern will appear to have two distinct levels onthe root. There is no way to interpret from a sin-gle radiograph whether the apically positionedbone level is on the buccal or the lingual side.This discrimination can only be made by clinicalexamination of the area.

Interpretation of discrete periapical or laterallesions and discrete periodontal lesions is of clin-ical importance in suggesting the cause of thelesion and the proper diagnostic procedures tofollow to confirm the cause. However, when thereis radiographic evidence that bone loss extends

from the level of crestal bone to or near the apexof the tooth, the radiograph is of little value indetermining the cause (Figure 26-3).

PULP TESTING PROCEDURES

The presence or absence of vital tissue in a toothwith a single canal can be determined with confi-dence with current pulp testing procedures. Theexact histologic status cannot be determined. Inteeth with multiple canals there may be vital tis-sue in one or more canals while pulp necrosismay have occurred in the remaining canal orcanals. Therefore the same degree of confidencecannot be ascribed to positive pulp test responsesin a tooth with multiple canals as can be attrib-uted to positive tests in a tooth with a singlecanal. Limitations related to the interpretation ofpulp test responses complicate diagnosis of thecause of a defect in the integrity of the gingivalsulcus. Chapter 4 of this text presents an in-depth discussion of the interpretation of pulptest responses.

PERIODONTAL PROBING

Considering the limitations in the diagnostic ar-mamentarium, discrimination of "perio-endo"

FIGURE 26-2A, Clear definition of the root and root canal space indicates bone loss on one side of the tooth down to the levelof the superimposed trabecular pattern. B, The image of the mesiobuccal root of the first molar demonstrates theclarity of definition of the root outline and of the root canal space up to the level of the superimposed trabecu-

l ar pattern. (A from Harrington GW: Dent Clin North Am 23:673, 1979.)

lesions must be made primarily on the basis ofthe critical examination of the area by means ofa periodontal probe. By development of acutetactile discriminations the nature and cause ofthe lesion can be determined. This determina-tion is made by identifying the physical charac-teristics of the lesion itself. Careful, accurateprobing all the way around the external rootsurface of the tooth is required. A fine peri-odontal probe must be used (Marquis periodon-tal probe, Marquis Dental Manufacturing Co.,Denver, CO). Differentiation must also be madebetween "probing" and "sounding." As used inthis chapter, probing is defined as the tactile dis-crimination of the level of the epithelial attach-ment through use of the periodontal probe. Incontrast, sounding implies penetrating throughthe attachment to define the most coronal levelof the alveolar bone. As there may be consider-able differences between the two, the clinicianmust understand and appreciate this clear dis-tinction to develop the quality of tactile dis-crimination required. In the descriptions to fol-low, probing is the procedure referred to in allinstances.

Definition of a Perio-Endo Lesion

A perio-endo lesion is defined as follows:1. The tooth involved must be pulpless.2. There must be destruction of the periodon-

tal attachment apparatus from the gingivalsulcus to either the apex of the tooth or tothe area of an involved lateral canal, i.e.,there must be a defect in the attachmentthat can be probed.

FIGURE 26-3These lesions have similar radiographic characteristics. A, Lesion is due solely to pulpal necrosis. B, Lesion isstrictly a periodontal lesion.


473

3. Both root canal treatment and periodontaltherapy are required to resolve the entiretyof the lesion.

The second and third criteria will be exten-sively described in the following clinical examples,but the first criterion requires some clarification.Clinical experience shows that if a tooth has anadvanced irreversible pulpitis, there is often mini-mal disruption of the lamina dura and periodon-tal ligament space at the apex of the tooth. Withsome teeth there may be radiographic evidence ofa very small periapical lesion, particularly inyoung patients. However, it is not common tofind irreversible pulpitis associated with a large ra-diolucent periapical lesion. In fact, if vital tissue isfound in the pulp chamber of a tooth with a sin-gle canal and there is a large radiolucent lesion as-sociated with the apex, it is incumbent to posi-tively identify the cause of the lesion. In a toothwith multiple canals at least one canal will havepulpal necrosis if there is a large lesion associatedwith the apex or apices. In summary, at least onenecrotic, not simply irreversibly inflamed, canal is to beexpected when a moderate-to-large periapical lesion ispresent.

Similarly, when a large lesion is associated withthe lateral surface of the root, the pulp of thetooth must be necrotic if there is an actual en-dodontic component to the lesion. The role, ifany, of inflammatory tissue in a lateral canal indevelopment of a lesion that can be probed alongthe lateral surface of the root must be questioned.Hence, it is inferred that some pulpal necrosismust be present for a lateral or apical lesion to de-velop. In the discussion to follow there must beevidence of pulpal necrosis for the lesion to beconsidered a true perio-endo lesion.

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26 I Periodontal-Endodontic Considerations

Clinical Situations ThatCan Be Identified

A periodontal-endodontic decision tree is pre-sented in Figure 26-4.

ACUTE OR "BLOW-OUT" LESIONS

When a patient presents with a localized swellingthat involves the gingival sulcus, it may be diffi-cult to determine if the swelling is due to a peri-odontal abscess or an abscess of endodontic ori-gin. The tooth must be pulpless. The swelling isusually on the labial or buccal side of the toothbut may be on the lingual side. As the sulcus isprobed there is usually normal sulcus depth allthe way around the tooth until the area of theswelling is probed. At the edge of the swellingthe probe drops precipitously to a level nearthe apex of the tooth, and the probing depth re-mains the full width of the swelling (Figure 26-5and Color Figure 26-1). At the opposite edge ofthe swelling, probing is once again within nor-mal limits. The width of the detached gingivacan be as broad as the entire buccal or lingualsurface of the tooth. This swelling can be charac-terized as having "blown out" the entire attach-ment on that side.

When probing carefully around the neck of thetooth in the area of swelling, intact crestal bone

may sometimes be felt. This would indicate thatthere has been a pathologic perforation of the cor-tical plate farther apically and that the perios-teum has been lifted off the coronal cortical plateby the swelling. If intact crestal bone is present,rapid reattachment can be expected after resolu-tion of the swelling. In some instances, on theother hand, careful probing will reveal the ab-sence of the buccal cortical plate to the depth ofapproximately the apical extent of the swelling.With this blow out type of probing, indicatingloss of bone along a broad front, rapid reattach-ment can also be expected. In furcations, however,healing may first proceed to what will be de-scribed later in this chapter as a "sinus tract typeof probing," but eventually complete reattach-ment can be expected.

Treatment for a blow out lesion involves cus-tomary endodontic emergency procedures thatwould be used if there were a similar swelling butthe entire sulcus were intact. The root surfaceneed not be curetted, nor the area surgicallyflapped. Endodontic treatment only is indicated.As the result of endodontic management of theswelling, complete periodontal reattachment oc-curs within 1 week in most cases. As mentionedearlier, however, the broad, precipitous probingmay resolve to a narrow, deep sinus tract type ofprobing, which may remain until after comple-tion of root canal treatment.

FIGURE 26-4Periodontal-endodontic decision tree. Appropriate tests and findings indicate both the diagnosis and etiology ofthe pathosis. CEJ, Cementum-enamel junction; WNL, within normal limits. (Courtesy Dr. D. Steiner, from Natkin E:An introduction to endodontic diagnosis and treatment, Seattle, 1989, University of Washington Press.)


47 5

It should also be apparent that probing inother areas around the root surface of a toothmay vary from what is considered to be withinnormal limits, but the blow out probing in thearea of the swelling will be distinctive.

TYPICAL PERIODONTAL LESIONS

In periodontal disease bone loss always begins at crestalbone level and progresses apically. The typical lesion isconical in contour. The probing may start from asulcus depth that is within normal limits, thengradually step down a slope to the apical extent ofthe lesion, and then step up again on the otherside to a sulcus depth within normal limits(Figure 26-6). The slope of the lesion will varyand may depend on the coronal width of thelesion. Regardless of the degree of the slope, adistinctive conical shape will be distinguishedby carefully feeling the increasing and then de-creasing depth of the attachment as the perio-dontal probe is stepped down into and then upout of the lesion.

Occasionally the clinical presentation of a peri-odontal lesion will have the sloping contour of aconical lesion on one side but a more precipitous,

sharp drop-off on the other. Such probing shouldbe considered to be of the "periodontal type" ofprobing.

A periodontal lesion will not resolve in re-sponse to root canal treatment even if the associ-ated tooth is pulpless. The prognosis for a toothwith conical shaped probing must be based on theprognosis for resolving the periodontal lesion. Ifit can be demonstrated that a tooth is pulplessand if the periodontal prognosis is favorable, rootcanal treatment should be completed before peri-odontal therapy. In summary, conical shaped prob-ing indicates periodontal patbosis.

RADIOLUCENT LESIONS IN WHICH

THE GINGIVAL SULCUS IS INTACT

Because bone loss from periodontal disease al-ways begins at crestal bone level and progressesapically, an intact gingival sulcus demonstratedby careful probing eliminates periodontal diseaseas the cause of a lesion. If a patient presents witha tooth with a necrotic pulp and the gingival sul-cus is intact, adequate nonsurgical root canaltreatment will resolve either a radiolucent lesionthat extends up the lateral root surface of the

FIGURE 26-5(Refer to Color Figure 26-1.) A, Periodontal probing in atypical "blow-out" type of lesion. Probings are within nor-mal limits on either side of the swelling. The lesion can beprobed to a level near the apices for the width of theswelling. B, After initiation of root canal treatment theswelling has resolved and the probing is reduced to a nar-row sinus tract type probing in the furcation. C, After com-pletion of root canal treatment the sulcus is intact. (FromHarrington GIN: Dent Clin North Am 23:673, 1979.)

476


FIGURE 26-6(Refer to Color Figure 26-3.) A, Probing in atypical periodontal lesion demonstrates the conicalcharacteristics of the lesion. B, Pretreatment radio-graph of a periodontal lesion. All teeth respondwithin normal limits to pulp tests. C, Two-year recallradiograph of successful periodontal treatment.( A from Harrington G)N: Dent Clin North Am 23:673,1979.)

tooth to involve crestal bone or a radiolucent le-sion in the furcation (Figure 26-7).

If there is radiographic evidence of a radiolu-cent lesion as described, but there is no evidenceof pulp necrosis in at least one canal, then abiopsy should be performed to determine the na-ture of the lesion (see Chapter 3).

LESIONS WITH NARROW SINUS

TRACT TYPE PROBING

An apparent periodontal lesion may or may notbe detectable radiographically. Clinically, a lesionmay be probed for some distance down the rootsurface of the involved tooth, but the defect is infact a sinus tract. Typically, probing reveals a sul-cus depth within normal limits with the excep-tion of one very narrow area that can be probedsome distance down the root surface of the toothand in many cases all the way to the apex of thetooth (Figure 26-8 and Color Figure 26-2). Usuallythe break in the attachment is only about 1 mmwide, and probing 1 mm to either side of the le-

sion will be within normal limits. A lesion thatprobes in this manner is in fact a sinus tract, andthe probing represents a typical sinus tract typeof probing.

The tooth is pulpless. Customary root canalprocedures are indicated. The lesion need nor becuretted or surgically flapped. It is strictly a sinustract similar to a sinus tract exiting in the alveolarmucosa or attached gingiva. Simply passing aperiodontal probe down through the sulcus alongthe lateral root surface of the tooth does notmean that a lesion is the result of periodontal dis-ease. When a sinus tract occurs over the lateralroot surface of a tooth, it will respond to rootcanal treatment like any other sinus tract. Typi-cally the orifice into such a sinus tract will closewithin 1 week after the cleaning and shapingappointment.

Occasionally this lesion will have the same typeof probing except that the sinus tract is muchwider than usual (Figure 26-9). In some instancesthe disruption in the gingival sulcus may be up to5 or 6 mm wide. There is no swelling in the area.

FIGURE 26-7A, This radiolucent lesion has the radiographic appearance of a periodontal lesion. Careful periodontal probingdemonstrates that the gingival sulcus is intact. B, The initial radiograph indicates bone loss from the crest of theridge around the apices of the tooth. Periodontal probing demonstrates that the gingival sulcus is intact. There isno response to pulpal tests. C, Root canal treatment completed. D, Four-year recall shows resolution of theradiolucency. (A from Harrington GW: Dent Clin North Am 23:673, 1979.)

Typically the sulcus probes within normal limitsto the very edge of the sinus tract, then falls offprecipitously to approach the apex of the tooth.Approximately the same depth is probed acrossthe entire 3 to 6 mm width of the sinus tract, and


47 7

then sharply at the demarcation of the sinus tractthe probing is again within normal limits.

There are some indications that the increasedwidth is associated with chronicity, although thishas not been documented. In any case, the treat-

478


FIGURE z6-sA, (Refer to Color Figure 26-2) A typical narrow sinus tractthrough the sulcus. B, The initial radiograph indicates boneloss from the crest of the ridge around the apices, includ-i ng the furcation. C, Sinus tract probing at the initial ex-amination. The sulcus is intact with the exception of thesinus tract. D, Root canal treatment completed. E, A 1-yearrecall shows resolution of the radiolucency. Probing iswithin normal limits. (A from Harrington GIN: Dent ClinNorth Am 23:673, 1979.)


479

FIGURE 26-9Periodontal probing of a typical wide sinus tract through thesulcus.There is no swelling in the area. (From Harrington GIN:Dent Clin North Am 23:673,1979.)

ment is once again nonsurgical root canal treat-ment. The lesion need not be curetted, and a sur-gical flap is not necessary for resolution. However,closure of the orifice into the sinus tract may re-quire somewhat more time than closure of a sim-ilar sinus tract of smaller width.

An exception to the above is a wide sinus tracttype of probing on the direct palatal surface ofmaxillary teeth. Experience has shown that thistype of probing does not resolve by root canaltreatment. In such instances, prognosis is deter-mined by the prognosis for the periodontal pro-cedure required to resolve such a defect.

Special consideration must be given to probingthe furcations of multirooted teeth. A verticalsinus tract type of probing in the furcation downthe distal aspect of the mesial root or the mesialaspect of the distal root of a pulpless mandibularmolar will respond to adequate root canal treat-ment by closure of the sinus tract. However, clo-sure may be somewhat slower in the furcationarea than on a lateral root surface of a tooth, andcomplete closure of the sinus tract may not occuruntil 2 to 3 months after obturation of the canals.Again, neither curettage nor a surgical procedurewill be required for resolution of a lesion with atypical sinus tract type of vertical probing in thefurcation. Although the example refers to a man-dibular molar specifically, the same holds true foreach furcation area of a maxillary molar.

Careful attention must also be given to probingthe furcation areas in a horizontal direction (Fig-ure 26-10). Because of the height of the soft tissue

FIGURE 26-10A, Vertical sinus tract type probing down the distal side ofthe mesial root in the furcation. B, Horizontal probing intothe furcation.

and the contour of the furcation, this proceduremay not be adequately carried out with a peri-odontal probe in many cases. A special curvedprobe or a thin periodontal curette may be requiredto follow the contour of the furcation to ade-quately explore the horizontal component of a fur-cation involvement. In many instances in whichthere is furcation involvement, there will be a hori-zontal as well as a vertical component to the lesion.

In younger patients, a lesion with a horizon-tal type of sinus tract probing in the furcationresolves with no complications after root canal

480


treatment. In older patients, if a lesion with ahorizontal component in the furcation is associ-ated with a pulpless tooth, resolution is unlikely.Although such lesions may occasionally fill inslowly after adequate root canal treatment, reso-lution of the horizontal component by means ofendodontic treatment alone occurs rarely in olderpatients. Therefore resolution of a lesion with ahorizontal probing into a furcation associatedwith a pulpless tooth must be viewed with skepti-cism in an older patient. The prognosis in suchcases should be determined by consideration ofthe typical periodontal criteria for determiningprognosis of a furcation involvement.

There are several other clinical situations inwhich a sinus tract type of probing may occur butdo not indicate a typical sinus tract. These excep-tions include the presence of enamel spurs, devel-opmental grooves, vertical root fractures, andperiodontal defects after trauma.

Enamel Spurs

Enamel spurs or extensions into the furcation areaof multirooted teeth usually are identified by visualexamination of the furcation during flap reflection.

Developmental Grooves

Developmental grooves occur most often on thelingual surface of maxillary lateral incisors but mayinvolve central incisors and less often other teeth.Developmental grooves are identified by carefulevaluation of radiographs, visual examination, andtactile discrimination. The pulp of a tooth with adeep developmental groove may become necroticand develop a periapical lesion. Adequate root canaltreatment will resolve the periapical lesion but willnot resolve the periodontal defect associated withthe developmental groove. Prognosis should be de-termined by the extent of the periodontal defect.


A sinus tract type of probing is not pathogno-monic of a vertical root fracture in a tooth thathas previously had root canal treatment, but asinus tract type of probing is very often associatedwith such fractures. Visual confirmation of a frac-ture is required to make the diagnosis. If a sinustract type of probing occurs on both the buccaland lingual aspects of such a root, it is highly sug-gestive of a vertical root fracture. The prognosisfor teeth with confirmed vertical root fracturesthat extend to the level of crestal bone is poor.

Similarly, a sinus tract type of probing may befound in the proximal areas of posterior teeth

that have incomplete coronal fractures that ex-tend into the roots. More information on theselongitudinal fractures is in Chapter 28.

Periodontal Defect After Trauma

Occasionally a sinus tract type of probing may beassociated with a tooth that has been involved in atraumatic incident. This defect usually occurs onthe lingual surface of anterior teeth. The tooth in-volved will usually respond within normal limitsto pulp testing procedures, although occasionallysuch traumatized teeth may not respond to pulptests for a period of time after trauma. The defectwill gradually resolve but may be present for aslong as several months after the impact injury. Notreatment is required for resolution of this lesion.

With the exception of the above four circum-stances, a sinus tract type of probing indicates alesion associated with a pulpless tooth. The sinustract may be coming from either a periapical orlateral lesion. Although it is rare, a sinus tract maydevelop through the periodontal ligament of atooth other than the tooth that is pulpless. Care-ful pulp testing reveals this situation. In such acase, adequate root canal treatment for the pulp-less tooth will resolve the sinus tract associatedwith the adjacent tooth.

In many instances, a sinus tract type of probingwill be associated with a lateral lesion involving apulpless tooth that has a root perforation or a re-sorptive lesion. Such lesions on the lateral surfaceof the root seem predisposed to development ofsinus tracts through the periodontal ligament. Asinus tract type of probing itself is not diagnostic ofsuch defects but should alert the clinician towardcareful evaluation for the cause of the sinus tract.

In all cases, a sinus tract should be considereda sign associated with the problem and shouldnot be considered to be a pathologic entity in it-self. If adequate endodontic treatment can beaccomplished, a sinus tract will resolve withoutany further definitive therapy directed toward itselimination. In summary, then, pulpal necrosis doesnot cause periodontal disease. It may cause the formationof a sinus tract througb the periodontal ligament. Boneloss resulting from pulpal necrosis is reversible. The pe-riodontal attachment apparatus will regenerate com-pletely after adequate root canal treatment.

INDEPENDENT PERIODONTAL ANDPERIAPICAL OR LATERAL LESIONSTHAT DO NOT COMMUNICATE

A tooth with periodontal disease may also be pulp-less and present with radiographic evidence of adiscrete periapical or lateral lesion (Figure 26-11).


481

FIGURE 26-11A, The lesion associated with the distal root surface hasthe conical-shaped probing of a typical periodontal lesion.A periapical lesion is evident. The lesions do not communi-cate. Prognosis is determined by the prognosis for resolu-tion of the periodontal pathosis. B, The initial radiographdemonstrates a large radiolucency involving the distal rootsurface. The radiolucency extends around the apices andup the mesial side of the mesial root. There is an angularcoronal radiolucency at the mesial root surface. Clinically,the mesial lesion probes in a conical manner. The conicall esion does not communicate with the apical radiolucency.There is also a narrow sinus tract type probing at the dis-tobuccal line angle. C, Completed root canal treatment.D, An 8-month recall shows marked reduction of the distalradiolucency caused by the necrotic pulp. Probing is withinnormal limits around the distal sulcus. E, The mesial lesionprobes in the same conical manner and to the same depthas before root canal treatment, indicating a periodontal le-

sion. (A from Harrington GW: Dent Clin North Am 23:673,

1979.)

482


FIGURE 26-12

A, Periodontal probing in a true combined perio-endo lesion. B, Communication between a periodontal lesionand a lesion caused by a necrotic pulp in a combined perio-endo lesion. C, Mandibular incisor with a large lesionat the distal. The lesion probed with a conical contour. Within the conical lesion there was a defect that probedto the apex, demonstrating communication. D, An 11-year recall demonstrates resolution of the lesion around theapex. An angular defect remains at the distal. (A and B from Harrington GW: Dent Clin North Am 23:673, 1979.)


483

The periodontal lesion probes in a manner consis-tent with the typical conical periodontal type ofprobing. The tooth is pulpless. The prognosis forthe tooth depends upon the periodontal progno-sis. Adequate root canal treatment will resolve thediscrete periapical or lateral lesion. Although bothperiodontal and periapical lesions are present, thefindings are not consistent with a true combinedperio-endo lesion as there is no demonstrablecommunication between the two lesions.

TRUE COMBINEDPERIO-ENDO LESIONS

True combined perio-endo lesions occur when in-dependent periodontal and periapical or laterallesions are present and do communicate. Eithersuch combined lesions are extremely rare, or thecriteria to make the discrimination have not beenfully elaborated. The typical combined perio-endolesion that can be identified presents radiographicevidence of bone loss, which appears to extendsome distance down the lateral root surface fromcrestal bone. Probing reveals the typical conicalperiodontal type of probing with the exceptionthat at the base of the periodontal lesion theprobe will abruptly drop farther down the lateralroot surface and may even extend to the apex ofthe tooth (Figure 26-12). The lesion can be char-acterized as a typical sinus tract type of probing atthe base of a periodontal lesion.

Adequate root canal treatment will resolve theperiapical lesion up to the extent of the periodon-tal lesion either with or without periodontal ther-apy. The overall prognosis for the tooth, there-fore, depends on the likelihood of resolution ofthe periodontal aspects of the lesion. In all suchinstances, if the periodontal prognosis is satisfac-tory, root canal treatment should be completedbefore initiation of definitive periodontal ther-apy. Otherwise, drainage from the periapical le-sion through the sinus tract into the periodontalaspect of the lesion will interfere with periodontalrepair if definitive periodontal therapy is initiatedbefore root canal treatment.

Basis for Patient Referral

When clinical diagnostic criteria as defined in thischapter are applied to dental patients, distinguish-ing between lesions of periodontal origin andthose resulting from pulpal necrosis is very oftenstraightforward. In many cases, however, discrimi-nations are difficult and appropriate treatmentplanning may prove to be quite complex. Requiredtreatment procedures and sequencing may also be

complicated. The interest of the patient is para-mount. If the etiology of a defect is unclear, a con-sultation with or referral to a specialist for appro-priate diagnosis and treatment is indicated.

REFERENCES

1. Mjbr IA, Nordahl 1: The density and branching ofdentinal tubules in human teeth, Arch Oral Biol 41:401,1996.

2. Garberoglio R, Brannstrbm M: Scanning electron mi-croscopic investigation of human dentinal tubules,Arch Oral Biol 21:355, 1976.

3. Furseth R, Mjbr IA: Cementum. In Mjbr I, PindborgJJ, editors: Histology of the human tooth, Copenhagen,1973, Munksgaard, Scandinavian University Books.

4. DeDeus DD: Frequency, location, and direction of thelateral secondary and accessory canals, J Endod 1:361,1975.

5. Kirkham DB: The location and incidence of accessorypulpal canals in periodontal pockets, J Am Dent Assoc91:353, 1975.

6. Vertucci FJ, Williams RG: Furcation canals in thehuman mandibular first molar, Oral Surg Oral Med OralPathol 38:308, 1974.

7. Gutmann JL: Prevalence, location, and patency of ac-cessory canals in the furcation region of permanentmolars, JPeriodontol 49:21, 1978.

8. Pineda F, Kuttler Y: Mesiodistal and buccolingualroentgenographic investigation of 7,275 root canals,Oral Surg Oral Med Oral Pathol 33:101, 1972.

9. Sjogren U, Hagglund B, Sundqvist G, Wing K: Factorsaffecting the long-term results of endodontic treat-ment,JEndod 16:498,1990.

10. Harrington GW, Natkin E: External resorption associ-ated with bleaching of pulpless teeth, J Endod 5:344,1979.

11. Madison S, Walton RE: Cervical root resorption fol-lowing bleaching of endodontically treated teeth,JEndod 16:570, 1990.

12. Rotstein I, Friedman S, Mor C, et al: Histological char-acterization of bleaching-induced external root re-sorption in dogs, JEndod 17:436, 1991.

13. Kornman KS, Robertson PB: Fundamental principlesaffecting the outcomes of therapy for osseous lesions,Periodontol 2000 22:22, 2000.

14. Jansson L, Ehnevid H, Lindskog S, Blomlof L: Rela-tionship between periapical and periodontal status. Aclinical retrospective study, J Clin Periodontol 20:117,1993.

15. Ehnevid H, Jansson L, Lindskog S, Blomlof LB: Peri-odontal healing in teeth with periapical lesions. A clin-ical retrospective study, J Clin Periodontol 20:254, 1993.

16. Jansson LE, Ehnevid H, Lindskog SF, Blomlof LB: Ra-diographic attachment in periodontitis-prone teethwith endodontic infection, J Periodontol 64:947,1993.

17. Ehnevid H, Jansson LE, Lindskog SF, Blomlof LB:Periodontal healing in relation to radiographic attach-ment and endodontic infection, J Periodontol 64:1199,1993.

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18. Jansson L, Ehnevid H, Lindskog S, Blomlof L: Theinfluence of endodontic infection on progression ofmarginal bone loss in periodontitis, J Clin Periodontol22:729, 1995.

19. Newman MG, Sanz M: Advanced diagnostic tech-niques. In Carranza FA, Newman MG, editors: Clinicalperiodontology, ed 8, Philadelphia, 1996, WB Saunders.

20. McGuire MK: Prognosis versus actual outcome: along-term survey of 100 treated periodontal patientsunder maintenance care,JPeriodontol62:51, 1991.

21. McGuire MK, Nunn ME: Prognosis versus actual out-come. 11. The effectiveness of clinical parameters in de-veloping an accurate prognosis, J Periodontal 67:658,1996.

22. McGuire MK, Nunn ME: Prognosis versus actualoutcome. III. The effectiveness of clinical parametersin accurately predicting tooth survival, J Periodontol67:666, 1996.

23. McGuire MK: Prognosis vs outcome: predicting toothsurvival, Compend Contin Educ Dent 21:217, 2000.

24. Jaoui L, Machtou P, Ouhayoun JP: Long-term evalua-tion of endodontic and periodontal treatment, IntEndod J 28:249, 1995.

25. Carnevale G, Di Febo G, Tonelli MP, et al: A retrospec-tive analysis of the periodontal-prosthetic treatmentof molars with interradicular lesions, Int J PeriodonticsRestorative Dent 11:188, 1991.

26. Basten CH J, Ammons WF, Persson R: Long-term eval-uation of root resected molars: a retrospective study,IntJPeriodonticsRestorative Dent 16:207, 1996.

27. Buhler H: Survival rates of hemisected teeth: an at-tempt to compare them with survival rates of alloplas-

tic implants, Int J Periodontics Restorative Dent 14:537,1994.

28. Carnevale G, Pontoriero R, Lindhe J: Treatment offurcation-involved teeth. In Lindhe J, Karring T, LangNP, editors: Clinical periodontology and implant dentistry,ed 3, Copenhagen, 1997, Munksgaard.

29. Adell R, Lekholm U, Rockler B, Branemark P-I: A15-year study of osseointegrated implants in the treat-ment of the edentulous jaw, Int J Oral Surg 10:387,1981.

30. Tagger M, Smukler H: Microscopic study of the pulpsof human teeth following vital root resection, Oral SurgOral Med Oral Patbol 44:96, 1977.

31. Ross IF, Thompson RH: A long term study of root re-tention in the treatment of maxillary molars with fur-cation involvement,JPeriodontol49:238, 1978.

32. Czarnecki RT, Schilder H: A histological evaluation ofthe human pulp in teeth with varying degrees of peri-odontal disease, JEndod 5:242, 1979.

33. Haskell EW, Stanley H, Goldman S: A new approach tovital root resection, JPeriodontol 51:217, 1980.

34. Bergenholtz G, Nyman S: Endodontic complicationsfollowing periodontal and prosthetic treatment of pa-tients with advanced periodontal disease, J Periodontol55:63, 1984.

35. Torabinejad M, Kiger RD: A histologic evaluation ofdental pulp tissue of a patient with periodontal dis-ease, Oral Surg Oral Med Oral Patbol 59:198, 1985.

36. Langeland K, Rodrigues H, Dowden W: Periodontaldisease, bacteria and pulpal histopathology, Oral SurgOral Med Oral Patbol 37:257, 1974.

COLOR FIGURE 27-1Orthodontic extrusion. A, Tooth with prior endodontic procedures experienced trauma, resulting in a deep shear-i ng fracture. B, Post space has been prepared, and a temporary post is cemented. C, A temporary crown is placed.An omega-shaped loop with elastic bands is attached to the TMS pin in the temporary crown. D, Extrusion is nearcompletion; occlusion of the temporary restoration is relieved as the tooth erupts. Extrusion is complete becausethe gingival margin of the TMS pin is level with interdental gingival margin of the anchorage wire. Note the levelof gingival margin on the facial surface. E, After several weeks of stabilization, periodontal surgery is necessaryto modify alveolar bone height and gingival contour. F, New position permits restoration with a permanent post,core, and crown. (Courtesy Dr. M. Messersmith.)

COLOR FIGURE 27-2Crown lengthening. A, Acrylic temporary crown on the first molar is encroaching on the lingual gingiva and bio-

l ogic width by extending to 0.5 mm from alveolar bone. B, After crown removal, full-thickness flaps were ele-vated, exposing a collar of excess tissue. C, Ostectomy and osteoplasty remove bone at the lingual and mesialsurfaces to a distance of at least 3 mm from the future crown margins. D, An apically positioned flap sutured; suf-ficient biologic width is now established. (From Freeman K, Bebermeyer R, Moretti A, Koh 5: l Gt Houst Dent Soc71:14, 2000.)

Endodontic Adjuncts

LEARNING OBJECTIVES


1 / Define the endodontic adjunct treatments described herein.

2 / Describe indications and contraindications for these treatments.

3 / Describe briefly the clinical technique, step-by-step, for each adjunct procedure.

4 / Discuss the prognosis for each adjunct procedure, both short-term and long-term.

s / Identify findings that would indicate failure both short-term and long-term.

6 / Identify the appropriate general treatment options if the adjunct treatment fails.

7 / Briefly describe what the treatment entails for the patient (time, orthodontic appliances, surgical trauma, and

so forth).

s / Determine when consultation is indicated to devise a treatment plan.

s / Determine when a patient should be referred to the appropriate specialist for treatment.

485

486

27 / Endodontic Adjuncts

Intentional Replantation

Definitions

Case Selection

Clinical Technique

Evaluation

Prognosis

Transplantation

Definitions

Case Selection

Clinical Technique

Evaluation

Prognosis

Orthodontic Extrusion

Definition

Case Selection

Clinical Technique

Evaluation

Prognosis

Crown Lengthening

Definition

Case Selection

Clinical Technique

Root Submersion

Definition

Case Selection

Clinical Technique

Evaluation

Prognosis

Endodontic Implants

Definition

Prognosis

ypes of therapy not performed rou-tinely but considered an integral partof endodontics include intentional re

plantation, transplantation, orthodontic extru-sion, crown lengthening, root submersion, andendodontic implants. Patients have changing pro-files and expectations. Their dental needs anddemands necessitate familiarity with treatmentsthat have been considered radical or last-resortoptions. This chapter discusses those options.Also included are case selection, a summary oftechniques, evaluation of success or failure, andprognosis.

The general practitioner may or may not per-form the procedures described in this chapter;however, the generalist should know the indica-tions and contraindications for such treatments,understand the techniques, and know how toapply this knowledge in case selection. Referralto an endodontict may then be considered, orthe general practitioner may choose to treat thepatient in accordance with his or her level oftraining and experience. Most important, thegeneralist needs to understand these proceduressufficiently to be able to explain them to thepatient, regardless of who performs the actualtreatment.

I ntentional Replantation

DEFINITIONS

Replntation is the return of a tooth to its alveolus.Intentional replantation is the insertion of a toothinto its alveolus after the tooth has been extractedfor the purpose of performing root-end surgery.'Replantation is not a new procedure; it was firstreported in 1593, when Pare replanted threeavulsed teeth .2

CASE SELECTION

Indications

These root canal treatments cannot be performedconventionally because of calcifications or otherblockages or because the patient cannot open hisor her mouth sufficiently. Also included are treat-ment failures that cannot be retreated by con-ventional means because of unusual anatomy(Figure 27-1); canals that are blocked with brokeninstruments, crowns, ledges, or restorative mate-rials such as posts; areas that are inaccessible; orroots that have unmanageable perforations. Ordi-narily, surgery would be indicated but cannot beperformed owing to anatomic restraints such asthe external oblique ridge or nerve bundle prox-i mity (inferior alveolar, lingual, or mental nerves).


487

FIGURE 27-1I ntentional replantation. A, Three years after root canaltreatment. Treatment has failed because the C-shapedcanal cannot be debrided and obturated. Periapical sur-gery is not feasible. B, After extraction, the tooth is keptmoist with gauze soaked in sterile saline. After root-endresection note the C-shaped canal system (arrows).C, Root-end preparation and amalgam placement im-

mediately before replantation. D, Radiograph of thereplanted tooth showing it to be in the correct position.E, Three-year recall: the tooth is stable and functional.Long-term prognosis is good. (Courtesy Dr. T. Erickson.)

488


In essence, intentional replantation is indicatedwhen there is no other treatment alternative tomaintain a strategic tooth (Figure 27-1, A).

of the day. He or she may release for short periodsto ingest soft foods; fluids are taken through astraw.

Contraindications EVALUATION

Intentional replantation is not a substitute for endo-dontic surgery if that procedure can be successfullyperformed. Replantation is contraindicated in pa-tients who have a major comminution or fractureof the jaws or alveolus or an extensive medical his-tory resulting in poor healing capacity. Replanta-tion is not indicated for a tooth with advancedperiodontal disease with mobility or furcation in-volvement. Caution is the rule for extractions ofteeth if there is a strong possibility of fracturingthe tooth or supporting bone.

CLINICAL TECHNIQUE

Important for success of this procedure are mini-mizing the out-of-socket time for the extractedtooth and minimizing damage to the root sur-face while the tooth is held. Adherence to theseprinciples will decrease periodontal ligament celldeath and decrease future ankylosis/resorption.The procedure of replantation involves first anes-thesia, then luxation, and then gentle extractionwith forceps that do not damage the root surfacecervically. The tooth is held carefully by the crownin saline-soaked gauze and inspected closely forfractures, perforations, or other damage. Threeto 4 mm of the apex is resected with a high-speedfissure bur using copious saline irrigation (Fig-ure 27-1, B). An apical root-end preparation ismade with small burs or an endodontic ultrasonichandpiece. This is followed by condensation of aroot-end filling material (Figure 27-1, C). It is im-portant not to damage the root and to keep thetooth moist, thus maintaining viable cells on theroot surface. Apical pathosis may be curetted, tak-ing care not to damage the socket walls; however,this procedure is probably unnecessary. The toothis then carefully replanted, usually with finger orwith forceps.

A perforation, resorptive defect, or other prob-lem also may be repaired after extraction and be-fore replantation using similar techniques.

Stabilization (if needed) after replantation maybe done with sutures and/or a periodontal pack-ing or with an acid-etch composite and orthodon-tic wire splinted to adjacent teeth; the splint is re-moved within 7 to 14 days. A radiograph is madeimmediately after replantation (Figure 27-1, D).

A very effective and simple stabilization ap-proach is to have the patient close in centric oc-clusion and hold this position for the remainder

Recall evaluations are performed to search forsigns of mobility, periodontal defects, root resorp-tion, persistent periradicular pathosis, and evi-dence of healing (Figure 27-1, E).

PROGNOSIS

Intentional replants tend to be more successfulshort-term than long-term. Usually connectivetissue and epithelial reattachment and stabiliza-tion occur initially. Problems may appear later,sometimes after several years.

However, intentional replants often are suc-cessful long-term. Some authors," includingGrossman,5 have reported good success rates for5 years or more. Factors affecting prognosis in-clude the time the tooth is out of the socket,damage to the socket wall or roots, or problemsduring extraction.

Serious complications include periodontaldefects or, most often, ankylosis with severe re-placement resorption. Thus long-term follow-up is necessary. 6.7 If these problems develop, ex-traction is indicated.

TransplantationDEFINITIONS

Transplantation is the transfer of a tooth from onealveolar socket to another either in the same or inanother person.' An autogenous transplant is thetransfer of a tooth from one alveolar socket to an-other in the same patient.8.9 Homogeneous (allo-geneic) transplantation is the transfer of a toothfrom one patient to another. This can be per-formed immediately or after storage of the toothin physiologic media or with cryopreservation."Heterogeneous transplantation is a transfer fromone species to another (for example, from monkeyto human)"; this process is not feasible clinically.

CASE SELECTIONIndications

Usually autogenous tooth transplants involvethird molars or premolars. Canine or incisor loca-tions that were congenitally missing or lost owingto caries, trauma, juvenile periodontitis, or im-paction are often the recipient sites for trans-planted premolars. Posterior teeth may be re-

placed after extraction because of severe caries ora procedural accident (Figure 27-2).

A transplanted tooth should possess an intactcrown. Ideally, there is partial root formation ap-proximately equal to crown length, althoughteeth with more developed roots may also be can-didates to transplant. Donor dimensions shouldbe similar to those of the recipient site. An imma-ture root often has an epithelial root sheath; pulpsurvival and root formation may then continue.Transplants of donor teeth with partial root de-velopment generally are easier and have a betterprognosis; usually the pulps survive.

Contraindications

The same systemic contraindications apply aswith intentional replantation. Local considera-tions are anatomic and may prevent transplan-


489

tation. For example, a relatively narrow alveolarridge may not accommodate a molar with diver-gent roots.

CLINICAL TECHNIQUE

Transplantation involves four steps: (1) at the re-cipient site, extraction and/or surgical preparationof the socket to receive the transplant; (2) extrac-tion and placement of the transplant; (3) stabiliza-tion; and then (4) root canal treatment (if needed).

Socket Preparation

Preparation of the recipient socket is related totransplant shape as well as to time. If root mor-phology and length are similar and the extractionis performed at the same visit, the recipient socketoften requires minimal preparation (Figure 27-3).

FIGURE 27-2Transplantation. A, First molar requires extraction because of a large furcation perforation. B, Earlier panelipseradiograph shows a partially erupted third molar with root formation almost complete-a suitable donor. Thethird molar is transplanted to the first molar site after extraction. C, Two years post-transplantation. The donor isi n occlusion and the pulp responds to pulp testing. (Courtesy Dr. H. Perinpanayagam.)

490


FIGURE 27-3Transplantation. A, Tooth 30 is unsalvageable. B, Removalof tooth and interradicular bone to accommodate trans-plant. C, Tooth 32 after extraction. Note the root surface;soft tissue remnants are undisturbed. D, Tooth 32 immedi-ately after transplantation to extraction site of tooth 30.E, Cross suture maintains the position of transplant allow-i ng physiologic movement. F, After transplantation. G, Sixmonths post-transplantion after interim calcium hydroxidetherapy and root canal obturation with gutta-percha. Be-cause access is minimal and the crown is relatively intact,only an amalcore is needed. Careful monitoring is neces-sary; bone is forming apically, but there is evidence of fur-cal bone resorption. Prognosis is questionable. (CourtesyDr. L. Wilcox.)

If transplantation is done at a separate appoint-ment from socket preparation, or if socket sizeand transplant size do not match, the socket re-quires shaping. This is best accomplished with anelectric slow-speed handpiece and copious salineirrigation. Socket size is measured and comparedto transplant size with a periodontal probe, andthe socket is surgically adjusted until a fit is ob-tained. The tooth is placed gently in the socketand stabilized (see under "Intentional Replanta-tion") if necessary.

If the area to receive the transplant is edentu-lous, preparation of both soft and hard tissue isnecessary. A full-thickness flap is elevated fromthe alveolar crest buccally and lingually. Osseoustissue is removed (as in socket preparation) toallow the transplant to fit passively but snugly inthe socket.

Extraction

Extraction should be performed as atraumaticallyas possible to maintain periodontal ligament fibersand cells. After extraction the donor site is managedcarefully. The transplanted tooth is kept moist bywrapping and holding it in saline-soaked gauze.

TransplantationThe prepared socket is rinsed with sterile saline.The tooth is gently positioned in the socket andthe flap is sutured snugly.

Stabilization

if the transplant exhibits mobility (usually) or ifcontinued hemorrhage causes supraeruption, sta-bilization should be used to maintain the toothin position, as with replantation. An alternativemethod is to suture over the occlusal surface andplace periodontal packing. Certain situations mayrequire more elaborate long-term splints, such aswire and bonded composite.

Follow-up

Conventional postsurgical instructions are given.The patient should return in 7 to 10 days for eval-uation of healing and splint removal. If the trans-plant has roots that are incompletely developed,periodic radiographic evaluation is performed at3- to 6-month intervals to monitor development.Arrested development and appearance of a re-sorptive lesion is a sign of pulp necrosis, requiringroot canal treatment.

Teeth with fully developed roots require rootcanal treatment soon after transplantation. The

protocol is similar to that used for traumaticallyavulsed and replanted teeth (see Chapter 25).After stabilization, the canals should be cleaned,shaped, and obturated, and the tooth is restored.Calcium hydroxide placement is probably unnec-essary. This agent was once believed to inhibitroot resorption, but evidence indicates that this isnot true.12

EVALUATION

Transplants may not manifest signs of failure(periodontitis or resorption) for several years.Therefore, they should be evaluated clinically andradiographically for a minimum of 5 years for evi-dence of pathosis. The criteria for success are ab-sence of pathosis, no adverse signs and symptoms,and no evidence of severe progressive external re-sorption (which is common in transplants).

Pulps that become necrotic in a transplantdonor with immature roots require root-endclosure (see Chapter 22) followed by root canaltreatment.

PROGNOSISThe prognosis for autogenous transplants varieswidely.13.14 Factors identified as most importantfor success are preservation of the periodontiumon the roots and socket walls, developmentalroot stage (immature roots are best), and loca-tion of the donor tooth in the arch. The ipsilat-eral or contralateral third molar is the donortooth of choice for replacement of molars.15 Pre-molars can replace premolars or anterior teeth."Failure of transplantation (replacement resorp-tion, periodontal lesions, or adverse signs andsymptoms) requires extraction.

Orthodontic ExtrusionDEFINITION

Orthodontic extrusion is defined as forced-controlledvertical tooth movement occlusally in the socket."Vertical orthodontic repositioning after root canaltreatment has been suggested in situations in whichloss of tooth structure cervically makes restora-tion and periodontal maintenance impossible."Through extrusion the area in question becomes ac-cessible for restoration; thus surgery (which oftencreates a periodontal defect) is avoided. However,because gingival tissues and alveolar bone of the ex-truding tooth move coronally, a surgical periodon-tal procedure is often needed to reestablish biologicwidth and to restore the tooth's normal bony andgingival contour.19.20 These procedures tend to be


491

492


complex and may require cooperative treatment bythe generalist, endodontist, periodontist, prostho-dontist, and orthodontist.

CASE SELECTION

Indications

Indications are subgingival pathoses that are un-treatable by standard restorative techniques, in-cluding coronal or root fractures in the cervicalarea, caries, deep marginal preparations, periodon-tal defects, resorptive lesions, and perforations.19.20Some of these lesions may be corrected by crownlengthening; however, the resultant periodontaldefect may be impossible to treat or may be unat-tractive or unmaintainable. In these situations, ex-trusion provides a more desirable treatment andrestorative environment. Orthodontic extrusion isalso a common indication prior to implant place-ment. Forced occlusal movement results in an in-crease in vertical bone height, thereby providingmore implant support. The tooth is first extruded,then extracted.

Contraindications

Orthodontic extrusion should not be consid-ered if (1) there is such extensive loss of struc-ture that vertical extrusion would result in apoor crown-root ratio or (2) the new tooth posi-tion would expose and create unmanageablefunation problems.

Other Considerations

An additional factor is patient acceptance of theprocedure, because orthodontic appliances are in-volved. Time and expense may also be factors; the

tooth has to be orthodontically repositioned andthen stabilized before it is restored. Finally, arestoration may be somewhat difficult to designbecause the available root surface is smaller andmay have proximal concavities.

Alternative treatment options include sur-gical crown lengthening, surgical repositioningof the tooth, and extraction with prostheticreplacement.

CLINICAL TECHNIQUE

The technique involves several phases: (1) rootcanal treatment, (2) post space preparation, (3) postand core fabrication with a hook on the occlusalsurface (or a pin or bracket on the facial surface),(4) extrusion, (5) crown lengthening, (6) stabiliza-tion, and (7) restoration. Adjacent teeth function asanchors during extrusion or, in some cases, a re-movable appliance is used. After root canal treat-ment various approaches can be used depending onthe situation.

One technique is a modification of the T-loopto prevent tipping (Figure 27-4) . 2 ' A more com-mon approach is to fabricate a hook to accom-modate an orthodontic appliance or elastic. Alarge-gauge wire with an occlusal hook may beused as a temporary post. Brackets are placed onthe facial surfaces of adjacent teeth. A horizontalwire engages the brackets, and the hook is acti-vated to exert a vertical extrusive force. Alterna-tively, an orthodontic wire is bonded to the facialsurfaces and an elastic force is used (see Color Fig-ure 27-1 immediately following page 484). If thefacial surface of the tooth to be extruded is intact,a post and hook may not be necessary. A bracketis bonded to the enamel and abutments, and thehorizontal wire is attached to all brackets.

FIGURE 27-4A, Orthodontic appliance used for extrusion; this is not a good design because it tends to tip adjacent teeth intothe extrusion site. B, T-loop appliance used for extruding a terminal tooth. This design prevents tipping of anchors.(From Tuncay 0, Cunningham C: J Endod 8:368, 1982.)


493

The patient should be evaluated often (every1 to 2 weeks) during eruption. The tooth usuallymoves quickly; the occlusion usually requires ad-justing, or the wire may have to be reactivated.The forced eruption period lasts approximately4 to 6 weeks. Alveolar crestal bone and gingivausually move coronally with the tooth. Periodon-tal procedures (bony recontouring or gingivec-tomy) may be required during or after orthodon-tic extrusion to correct gingival contours. Theseprocedures may be unnecessary or minimized if,during extrusion, an intrasulcular incision (gingi-val fiberotomy) of the supracrestal attachment isperformed every 2 weeks . 22

Stabilization with a passive arch wire is re-quired for 6 to 8 weeks to prevent intrusion. Thisallows time for the periodontal tissues to estab-lish new attachments . 23

The area involved is often of cosmetic concern.The following techniques improve appearance dur-ing movement and stabilization. Hollow-groundacrylic or a natural crown may be positioned faciallyto the root. Also, removable appliances may replacethe missing tooth structure without interferingwith movement 24 When extrusion is complete andgingival appearance is satisfactory, the tooth is per-manently restored. Importantly, the patient mustbe trained to follow special oral hygiene proceduresboth during and after movement and restoration.

EVALUATION

The patient should be recalled periodically. Aminimal follow-up period is 1 year; however, long-term evaluation is recommended. Both radio-graphic and clinical examinations are necessary toassess periodontal status and mobility and checkfor the presence of caries as well as for periradicu-lar pathoses.

PROGNOSIS

The outcome of orthodontic extrusion is good,provided periodontal attachment remains intactand the crown-root ratio is acceptable.25 Becauseperiodontal ligament fibers are reorganized (but

not destroyed) during extrusion and alveolarbone moves with the tooth, root resorption israrely a problem.25 Developing periradicular andperiodontal pathoses usually are correctable.Again, meticulous oral hygiene is critical.

Crown LengtheningDEFINITION

Crown lengthening is a surgical procedure used toincrease the extent of supragingival tooth struc-ture for restorative or esthetic purposes. The basicprocedure is apical positioning of the gingivalmargin and/or reducing cervical bone . 26

CASE SELECTION

Indications

Crown lengthening is generally used for restoringteeth with subgingival defects such as caries, per-forations, or resorptions. Other indications arecosmetic factors or short clinical crowns that maybe lengthened to improve retention and appear-ance. To repeat, with orthodontic extrusion, theperiodontium usually accompanies the tooth;surgical crown lengthening is necessary for ap-pearance and function.

I mpingement by restoration margins on the at-tachment apparatus may result in inflammation,pain, and loss of periodontal attachment (see ColorFigure 27-2 immediately following page 484) .2'Margins should not be placed near or at the alveo-lar crest. Preferably, the relationship should allow atleast 2 mm of root surface between the alveolar crestand the restoration; such is the concept of the "bio-logic width. "28 Biologic width (Figure 27-5) has twocomponents cervical to the margin of the alveolarcrest, each averaging 1 mm in width: (1) the con-nective tissue attachment and (2) the epithelial at-tachment.29 Sulcus depth varies.

Many factors are considered in planning treat-ment. These include extent and location of frac-tures, perforations, caries, root length, periodon-tal support, periodontal status of adjacent teeth,tooth position, and esthetics.

FIGURE 27-5Levels of factors related to biologic width. Each anatomic division is approximately 1 mm.

494


Contraindications

Usually adverse factors can be determined beforethe procedure is undertaken. However, occasion-ally some situations are encountered during sur-gery, including creation of an unattractive gin-gival deformity, production of an unfavorableroot-to-crown ratio, compromise of bone supportfor adjacent teeth, and exposure of the furcation.

CLINICAL TECHNIQUE

Root SubmersionDEFINITION

Root submersion is a surgical procedure in whichthe tooth roots are resected approximately 3 mmbelow the alveolar crest and then covered with amucoperiosteal flap. Eventually the area is shapedby hard tissue. Root submersions are generally notcomplex; the more straightforward proceduresmay be managed by the general practitioner.

Studies have shown no correlation between thewidth of the attached gingiva and periodontalhealth except in association with restorations;however, the attached gingiva should not be in-discriminately removed .30.32 In patients with sub-gingival restorations it is recommended that atleast 2 mm of attached keratinized gingiva be leftto maintain periodontal health and protect therestoration.33 This requires an internal bevel inci-sion with elevation of a full-thickness flap. Thencrestal bone is removed to at least 2.5 to 3.0 mmbelow the level of the free gingival margin desired(Figure 27-G). Thorough root planing follows theosteotomy. Then the flap is sutured at this level(apical to its original height).

On anterior teeth, for esthetic purposes, crownpreparation should be delayed for approximately14 weeks after surgery. The best method of deter-mining preparation time is to measure from theprovisional crown margin to the free gingivalmargin; final restoration is done when the areawithin this measurement has stabilized for atleast 1 month .34 Posterior crown preparation maybe done 2 to 4 weeks after crown lengthening be-cause appearance is not a factor, and crown mar-gins are supragingival.

CASE SELECTION

Indications

After tooth extraction the alveolar ridges resorb,approximately 0.1 mm/yr for the maxilla and0.4 mm/yr for the mandible .35.36 Alveolar bone re-sorption is prevented by maintaining the roots.Proprioception is also retained . 3 ' Three consider-ations related to root submersion are (1) rootswith vital pulps,38 (2) root canal treatment insitu,39 and (3) root canal treatment after extrac-tion and replantation to encourage ankylosis."The first method has been most successful be-cause it results in a blending of healthy pulpaltissue with overlying connective tissue followedby osteodentin covering the root face and even-tual bone formation. The second technique hasshown similar results in some patients. The thirdmethod shows little promise because no boneforms coronally and many roots are resorbed.

Conditions that indicate root submersion in-clude rampant caries, poor periodontal condi-tions, poor oral hygiene, and repeated prostheticfailures. These types of conditions tend to be seenin aged, medically compromised or handicapped,or financially compromised patients who require

FIGURE 27-6

Crown lengthening after orthodontic extrusion. A, Full-thickness flap exposes bony margin. B, Reduction andrecontouring of crestal bone reestablishes biologic width. Often some removal of bone from adjacent teeth isnecessary.


49 5

denture support and have a need for propriocep-tion. Roots are occasionally retained when extrac-tion would produce surgical or esthetic defects(Figure 27-7).

fenestration is likely. These patients often developa soft tissue fenestration with root exposure (fail-ure) at varying times after root submersion, whichrequires resubmergence or extraction.

Contraindications CLINICAL TECHNIQUE

Root resorption, unresolved endodontic pathosis,and inadequate bone support are contraindica-tions. Loss of vestibular depth may result fromsurgery (which may interfere with prosthetic re-tention and use); this may be treated with vestibu-loplasty or a free gingival graft. An anatomicproblem occurs when the facial gingiva is thin,the root is prominent, and a bony dehiscence or

Preferably, healthy pulp should not be removedbefore submersion. However, in patients withpulp or periradicular pathosis, root canal treat-ment is first necessary. Both situations require asimilar surgical approach. An inverse beveled in-trasulcular incision is made to remove the sulcu-lar (or pocket) epithelium. A mucoperiosteal flap,extending both buccally and lingually, is elevated

FIGURE 27-7Root submergence. A, Carious, partially impacted max-illary canine tooth (arrow). B, Flap is reflected, and thenroot canal treatment is performed because of pulppathosis. The root is submerged by bur reduction 3 mmbelow the alveolar crest and the flap is sutured forprimary closure. C, Postendodontic treatment, submer-sion, and amalgam seal.

496


far enough apically to allow reapproximation (pri-mary closure) of the flap margins. The root is re-sected at least 3 mm below the alveolar crest. If thepulp is to be retained, the resection is done withcopious water spray and gentle reduction. If rootcanal treatment was performed, an amalgam sealmay be placed in the canal, although this is gener-ally unnecessary.

Flap margins are apposed (primary closure)with mattress sutures. Postoperative instructionsare the same as those given for surgical extrac-tions (Figure 27-7). Sutures are removed in 5 to7 days.

EVALUATION

Postoperative evaluation is critical and is recom-mended initially every 3 months for 1 year; there-after, recall is performed yearly. Failures generallyresult from four factors: (1) flap breakdown im-mediately after the procedure; (2) denture im-pingement with ulceration and fenestration (rootexposure) through overlying tissue; (3) passive

eruption or crestal bone resorption, also resultingin soft tissue fenestration; and (4) obliteration ofthe vestibule. This decrease in vestibular depth isa major disadvantage of this technique because itlimits prosthesis retention.

PROGNOSIS

Short-term success tends to be much better thanlong-term success. Good results continue for anaverage of about 2 years, after which the rate offailure increases.41 Success with vital pulp rootsubmersion is higher than when the roots haveroot canal treatment; the latter have an overallmoderate success rate . 42 Presently, root submer-sion cannot be recommended as a routine proce-dure, but for selected patients it is a practicalmeans of retaining alveolar bone .43

The major reasons for failure are soft tissuefenestration with exposure of roots or loss ofvestibular depth. Endodontic failure with apical orcoronal pathosis may occur as well. Failures gener-ally require surgical removal of the tooth or reop-eration to submerge the root further into bone.

Endodontic ImplantsDEFINITION

FIGURE 27-8Seventeen years after implant placement. Note the apical radio-lucencies. There is a sinus tract associated with tooth 9, anddeep probing defects. Despite eventual failure, the implantsserved the patient for many years. (Courtesy Dr. S. Madison.)

Endodontic implants are metallic extensions of atooth root using a post prepared for that purpose.The tooth first has root canal treatment, then ametallic post is placed into the canal and out theapex, extending beyond the root apex and in-serted into a previously prepared channel in bone.The purpose is to increase the root-crown ratio,thus stabilizing the tooth. A potential advantageover osseous integrated implants is the absence ofcommunication (direct contact) of a materialwith the tissues of the oral cavity; epithelium andconnective tissue remain attached to the toothsurface.44 Offsetting major disadvantages are thedifficulty of achieving anatomic adaptability andcreating and maintaining an apical seal of theimplant.

PROGNOSIS

Under good conditions, the success rate for en-dodontic implants is reasonable for several years,but they usually show problems with time .

44,45

Usually the initial evaluation is very good; thetooth feels solid, and periradicular findings arefavorable. These positive findings generally donot persist and with time periodontal lesions,increasing mobility, or periradicular pathosis(often) may be seen (Figure 27-8). Long-term


497

failure is often related to coronal or apical teak-age 46.47 or periodontal communication with theapex . 48 The poor long-term prognosis for en-dodontic implants has discouraged their use.Most patients are now treated with extractionand immediate insertion of a single-tooth os-seous integrated implant.

REFERENCES

1. American Association of Endodontists: An annotatedglossary of terms used in endodontics, ed 6, Chicago, 1998,American Association of Endodontists.

2. Kupfer 1J, Sidney R, Kupfer BS: Tooth replantation fol-lowing avulsion, NY State Dent) 19:80, 1952.

3. Kingsbury BC, Wiesenbaugh JM: Intentional replanta-tion of mandibular premolars and molars, J Am DentAssoc 83:1053, 1971.

4. Bender I, Rossman L: Intentional replantation of en-dodontically treated teeth, Oral Surg Oral Med OralPatbol76:623, 1993.

5. Grossman L: Intentional reimplantation of teeth, JAmDentAssoc 72:1111, 1966.

6. Holland G, Robinson P: Pulp reinnervation in reim-planted canine teeth of the cat, Arch Oral Biol 32:593,1987.

7. Andreasen J: Atlas of replantation and transplantation ofteeth Philadelphia, 1992, WB Saunders.

8. Apfel H: Autoplasty of enucleated perfunctional thirdmolars, J Oral Surg 8:289, 1950.

9. Miller HM: Transplantation: a case report, J Am DentAssoc 40:237, 1950.

10. Andreasen J, Schwartz O: Atlas of replantationand transplantation of teeth, Philadelphia, 1992, WBSaunders.

11. Natiella J, Armitage J, Green G: The replantation andtransplantation of teeth: a review, Oral Surg Oral MedOral Pathol 23:397, 1970.

12. Dumsha T, Hovland E: Evaluation of long-term cal-cium hydroxide treatment in avulsed teeth, Int Endod J28:7, 1995.

13. Tsukibashi M: Autogenous tooth transplantation: areevaluation, Int J Periodontics Restorative Dent 13:121,1993.

14. Akiyama Y, Fukuda H, Hashimoto K: A clinical and ra-diographic study of 25 autotransplanted molars, J OralRebabil 25:640, 1998.

15. Andreasen J: Third molar autotransplantation relationbetween successful healing and stage of root develop-ment at time of grafting. Presented at the annualmeeting of the Scandinavian Association of Oral andMaxillofacial Surgeons, Nyborg, Denmark, August IS-19, 1990.

16. Andreasen J, Paulsen H, Yu Z, et al: A long-term studyof370 autotransplanted premolars. Part 11. Tooth sur-vival and pulp healing subsequent to transplantation,EurJOrtbod 12:14, 1990.

17. Berglundhl T, Marinello CP, Lindhe J, et al: Periodon-tal tissue reactions to orthodontic extrusion: an exper-imental study in the dog, J Clin Periodontol 18:330,1991.

18. Heathersay G: Combined endodontic orthodontictreatment of transverse root fractures in the region ofthe alveolar crest, Oral Surg Oral Med Oral Pathol 36:408,1973.

19. Stevens H, Levine R: Forced eruption: a multidiscipli-nary approach for form, function, and biologic pre-dictability, Compend Contin Educ Dent 19:994, 1998.

20. Ingber J: Forced eruption. Part I. A method of treatingisolated one and two walled infrabony osseous defectsrationale and case report, JPeriodontol 45:199, 1974.

21. Tuncay O, Cunningham C: T-loop appliance inendodontic-orthodontic interactions, J Endod 8:367,1982.

22. Kozlorsky A, Tal H, Lieberman M: Forced eruptioncombined with gingival fiberotomy: a technique forclinical crown lengthening, J Clin Periodontol 15:534,1988.

23. Simon J, Lythgoe J, Torabinejad M: Clinical and histo-logical evaluation of extruded endodontically treatedteeth, Oral Surg Oral Med Oral Pathol 50:361, 1980.

24. Delivanis P, Delivanis H: Esthetic solutions in ortho-dontic extrusion of compromised teeth, J Endod 10:221, 1984.

25. Hamilton R, Gutmann J: Endodontic-orthodontic re-lationships: a review of integrated treatment planningchallenges, Int Endod J 32:343, 1999.

26. American Academy of Periodontology: Glossary of peri-odontal terms, ed 3, Chicago, 1992, American Academyof Periodontology.

27. Freeman K, Bebermeyer R, Moretti A, Koh S: Single-tooth crown lengthening by the restorative dentist: acase report, J Gt Houst Dent Soc 71:14, 2000.

28. Eissman H, Radke A, Noble W: Physiologic designcriteria for fixed dental restoration, Dent Clin North Am15:543, 1971.

29. Gargiulo A, Wentz F, Orban B: Dimensions and rela-tions of the dentogingival junction in humans, J Peri-odontol 32:261, 1961.

30. Hangorsky W, Bissada N: Clinical assessment of freegingival grafts' effectiveness on the maintenance ofperiodontal health, JPeriodontol 51:274, 1980.

31. Dorfman H, Kennedy J, Bird W: Longitudinal evalua-tion of free autogenous gingival grafts, J Clin Periodon-

tol 7:316, 1980.32. Wennstrom J, Lindhe J, Myman S: Role of keratinized

gingiva for gingival health, J Clin Periodontol 8:311,1981.

33. Statler K, Bisada N: Significance of the width of kera-tinized gingiva in the periodontal status of teeth withsubmarginal restorations, JPeriodontol 58:698, 1987.

34. Wise MD: Stability of gingival crest after surgery andbefore anterior crown placement, JProstbetDent 53:20,1985.

35. Tallgren A: The continuing reduction of the residualalveolar ridges in complete denture wearers: a mixedlongitudinal study covering 245 years, J Prosthet Dent27:120, 1972.

36. Atwood D, Clay KW: Clinical cephalometric and den-sitometric study of reduction of residual ridges, J Pros-thetDent26:280, 1971.

37. Simpson HE: Histologic changes in retained roots, JCan Dent Assoc 25:287, 1989.

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38. Poe GS, Johnson DL, Hillenbrand DJ: Vital root reten-tion in dogs, Technical report 019, Bethesda, MD,1971, Naval Dental School.

39. Bjorn H, Hollender L, Lindhe J: Tissue regeneration inpatients with periodontal disease, Odontol Rev 16:317,1965.

40. Simon JH, Kimura JT: Maintenance of alveolar bone bythe intentional replantation of roots, Oral Surg OralMed Oral Pathol 37:963, 1974.

41. Goska FA, Vandrak RK: Roots submerged to preservealveolar bone: a case report, Milit Med 137:446, 1972.

42. Whitaker DD, Shankle RJ: A study of the histologicreaction of submerged root segments, Oral Surg OralMed Oral Pathol 37:819, 1974.

43. Wallace J, Carman J, Jimenez J: Endodontic therapyand root submergence of an impacted maxillary ca-nine, Oral Surg Oral Med Oral Pathol 77:519, 1994.

44. Madison S, Bjorndal A: Clinical application of en-dodonticimplants, JProsthetDent 5:603, 1988.

45. Cranin AN, Robin MF: A statistical evaluation of 952endosteal implants in humans, J Am Dent Assoc 94:315,1977.

46. Frank AL, Abrams MF: Histologic evaluation of en-dodontic implants, JAm DentAssoc 78:520, 1969.

47. Simon JH, Frank AL: The endodontic stabilizer: addi-tional histologic evaluation, JEndod 6:450, 1980.

48. Perel ML: Dental implantology and prosthesis, Philadelphia,1977, JB Lippincott.

Longitudinal Tooth Fractures

LEARNING OBJECTIVES


1 / Define and differentiate craze line, cusp fracture, cracked tooth, split tooth, and vertical root fracture.

2 / Describe the causes of these fractures of tooth structure.

a / List and describe the five considerations (characteristics) of fractures in dentin.

4 / Describe in general each of the five categories of fracture in regard to

a. Incidence

b. Pathogenesis

c. Clinical features

d. Etiologies

e. Diagnosis

f. Treatment

g. Prognosis

h. Prevention

s / Identify patients with difficult situations who should be considered for referral.

499

500

28 / Longitudinal Tooth Fractures

Incidence

Categories

Craze Lines

Fractured Cusp

I ncidence

Pathogenesis

Clinical Features

Etiologies

Diagnosis

Treatment

Prognosis

Prevention

Cracked Tooth

I ncidence

Pathogenesis

Clinical Features

Etiologies

Diagnosis

Treatment

Prognosis

Prevention

Split Tooth

I ncidence

Pathogenesis

Clinical Features

Etiologies

Diagnosis

Treatment

Prognosis

Prevention


I ncidence

Pathogenesis

Clinical Features

Etiologies

Diagnosis

Treatment

Prognosis

Prevention

racked teeth and their related en-tities as well as vertical root fracturesare longitudinal fractures of the crown

and/or root. These contrast with horizontal frac-tures, which predominate in anterior teeth and re-sult from impact trauma. Longitudinal (vertical)fractures occur in all tooth groups and are causedby occlusal forces and by dental procedures.

There is relatively little research on longitudinaltooth fractures, particularly on clinical outcomesrelated to diagnosis and treatment. Most treatmentmodalities are based on opinion and anecdotalinformation:' Therefore many recommendationshave not been substantiated in controlled clinicaltrials but are based on experience. This chapterdeals with longitudinal fractures in the verticalplane, that is, the long axis of the crown or root.

Treating longitudinal fractures is usually chal-lenging. Sometimes they are not difficult to diag-nose or manage, whereas at other times they are sodevastating that the involved tooth must be ex-tracted. Notwithstanding, many situations presentproblems with both diagnosis and treatment andthese patients should be considered for referral.

I ncidence

The incidence of longitudinal fractures is appar-ently increasing. There are several reasons for thisunfortunate occurrence. One is the increasing ageof patients with decreased numbers of tooth ex-tractions. Therefore more teeth undergo complexprocedures and are present for longer periods oftime. These procedures include restorative and en-dodontic treatments that remove dentin, therebycompromising internal strength. Also, the teethabsorb external forces, usually occlusal, that ex-ceed the strength of dentin and gradually altertooth structure. When the destructive force is be-yond the elastic limit of dentin or enamel, a frac-ture occurs .2; Therefore the longer a tooth is pre-sent and the more forces it undergoes, the greaterthe chances of an eventual fracture. Another rea-son for the increased incidence is more awarenessand better diagnosis and identification of theproblem. Importantly, such fractures are not con-fined to elderly patients and do not occur only inrestored teeth. 4-6

Categories

There are five categories of longitudinal fractures.From least to most severe they are (1) craze lines,(2) fractured cusp, (3) cracked tooth, (4) splittooth, and (5) vertical root fracture. These types offracture differ but they are often confused or

combined in clinical articles.7 - 10 This leads to mis-understanding, with incorrect diagnosis and in-appropriate treatment. Table 28-1 identifies fourof the five entities by findings, diagnostic meth-ods, and treatment. The reader is referred to thistable throughout the chapter.

Fractures occur primarily in two areas, crownand root. Either area may be the site of initiation aswell as the region of principal damage. In the crown(usually extending to the root), these lesions takethe form of a craze line, fractured cusp, crackedtooth, or split tooth (Figure 28-1); the latter threeusually extend to the root. Roots show vertical rootfracture (Figure 28-2). The remainder of the chapteris subdivided into these five categories.

Craze LinesCraze lines are common, particularly in perma-nent teeth in adults. They usually extend over

28 I Longitudinal Tooth Fractures

501

TABLE 28-1

50 2


marginal ridges and along buccal and lingual sur-faces in posterior teeth but also appear as longvertical defects from incisal to cervical aspect onanterior teeth (Figure 28-3). Craze lines are con-fined to enamel.''

Craze lines occur naturally but their inci-dence increases in patients who have had res-torations or impact injuries. It is unknown (butunlikely) whether they are precursors to dentinfractures. Craze lines are unimportant otherthan as a common source of misidentificationand confusion with cracked teeth. Because oftheir insignificance, they are not included inTable 28-1.

Fractured Cusp

Fractured cusps are usually relatively easy to diag-nose and treat and generally have a good progno-sis (see Table 28-1).

INCIDENCE

Fractured cusps are more common than theother major entities discussed in this chapter,which is fortunate because these are the least dev-astating and are the most manageable.' This frac-ture occurs often in teeth with extensive cariesor large restorations that do not protect under-mined cusps."

FIGURE 28-2This fracture begins and ends on the root. Usually the fracture extends facially and lingually, but may not extendto both surfaces or from apical to cervical.

FIGURE 28-1The three fracture types that originate occlusally and then ex-tend toward the root.

PATHOGENESIS

These fractures are related to lack of cusp sup-port. A second, but uncommon, cause is a trau-matic upward blow to the mandible, resulting in asharp impact between the maxillary and man-dibular teeth. Fortunately, this mishap does nothappen often; a single injury may cause fractureor loss of several cusps.

CLINICAL FEATURES

Cusp fractures are usually associated with a weak-ened marginal ridge in conjunction with an un-dermined cusp. These compromise dentin sup-port for the cusp, which is supplied primarily bythe marginal ridge." Either a single cusp or twocusps (in molars) are involved. The fracture in-cludes a mesial-distal and a facial-lingual compo-nent (Figure 28-4). Therefore the crack lines (seeFigure 28-1) cross the marginal ridge and then ex-tend, down a facial or lingual groove and ofteninto the cervical region parallel to the gingivalmargin (or somewhat subgingivally, which ismore common). If two cusps are involved, thefracture lines will be mesial and distal, without afacial or lingual component. Very rarely are twomesial or two distal cusps fractured together.

These are oblique shearing fractures extendingfrom the occlusal, often at the base of a cavity


503

(Figure 28-5). The defect often includes the regionof epithelial attachment and does not extend be-yond the cervical third of the root. 13 There usuallyis no pulp exposure, particularly in older teethwith smaller pulp chambers.

ETIOLOGIES

Typically there is a history of extensive deep inter-proximal caries or a subsequent class II restoration.Occasionally these cusp fractures occur in nonre-stored teeth with extensive undermining caries.

DIAGNOSIS

Subjective Symptoms

Often the patient reports brief, sharp pain onmastication or with temperature changes, partic-ularly cold. Often the pain is more distinct withmasticatory release (not with closure but withseparation of teeth after biting). Pain is neither se-vere nor spontaneous and occurs only on stimu-lus. Interestingly, the symptoms are often relievedwhen the cusp finally breaks off.

Objective Tests

The most indicative test is biting. The patientmay close onto a cotton swab applicator, a rubber

FIGURE 28-3Craze lines are common. These are fractures that are limited to the enamel and do not extend to dentin. A, Thismolar shows craze lines over marginal ridges and through buccal and lingual grooves (arrows). B, Vertical crazeli nes are common in anterior teeth (arrow), particularly in older patients.

504


FIGURE 28-4Cusp fracture. A, This fracture is usually associated with a class II restoration, extending across at least one mar-ginal ridge (arrow) and often (B) down a lingual or buccal surface. These fractures tend to acquire stain with time,are usually symptomatic, and will stop light with transillumination.

polishing (burlew) wheel, or a specially designedbite-testing instrument (Figure 28-6). An oc-clusal, gnashing force on the involved cusp elicitspain. Ordinarily, pulp tests indicate vitality.


Radiographs are not useful because cusp fracturesare not visible radiographically.

Other Findings

The restoration may have to be removed to ob-serve the underlying dentin. The fracture maythen be readily visible, or it may be disclosedby either staining or transillumination. Olderfractures may have already acquired stain (seeFigure 28-4). The cusp fracture line usually orig-inates at the cavity floor at a line angle.

TREATMENT

Retaining the fractured cusp is often not indi-cated. The cusp is removed, and the tooth is re-stored as appropriate. The restoration will prob-ably be a three-fourths or full crown extendingbelow or to the fracture margin. Root canaltreatment is often not required, because thepulp is not exposed. Occasionally, restoration isunnecessary.

If the cusp is not mobile, the fracture lineprobably does not extend to a root surface sub-

gingivally. In these cases, the cusp need not beremoved; a crown should be placed to hold thesegments.

PROGNOSIS

Long-term success is good because fractures tendto be shallow. Cusp fractures occasionally extenddeeper, below the gingival attachment; treatmentof these is more challenging. An approach torestoring deep-extending cusp fractures is de-scribed later in this chapter.

PREVENTION

Extensive removal of dentin support should beavoided. The width and particularly the depth ofrestorations should be minimized. 14 Those thatwedge, such as inlays, require adequate dentinsupport. Cusps should be reduced and onlayedif undermined; both amalgam and gold onlaysprovide fracture resistance." Composite resinsthat are bonded to enamel or dentin and improp-erly placed may shrink excessively upon polymer-ization; this contraction may displace and weakencusps, rendering them susceptible to occlusalforces and fracture.

In terms of bonding, adhesive resins, if placedwith special techniques, may reinforce weakenedcusps.16-18 However, studies are still short-termand "bench-top" and do not include long-termevaluations made under clinical conditions. In


505

FIGURE 28-SCusp fracture. Typically, the separation occurs from the lineangle of the cavity to the cervical surface.

other words, such bonded restorations may pro-vide only temporary reinforcement.

Cracked Tooth

Cracked teeth are also described as "incomplete(greenstick) fractures," which describes theirform.19 Cracked tooth is a variation of the cuspfracture, but the associated fracture is centeredmore occlusally (see Figure 28-1). The effects ofcracked teeth tend to be more devastating be-cause their extent and direction are more cen-tered and more apical (see Table 28-1).

I NCIDENCE

The occurrence of cracked tooth is unknownbut is apparently increasing.5.8 Cracked teeth arepredominantly seen in older patients, althoughthey may occur at any age in adults.', ' The lon-gevity and complexity of restorations are relatedfactors, although cracked teeth often are mini-mally restored or not restored at all.8 Mastica-tion for many years, particularly of hard objects,is also a factor. Continued and repeated forces fi-nally cause fatigue of tooth structure resultingin fracture followed by continued growth of thatfracture.

The teeth usually involved are mandibularmolars (both restored and nonrestored) followedby maxillary premolars and then by maxillaryfirst molars.' Anterior teeth do not develop truecracks, and true cracks are seen rarely on man-

FIGURE 28-6Special diagnostic "biting" instruments (Tooth Slooth) areplaced on one cusp at a time while the patient grinds withopposing teeth. Sharp pain on pressure or release may indi-cate a cusp fracture or cracked tooth,

dibular premolars. Furthermore, class I restoredteeth fracture as often as do class II restoredteeth, particularly molars. Therefore the phe-nomenon is not always dependent on violationof tooth structure by access preparations, caries,or restorations. There has been speculation thatteeth treated by root canals are more brittle andweakened and therefore are more susceptible tofracture. Evidence does not support this as-sumption." ,"`

PATHOGENESIS

As stated previously, cracks in teeth tend todepend on time and patient habits. Obviously,forces in excess of dentin strength are responsi-ble; these forces are greater in the posterior re-gion, i.e., close to the fulcrum of the mandible,invoking the "nutcracker" effect. 6,23

Although occlusal anatomy (deep fissures orprominent or functional cusps) and occlusaldysfunction might render a tooth more suscepti-ble to cracking, these factors are only specula-tive; no relationship with cracked teeth has beendemonstrated.

CLINICAL FEATURES

Cracks in teeth are almost invariably mesiodistalfractures (Figure 28-7), although mandibularmolars occasionally (rarely) fracture toward thefacial-lingual surface. The diagnosis of a facial-lingual cracked molar is a common misinterpre-tation because of visualization of facial and lin-gual fractures (see Figure 28-3, A). These areactually craze lines, which follow the buccal and

506


FIGURE 28-7Cracked tooth. The fracture extends across both marginalridges and across the cavity floor (arrows). Fractures in themesial-distal direction are by far the most common.

FIGURE 28-8Cracked tooth. The fracture extends across the marginal ridgeand down the proximal close to the furcation (greenstickfracture).

lingual grooves. Cracks cross one or both mar-ginal ridges. They generally shear toward the fa-cial or lingual side toward a root surface, usuallylingual. Because the fracture begins on the oc-clusal surface, it grows from this surface towardthe cervical surface and down the root. Impor-tantly, the more centered the fracture (initiatedon the midocclusal surface), the more it has atendency to extend deeper before it shears to-ward the root surface. The fracture is consideredgreenstick because it is incomplete (either to themesial or distal surface) or does not extend to thefacial or lingual root surface.8 The direct midoc-clusal fracture may be very deep; on maxillarymolars it may extend toward the furcation (Fig-ure 28-8) or occasionally toward the apex onmandibular molars (Figure 28-9).

The fracture may or may not include the pulp.The more centered the fracture is, the greater is thechance of pulp exposure now or later. Occasion-ally, fractures oriented toward the facial-lingualsurface shear away from the pulp, although this isnot likely and is difficult to determine clinically.Therefore many cracked teeth require root canaltreatment, preferably before restoration for coro-nal protection. Wedging forces must be minimized

during both root canal treatment and restorationto avoid aggravating the fracture.

ETIOLOGIES

Cracked teeth are often found in patients whochew hard, brittle substances (ice, unpopped pop-corn kernels, hard candy, and so on). These pa-tients may have prominent masticatory musclesand show excessive occlusal wear as a result ofheavy occlusal forces.23 If these teeth are restored,the restorations may be class I or a deep class II.Interestingly, cracks associated with wide class IIrestorations are more likely to be cusp fracturesand their effects are not as devastating.2 4

Thermal stresses are also thought to be a causeof fractures, although the evidence of this is in-conclusive. Supposedly, differences in expansionand contraction of restorations versus toothstructure may weaken and crack dentin.25,26

DIAGNOSIS

Cracked teeth show a variety of test results, radio-graphic findings, and signs and symptoms, de-pending on many factors.' This variety and un-


507

FIGURE 28-9Centered fracture on this lightly restored second molarextends toward the apex. Treatment of these fractures ishopeless.

predictability often make the cracked tooth aperplexing diagnostic and treatment entity.

Subjective Findings

Often cracked teeth manifest as the so-calledcracked tooth syndrome.27 This syndrome is charac-terized by acute pain on mastication (pressure or re-lease) of grainy, tough foods and sharp, brief painwith cold.24 These findings are also related to cuspfracture. However, there may be a variety of symp-toms ranging from slight to very severe sponta-neous pain consistent with irreversible pulpitis,pulp necrosis, or apical periodontitis. Even an acuteapical abscess may be present if the pulp has under-gone necrosis. There may be apical pathosis relatedto acute apical abscess (with or without swelling) ora draining sinus tract. In other words, once the frac-ture has extended to and exposed the pulp, severepulp or periradicular pathosis will be present. Thisexplains the variation in signs and symptoms.

Objective Tests

Pulp and periradicular tests also have variable re-sults. The pulp is usually responsive (vital) but

may be nonresponsive (necrosis). Periapical testsalso vary, but usually pain is not elicited with per-cussion or palpation if the pulp is vital. Direc-tional percussion is also advocated. Percussionthat separates the crack may cause pain. Opposite-direction percussion usually is asymptomatic.This pain is probably related to stimulation of theperiodontal ligament proprioceptors.


Because of the mesiodistal direction of the frac-ture, it is not visible. Radiographs are to helpdetermine the pulp-periradicular status. Usuallythere are no significant findings, although occa-sionally different entities also occur. At times, lossof proximal (horizontal, vertical, or furcal) bone isrelated to the fracture; bone loss increases as theseverity of the crack increases.

Other Findings

Craze lines in posterior teeth that cross marginalridges or buccal and lingual surfaces must be dif-ferentiated with transillumination.

With craze lines, transilluminated light fromthe facial or lingual surface is not blocked or re-flected; the entire tooth in a facial-lingual orienta-tion is illuminated.

When a crack is suspected, it is important totry to visualize the length and location of the frac-ture. Occlusal and proximal restorations are firstremoved. Then transillumination (Figure 28-10),which often shows a characteristic abrupt block-age of transmitted light, is performed. With trans-illumination the portion of the tooth where thelight originates illuminates to the fracture. A frac-ture contains a thin air space, which does notreadily transmit light. Therefore the crack (orfracture) blocks or reflects the light, causing theother portion to appear dark.

Staining with methylene blue or iodine mayalso disclose the fracture, although not pre-dictably. A cotton pledget soaked with methyleneblue or other dye is placed against the cavity floor;the dye is held in by a sealing temporary such asIRM. The temporary restoration and pledget areremoved after a few days. The dye may have con-tacted the crack long enough to disclose it clearly(Figure 28-11). Patients should be advised thatthe tooth will temporarily turn blue, they maywish to forgo this test.

If a fracture is detected, an instrument isplaced in the cavity with moderate pressure ex-erted on opposing walls to try to separate the seg-ments. If no movement is detected, the classifi-cation is a cracked tooth; when the segments

508

28 I Longitudinal Tooth Fractures

FIGURE 28-10Cracked tooth. A, Fracture through dentin reflects transilluminated light showing abrupt change in brightness.B, For comparison, an adjacent noncracked premolar transmits light readily.

separate it is a split tooth (discussed later). It isdebatable whether wedging should be performed;wedging may split the tooth iatrogenically. How-ever, if controlled force exacerbates the crack,certainly the tooth is predisposed to a later splitanyway.

Occasionally (particularly if the crack is cen-tered), an access preparation is necessary to dis-close the extent (Figure 28-12) of the crack. Afterthe chamber roof and coronal pulp have been re-moved, the floor is transilluminated as for a frac-ture (not to be confused with anatomic grooves).Sealing in a disclosing dye for a few days may behelpful.

Periodontal probing is important and may dis-close the approximate depth and severity of thefracture. Removal of interproximal restorationsis helpful because it allows improved access forplacement of the periodontal probe. However,subgingival fractures often do not create a prob-ing defect. Therefore the absence of deep probingdoes not preclude a cracked tooth. The presenceof deep probing is serious and indicates an ad-verse prognosis.

Selective biting on objects (as described ear-lier under "Fractured Cusp") is helpful (see Fig-ure 28-6), particularly when pain is reported onmastication.

TREATMENTPrognosis

The five important considerations listed in thebox on p. 501 should be reviewed. When bothclinician and patient are aware of the compli-cations and questionable outcomes, a treatment

plan is formulated. Extraction is a reasonable so-lution in many situations. Much depends on thenature (depth and location) of the fracture. Again,the segments must not separate on wedging. Ifthey do not separate, there are many treatmentalternatives to retain the tooth intact. If theocclusal-proximal fracture is centered in the facial-lingual aspect and involves the floor of the cavitypreparation, there are treatment options. If thereare no symptoms of irreversible pulpitis, a crownmay be placed, although some of these teeth willeventually manifest irreversible pulpitis or pulpnecrosis. They will then require treatment throughthe crown.28

Further Examination

After access has been gained, the chamber floor isexamined. If the fracture extends through thechamber floor, generally further treatment is hope-less and extraction is preferred (Figure 28-12). 29 Anexception is the maxillary molar, which may behemisected along the fracture, saving half (or bothhalves) of the crown and supporting roots. Manyof these treatments are complex, and the patientshould be considered for referral to an endodon-tist. If a partial fracture of the chamber floor isdetected, the crown is bound with a well-fitting ce-mented orthodontic band (Figure 28-12) or tem-porary crown to protect the cusps until finalrestoration is performed.30 This also helps to deter-mine whether symptoms decrease during rootcanal treatment. The rationale (unsupported) isthat if pain symptoms are not relieved, the progno-sis is significantly poorer and extraction may benecessary.

FIGURE 28-11A, Disclosing solution on a cotton pellet (in this case, methylene blue) is placed in the cavity for a few minutesor sealed in for a week. B, This technique may clearly disclose the fracture (arrow) and its extent.

Restoration

If the fracture appears to be incomplete (not ter-minating on a root surface), the tooth is restoredto bind the fractured segments (barrel-stave ef-fect) and also to protect the cusps. For a per-manent restoration, a full crown is preferred, al-though an onlay with bevels may suffice. Postsand internally wedging foundations are to beavoided. Acid-etch dentin bonding resins orbonded amalgams may help to provide a founda-tion for the crown to prevent crack propagation,although this approach is unproven. 31

One suggested approach has been to removedentin with burs until the crack disappears in aneffort to eliminate or determine the extent ofthe crack. This is not rational; the fracture is smalland invisible at the furthest extent (even afterstaining). Therefore the crack probably continuesdeeper into dentin than can be visualized. Thisprocedure removes sound tooth structure unnec-essarily, thereby further decreasing tooth strength.

PROGNOSIS

The overall prognosis depends on the situationbut is always questionable at best. The patient isinformed about the possible outcomes and theunpredictability of duration of treatment. The


509

FIGURE 28-12Managing a cracked tooth. To minimize movement of seg-ments, an orthodontic band has been placed. The access isnow completed to determine the depth of the fracture. Thefracture (arrow) extends across the floor; the prognosis is poor.

fracture may continue to grow with eventuallydevastating consequences, requiring tooth extrac-tion or additional treatments (Figure 28-13). Fur-thermore, the patient should be informed thatcracks may be present in other teeth as well andcould manifest in the future.

510


FIGURE 28-13Cracked tooth resulting in eventual split tooth. A, A cracked tooth was identified, root canal treatment was com-pleted, and a full crown was placed. B, After 3'h years the fracture became manifest with extensive bony de-struction. C, The fracture had grown over time to become a split tooth.

In general, the more centered the origin of thefracture is on the occlusal surface, the poorer thelong-term prognosis; these fractures tend to re-main centered and grow deeper. The result is majordamage to the tooth and periodontium. In otherwords, the cracked tooth may ultimately evolve toa split tooth or develop severe periodontal defects.

PREVENTION

Generally, patients are encouraged to forego de-structive habits such as ice chewing. In addition,most suggestions made earlier for prevention ofcusp fractures apply here. The use of deep class Ior class II restorations should be minimized, par-ticularly on maxillary premolars (cusp protectionmay be helpful) .32 Altering the occlusal anatomyor changing occlusal relationships is not useful.

Split Tooth

A split tooth is the evolution of a cracked tooth.The fracture is now complete and extends to a sur-face in all areas.' The root surface involved is prob-ably in the middle or apical third. There are nodentin connections; tooth segments are entirelyseparate (Figure 28-13, C). The split may occursuddenly, but it more likely results from long-termgrowth of an incomplete fracture (see Table 28-1).

INCIDENCE

As with cracked tooth, the occurrence of splittooth is apparently increasing." Obviously, manyfactors related to cracked tooth are endemic tosplit tooth. An assumption is that root canaltreatment weakens dentin and renders teeth moresusceptible to severe fractures, this is unlikely.21.33

PATHOGENESIS

Causative factors related to cracked tooth alsoapply to split tooth. Why some cracked tooth frac-tures continue to grow to a complete split is un-known. Two major causes are probably persistentdestructive wedging or displacing forces on existingrestorations and new traumatic forces that exceedthe elastic limits of the remaining intact dentin.

CLINICAL FEATURES

These are primarily mesiodistal fractures thatcross both marginal ridges and extend deep toshear onto the root surfaces. The more centeredthe fracture is occlusally, the greater the tendencyto extend apically. These fractures are more devas-tating. Mobility (or separation) of one or bothsegments is present.

These fractures usually include the pulp. Themore centered the fracture is, the greater theprobability of exposure.

FIGURE 28-14Split tooth. A, Often split teeth demonstrate marked horizontal and vertical bone loss (arrows) interproximallyand in the furcation. B, This molar shows the definitive sign: separation of the segments on wedging.

ETIOLOGIES

Split tooth has the same causes as crackedtooth. Split tooth may be more common in rootcanal treated teeth. However, this is not becausethe treatment per se weakens the tooth by dehy-drating or altering dentin.33 Rather, the strengthof these teeth has already been compromisedby caries, restorations, or overextended accesspreparations.

DIAGNOSIS

Split tooth does not have the same variety ofconfusing signs, symptoms, and test results ascracked tooth. Generally, split teeth are easierto identify." Damage to periodontium is usuallysignificant and is detected by both patient anddentist.

Subjective Findings

Commonly, the patient reports marked pain onmastication. These teeth tend to be less painfulwith occlusal centric contacts than with mastica-tion. A periodontal abscess may be present, oftenresulting in mistaken diagnosis.

Objective Findings

Objective findings are not particularly helpfulbut should include both pulp and periradiculartests.


511


Findings on radiographs depend partially on pulpstatus but are more likely to reflect damage to theperiodontium. Often there is marked horizontalloss of interproximal or interradicular bone (Fig-ures 28-13, B, and 28-14, A).

Other Findings

The most important consideration is to identifythe extent and severity of the fracture, whichoften requires removal of a restoration. With splittooth the fracture line is usually readily visibleunder or adjacent to the restoration; it includesthe occlusal surface and both marginal ridges.

Separability of the segments is also important.As with cracked tooth, an instrument is placedin the cavity. Wedging against the walls is donewith moderate pressure; the walls are then visual-ized for separation (Figure 28-14, B). A separat-ing movement indicates a through-and-throughfracture.

Periodontal probing generally shows deep de-fects; probings tend to be adjacent to the fracture.Here again, removal of existing restorations ishelpful in visualizing interproximal areas.

TREATMENT

Maintaining an intact tooth is impossible. If thefracture is severe (that is, deep apically), the toothmust be extracted. If the fracture shears to a root

512

28 1 Longitudinal Tooth Fractures

FIGURE 28-15

A technique for managing certain split teeth and cusp fractures. From upper left to lower left: Separable segmenti s held with a matrix or band. Root canal treatment is followed by an amalcore onlay. The fractured segment isremoved and the amalgam is contoured. The tissue will heal and usually reattach; the nature of the attachment(connective or epithelial tissue) is unknown. Usually, normal sulcus depth is reestablished.

surface that is not too far apical (middle to cervi-cal 1/3 of the root), the smaller segment will be verymobile. Then there is a good possibility that thesmall segment can be removed and the remainderof the tooth salvaged.

Different approaches to maintenance are used,depending on conditions. Some choices are thefollowing.

Remove the fractured segment. Then the type oftreatment and restoration are determined. How-ever, the following choice (retention of fracturedsegment temporarily) is preferred and is generallyless complicated.

Retain the fractured segment temporarily (Fig-ure 28-15). First, a rubber dam is applied with astrong rubber dam clamp to isolate and hold thesegments together. Root canal treatment is com-pleted (if not already performed), and restora-tion with a retentive amalcore (onlaying theundermined cusps) is performed. Then the frac-tured segment is removed. Granulation tissueproliferates to occupy the space and reattach theperiodontium to the root dentin surface. Thefinal restoration usually is the amalcore but maybe a full crown with a margin related to the newattachment.

Remove the fractured segment and perform crownlengthening. The mobile segment is removed first,

and root canal treatment is performed next fol-lowed by crown lengthening and appropriaterestoration. This is not feasible in most situa-tions because the fracture is too deep on the rootsurface.

Remove the fractured segment and perform no fur-ther treatment. This choice is appropriate whenroot canal treatment has been completed previ-ously and the tooth already restored. All pulpspace areas must be filled to the margins with per-manent restorative material (for example, amal-gam) with no obturating material (e.g., gutta-percha) exposed (Figure 28-16). The defect oftengranulates in, and reattachment to the fractureddentin surface occurs.

In summary, treatment may be complex or rela-tively simple depending on the situation. Becauseof the complexity of their situations, these pa-tients should be considered for referral to a spe-cialist for diagnosis or treatment.

PROGNOSIS

As expected, prognosis is variable. Some treat-ments of split tooth are successful, whereas othersare doomed to failure if attempted. When thefracture surfaces in the middle to cervical third ofthe root, there is a reasonable chance of successful

FIGURE 28-16A technique for managing fractures. Root canal treatment and amalcore onlay had been done earlier; the fractureoccurred after treatment. A, The mobile segment is removed. B, A space is created with raw root dentin exposed(arrow). Tissue usually granulates in and is reattached to the dentin (but not to the amalgam). No further treat-ment is needed.

treatment and restoration. If the fracture surfacesin the middle to apical third, the prognosis ispoor. With these deep fractures, usually too muchof the pulp space is exposed to the periodontium;root canal treatment with restoration of thisspace would result in deep periodontal defects.

Sometimes prediction of success or failurecannot be determined before treatment is com-pleted if the more conservative approach is taken,that is, if the segment is temporarily held in placeduring root canal treatment and restoration.After root canal treatment has been completedand the segment has been removed, the dentistmay discover that, unfortunately, the fracture isindeed very deep and the tooth is unsalvageable.The patient must be informed of all these possi-bilities before treatment is begun.

PREVENTION

Generally, preventive measures are similar tothose recommended for cracked tooth, that is,eliminating oral habits that damage tooth struc-ture and impose wedging forces. Teeth requir-ing large, deep access preparations should beprotected by an onlay or full crown. Large ac-cess preparations also require appropriate cuspprotection."


513


Vertical root fracture (VRF) differs from the enti-ties (see Table 28-1) described previously in thischapter because the treatment plan is easy, butdiagnosis often is tricky and elusive because theVRF mimics other conditions.34-35 Because treat-ment invariably consists of tooth extraction or re-moval of the fractured root, an error in diagnosishas serious consequences.

I NCIDENCE

The overall occurrence is unknown, but VRF iscommon . 36 These defects occur more often inteeth that have undergone complex restorativeprocedures, that is, root canal treatment and in-traradicular post retention.

PATHOGENESIS

This fracture results from wedging forces withinthe canal. These excessive forces exceed the bind-ing strength of existing dentin, causing fatigueand fracture. Irritants that induce severe inflam-mation in the adjacent periodontium result fromthe fracture.37 Generally, this periodontal de-struction and the accompanying findings, signs,

514


FIGURE 28-17Vertical root fracture extends facially and lingually and, inthis case, in an apical to cervical direction.

FIGURE 28-18Vertical root fracture of the distal root. A common radio-graphic pattern of bone resorption is seen. The defect extendsalong the fractured root and into the furcation.

and symptoms bring the fracture to the attentionof the patient or dentist.

CLINICAL FEATURES

These fractures occur primarily in the facial-lingualplane (see Figure 28-2). They are longitudinal andmay either be short or extend the length of theroot, that is, from apical to cervical (Figure 28-17).The fracture probably begins internally (canal wall)and grows outward to the root surface. In addition,the fracture may begin at the apex or at midroot. 38Therefore it may be incomplete (see Figure 28-2),extending neither to both facial and lingual rootsurfaces nor from apical to cervical root surfaces.

Although VRFs usually show only mild clinicalsigns and symptoms, the effects on the periodon-tium are eventually devastating and irresolvable.

ETIOLOGIES

There are two major causes (the only demonstratedones) of VRFs. These are (1) post placement (ce-mentation) and (2) condensation during obtura-tion." The only reported cases of VRF occurring innonendodontically treated teeth are in Chinesepatients.40-41 Other causes, such as occlusal forces,wedging of restorations, corrosion and expansionof metallic posts, and expansion of postsurgicalretrograde restorations, have been mentioned butnot convincingly shown . 42

Condensation, both lateral and vertical, maycause excessive wedging forces, creating a VRF.43-44Intraradicular retentive posts have also been im-plicated.34-39-45 Two aspects of posts cause wedgingforces. Wedging occurs during cementation ofposts and also during the seating of tapered postsor with posts that depend on frictional reten-tion.39-46 Occlusal forces exerted on the post aftercementation and restoration may also be a factorbut probably a minor one. Post placement hasbeen shown to exert a greater wedging force thanlateral condensation.46

Certain root shapes and sizes are more suscepti-ble to VRF. Roots that are deep facially and lin-gually but narrow mesially and distally are particu-larly prone to fracture.38 Examples are mandibularincisors and premolars, maxillary second premo-lars, mesiobuccal roots of maxillary molars, andmesial and distal roots of mandibular molars.Round, oval, or bulky roots are resistant to frac-ture, examples are maxillary central incisors, lingualroots of maxillary molars, and maxillary canines.

Susceptibility of any root to fracture is markedlyincreased by excessive dentin removal during canalinstrumentation or post preparation.47.48 An addi-tional factor occurring during condensation is theplacement of excessive numbers of accessory conesrequiring multiple spreader insertions .38,49 Also, theinsertion of tapered, inflexible condensing instru-ments into curved canals creates root distortionand the potential for fracture.50

28 1 Longitudinal Tooth Fractures

515

FIGURE 28-19Vertical root fracture. A, At the time of root canal treatment and restoration. B, Several years later the fracturemanifests devastating results. Visualizing the fracture on a radiograph is unusual.

DIAGNOSIS Objective Tests

Vertical root fractures become manifest by a vari-ety of signs, symptoms, and other clinical find-ings. They may mimic other entities such as peri-odontal disease or failed root canal treatment.This variety of findings often makes VRF a per-plexing diagnosis.51.52 Interestingly, because VRF-'are often mistaken for periodontal lesions or forfailed root canal treatment, the dentist may referthese difficult diagnosis patients to the periodon-tist or endodontist, presumably for periodontaltherapy or endodontic retreatment.

Diagnostic findings of VRF were reported in aseries of 42 clinical cases in a study performed byMichelich et al .35 Much of the information thatfollows is derived from the findings in that studyin conjunction with other reports.

Subjective Findings

Symptoms tend to be minimal. Seldom is the VRFpainful, and it is often asymptomatic or showsmild, insignificant signs and symptoms. Often,some mobility is detectable, but many teeth arestable. Periradicular symptoms (pain on pressureor mastication) are common but mild.

Because many VRF-' resemble periodontal le-sions, a periodontal-type abscess (either as a pre-senting sign or in the history) is a common occur-rence. 37-45 In fact, this localized swelling is oftenwhat brings the patient to the dentist's office.

Periradicular tests of palpation and percussionare not particularly helpful. Periodontal probingpatterns are more diagnostic. Significantly, someteeth with VRF-' have normal probing patterns.'-'Most show significant probing depths with nar-row or rectangular patterns, which are more typi-cal of endodontic-type lesions. 45,53 These deepprobing depths are not necessarily evident onboth the facial and lingual aspects. Overall, prob-ing patterns are not in themselves totally diagnos-tic, but they are helpful.


Radiographs also show a variety of patterns. Attimes there are no significant changes.35 How-ever, when present, bone resorptive patternstend to be marked, extending from the apexalong the lateral surface of the root and ofteninclude angular resorption at the cervical root(Figure 28-18). 54 However, many of the resorp-tive patterns related to VRF mimic other enti-ties. Lesions may resemble failed root canaltreatment; that is, they have an apical "hangingdrop" appearance. In only a small percentageof teeth is there a visible separation of frac-tured root segments (Figure 28-19). Interest-ingly, VRF-' may be more readily identified usingcomputed tomography rather than conventionalradiography. 55

51 6


The idea that a radiolucent line separating thefilling (i.e., gutta-percha) from the canal wall is di-agnostic has been advocated. However, this radio-lucent line may be a radiographic artifact, incom-plete obturation, an overlying bony pattern, orother radiographic structure that is confusedwith a fracture. Therefore radiographs are helpfulbut are not solely diagnostic except in those fewinstances in which the fracture is obvious.

Dental History

Virtually all teeth with a VRF have had rootcanal treatment; many have been restored withcast or prefabricated posts. Potentially greaterdestructive forces exist with tapered, wedgingposts.56,57

Interestingly, endodontic and restorative treat-ment may have been done months or years be-fore the fracture. Forces (without fracture) areestablished at the time of treatment or restora-tion .41.45.46 These forces are stored in root dentin

but may not result in an actual fracture untillater; neither patient nor dentist may relate thefracture to earlier procedures.

Other Findings

signs, symptoms, and radiographs all give vari-able findings. Flap reflection is the only reliablediagnostic approach. Surgical exposure of boneoverlying the root surface is the best method ofidentification . 34,35 VRFs have consistent patterns(Figure 28-20). There is usually a "punched-out"bony defect that tends to be oblong and overliesthe root surface. This defect may take the form ofa dehiscence or fenestration at various root levels.The defect is filled with granulomatous tissue.

After inflammatory tissue has been removed,the fracture is usually (but not always) visible onthe root (Figure 28-21). If it is not obvious, thefracture line may be hidden or very small and un-developed. However, the characteristic punched-out, granulomatous tissue filled defect is fairlydiagnostic of VRF, which should be strongly sus-pected." Transillumination or staining with dyesare helpful. Also, the root-end could be resectedand examined under magnification to detect thefracture.

FIGURE 28-20Vertical root fracture. After flap reflection and visualization, thepattern of bony changes tends to be consistent with oval or ob-l ong "punched-out" defects filled with granulomatous tissue(VRF). This is differentiated from the normal bony fenestration.

FIGURE 28-21Vertical root fracture is usually but not always identified (arrow)after flap reflection. Usually (as in this case), the bone has beenresorbed, showing a long defect. This molar has been hemi-sected; the fractured mesial segment will now be removed.

Fracture Characteristics

Histologic fracture characteristics have been de-scribed with VRF after removal.37 All fractures ex-tended from the canal to at least one root surfacebut not necessarily to both (Figure 28-22). Simi-larly, fractures often extended only the partiallength of the root, usually to the apex but not al-ways to the cervix.

Many irritants occupy the fracture space andadjacent canal.37 Fractures usually harbor bac-teria, sealer particles, and amorphous material.Canals adjacent to the fracture often containnecrotic tissue as well as concentrations of bacte-ria. Periodontal tissues adjacent to the fractureare chronically inflamed. Occasionally, connectivetissue grows into the fracture toward the canal;this is often associated with resorption at the rootsurface (Figure 28-23).

Thus profound irritants related to the frac-ture with resulting inflammation at the surfacewere identified in the study.37 VRFs resemble avery long apical foramen that communicates

FIGURE 28-22Vertical root fracture. This histologic cross section shows afracture extending to only one surface and to the canal. Thefracture space and root surface show inflammatory tissue

(arrows).


51 7

with necrotic pulp containing bacteria-thusthe hopeless prognosis.

TREATMENT

As stated earlier, the only treatment is removal ofthe fractured root. In multirooted teeth, thiscould be done by root amputation or hemisection(see Figure 28-21).

Other modalities have been suggested in at-tempts to reduce the fracture or retain the root,such as placement of calcium hydroxide, ligationof the fractured segments, or cementation of thefractured segments, trying to bind them by adhe-sive resins, epoxies, or glass ionomer.58 A uniqueapproach is to extract the tooth, repair the frac-ture with a laser or with a cement, and then re-plant the tooth. Many of these suggested methodsare impractical and have not been shown to be ef-fective long-term. Surgical repairs such as removalof one of the fractured segments or repair withamalgam or resin after surgical exposure and

FIGURE 28-23Vertical root fracture extends to both surfaces (facial and lin-gual). The facial surface shows resorption (arrows) and in-growth of connective tissue. The lingual component containsnecrotic debris and bacteria.

51 8


preparation have also been suggested, but no suc-cessful results have been documented.

PROGNOSIS

At present, prognosis is virtually hopeless fortooth with a vertically fractured root.

PREVENTION

Because the causes of VRF are well known, pre-vention should not be difficult. The cardinalrules for safety are to (1) avoid excessive removalof intraradicular dentin and (2) minimize internalwedging forces. The binding strength of root den-tin is considerable but it is easily compromised.Treatment and restorative procedures that re-quire minimal dentin preparation should be se-lected. Condensation of obturating materialsshould be carefully controlled. More flexible andless tapered finger pluggers or spreaders are pre-ferred because they are safer than stiff, conven-tional hand-type spreaders.49.50

Posts weaken roots and should not be used un-less they are necessary to retain a foundation (seeChapter 15). The post design least likely to causestress and fracture dentin is the flexible (includingcarbon-fiber carbon) or cylindrical (parallel-sided)preformed post,39.56 although these designs arenot suitable in all restorative situations. Castposts or some of the tapered preformed postsmay be necessary. Their shape may exert wedgingforces that readily split roots or cause dentinstrain, particularly if they lack a stop or ferrule onthe root seat .59-60 Any post used should be as smallas possible, have a passive fit, and not lock or gripthe root internally with threads .39 Cementationshould be done carefully and slowly; an escapevent for the cement is probably helpful.

REFERENCES

1. American Association of Endodontists: Cracking thecracked tooth code, Endodontics: Colleagues forExcellence,Nov 1997.

2. Renson CE, Braden M: The experimental determina-tion of the rigidity modulus, Poisson's ratio and theelastic limit in shear of human dentin, Arch Oral Biol20:43, 1975.

3. Carter J, Sorenson S, Johnson R, et al: Punch sheartesting of extracted vital and endodontically treatedteeth, JBiomech 16:841, 1983.

4. Eakle W, Maxwell E, Braley B: Fractures of posteriorteeth in adults, JAm DentAssoc 112:215, 1986.

5. Ehrmann E, Tyas M: Cracked tooth syndrome: diag-nosis, treatment and correlation between symptomsand post-extraction findings, AustDentJ 35:105, 1990.

6. Hiatt W: Incomplete crown-root fracture in pulpal-periodontal disease, JPeriodontol 44:369, 1973.

7. Rosen H: Cracked tooth syndrome, J Prosthet Dent47:36, 1982.

8. Abou-Rass M: Crack lines: precursors of toothfractures-their diagnosis and treatment, QuintessenceInt 4:437, 1983.

9. Gehr M, Denlap R, Anderson M, Kuhl L: Clinicalsurvey of fractured teeth, J Am Dent Assoc 114:174,1987.

10. Schweitzer J, Gutmann J, Bliss R: Odonto-iatrogenictooth fracture, Int Endod j 22:64, 1989.

11. Silvestri A, Singh I: Treatment rationale of fracturedposterior teeth, J Am Dent Assoc 97:806, 1978.

12. Reeh E, Messer H, Douglas W: Reduction in toothstiffness as a result of endodontic and restorative pro-cedures, JEndod 15:512, 1989.

13. Cavel W, Kelsey W, Blankenau R: An in vivo study ofcuspalfracture, JProsthetDent 53:38, 1985.

14. Re G, Norling B, Draheim R: Fracture resistance oflower molars with varying facio-occlusolingual amal-gam restorations, JProsthetDent 47:518, 1982.

15. Salis S, Hood J, Kirk E: Impact-fracture energy ofhuman premolar teeth, JProsthetDent 58:43, 1987.

16. Trope M, Langer 1, Maltz D, Tronstad L: Resistance tofracture of restored endodontically treated premolars,Endod Dent Traumato12:35, 1986.

17. Reeh E, Douglas W, Messer H: Stiffness of endodonti-cally-treated teeth related to restoration technique,JDentRes 68:1540, 1989.

18. Trope M, Tronstad L: Resistance to fracture of en-dodontically treated premolars restored with glassionomer or acid-etched composite resins, J Endod 17:257, 1991.

19. Burke F: Tooth fracture in vivo and in vitro, J Dent20:131, 1992.

20. Howe C, McKendry D: Effect of endodontic accesspreparation on resistance to crown-root Fracture, JAmDentAssoc 121:712, 1990.

21. Rivera E, Yamauchi M: Site comparisons of dentinecollagen cross-links from extracted human teeth, ArchOral Biol 38:541,1993.

22. Huang T -J, Schilder H, Nathanson D: Effect of mois-ture content and endodontic treatment on some me-chanical properties of human dentin, J Endod 18:209,1992.

23. Cameron C: The cracked tooth syndrome: additionalfindings, JAm Dent Assoc 93:971, 1976.

24. Homewood C: Cracked tooth syndrome-incidence,clinical findings, and treatment, Aust Dent J 43:217,1998.

25. Brown W, Jacobs H, Thompson R: Thermal fatigue inteeth, JDentRes 51:461, 1972.

26. Harper R, et al: In vivo measurement of thermal diffu-sion through restorative material, J Prosthet Dent42:180, 1980.

27. Christensen G: The cracked tooth syndrome: a prag-matic treatment approach, J Am Dent Assoc 124:107,1993.

28. Krell K, Rivera E: Six-year evaluation of cracked teethdiagnosed with reversible pulpitis, J Endod 26:540,2000 (abstract).


51 9

29. Turp J, Gobetti J: The cracked tooth syndrome: an elu-sive diagnosis, JAmDent Assoc 127:1502, 1996.

30. Ailor J: Managing incomplete tooth fractures, J AmDent Assoc 131:1168, 2000.

31. Franchi M, Breschi L, Ruggeri O: Cusp fracture resis-tance in composite-amalgam combined restorations,JDent 27:47, 1999.

32. Blaser P, Lund M, Cochran M, et al: Effects of designsof class 11 preparations on resistance of teeth to frac-ture, Oper Dent 8:11, 1983.

33. Sedgley C, Messer H: Are endodontically treated teethmore brittle? J Endod 18:332, 1992.

34. Pitts D, Natkin E: Diagnosis and treatment of verticalroot fractures, JEndod 9:338, 1983.

35. Michelich R, Smith G, Walton R: Vertical root fracture:clinical features (unpublished).

36. Fuss A, Lustig J, Tamse A: Prevalence of vertical rootfractures in extracted endodontically treated teeth, IntEndod J 32:283, 1999.

37. Walton R, Michelich R, Smith G: The histopathogene-sis of vertical root fractures, J Endod 10:48, 1984.

38. Holcomb Q, Pitts D, Nicholls J: Further investigationof spreader loads required to cause vertical root frac-ture during lateral condensation, JEndod 13:277, 1987.

39. Ross R, Nicholls J, Harrington G: A comparison ofstrains generated during placement of five endodonticposts,JEndod 17:9, 1991.

40. Yang S, Rivera E, Walton R: Vertical root fractures innon-endodontically treated teeth, J Endod 21:337,1995.

41. Chan C, Lin C, Tseng S, et al: Vertical root fracturein endodontically versus nonendodontically treatedteeth: a survey of 315 cases in Chinese patients, OralSurg Oral Med Oral Pathol Oral Radiol Endod 87:504,1999.

42. Rud J, Onmell D: Root fractures due to corrosion: di-agnostic aspects, Scand jDent Res 78:397, 1970.

43. Ricks-Williamson L, Fotos P, Goel V, et al: A three-dimensional finite-element stress analysis of an en-dodontically prepared maxillary central incisor, JEndod 21:362, 1995.

44. Harvey T, White J, Leeb 1: Lateral condensation stressi n root canals, JEndod 7:151, 1981.

45. Meister F, Lommel T, Gerstein H: Diagnosis and pos-sible causes of vertical root fractures, Oral Surg OralMed Oral Pathol 49:243, 1980.

46. Obermayr G, Walton R, Leary M, Krell K: Vertical rootfracture and relative deformation during obturationand post-cementation, JProsthetDent 66:181, 1991.

47. Sornkul E, Stannas J: Strength of roots before andafter endodontic treatment and restoration, J Endod18:440, 1992.

48. Trope M, Ray H: Resistance to fracture of endodonti-cally treated roots, Oral Surg Oral Med Oral Pathol73:99,1992.

49. Dang D, Walton R: Vertical root fracture and root dis-tortion: effect of spreader design, JEndod 15:294, 1989.

50. Murgel C, Walton R: Vertical root fracture and dentindeformation in curved roots: the influence of spreaderdesign, Endod Traumatol 6:273, 1990.

51. Moule A, Kahler B: Diagnosis and management ofteeth with vertical root fractures, Aust Dent J 44:75,1999.

52. Tamse A, Fuss, Z, Lustig J, Kaplavi J: An evaluation ofendodontically treated vertically fractured teeth, JEndod 7:506, 1999.

53. Harrington G: The perio-endo question: differentialdiagnosis, Dent Clin North Am 23:673, 1979.

54. Tamse A, Fuss Z, Lustig J, et al: Radiographic featuresof vertically fractured, endodontically treated maxil-lary premolars, Oral Surg Oral Med Oral Pathol Oral Ra-dial Endod 88:348, 1999.

55. Youssefzadeh S, Gahleitner A, DorfFner R, et al: Dentalvertical root fractures: value of CT in detection, Radiol-ogy 210:545, 1999.

56. Standlee J, Caputo A, Collard E, Pollack M: Analysis ofstress distribution by endodontic posts, Oral Surg OralMed Oral Pathol 33:952, 1972.

57. Johnson J, Schwartz H, Blackwell R: Evaluation andrestoration of endodontically treated posterior teeth,JAm Dent Assoc 93:597, 1976.

58. Trope M, Rosenberg E: Multidisciplinary approach torepair of vertically fractured teeth, J Endod 18:460,1992.

59. Sorenson J, Englemen M: Ferrule design and fractureresistance of endodontically treated teeth, J ProsthetDent 63:529, 1990.

60. Milot P, Stein R: Root fracture in endodonticallytreated teeth related to post selection and crown de-sign, JProsthet Dent 68:428, 1992.

Differential Diagnosisof Orofacial Pain

LEARNING OBJECTIVES


1 / Describe the basic components of pain mechanisms while recognizing that current knowledge is

i ncomplete.

z / Explain why an understanding of physiology, psychology, and pathology of pain is important to dental

practice.

3 / Explain the mechanisms of referred and spreading pain and how these may lead to misdiagnosis.

a / Describe the difference between acute and chronic pain.

s / Recognize the bases for migraine, neuritis, and neuralgia and explain how these syndromes may mimic

tooth pain.

6 / Understand that pain may be largely or entirely of psychogenic origin.

7 / Differentiate between deep and superficial pain, and relate this to the difference between pain of pulpal or

periradicular origin and that of periodontal origin.

s / List the main characteristics of pulpal, periradicular, periodontal, and mucosal pain.

9 / Describe how history and diagnostic tests help clarify difficult diagnoses.

10 / Describe procedures to be followed when a definitive diagnosis and localization of pain are not possible.

520

29 I Differential Diagnosis of Orofacial Pain

521

Significance of Pain Diagnosis

Significance of Pain Diagnosis

Pain Mechanisms

Specificity

Gating

Pain as an Experience

The Versatility of Pain

Superficial Versus Deep Pain

Periodontal Pain

Pulpal Pain

Phenomena Complicating the Diagnosis

of Dental Pain

Referred Pain

Spreading Pain

Psychogenic pain

Headaches

Neuritis

Trigeminal Neuralgia

Atypical Oral and Facial Pain

Diagnostic Procedures

Recognition of Difficult Diagnoses

Approach to Difficult Diagnoses

I mportant Clues

Many dental patients are in pain when they areseen. The most common cause of pain in the oro-facial region is inflammatory disease of either thepulp or the tooth's supporting structures. Effec-tive treatment is based on careful, accurate diag-nosis. However, diagnosis and identification ofthe source of pain are not simple. Pain originatingfrom the teeth may be referred to or spread toother structures; conversely, pain from nondentalsites can be referred to teeth. Because rationaltreatment involves removal of the cause or causesof pain rather than merely addressing the symp-toms, it is imperative to establish first whetherpain is of dental origin. When pain is dental, de-termination of which tooth or teeth are involvedis the most important consideration. Difficultiesin the localization of pain may result in extractionor endodontic treatment of the wrong tooth. Thepain may originate from other sources such as themuscles of mastication or mucosa of the nose andsinuses; again, neither tooth extraction or rootcanal therapy will resolve the symptoms. Unfortu-nately, such inappropriate treatments in attemptsto relieve pain are all too common. Not only aresuch misadventures ineffective in resolving pain,they may also lead to litigation.

Thus before a practitioner treats a patientin pain, a correct diagnosis is essential. Whendiagnosis is difficult, two measures are recom-mended. One is to provide symptomatic reliefand to observe the patient. When pain intensifies,identification is easier; an example is when pulpalinflammation invades the periradicular tissues.The second option is to seek an expert opinion.Pain is a versatile phenomenon; many forms ofchronic pain and myofascial pain elude simplediagnosis and may be beyond the expertise of ageneral dentist. For example, temporomandibu-lar joint and muscle disorders are often found inconjunction with other, more generalized condi-tions such as fibromyalgia. Complete diagnosisof orofacial pain may necessitate input from spe-cialists from several disciplines.

This chapter does not provide a complete orcomprehensive discussion of the complexities ofdiagnosis of orofacial pain. This warrants an en-tire text.1,2 It does provide a guide to (1) deter-mining whether a pain is of dental origin and(2) locating the site and nature of the origin ofthe pain (Box 29-1). Importantly, although mostdental pain results from inflammatory changes,such inflammation of pulp and periradicular tis-sues is often not painful. In fact, pain severeenough for the patient to seek dental treatmentmay occur only a small proportion of the time.

522

29 / Differential Diagnosis of Orofacial Pain

Many inflammatory pulpal or periradicular le-sions are detected by chance in a patient with nohistory of previous pain.

Pain Mechanisms

Differential diagnosis must be based on an un-derstanding of pain mechanisms. This is still anarea of discovery; a comprehensive account is notcurrently possible. Only a very brief summary ofcontemporary knowledge is possible here. Moredetails may be sought elsewhere.3-7

Many hypotheses have been developed in at-tempts to explain the mechanics of pain. Themost distinct and distinguished of these are the

"specificity theory" and the "gate control theory."Although originally developed as alternatives, thekey elements of "specifity"3,5 and "gating"3.6.8 arecompatible.

SPECIFICITY

A longstanding belief is that a specific part of thenervous system is responsible for carrying painfrom pain receptors to a pain center in the centralnervous system. There are, in fact, some nervefibers that respond only (or maximally) to stimuliin the noxious range. However, the existence ofsuch a dedicated "pain system" is not sufficient, initself, to explain all experimental and clinical fea-tures of pain. Referred pain (in which the sensation


523

FIGURE 29-1Gating in the central nervous system. Large and small afferent fibers interact through a gating mechanism in thedorsal horn of the spinal cord and trigeminal nucleus (dorsal horn gate). Branches of the afferent fibers act onspecialized interneurons, the spinal gating cells (SG), which, by presynaptic inhibition, control input to the trans-mission cells (T cell). These cells are the second-order sensory neurons responsible for passing on sensory inputto higher nerve centers where motivational/affective factors and the sensory discriminative components interact,which may result in perception of a pain experience and lead to motor activity. The dorsal horn gate is alsoi nfluenced by descending central control. (Adapted from Melzack R, Wall PD: Science 150:971-979, 1965.)

is incorrectly localized) and pathologic pain (suchas trigeminal neuralgia, which is initiated by mildnonnoxious stimuli) as well as the clearly docu-mented effects of emotional and motivational fac-tors require an explanation. The best explanationincludes mechanisms such as summation and in-hibition acting on a "gate' which controls theprogress of potentially painful input.3.8

GATING

All incoming afferent activity from the peripheralnervous system is subject to modulating effectsupon entering the central nervous system (Fig-ure 29-1). The central nervous system actually fil-ters and integrates a vast amount of sensory in-formation, only a very small proportion of whichwill reach the level of consciousness. Much ofthe information is discarded and much is used inunnoticed autonomic reflex activities. Incomingnoxious information is a part of this overall pat-tern. The integrating process has been describedas analogous to a gate. When the gate is open, in-coming sensory activity passes through and goeson to the next level.

The anatomic substrate of the gating mecha-nism for pain is in the dorsal horn of the gray

matter of the spinal cord and brainstem. The gateeither inhibits or facilitates the activity of trans-mission cells that carry activity further along thenervous pathway. A number of factors determinewhether the gate is open or not. One importantfactor is the relative degree of activity in large di-ameter AB fibers and small diameter A8 and Cfibers. The large diameter AB fibers are activatedby nonnoxious stimuli, and the small A8 and Cfibers by noxious stimuli. Large fiber activitytends to close the gate, whereas small fiber activityopens the gate. Descending control mechanismsfrom higher levels in the central nervous systemare influenced by cognitive, motivational, and af-fective processes. These higher level mechanismsalso modulate the gate. Activity in large afferentfibers not only tends to close the gate directly butalso activates the central control mechanisms,which may also close the gate.

When the gate is open and activity in the in-coming afferents is sufficient to activate the trans-mission system, two main ascending pathways areactivated. One is the sensory-discriminative path-way, which connects to the somatosensory cortexby way of the ventroposterior thalamus. Thispathway allows the localization of pain. Thesecond ascending pathway involves the reticular

524


information through the medial thalamic andlimbic system, which deals with the unpleasant,aversive, and emotional aspects of pain. Descend-ing pathways, as well as acting on the dorsal horngate, may also interact with these two ascendingsystems. One of the principal descending path-ways uses endogenously secreted opioid-like pep-tides (e.g., endorphin) to suppress or reduce trans-mission in pain pathways.

Pain as an Experience

This overall description of the processing of nox-ious information integrates the presence of recep-tors and pathways specialized to conduct pain. Italso explains how this noxious information maybe suppressed, amplified, or altered by other affer-ent input as well as by the influence of higher cen-ters. Hence pain is not a simple sensation such astouch, heat, or taste but an "experience," resultingfrom extensive integration.'

This outline explains the versatility of pain.Why, for example, do similar tissue injuries pro-duce different degrees of pain either in differentindividuals or in the same individual on differentoccasions? This difference occurs because of vari-ations in the magnitude and effect of other inputsand higher nerve centers. The involvement ofhigher centers can also explain why the pain expe-rience can vary with age9.10, gender,10 and culturalbackground. 11-13 The flexible pain "system" alsoallows recognition of the difference between acuteand chronic pain. Acute pain provides a warn-ing of actual or impending tissue damage and isessential to survival. Significantly, subjects whoshow congenital insensitivity to pain have a shortlife expectancy. Chronic pain such as trigeminalneuralgia has no survival value but is interpretedas a disease of the pain system.

pulp14 (e.g., substance P, calcitonin gene-relatedpeptide, neuropeptide Y) primarily regulate bloodflow." Many peptides are released from sensoryterminals by axon reflexes in neurogenic inflam-mation. The principal role of the afferent innerva-tion of the dental pulp may not be sensory but va-somotor and possibly trophic.

Other mechanisms such as referred and psy-chogenic pain require the inclusion of central in-teractions. In general, the differential diagnosis ofdental pain requires identifying pain from othersources (real or imagined), such as psychogenicand chronic pain, as well as from other sites, suchas pain from the muscles of mastication.

Social, cultural, and sex- and age-related fac-tors all affect the pain experience through theemotional-motivational component. For exam-ple, the pain threshold is similar in different racialgroups but pain perception may differ betweendifferent groups.9,11 Social and cultural factors de-termine the symptoms that patients emphasize.12

The characteristics of pain can change with timebecause of the adaptation of peripheral receptors,facilitation or fatigue among central connections,or a number of other causes. The central nervoussystem exhibits considerable plasticity. Persistingnoxious input, particularly from C fibers, can pro-duce changes in the dorsal horn neurons, especiallyin the presence and distribution of membrane re-ceptors." The changes in these altered neurons canpersist long after the original stimulus, a phenom-enon known as central sensitization or "wind-up."" These long-term changes in excitability canlead to spontaneous pain or decreased pain thresh-olds and may be a component of some chronicpain syndromes. It is also possible that the so-called "hot tooth" syndrome in which a tooth withlongstanding, intense pulpitis is difficult to anes-thetize may be the result of this effect.

The Versatility of Pain

Many elements contribute to the experience ofpain. Therefore the presentation of pain may behighly variable and the identification of the sourceand cause may be difficult.

Some pain characteristics arising from andaround the teeth (for example, the hyperalgesiathat occurs with inflammation) may be explainedby the sensitization of nociceptors. Many inflam-matory mediators, neuropeptides, growth factors,and other cyrokines are involved in tissue injuryand the body's response. This array of factorsgives wide variability in the response to tissue in-jury. Many of the peptides present in the dental

Superficial Versus Deep Pain

Pain arising from damage to deep visceral tissuediffers from that arising from superficial tissues.Viscera are insensitive to procedures such as cut-ting or burning but are highly sensitive to disten-sion, pressure, and inflammation. Pain from deeptissues is poorly localized. In contrast, larger, fasternerve fibers in superficial tissues and less centralconvergence allow more precise localization of su-perficial pain. Pulpal pain may be considered deep(visceral). Periradicular pain is superficial (periph-eral). Thus extension of inflammation from a deepsite (pulp) to a superficial one (periradicular tis-sues) often allows localization of the tooth that isthe culprit.

PERIODONTAL PAIN

Periodontal disease is widespread primarily be-cause it is largely painless. It may occasionallymanifest with acute pain such as that associatedwith a lateral periodontal abscess. Periradicularinflammation extending from a necrotic or in-flamed pulp may be painful when acute but notwhen chronic. Mild inflammation arising fromthe early stages of the extension of pulpal diseaseor from a high restoration may result in tender-ness without spontaneous pain. Locating a toothwith periodontal pain is usually straightforwarddue to the presence of proprioceptors whose posi-tion the nervous system is able to identify.'

PULPAL PAIN

Pulpal inflammation is often not painful. Manypatients with pulpal necrosis and periradicularpathosis relate no history of endodontic pain.However, at times, an inflamed pulp may be ex-quisitely painful, causing spontaneous, throb-bing, and intense pain that is worsened by hotand cold stimuli.' When pain is not spontaneousbut evoked by a stimulus, it may outlast the stim-ulus. It is unclear why pulpal inflammation is,on some occasions, painful and, on other occa-sions, not painful. If evoked pain from pulpitissignificantly outlasts the stimulus, the pulpitis isdeemed "irreversible." If the pain subsides quickly,the inflammation is more likely "reversible."

Unfortunately the correlation between symp-toms and the histologic condition of the pulp isnot consistent. Patients describe pain from pulpi-tis in a variety of ways. It may increase and throbwhen they are lying down. It may present as a con-tinuous dull ache that is increased by a stimulus.The pain is intermittent and may abate suddenlyfor no apparent cause or, conversely, awaken thepatient.

Pulpal pain tends to be diffuse and to be re-ferred. As the pain increases in intensity it mayspread to the ear, temple, cheek, or other teeth, al-though never across the midline." If the inflam-mation extends into the periradicular tissues, lo-calization is usually easier, presumably because ofproprioceptors.

Phenomena Complicatingthe Diagnosis of Dental PainREFERRED PAIN

Referred pain in the oral and perioral region iscommon and important." By definition, referredpain comprises input from a site of tissue damage


525

FIGURE 29-2Referred pain mechanism. Afferent nerves from a variety of

tissues converge on the cell body of the second-order neuron(the transmission T cell) in the brainstem, which stimulatesthe action system. Once the T cell is activated, it may be dif-ficult for higher centers to determine the exact location of the

i nitiating pain, which may be wrongly assigned. A higher cen-ter may assume that the painful input comes from a recentlyactivated pathway, resulting in the assignment of painful

i nput to a recently restored tooth.

combined with input from another site wherethere is no tissue damage; therefore the pain is re-ferred and is perceived to originate from the site ofno damage. The convergent neurons are the cellsin the dorsal horn gate. When the transmissionsystem is activated and nerve impulses pass alongthe sensory discriminative pathway, the highercenters in the brain are unable to distinguish thesource of the noxious stimuli (Figure 29-2). There-fore the brain may interpret the source wrongly,particularly when previous non-noxious stimulihave been received from the same (referred) site.

This pattern explains the not uncommon phe-nomenon of pain being referred to a recently re-stored tooth. Pain from a tooth may then seem tooriginate from a different tooth. Tooth pain mayalso appear to originate from a nondental site or,conversely, a tooth may be identified as the sourceof pain when the origin is nondental. A good ex-ample (and a common occurrence) is pain fromsinusitis being referred to a maxillary molar.

Odontogenic pain is more likely to be referredwhen it is more intense, but duration and qualitydo not seem to be related to referral. The associa-tion of intensity to referral is attributed to centralnervous system hyperexcitability (central sensiti-zation), causing the expansion of receptive fields.Pain is never referred across the midline but read-ily from arch to arch.

Some referral patterns are more common thanothers; it is important to be aware of these possi-bilities. When the offending tooth is not obviousand cannot be stimulated to reproduce the pa-tient's symptoms, examination should be ex-tended to include these other possibilities. For ex-ample, muscles of mastication, the ear, sinuses,the heart, and other teeth may be the source of thereferred pain.

526


Muscles of Mastication Ear, Nasal, and Sinus Mucosa

Many patients with myofascial pain dysfunctionsyndrome describe toothache among their symp-toms. Some may describe a toothache but be un-aware that the problem is a joint/muscle disorder.This pattern of referral is common and may resultin unnecessary extraction or root canal therapy. Itis important to examine the temporomandibularjoint and muscles of mastication in the diagnosisof all but the most obvious toothaches. 19-22

CASE

PAIN REFERRED TO A TOOTH

FROM MUSCLES OF MASTICATION

Referred pain from respiratory mucosa to teethhas been demonstrated by stimulating the mu-cosa 1 week after cavity preparation. Clinically,posterior maxillary teeth are tender to mastica-tion and hypersensitive to cold. The patient oftengives a history of an upper respiratory tract infec-tion or recent pollen allergies. The inflamed, fluid-filled sinus may be tender to pressure anterior tothe zygomatic buttress. Pain increases when thepatient lowers his or her head or jumps and landson the heels with a jarring motion. Pain of dentalorigin can also be referred to the ear and preauric-ular region and may present as tinnitus. 23-25

Complaint: Moderately severe but continuous dullache in left lower jaw.History: The pain has lasted several weeks, beingmost severe in the morning. It is not intensifiedby hot and cold stimuli and is relieved temporar-ily by mild analgesics. A three-unit mandibular-posterior bridge had been placed a few days ear-lier. There was neither recent acute infection nortrauma. The referring dentist had completed rootcanal treatment on the premolar abutment withno change in symptoms.Examination: No visible or palpable intraoral softtissue abnormalities are present. All teeth on theleft side respond within normal limits to vitalitytests and percussion. Radiographs show no hardtissue lesions. Discomfort is not relieved by an in-ferior alveolar nerve block. Palpation of the leftmasseter muscle shows it to be acutely tender, par-ticularly on the anterior border. Occlusal examina-tion shows imbalances and premature contacts onthe left side. Injecting a local anesthetic into thetender region of the muscle relieves the pain.Diagnosis: Acute myofascial pain in the left mas-seter muscle after dental treatment.Etiology: Afferents from the muscle (probably intendons or fascia) converge on the same second-order neuron in the brainstem trigeminal nucleusas periodontal afferents from the mandibularabutment teeth. The higher centers to which thesecond-order neuron projects are unable to differ-entiate between the two inputs. The higher nervecenters "assume" that the new input (from themuscle) originates from the same site as the orig-inal input (the teeth).Treatment: A night guard was worn for 1 weekfollowed by occlusal adjustment. Short-termsplint therapy was necessary to ensure that oc-clusal changes did not occur while the musclewas in spasm.

Complaint: Continuous, dull, widespread tooth-ache from the maxillary molars bilaterally.History: Symptoms have recurred on several occa-sions over a period of years; the discomfort at timesspreads over the cheek. Teeth are tender to masti-cation and somewhat sensitive to cold. Symptomsseem to resolve spontaneously. The patient has fre-quent colds and often feels "stuffed up."Examination: Nasal and oropharyngeal dischargeand inflamed mucosa are seen. Tenderness is re-ported with strong pressure to the cheek. Soft tis-sues around the teeth are normal. The molars re-spond briefly and sharply to a cold stimulus but notwith lingering pain. Other teeth test within normallimits. Maxillary molars on both sides are slightlytender to pressure. Radiographs reveal no caries,deep restorations, nor periradicular pathosis.Diagnosis: Acute upper respiratory tract infectionwith involvement of the maxillary sinuses.Etiology: Afferents from both mucosa and teethconverge on the same second-order neurons inthe brainstem. Possibly, some afferents supplyingthe teeth that travel along the wall of the sinus arealso stimulated "en passant" by sinus pressure.Treatment: No dental treatment was indicated.The patient was referred to her medical practi-tioner to treat the respiratory complaint. On re-call, the "toothaches" had resolved; all molars re-sponded within normal limits to vitality andpercussion tests.

Cardiac Origin

Cardiac disease may refer pain to the teeth. Painarising from both narrowing of the coronary

CASE

PAIN REFERRED FROM NASAL

AND ANTRAL MUCOSA

artery (angina pectoris) and myocardial infarctionmay refer to either arch but most commonly tothe left mandible .26.28 Occasionally the oral symp-toms are not accompanied by chest pains; cardiacpain is felt only in the face and jaws.

CASE

REFERRED PAIN OF CARDIAC ORIGIN

Complaint: Dull toothache in tooth No. 20, usu-ally after physical exertion.History: The patient has a long history of cardiacdisease with previous infarctions and two bypassoperations. The hospital cardiac unit referred himfor dental evaluation and treatment before per-forming a third surgical procedure. Radiographsreveal a periradicular lesion on tooth No. 20, al-though the tooth is asymptomatic. Neither as-pirin nor acetaminophen relieves the pain, butamyl nitrite does.Diagnosis: Angina pectoris referred to a toothwith an otherwise asymptomatic lesion.Etiology: Cardiac pain is a "deep" pain and as suchis poorly localized. Oral and cardiac afferents arelikely to converge above the brainstem level.Treatment: Tooth No. 20 was treated endodonti-cally with appropriate medical precautions. Thepatient was warned that the discomfort mightcontinue with referred pain until his cardiac prob-lems were resolved.

Other Teeth

Toothache may refer not only to nondental sitesbut to other teeth as well .29

CASE

TOOTH-TO-TOOTH REFERRAL

Complaint: Intermittent, poorly localized, dullpain in the upper right quadrant.History: The pain has lasted several weeks, follow-ing no fixed pattern. Root canal treatment oftooth No. 4 was completed 1 year ago and treat-ment of tooth No. 3 was done 2 months ago. Thereferring dentist suspected that tooth No. 3 wasthe problem and retreated the tooth, but symp-toms did not resolve.Examination: No soft tissue abnormalities are visi-ble or palpable in the area. None of the teeth aretender to percussion and palpation. Teeth with-out root canal treatment respond within normallimits to vitality tests, although a response intooth No. 2 is slow to develop. Radiographs reveal


527

apparently successful root canal treatment ontooth No. 3 and tooth No. 2 has a crown withthree pins visible.

The patient was treated symptomatically withanalgesics and advised that a definitive diagnosiswas not possible until symptoms were focused.The discomfort level increased 2 weeks later. Onexamination tooth No. 2 is very tender to pressureand responds to electrical and thermal stimuli, al-though now with lingering pain. All other teethremain asymptomatic.Diagnosis: Irreversible pulpitis and acute apicalperiodontitis in tooth No. 2 that became localizedas inflammation spread from the pulp to peri-radicular tissues.Etiology: Afferents from teeth Nos. 2, 3, and 4converge on the same brainstem neuron. Possiblywhen the origin and site of referral are close to-gether, afferent fibers branch and supply twoteeth.Treatment: Pulpectomy of tooth No. 2 resolvedthe symptoms. This was followed by full rootcanal treatment. Symptoms have not returned.

SPREADING PAIN

As inflammation increases and mediators spreadthrough the adjacent tissues, pain may diffusein an increasingly wider area.""' The pain maynot be localizable because the origin is some-where within that area. This is primary spread-ing pain. The term secondary spreading pain de-scribes pain from muscle spasms. These mayresult from masticatory function disturbed by apainful tooth.

CASE

SPREADING PAIN

Complaint: Soreness of the temporomandibularjoint and stiffness in the jaw musculature result-ing in trismus.History: Two months earlier a periradicular ab-scess on tooth No. 14 had spread through softtissues, causing extensive swelling. Incision anddrainage followed by root canal treatment re-sulted in resolution of tooth symptoms, althoughjoint soreness and stiffness persisted.Examination: Tooth No. 14 is asymptomatic afterapparently successful root canal treatment. Open-ing of the jaw is limited with tenderness of theanterior border of the right masseter muscle.Diagnosis: Spasms in the right masseter muscle.Etiology: The spread of inflammatory mediatorsfrom the periradicular abscess induced spasms in

528


the masseter muscle. These spasms often persistafter resolution of the inflammation.Treatment: Therapy is focused on the musclespasm. Heat, exercise, and possibly muscle relax-ants should be effective.

PSYCHOGENIC PAIN

Pain has strong emotional and affective compo-nents .32 The gate control theory helps to explainthis by incorporating the role of higher nervecenters in the overall description of pain mecha-nisms. Support comes from the finding that anti-depressant drugs, particularly tricyclic antidepres-sants are often effective for treating chronic painsyndromes. Importantly (and confusingly), painmay originate in higher centers even withoutinput from peripheral nerves. A patient sufferingfrom psychogenic pain often indicates a painfulsite. Because the mouth and face have unusualemotional significance, these sites are commonlyindicated as major sources of pain. The complexpsychology of psychogenic pain is beyond thescope of this chapter. Accurate diagnosis andtreatment are difficult. Importantly, psychogenicpain is common and should be included in a dif-ferential diagnosis. A psychologic component issuspected when the pain does not fit known phys-iologic patterns:

No identifiable originMultiple (particularly when bilateral) painsitesNo predictable response to therapy (espe-cially analgesics)Unusual, inconsistent, nonanatomically log-ical pain patternsNo demonstrable etiology for the pain

As a clue, patients suffering from psychogenicpain often focus on social and emotional prob-lems when giving their history. Although all painhas an emotional component, with psychogenicpain it is the predominant component. Psycho-genic pain is a tentative diagnosis of last resortand an indication for referral. Often there is a truecause for the pain, but the dentist is unable tomake a definitive diagnosis and mistakenly dis-misses the problem as being of emotional or psy-chogenic origin.

CASE

PSYCHOGENIC PAIN

Complaint: A 45-year-old woman was seen with acontinuous, moderate, dull, but occasionally severeache from bilateral temporomandibular joints and

molars. Discomfort began with the onset of mari-tal problems and financial hardship. Root canaltreatment of tooth No. 3 provided temporary relief,as did occlusal splint therapy and pharmacologictreatment for depression. However, the discomfortreturned.Examination: Clinical and radiographic examina-tions of teeth show no abnormalities. Treatmentof tooth No. 3 appears successful. Palpation of thetemporomandibular joint reveals no abnormality.Further questioning reveals extended emotionalstress after marital break-up.Diagnosis: Orofacial pain of psychogenic origin(tentative).Etiology: Pain originates from higher nerve cen-ters and is probably entirely affective. Variousforms of treatment are transiently effective be-cause they affect higher central nervous systemcenters.Treatment: Long-term relief depends on the emo-tional problems sustaining the central nervoussystem changes being removed or on the patientadopting suppressive strategies. A careful non-judgmental explanation of psychogenic pain wasgiven to the patient. In particular, the contribu-tion of both organic and psychologic componentsto the pain experience was described. Clearly thepatient was experiencing pain, but, because noorganic cause was evident, interventional dentaltreatment would not bring long-term relief. Ad-dressing the emotional component of the painwith the help of a physician, family, and othersupport services may eliminate it. The prescrip-tion of antidepressants by the physician is virtu-ally always a component of treatment.

HEADACHES

Headaches are the most common painful entitiesof the head and neck .33 The pain is often referredto teeth and may be confused with toothache.Headache presents in many forms. There are manyclassifications but two primary groups of head-aches: functional and organic.

Functional

Functional headaches are caused by vascular (mi-graine, cluster, toxic vascular, and hypertensive),musculoskeletal, and emotional disturbances.

Migraine headaches. These may be referred tothe teeth (commonly the maxillary canine teethand premolars), although the principal experienceis headache.34 Classic migraine is readily diag-nosed (unilateral throbbing associated with pho-tophobia and nausea); patients usually have a his-

29 I Differential Diagnosis of Orofacial Pain

529

tory of recurrent episodes. Atypical variants mayconfuse diagnosis.

Cluster headaches. These are severe. The patientexperiences several (sometimes daily) within a2- or 3-month period, each lasting up to anhour . 3s The pain is usually limited to the distri-bution of the first and second divisions of thetrigeminal nerve and may be manifest in the max-illary and occasionally the mandibular teeth.

Tension headache. This is the most commonform of headache. Involved are muscle spasmsthat induce pain, which may be referred over awide area, including the forehead, temples, andback of the neck.1

Organic

These headaches are caused by mass lesions (tu-mors, hematomas, and so on), infection, arteritis,phlebitis, vascular occlusion, cranial neuralgias,and diseases of the eye, ear, nose, throat, and teeth.

Brain tumors may produce a range of no to se-vere headache. When present, the headache ismost often a deep, aching, steady, dull pain. Themost severe head pains are associated with neu-ralgias and vascular headaches. Headaches causedby intracranial hematomas usually are seen afterinjury.

NEURITIS

Neuritic pains from nerves supplying teeth oftencause or mimic toothache.' A neuritis may arisefrom trauma or spread of disease (inflammatoryor neoplastic) from adjacent structures. Neuritisis best distinguished from pain originating fromthe teeth by the history, which usually includestrauma, other disease processes, or other neuro-logic symptoms such as anesthesia, paresthesia,or occasional muscle weakness and paralysis.

TRIGEMINAL NEURALGIA

Trigeminal neuralgia is is initiated by innocuousstimuli from a trigger zone and causes severepain.1,36-38 More common in older patients, it hasa neuroanatomic pattern, usually being limited toone division of the trigeminal nerve, most oftenthe mandibular branch. Most trigger sites are ex-traoral but may be intraoral and therefore con-fused with tooth pain. The cause of trigeminalneuralgia is controversial.

ATYPICAL ORAL AND FACIAL PAIN

This poorly defined group includes conditionssuch as atypical facial neuralgia, atypical odontal-

gia, phantom tooth pain, and burning mouth. 6,39-41

Their most consistent characteristic is chronicpain of a steady intensity (usually burning butsometimes throbbing) that is poorly localized. Thepain often changes location and may cross themidline. Most patients are female. Because theseconditions may include tooth pain in their presen-tation, they are a source of possible misdiagnosis.Multiple dental procedures have often been con-ducted on patients with these conditions. Theetiology is unknown but a psychiatric basis isstrongly suspected. Treatment with antidepres-sants, commonly tricyclics, has been reported tobe successful though topical capsaicin may also beeffective.

Failure to recognize chronic pain may leadto inappropriate and ineffective treatment. In arather extreme example,41 a 22-year-old womanunderwent 38 separate root canal treatments,22 apicoectomies, and 12 extractions, all in a fu-tile attempt to relieve perceived oral pain. Herproblem was probably psychogenic.

Diagnostic Procedures

Thorough diagnosis of orofacial pain in some pa-tients may be difficult and time-consuming 1,42

and is beyond the scope of this chapter. The dis-cussion here is limited to determining whetherthe presenting pain is of dental or other originand, if dental, to locating its origin. The proce-dures and tests used in endodontic diagnosis weredescribed in Chapter 4. There is a definite ten-dency to attribute orofacial pain to a pulpal orperiradicular cause. Root canal treatment is notinitiated until indicated by a definitive diagnosis.

RECOGNITION OFDIFFICULT DIAGNOSES

In most cases the diagnosis of dental pain is rela-tively straightforward. The history identifies a con-sistent, logical pattern of symptoms. The patientindicates a particular tooth, which, when exam-ined, reveals a diseased pulp or periradicular tissuesand when stimulated, appropriately reproduces thesignificant symptoms described in the history. Anydeparture from this pattern should alert the den-tist (Table 29-1, Box 29-2 and Box 29-3).

APPROACH TODIFFICULT DIAGNOSES

The major weapons are knowledge, an under-standing of the mechanisms of pain, and, in par-ticular an appreciation of the phenomena of


531

referred and spreading pain and their patterns.Dental pains are extremely versatile and have thepropensity to simulate nearly any pain syndrome.

IMPORTANT CLUES

The following items are important clues in thedifferential diagnosis of orofacial pain:

Recent medical history may include colds orflu with suspected sinusitis and ear infec-tions. The symptoms may become worsewhen the head is lowered. Examination shouldinclude the oropharynx, sinuses, and ears for signsof inflammation.Stress and insomnia are correlated with brux-ism and myofascial pain syndromes. The pa-tient should be questioned about these condi-tions and habits; include an examination of themuscles of mastication and temporomandibularjoint.Recent dental treatment suggests that a com-promised pulp has succumbed to the finalinsult of cavity preparation and restoration.Pain is commonly referred to the most re-cently treated tooth or teeth. Pain in recentlytreated teeth should always be approached withsuspicion.The true origin of pain is sometimes silent,but pain may be initiated by direct stimula-tion. Stimulating the site of perceived pain nei-ther initiates nor worsens pain that has beenreferred from another source.Anesthetizing the site to which pain is referredmay reduce but not eliminate the pain. Anes-thetizing the true origin of the pain eliminatesthe pain. Selective infiltration anesthesia shouldbe conducted on maxillary teeth beginning withthe anterior teeth because these are more easilyanesthetized individually.

More than one source of pain is possible; thesources may be related. For example, atender tooth may cause an occlusal imbal-ance. Avoiding this tooth could lead to asecondary, painful muscle spasm. Pulpitis inmore than one tooth is uncommon, but in oc-clusal derangements several teeth may becometender.Pain from the pulp is poorly localized because itis a deep tissue. When the inflammationspreads to the superficial periodontium itbecomes well localized. Ifpain is poorly local-ized and pulpitis is suspected, allow for inflamma-tion to spread to the periodontal tissues, at whichtime localization will be clear.

REFERENCES

1. Okeson J: Bell's orofacial pains, Chicago, 1995, Quintes-sence Publishing.

2. Dubner R, Sessle B, Lavigne G: Physiology, diagnosis andmanagement of oro facial pain, Chicago, 2000, Quintes-sence Publishing.

3. Melzack R, Wall P: The challenge ofpain, ed 2, New York,1988, Penguin Viking.

4. Dubner R, Sessle B, Storey A: The neural basis of oral andfacial function, New York,1978, Plenum.

5. Willis W: The pain system, Basel, 1988, Karger.6. Wall P, Melzack R: Textbook of pain, ed 4, Edinburgh,

1999, Churchill Livingstone.7. Sessle B: Acute and chronic craniofacial pain: brain-

stem mechanisms of nociceptive transmission andneuroplasticity, and their clinical correlates, Crit RevOral Biol Med 11:57, 2000.

8. Melzack R, Wall P: Pain mechanisms: a new theory,Science 150:971, 1965.

9. Isberg A, Hagglund M, Paesani D: The effect of ageand gender on the onset of symptomatic temporo-mandibular joint disk displacement, Oral SurgOral MedOral Pathol Oral Radiol Endod 85:252, 1998.

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10. Riley J, Gilbert G, Heft M: Orofacial pain symptomprevalence: selective sex differences in the elderly? Pain76:97,1988.

11. Zola I: Culture and symptoms-an analysis of patients'presenting complaints, Am Soc Rev 31:615, 1966.

12. Craig K, Wycoff M: Cultural factors in chronic painmanagement. In Burrows GD, Elton D, Stanley G, ed-itors, Handbook of chronic pain management, Amsterdam,1987, Elsevier.

13. Moore R, Miller M, Weinstein P, et al: Cultural percep-tions of pain and pain coping among patients anddentists, Community Dent Oral Epidemiol 14:327, 1986.

14. Casasco A, Calligaro A, Casasco M, et al: Peptidergicnerves in human dental pulp: an immunocytochemi-cal study, Histochemistry 95:115, 1990.

15. Olgart L: Neural control of pulpal blood flow, CritRevOral Biol Med 7:159, 1996.

16. Bennett G: Update on the neurophysiology of paintransmission and modulation: focus on the NMDA-receptor, Pain 19:S2, 2000.

17. Mannion R, Costigan M, Decosterd 1, et al: Neu-rotrophins: peripherally and centrally acting modula-tors of tactile stimulus-induced inflammatory pain hy-persensitivity, Proc Natl Acad Sci USA 96:9385, 1999.

18. Falace D, Reid K, Rayens MK: The influence of deep(odontogenic) pain intensity, quality, and duration onthe incidence and characteristics of referred orofacialpain, JOrofac Pain 10:232, 1996.

19. Travell J: Temporomandibular joint pain referred frommuscles of the head and neck, J Prosthet Dent 10:745,1960.

20. Fricton J, Kroenig R, Haley D, Siegert R: Myofascialpain syndrome of the head and neck: A review of clin-ical characteristics of 164 patients, Oral Surg Oral MedOral Pathol 60:615, 1985.

21. Reeh E, El Deeb M: Referred pain of muscular originresembling endodontic involvement, Oral Surg OralMed Oral Pathol 71:223, 1991.

22. Raphael K, Marbach J, Klausner J: Myofascial pain:clinical characteristics of those with regional vs. wide-spread pain, J Am Dent Assoc 131:161, 2000.

23. Wright E, Gullickson D: Dental pulpalgia contribut-ing to bilateral preauricular pain and tinnitus, J OrofacPain 10:166, 1996.

24. Hutchins H, Reynolds O: Experimental investigationof the referred pain of aerodontalgia, J Dent Res 26:3,1947.

25. Silverglade D: Dental pain without dental etiology: amanifestation of referred pain from otitis media, JDent Child 47:358, 1980.

26. Matson M: Pain in the orofacial region associated withcoronary insufficiency, Oral Surg Oral Med Oral Pathol16:284,1963.

27. Natkin E, Harrington G, Mandel M: Anginal pain re-ferred to the teeth, Oral Surg Oral Med Oral Pathol 40:678, 1975.

28. Kreiner M, Okeson J: Toothache of cardiac origin, JOrofac Pain 13, 201, 1999.

29. Glick D: Locating referred pulpal pains, Oral Surg OralMed Oral Pathol 15:613, 1962.

30. Okeson J: Orofacial pain: guidelines for assessment, diag-nosis, and management, Chicago, 1996, QuintessencePublishing.

31. Sharav Y, Leviner E, Tzukert A, McGrath P: The spatialdistribution, intensity and unpleasantness of acutedental pain, Pain 20:363, 1984.

32. Baron R, Logan H, Hoppe S: Emotional and sensorfocus as mediator of dental pain among patients dif-fering in desired and felt control, Health Psychol 12:381,1993.

33. Dalessio D: Wolf's headache and other head pain, ed 4,New York, 1980, Oxford University Press.

34. Brooke R: Periodic migranous neuralgia: a cause ofdental pain, Oral Surg Oral Med Oral Patbol 46:511,1978.

35. Bittar G, Graff-Radford S: A retrospective study of pa-tients with cluster headaches, Oral Surg Oral Med OralPathol73:519, 1992.

36. Loser J: Tic douloureux and atypical facial pain, J CanDent Assoc 12:917, 1985.

37. Law A, Lilly J: Trigeminal neuralgia mimicking odon-togenic pain: a report of two cases, Oral Surg Oral MedOral Patbol 80:96, 1995.

38. Turp J, Gobetti J: Trigeminal neuralgia-an update,Compend Contin Educ Dent 21:279, 2000.

39. Brooke R: Atypical odontalgia, Oral Surg Oral Med OralPatho149:196, 1980.

40. Bates R, Stewart C: Atypical odontalgia: phantomtooth pain, Oral Surg Oral Med Oral Patbol 72:479, 1991.

41. Marbach J, Hulbrook J, Hohn C, Segal A: Incidence ofphantom tooth pain: an atypical facial neuralgia, OralSurg Oral Med Oral Patbol 53:190, 1982.

42. Okeson JP, Falace DA: Nonodontogenic toothache,Dent Clin North Am 41:367 1997.

Endodontic Therapeutics

LEARNING OBJECTIVES


/ Identify patients with a higher risk for experiencing pain after endodontic procedures.

2 / Understand the indications and contraindications for prescribing analgesics, antibiotics, anti inflammatory

agents and anxiolytics.

a / Develop a treatment plan consisting of appropriate endodontic and pharmacologic strategies for managing

pain, anxiety, and infection.

4 / Diagnose and treat odontogenic infections.

s / Monitor patient response to treatment.

6 / Make alternative therapeutic selections when required.

533

534

30 1 Endodontic Therapeutics

OUTLINE

Odontalgia

Predictors of Post-Treatment

Endodontic Pain

Risk Factors for Post-Treatment

Endodontic Pain

Flare-up

Pain Management Strategies: the "Ws"

Diagnosis

Definitive Treatment

Drugs

Antibiotics

Prophylactic Antibiotics for Medically

Compromised Patients

Antibiotics Used in Treatment

Selection of an Antibiotic Regimen

Role of Bacteria and Their Control

Anxiolytics

Oral

I nhalation

his chapter is not a complete reviewof the pharmacology of certain drugclasses. Instead, it reviews therapeutic

strategies for combining both pharmacologic andendodontic treatments for managing pain, infec-tion, and anxiety.

0dontalgia

The management of the endodontic patient doesnot end at the completion of the appointment.Continuing treatment includes strategies to con-trol pain and/or infection both before and aftertreatment. Thus endodontic therapeutics includesclinical procedures as well as appropriate adjunc-tive pharmacotherapy. Indeed the most commonform of orofacial pain is toothache (odontalgia),yearly affecting 12% of the population or about22 million citizens in the United States.' Thusstrategies for managing odontalgia are importantcomponents of root canal treatment.

Predictors of Post-TreatmentEndodontic Pain

Fortunately not all endodontic patients experiencepain after treatment. Studies have shown thatmore than one-half of endodontic patients do notreport post-treatment pain.2-4 However, this alsomeans that approximately 40% of patients expe-rience some pain after endodontic procedures,with about 20 percent of all patients reportingmoderate-to-severe pain .z 'Therefore patients whoare at increased risk for post-treatment pain shouldbe identified and receive additional pharmacother-apy for pain management.

RISK FACTORS FOR POST-TREATMENT ENDODONTIC PAIN

Unfortunately, there are no tests that reliably pre-dict which patients will experience pain; however,certain risk factors have been identified. Onemajor risk factor is the presence of preoperativepain or percussion sensitivity.-' This may be dueto hyperalgesia or allodynia initiated by pulpaland/or periradicular inflammation. Hyperalgesia(exaggerated pain response) is due to both pe-ripheral and central mechanisms and, signifi-cantly, can persist with little-to-no peripheralinput." Allodynia (a reduction in pain threshold)is identified by the symptom of painful chewingor a positive percussion rest, in which a normallyinnocuous stimulus (e.g., gentle tapping of atooth with a mirror handle) is now perceived as

30 / Endodontic Therapeutics

53 5

painful. As summarized in Box 30-1, patients withpreoperative hyperalgesia or allodynia have anincreased risk for developing post-treatment en-dodontic pain.9-11

FLARE-UP

A small proportion of patients (2% to 4%) experi-ence a post-treatment flare-up." A flare-up isthe development of severe post-treatment painand/or swelling that requires an emergency dentalvisit. Risk factors include apprehension, retreat-ment, female sex and age older than 40, a historyof allergy, and a diagnosis of pulpal necrosis. 10,11,14

Patients with an apical periodontitis who have en-dodontic treatment completed in one visit havean almost 10-fold increase in the risk of develop-ing a flare-up." Patients with risk factors shouldbe informed of this possibility; this may increasetheir compliance in taking analgesics and may de-crease the tendency to blame the clinician.

Pain ManagementStrategies: the "Ws"

A simple effective algorithm for managing thepatient with odontalgia is the "3D's": Diagnosis,Definitive treatment, and Drugs. First, the 3D'sprovides an easy mnemonic to summarize an in-tegrated approach. Second, this algorithm com-bines pharmacologic and nonpharmacologic ap-proaches to obtain maximal clinical benefit. Andthird, the order of the 3D's is a logical sequencefor developing a plan for management of post-treatment pain.

DIAGNOSIS

Diagnosis is the first "D" and is a critical initialstep in managing pain. Diagnosis of the cause andlocalization of the pain are critical in effectivepain management. Two general issues shouldbe considered in examining a patient with pain.First, can the chief complaint be reproduced? Ifthe chief complaint cannot be reproduced, thenpossibly the pain is originating from another lo-cation, including another tooth (see Chapter 29).This possibility can be evaluated by using a localanesthetic block to rule out pain referred fromdistant sites, although there are limitations in in-terpreting diagnostic local anesthetic injections(see Chapters 7 and 29).

The second general issue is identification of acause for the odontalgia. If the patient points to acertain tooth as the source of the pain, then clini-cal examination should reveal an etiologic factor.

In most cases odontalgia is due either to acutestimulation (i.e., dentinal hypersensitivity), totrauma, or to pulp inflammation. Thus clinicalexamination should reveal corresponding etio-logic factors such as exposed dentin, traumaticocclusion (or a history of trauma, bruxism, etc),caries, or a leaking restoration. If the suspectedtooth has no apparent etiologic factors that couldcontribute to the pain, then the differential diag-nosis should be expanded. It is appropriate andethical to consider referring the patient to a spe-cialist for more detailed clinical examination if ei-ther the chief complaint cannot be reproduced oretiologic factors are not apparent. Ignoring thesefactors may increase the risk of misdiagnosis andmistreatment.

DEFINITIVE TREATMENT

The second "D" refers to definitive dental treat-ment. Examples include pulpotomy, pulpectomy,incision for drainage, and even immediate extrac-tion for teeth with a hopeless prognosis. Definitivetreatment reduces or eliminates the peripheralcausative factors contributing to hyperalgesia, re-sulting in a significant reduction in pain levels.Figure 30-1 compiles data from studies of morethan 1000 patients with pain after endodonticprocedures. Whenever possible, data from thecontrol groups are shown (e.g., patients takingplacebo tablets instead of active analgesics); thusthe major source for the pain reduction presum-ably was the definitive dental treatment. Bothpulpotomy and pulpectomy substantially reducepost-treatment pain by 50% to 75%, comparedwith pretreatment pain values.

Figure 30-1 illustrates and reinforces an impor-tant therapeutic concept. The optimal method tocontrol post-treatment pain is to combine bothdefinitive treatment and appropriate drugs. Ef-fective treatment, such as canal debridement and

536


FIGURE 30-1

Evaluation of the effects of pulpotomy or pulpectomy on post-treatment pain in patients experiencing pain beforetreatment. Data are presented relative to the mean pre-treatment pain values reported for each study. Pre-treatmentpain values (solid lines at 100%) and mean post-treatment pain values (dashed arrows) are normalized by samplesize for each study. The first author, year, and reference number (in parentheses) are noted for each study.

irrigation, will reduce or eliminate many of the pe-ripheral factors that lead to activation of noci-ceptors innervating pulpal or periradicular tissue,thus altering the peripheral component of hyper-algesia. Prescribing drugs without dental treat-ment is unlikely to provide the same level of painrelief as compared to the combination of bothtechniques.

After definitive treatment, pain is often re-duced fairly quickly. An average time course ofpost-treatment endodontic pain is illustrated inFigure 30-2, as shown in a multicenter clinicaltrial." Two important concepts emerge from thisfigure. First, the best predictor of post-treatmentpain appears to be the magnitude of pretreat-ment pain. Figure 30-2 shows that patientswith moderate-to-severe pretreatment pain re-port greater pain after endodontic treatmentcompared with those who report no or mild pre-treatment pain. Second, on average, maximalpain is experienced in the first 24 hours of treat-ment with levels diminishing thereafter . 3,15-22

These pain predictors have important implica-tions for dispensing of analgesics. Patients who

are at increased risk (e.g., presenting with morepain) for post-treatment pain should take anal-gesics "by the clock" (e.g., every 6 hours) for thefirst 2 to 3 days. This maintains a more pre-dictable blood level of analgesics compared withthe traditional "take as needed" (prn) instruction.After 2 to 3 days, patients may then take anal-gesics as needed.

DRUGS

The third "D" refers to drugs. The three majorareas covered in this section on drugs are a flexibleprescription plan, the use of long-acting localanesthetics, and indications for steroids.

Analgesics

A flexible analgesic prescription strategy, based onresearch, has been developed. 5.23 The overall objec-tive of a flexible analgesic prescription strategy isto obtain maximal analgesia and minimal side ef-fects. Thus a flexible pain management plan se-lects the optimal analgesic based upon the pa-


537

FIGURE 30-2Time course of post-treatment pain in 53 patients. This was a multicenter clinical trial evaluating the effects ofvarious analgesics on post-treatment pain after anesthesia, isolation, and complete cleaning and shaping of theroot canal systems. Only patients given a placebo are presented in this figure. The patients are subdivided intofour groups depending on the magnitude of pre-treatment pain they reported before treatment. (Modifed fromTorabinejad M, Cymerman J1, Frankson M, et al: l Endod 20:345, 1994.)

tient's medical history, level of pain, and presenceof risk factors for post-treatment pain.

The selection of the appropriate analgesic isbased in part upon the observation that the non-narcotic component of a combination drug oftenprovides greater analgesia with fewer side effectsthan the opioid component. This is based on re-sults of studies evaluating both acetaminophen-codeine combinations (e.g., the equivalent of twotablets of Tylenol III and ibuprofen [200 mg]-hydrocodone [7.5 mg] combinations [i.e., theequivalent of Vicoprofen]).24.25 Thus analgesia canbe maximized with fewer side-effects by using thestrategy of first prescribing the most effectivedose of a nonnarcotic analgesic.

There are important dose-response considera-tions for the nonnarcotic drugs such as ibuprofenor acetaminophen, because they have a ceiling intheir dose-response curve. Thus after a maximallyeffective dose is ingested, additional amounts ofthe same drug will not provide a proportionateanalgesic benefit. This last point has importantclinical implications. Patients with endodonticpain should always be asked about how muchpain they have (i.e., estimated on a scale of 1 to 10)and about their recent history of analgesic use(type of analgesic, total dose, and time of lastdose). These factors will guide the selection of anappropriate analgesic treatment plan.

Figure 30-3 presents a simplified model of aflexible analgesic prescription plan. This plan is di-vided into two columns, for patients who can takenonsteroidal antiinflammatory drugs (NSAIDs)and for patients who cannot (e.g., those with activeulcers, ulcerative colitis, or asthma, or those witha potential interaction with certain concomitantdrugs). Each column is then divided into threegeneral categories of analgesic recommendationsbased on the level of pain or the clinician's assess-ment of risk factors for post-treatment pain. Theoverall strategy is to first obtain the best analgesiaas a result of the use of the nonnarcotic drug andthen to add narcotic drugs when needed for ad-ditional pain control. This approach maximizesanalgesia benefit while minimizing the potentialfor side effects.

NSAIDs alone are usually sufficient for patientswho can tolerate them because of the relatively lowincidence of post-treatment pain (most patientshave no to slight pain). 3,4 Thus a prescriptionfor an NSAID, such as ibuprofen 600 mg every6 hours, is optimal for the majority of patients. Ifpatients cannot tolerate an NSAID, a 1000 mgdose of acetaminophen is often suitable for man-aging post-treatment pain.

Some patients have moderate-to-severe post-treatment pain 4; these patients may not obtainadequate pain relief by a single drug approach.

538

30 1 Endodontic Therapeutics

FIGURE 30-3A simplified analgesic prescription plan to guide drug selection based upon patient history and level of presentpain or anticipated post-treatment pain. NSAID, Nonsteroidal anti inflammatory drug.

For these patients, there are two general analgesicapproaches. A first approach is to coprescribe thealternating schedule of NSAID described earlierwith an acetaminophen-opioid combination (Fig-ure 30-3). This provides predictable control for se-vere pain and can be used to modify a standardNSAID-only regimen if pain control is inade-quate.26-27 Moreover, all three drugs (the NSAID,acetaminophen, and the opioid) are active anal-gesics that can have additive effects when com-bined .25,27.28 A second general approach would beto switch to a fixed drug combination of ibupro-fen 200 mg with hydrocodone 7.S mg (e.g., Vico-profen); this combination is effective for pain ofinflammatory origin .25 In general, a flexible anal-gesic prescription strategy offers the best combi-nation of pain relief with minimal side effects, inaddition to providing the clinician with a rationalapproach for customizing an analgesic plan suit-able for the patient's needs.

Local Anesthetics

Another important element in a review of thethird "D" of pain control (drugs) is local anes-

thetics. Chapter 7 provides a detailed descriptionof the use of local anesthetics. Local anestheticsoffer the benefit of prolonged pain control aftercompletion of the endodontic appointment.Long-acting local anesthetics, etidocaine or bupi-vacaine, offer prolonged pain control for up to6 to 8 or more hours after injecrion.29,30

However, recent basic research on pain mecha-nisms have revealed the existence of a centralcomponent to hyperalgesia, which can be estab-lished by an intense barrage of activity from pe-ripheral nociceptors. 6,8 The preemptive analgesia hy-pothesis states that clinical pain is reduced if theperipheral barrage of nociceptors is reduced .31

Subsequent studies on orofacial pain have pro-vided support for this concept. For example, pa-tients given a bupivacaine injection for an inferioralveolar nerve block before an oral surgical proce-dure reported less pain at 2 days after the proce-dure compared with placebo-injected patients . 32

This result is not restricted to extraction pro-cedures because infiltration with bupivacaine be-fore tonsillectomy reduced postoperative painfor 7 days compared with placebo injections .33

Collectively, these studies indicate that long-


539

acting local anesthetics should be considered fortreating endodontic pain patients.

Steroids

Steroids represent another example of the third"D" of pain control (drugs). In general, the de-cision to use a drug depends on the risks, bene-fits, patient factors, and pharmacologic alter-natives. The decision to prescribe steroids isnot always simple because potential risks in-clude suppression of immune function andwound healing. Single-dose administration ofa steroid produces a reduction in circulatinglymphocytes and monocytes for 24 hours withno reduction in circulating neutrophils or anti-body response . 34

Controlled clinical trials for mild-to-moderatepain indicated that steroids provide analgesiain patients with endodontic pain after oral, in-tramuscular, or intracanal routes of adminis-tration .22,35,36 Short-term administration of ste-roids may have a place in management ofendodontic pain for patients in whom the bene-fits outweigh the potential modulation of infec-tion, wound healing, or other adverse effects.However, this benefit must be balanced againstthe known efficacy of alternative drugs (e.g.,NSAIDs) and the particular factors of each case.No evidence supports the prophylactic use ofsteroids for prevention of more severe levels ofendodontic pain.

AntibioticsAs described above, odontogenic pain is best man-aged by a combined approach using both localtreatment and pharmacotherapeutic measures.The same philosophy holds for odontogenicinfections-optimal management includes bothdefinitive treatment (e.g., canal debridement and,often, incision for drainage) and pharmacologicadjuncts (e.g., antibiotics) when indicated. Sys-temic antibiotics are not a substitute for properlocal treatment. Indeed, the vast majority of en-dodontic infections can be treated without antibi-otics. Pain and swelling are managed by debride-ment of the pulp space and drainage of the softand hard tissues. Healthy patients without sys-temic signs and symptoms of infection but withsymptomatic pulpitis, symptomatic apical peri-odontitis, a draining sinus tract, or localizedswelling do not require antibiotics .37.38

Likewise, the use of "prophylactic antibiotics"to prevent post-treatment pain or flare-ups afterroot canal treatment is neither effective, rational

nor justified . 394° Even if antibiotics were helpful,because only a small percentage of endodontic pa-tients experience a flare-up, the risk-benefit ratiowould not support their routine use. 12,14,41,42 Theuse of prophylactic antibiotics places patients atrisk for side effects. In addition, these patients aresubjected to the possibility of selection of resis-tant microorganisms and "superinfections." Also,antibiotics may be very costly.

PROPHYLACTIC ANTIBIOTICSFOR MEDICALLYCOMPROMISED PATIENTS

Medically compromised patients who have an in-creased risk of a secondary infection at a distantsite (metastatic) after a bacteremia include thosewith rheumatic or congenital heart disease, pros-thetic cardiac valves, mitral valve prolapse withregurgitation, previous infective endocarditis,systemic pulmonary shunts, indwelling arteri-ovenous shunts, uncontrolled diabetes, and animmunosuppressed or immunologically defi-cient status. These dental patients who are atrisk of metastatic infection after a bacteremiamust receive a regimen of antibiotics that eitherfollows the recommendations of the AmericanHeart Association (AHA) or is determined in con-sultation with the patient's physician. A team ap-proach by the patient, dentist, and physicianhelps to ensure compliance and adequate ther-apy." ," The regimens recommended by the AHAare given in Table 30-1.

The AHA recommends the use of antibiotics toprotect against endocarditis for canal instrumen-tation beyond the apex, for endodontic surgery,and for anesthesia delivered via the periodontalligament.43.44 Although the incidence of bac-teremia is low with root canal procedures, a tran-sient bacteremia can result from instrumentationconfined to the root canal45,46 Care must be takenwhen positioning rubber dam clamps and per-forming other procedures that may producebleeding with an accompanying bacteremia. Theuse of chlorhexidine, povidone-iodine, or iodine-glycerin on isolated and dried gingiva for 5 min-utes along with irrigation of the gingival sulcusbefore surgical procedures are performed hasbeen recommended .43,47

Antibiotic prophylaxis guidelines for patientswith total joint replacements have recently beenupdated .4s Patients considered to be at risk in-clude immunocompromised/immunosuppressedpatients, insulin-dependent (type I) diabetic pa-tients, patients who have had joint replacementsin the past 2 years, and those with previous jointinfections, malnourishment, and hemophilia .48,49

540


TABLE 30-1

Adapted from Dajani A, Taubert K, Wilson W, et al: Prevention of bacterial endocarditis: recommendations by the American Heart Association,

JADA 128:1142-1151, August 1997. Copyright 0 1997 American Dental Association. Reprinted by permission of ADA Publishing, a Division of

ADA Business Enterprises, Inc.IV, Intravenous; IM, intramuscular.

"Total children's dose should not exceed adult dose.tCephalosporins should not be used in individuals with immediate-type hypersensitivity reactions (urticaria, angioedema, or anaphylaxis) to

penicillins.

ANTIBIOTICS USED IN TREATMENT

An antibiotic regimen should be prescribed inconjunction with the appropriate endodonticprocedure when there is systemic involvement, apersistent infection, or a spreading infection. Thesigns and symptoms of systemic involvement andspread of infection include fever (>100° F or>38' C), malaise, cellulitis, progressive abscess,and unexplained trismus, alone or in combina-tion. Under these circumstances, an antibioticshould be given only as an adjunct to debride-ment and drainage or extraction when indicated.Patients with these signs and symptoms must beclosely followed on a daily basis, in person or bytelephone. After the source of infection has beentreated, improvement is usually rapid. Systemi-cally administered antibiotics will not be effectiveagainst a reservoir of microorganisms in an in-fected root canal system or a periradicular abscessbecause of absence of normal circulation.

Initial empirical selection of an antibiotic (an-timicrobial agent) is based on the microorgan-isms commonly associated with endodontic in-fections.50,51 The clinician must be thoroughlyfamiliar with the drug and inform the patient of

benefits, side effects, and possible sequelae of nottaking the proper dosage. If the patient's condi-tion does not rapidly improve, consultation or re-ferral to a specialist should be done immediately.

SELECTION OF AN

ANTIBIOTIC REGIMEN

Under ideal circumstances, susceptibility test-ing would be undertaken before the prescriptionof antimicrobial drugs. Unfortunately with thepolymicrobial nature of endodontic infections,it may take from several days to weeks to obtaina complete susceptibility profile of the bacteria.Therefore by necessity, the initial antibiotic pre-scribed is empiric. Penicillin VK remains the firstantibiotic (antimicrobial) of choice because ithas remained effective against most of the facul-tative and strict anaerobes commonly found inpolymicrobial endodontic infections .50-5 3 Bac-teria sensitive to penicillin include anaerobes(Porpbyromonas, Prevotella, Peptostreptococcus, Fu-sobacterium, and Actinomyces), and Gram-positivefacultative bacteria (e.g., streptococci and ente-rococci).50-53

Penicillin is inexpensive and has low toxicity,but importantly, approximately 10% of the popu-lation may be allergic to this medication. Most al-lergic reactions occur in patients with no reportedhistory of penicillin allergy.54 However, obtaininga careful history of the patient's drug reactions ismandatory. If a decision is made to prescribepenicillin, an adequate blood level must be ob-tained. An initial oral loading dose of 1000 mg ofpenicillin VK is followed by 500 mg every 6 hoursfor 7 days. A loading dose provides an adequatetherapeutic level and helps prevent developmentof resistant strains. Antibiotics should be contin-ued for 2 to 3 days after resolution of the signsand symptoms of the infection. When an antibi-otic is prescribed in conjunction with debride-ment of the root canal system and soft tissuedrainage, significant improvement should be seenwithin 2 to 3 days. If the infection is not resolving,referral to a specialist is indicated.

Amoxicillin has a broader spectrum than peni-cillin VK that includes bacteria not usually foundin endodontic infections. Thus it selects for resis-tant organisms commonly found in the gastroin-testinal tract. For patients with severe infectionsor if immunocompromised, the prescription ofthe broader spectrum amoxicillin may be war-ranted. An oral loading dose of 1000 mg is fol-lowed by 500 mg every 8 hours for 7 days. Thecombination of amoxicillin and clavulanate (Aug-mentin) may be indicated if tests demonstrate thepresence of /3-lactamase-producing bacteria or ifthe infection is life-threatening.

Metronidazole is bactericidal against strictanaerobes but does not have activity against aer-obes or facultative anaerobes. The addition ofmetronidazole to penicillin for combined therapyis indicated if the patient's condition is not im-proving after 72 hours. The patient should con-tinue to take the prescribed penicillin for its ef-ficacy against aerobes or facultative anaerobes.When the patient's condition is not improving,the initial diagnosis and treatment must be re-viewed and further treatment rendered if indi-cated. The recommended dose of metronidazoleis 500 mg every 6 hours for 7 days. Patients takingmetronidazole have an intolerance to alcohol.

Clindamycin is effective against many Gram-positive and Gram-negative microorganisms in-cluding both facultative and strict anaerobes. Clin-damycin is a good (but expensive) alternative topenicillin and is recommended for patients allergicto penicillin. It is well distributed throughout thebody and reaches bone concentrations similar tothose in plasma. Clindamycin therapy has been as-sociated (very seldom) with pseudomembranouscolitis. However, antibiotic-associated colitis is


541

now known to be caused by all antibiotics exceptthe aminoglycosides. Clindamycin, ampicillin/amoxicillin, and the cephalosporins each causeabout one-third of cases of antibiotic-associatedcolitis. The usual adult dose of clindamycin is a300 mg loading dose followed by 150 to 300 mgevery 6 hours for 7 days.

Clarithromycin and azithromycin are macro-lides like erythromycin with some advantagesover erythromycin.55 They may be prescribed forpatients allergic to penicillin with relatively mildindications for systemic antibiotic therapy. Theyproduce less gastrointestinal upset and have aspectrum of antimicrobial activity that includessome of the anaerobic bacteria associated with en-dodontic infections. Clarithromycin may be givenwith or without meals in a dose of 250 to 500 mgevery 12 hours for 7 days. Azithromycin should betaken 1 hour before meals or 1 hour after meals. Aloading dose of 500 mg is followed by 250 mgdaily for 5 to 7 days. These antimicrobials blockthe metabolism of warfarin and anisindione,which can lead to serious bleeding in patients tak-ing anticoagulant medication.56

Patients using oral contraception should bewarned to use alternative methods of contracep-tion after the prescription of antibiotics. Althoughrifampin seems to be the only antimicrobial provento be associated with reduced effectiveness oforal contraceptives, case reports have implicatedothers .56

ROLE OF BACTERIAAND THEIR CONTROL

Antimicrobials in the form of irrigants, intracanalmedicaments, and antibiotics have been an inte-gral part of endodontic practice. With the adventof improved microbiologic techniques, scientificdata suggest that diseases of endodontic originare either primarily or secondarily caused by mi-croorganisms. Clinicians must understand therole of microorganisms in the pathogenesis ofthese pathoses. Important treatment modalitiesare complete root canal debridement and incisionfor drainage in conjunction with appropriate useof antimicrobials.

AnxiolyticsA third realm of endodontic pharmacotherapy isthe control of anxiety. Surveys of dental patientsindicate that both endodontic and oral surgicalprocedures rank as the most fearful for patients,with many patients reporting that they are "ner-vous" when facing an impending endodontic

542


appointment.57.58 Similar to the control of painand infection, an integrated approach for the con-trol of anxiety includes both nonpharmacologicand pharmacologic techniques.

Several nonpharmacologic techniques for thecontrol of anxiety, ranging from behavioral man-agement techniques to distraction to hypnosishave been evaluated in endodontic patients. 59-60

These techniques reduce reports of pain or anxietyduring endodontic treatment. 61,62 Nonpharmaco-logic techniques are often combined with pharma-cologic techniques for control of anxiety. 63

Pharmacologic routes for control of anxiety in-clude oral, inhalation, and intravenous techniques;because of the scope of this topic, only the first twomethods will be reviewed. Advantages of oral routesof drug administration for control of anxiety in-clude demonstrated efficacy, reduced monitoring,and decreased likelihood of serious morbidity. 64,65

ORAL

Commonly and conveniently used oral benzo-diazepines include diazepam and triazolam. Di-azepam (Valium), at an adult dose of 5 to 15 mg,can be administered to reduce anxiety in endo-dontic patients.66 Triazolam (Halcion), at a 0.25 mgoral dose, is also effective. It has rapid onset and re-duces anxiety comparable to an intravenous doseof 19 mg of diazepam . 66,6' Unlike diazepam, triazo-lam does not have an active metabolite and pro-vides faster recovery; however, patients cannotdrive because they may experience transient reduc-tions in psychomotor impairment .6' Sublingualadministration of the triazolam tablet bypassesfirst-pass hepatic clearance of the drug and in-creases the peak anxiolytic effect; an indication forthis approach may be patients requiring a fasteronset of anxiolytic activity.68 Diazepam is availablein tablet form, or for a more rapid onset, maybe prepared as a liquid at 5 mg/ml and ad-ministered approximately one hour before the ap-pointment.

INHALATIONAL

The primary inhalational anxiolytic drug is ni-trous oxide (N2O). Although 40% N2O appears tohave marginal effects on anxiety, the delivery of50% N2O has been reported to be effective. 67,69 N2Odoes not appear to have additive effects when com-bined with either triazolam or diazepam. 17,70 Intra-operative scavenging of N2O is important becausechronic exposure to the gas has medical implica-tions .71^ ' 2 Although patient acceptance is oftenhigh with N2 O, the clinician should consider thepotential for effective gas scavenging as well as the

effectiveness of alternative drugs. Also there issome difficulty in completing endodontic proce-dures and radiographic examination because ofinterference from the inhalation apparatus.

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27. Breivik E, Barkvoll P, Skovlund E: Combining di-clofenac with acetaminophen or acetaminophen-codeine after oral surgery: a randomized, double-blind, single oral dose study, Clin Pharmacol Ther66:625, 1999.

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29. Dionne R: Suppression of dental pain by the preoper-ative administration of flurbiprofen, Am J Med 80:41,1986.

30. Dunsky JL, Moore PA: Long-acting local anesthetics: acomparison of bupivacaine and etidocaine in en-dodontics,JEndod 10:457, 1984.

31. Woolf C: Transcriptional and posttranslational plas-ticity and the generation of inflammatory pain, ProcNatl Acad Sci USA 96:7723, 1999.

32. Gordon S, Dionne R, Brahim J, et al: Blockade of pe-ripheral neuronal barrage reduces postoperative pain,Pain 70:209, 1997.

33. Jebeles J, Reilly J, Gutierrez J, et al: Tonsillectomy andadenoidectomy pain reduction by local bupivacaineinfiltration in children, Int J Pediatr Otorbinolaryngol25:149, 1993.

34. Haynes R: Adrenocorticotrophic hormone: adrenocor-tical steroids and their synthetic analogs; inhibitors ofthe synthesis and actions of adrenocortical hormones.In Gilman A, Rall T, Nies A, Taylor P, editors: Goodman


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and Gilman's the pharmacological basis of therapeutics,ed 8, New York, 1990, Pergamon.

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36. Liesinger A, Marshall FJ, Marshall JG: Effect of vari-able doses of dexamethasone on posttreatment en-dodontic pain, JEndod 19:35, 1993.

37. Fouad AF, Rivera EM, Walton RE: Penicillin as a sup-plement in resolving the localized acute apical abscess,Oral Surg Oral Med Oral Pathol 81:S90,1996.

38. Henry M, Reader A, Beck M: Effect of penicillin onpostoperative endodontic pain and swelling in symp-tomatic necrotic teeth, JEndod 27:117, 2001.

39. Walton RE, Chiappinelli J: Prophylactic penicillin:effect on posttreatment symptoms following rootcanal treatment of asymptomatic periapical pathosis,JEndod 19:466, 1993.

40. Pickenpaugh L, Reader A, Beck M et al: Effect of pro-phylactic amoxicillin on endodontic flare-up inasymptomatic, necrotic teeth, JEndod 27:53, 2001.

41. Pallasch T: Infectious disease at the millennium, J CalifDentAssoc27:367, 1999.

42. Pallasch T: Pharmacokinetic principles of antimicro-bial therapy, Periodontol2000 10:5, 1996.

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48. American Dental Association and American Academyof Orthopaedic Surgeons: Advisory statement: Antibi-otic prophylaxis for dental patients with total joint re-placements, J Am Dent Assoc 128:1004, 1997.

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Geriatric Endodontics

LEARNING OBJECTIVES


/ Identify those biologic aspects in the elderly patient that are similar to and different from those in the

younger patient.

z / Discuss age changes in the older dental pulp, both physiologic and anatomic.

a / Discuss differences in healing patterns in the older patient.

4 / Describe complications presented by the medically compromised older patient.

s / Describe, step by step, the process of diagnosis and treatment planning in the elderly patient.

6 / Identify factors that complicate case selection.

7 / Discuss why there are differences and what those differences are when root canal treatment is performed

i n the older patient.

s / Recognize the complications of endodontic surgery.

s / Select the appropriate restoration after root canal treatment.

10 / Identify those elderly patients who should be considered for referral.

545

546

31 / Geriatric Endodontics

Biologic Considerations

Pulp Response

Changes with Age

Nature of Response to Injury

Periradicular Response

Healing

Medically Compromised Patients

Diagnosis

Diagnostic Procedure


Differential Diagnosis

Endodontic Pathosis

Other Pathoses

Treatment Planning and Case Selection

Procedure

Prognosis

Number of Appointments

Additional Considerations


Treatment Considerations

I mpact of Restoration

Retreatment

Endodontic Surgery

Medical Considerations

Biologic and Anatomic Factors

Healing After Surgery

Bleaching

External Stains

I nternal Stains

Restorative Considerations

Overdenture Abutments

Coronal Seal

Trauma

ndodontic considerations in theelderly patient are similar in many waysto those in the younger patient, but

with differences. This chapter will discuss thosesimilarities as well as concentrating on the differ-ences. The topics will include the biologic aspectsof pulpal and periradicular tissues, healing pat-terns, diagnosis, and treatment aspects in the geri-atric patient.

The number of persons aged 65 and over in theUnited States exceeds 35 million. Not only is thisage group expanding in numbers, but their dentalneeds continue to increase.1.2 More elderly patientswill not accept tooth extraction unless there are noalternatives.3.4 Their expectations for dental healthparallel their demands for quality medical care. Aneven more important consideration is that theirdentitions will have experienced decades of dentaldisease as well as restoratives and periodontal pro-cedures (Figure 31-1). These all have compoundadverse effects on the pulp, periradicular, and sur-rounding tissues (Figure 31-2). In other words, themore injuries that are inflicted, the greater the like-lihood of irreversible disease and thus the greaterthe need for treatment.

The combination of an increase in pathosisand dental needs, coupled with greater expecta-tions, has resulted in more endodontic proce-dures among these aging patients (Figure 31-3).Furthermore, expanded dental insurance benefitsfor retirees as well as more disposable income hasmade complex treatment more affordable . 2

Endodontic considerations in elderly patientsinclude biologic, medical, and some psychologicdifferences from younger patients as well as treat-ment complications. These considerations will befurther discussed in the chapter.

Biologic Considerations

Biologic considerations are both systemic andlocal. The wide variety of systemic changes relatedto the patient's medical status are covered in othertextbooks. In the older patient, there are no sys-temic or local changes particularly unique to en-dodontics that are different from those for otherdental procedures. Similarly, pulp and periradicu-lar tissues do not respond markedly differently.

Pulp Response

CHANGES WITH AGE

There are two considerations: (1) structural (histo-logic) changes that take place as a function oftime; and (2) tissue changes that occur in response


547

FIGURE 31-1

Dentitions in older individuals often have multiple appearances and diverse problems caused by many years ofdisease, restorations, and oral and systemic changes. These dentitions often are a challenge to restore to accept-able function and esthetics.

to irritation from injury. These tend to have simi-lar appearances in the pulp. In other words, injurymay prematurely "age" a pulp. Therefore an "old"pulp may be found in a tooth of a younger person,i.e., a tooth that has experienced caries, restora-tions, etc. Whatever the etiology, these older (or in-jured) pulps react somewhat differently than doyounger (or noninjured) pulps.

Chronologic Versus Physiologic

Does a pulp in an older individual react differentlythan an injured pulp in a younger individual? Thisquestion has not been answered. Probably a previ-ously injured pulp (from caries, restoration, etc.) ina younger person has less resistance to injury thanan undamaged pulp in an older individual. At ahistologic level, there are some consistent changesin these older pulps as well as in irritated pulps.

Structural

The pulp is a dynamic connective tissue. It has beenwell documented that, with age, there are changesin both cellular, extracellular, and supportive ele-ments (see Chapter 2). There is a decrease in cells,including both odontoblasts and fibroblasts. Thereis also a decrease in the supportive elements, i.e.,

blood vessels and nerves.6.7 There is presumably anincrease in the percentage of space occupied by col-lagen, but less ground substance; these changes inproportions have not been measured, but onlyhave been observed histologically.8

Calcifications

These include denticles (pulp stones) and diffuse(linear) calcifications. These increase in the agedpulp9 as well as in the irritated pulp.'° Pulp stonestend to be found in the coronal pulp, and diffusecalcifications are in the radicular pulp. It has beenspeculated that the indices of calcification arisefrom degenerated nerves or blood vessels, but thishas not been proven. Another common specula-tion is that pulp stones may cause odontogenicpain; this is not true.

Dimensional

Pulp spaces generally progressively decrease insize and often become very small.1 1.12 Dentin for-mation is not necessarily continuous throughoutlife, but it often does occur and may be acceler-ated by irritation from caries, restorations, andperiodontal disease. Dentin formation with timeor irritation is not uniform. For example, in molar

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31 1 Geriatric Endodontics

FIGURE 31-2Cervical external resorption exposing the pulp. A free-end re-movable partial denture has settled posteriorly, exerting pres-sure on the gingiva and inducing inflammation and root re-sorption. (From Walton RE: Dent Clin North Am 41:795,1997.)

FIGURE 31-3Restorations, caries, and time have all combined to result indentin formation. The first premolar shows calcific metamor-phosis (a very small pulp space is present). The second pre-molar has dentin formation (arrow) in response to recurrentcaries. Both will be difficult to treat and restore. (From WaltonRE: Dent Clin North Am 41:795,1997.)

pulp chambers there is more dentin formation onthe roof and floor than on the walls. The result isa flattened (disc-like) chamber (Figure 31-4).

NATURE OF RESPONSE TO INJURY

The older patient does tend to have more adversepulpal reactions to irritation than those thatoccur in the younger patient. The reason for thesedifferences is debatable and not fully understood,but they are probably the result of a lifetime ofcumulative injuries.

From Irritation

There are reasons for pulp pathosis after restora-tive procedures. First, the tooth may have experi-enced several injuries in the past. Second, thereare likely to be more extensive procedures that in-volve considerable tooth structure, such as crownpreparation. There are multiple potential injuriesassociated with a full crown: foundation place-

ment, bur preparation, impressions, temporarycrown placement (often these leak), cementation,and unsealed crown margins. The coup de graceof a pulp that is already stumbling along may bethat final restoration.

Age

Although it would seem that a pulp with fewercells, blood vessels, and nerves would be less resis-tant to injury, this has not been proven. Pulp re-sponses to various procedures in different agegroups have not shown differences, although thelarge number of variables in these types of clinicalstudies make it difficult to isolate age as a factor.This is not necessarily the case with the immaturetooth (open apex), in which pulps have indeedbeen shown to be more resistant to injury. Thereare some who theorize that pulps in older teethmay, in fact, be more resistant because of de-

FIGURE 31-4Disc-like chamber (arrow). The chamber is flattened becauseof dentin formation on the roof and floor. These chambersand canals are a challenge to locate. (From Walton RE: Dent

Clin North Am 41:795,1997.)

creased permeability of dentin.13 Again this resis-tance to injury in old teeth has not been proven."The bottom line is that older pulps in older pa-tients do require more care in preparation andrestoration; this is probably due to a history ofprevious insults rather than age per se.

Systemic Conditions

There is no conclusive evidence that systemic ormedical conditions directly affect (decrease) pulpresistance to injury. One proposed condition is ath-erosclerosis, which has been presumed to directlyaffect pulp vessels'-; however the phenomenon ofpulpal atherosclerosis could not be demonstrated."

Periradicular ResponseLittle information is available on changes of boneand soft tissues with age, and how these might af-fect the response to irritants or to subsequent

31 1 Geriatric Endodontics

549

healing after removal of those irritants. The indi-cators are that there is relatively little change inperiradicular cellularity, vascularity, or nerve sup-ply with aging." Therefore it is unlikely that thereare significantly different periapical responses inolder compared with younger individuals.

Healing

There is a popular concept that healing in olderindividuals is impaired, compromised, or delayedcompared with that in younger patients. This isnot necessarily true. Studies in animals haveshown remarkably similar patterns of repair oforal tissues in young versus old, but with a slightdelay in healing response.'' Radiographic evi-dence of healing of younger versus older patientsafter root canal treatment demonstrated no ap-parent difference in success and failure.1 9 There isno evidence that vascular or connective tissuechanges in older individuals result in significantlyslower or in impaired healing. Overall, there is lit-tle difference in the speed or nature of healing be-tween the different age groups; this includes bothbone and soft tissue. Critical to healing is vascu-larity. In healthy individuals, blood flow is not im-paired with age .z°

Medically Compromised Patients

Certainly, systemic problems in the older patienttend to occur more often and with greater sever-ity. In general, medical conditions are no moresignificant for endodontic procedures in the olderpatient than for other types of dental treatment.In fact, there is little information on the relation-ship of medical conditions or medically compro-mised patients as to adverse reactions during orafter endodontic procedures.

It has been presumed that systemic conditionssuch as diabetes or immunosuppressant therapywould predispose an endodontic patient to infec-tion or to delayed healing. There is no evidencethat this presumption is true nor that these con-ditions will have more of an adverse effect in el-derly patients. There is concern, however, aboutthe person with severe, uncontrolled diabetes,who may require additional precautions and care-ful monitoring.21

Of interest is osteoporosis, a rather commoncondition of older women. There is evidence thatosteoporosis is associated with a decrease in tra-becular bone density in the jaws, particularly in theanterior maxilla and the posterior mandible . 22,23

However, it is not known whether patients with

55 0


osteoporosis have impaired bony healing after rootcanal treatment or surgery. As related to diagnosisof periapical pathosis, osteoporotic changes areprobably not of sufficient magnitude24 to confusepre- or post-treatment evaluation.

In summary, elderly medically compromisedpatients are at no more risk for complicationsthan are other age groups. In fact, for any med-ically compromised patient, root canal treatmentor other endodontic procedures are far less trau-matic and damaging than extraction. However,one important consideration is that older patientsare more likely to be taking more and strongermedications.25 Caution is required, particularlywhen prescribing additional medications.

Diagnosis

Again, the same basic principles apply with olderas with younger patients.

DIAGNOSTIC PROCEDURE

It is important that a routine sequence be appliedto diagnosis, particularly with elderly patients.The most important findings are from the subjec-tive examination to determine symptoms and his-tory. Careful questioning and then allowing suf-ficient time for the older patient to recall andanswer often yields valuable information.

Chief Complaint

Allow the patient to express the problem(s) in his orher own words. Not only will this divulge symp-toms, but also it provides an opportunity to deter-mine the patient's dental knowledge and ability tocommunicate; this ability may be impaired becauseof problems with sight, hearing, or mental status.

Medical History

The prudent diagnostician not only discussespositive responses marked on the medical historyform but repeats important items that may nothave been marked or were overlooked by thepatient. Systemic conditions, medications, andrelated considerations should be discussed indepth. It is now appropriate to explain how thepatient's condition might affect diagnosis, treat-ment planning, treatment, and outcomes.

Dental History

In general, elderly patients have a lot of history toreview and recall. There may have been important

dental occurrences that are only a dim memory,which require prompting by the examiner. Exam-ples include a history of traumatic injury, frac-tures, caries, or pain and/or swelling.

Subjective Findings

By definition, subjective findings include infor-mation obtained by questioning the patient's de-scription of current signs and symptoms. Manyolder patients are stoic. They do not readily ex-press adverse symptoms and may consider themto be minor relative to other systemic problems orpains. A careful, concerned discussion about theseseemingly minor problems also helps establishrapport and confidence.

Overall, symptoms of pulpitis do not seem tobe as acute in the older patient. One reason maybe that there is a reduced pulp volume and a de-crease in sensory nerves, 26 particularly in dentin.

The absence of significant signs and symp-toms is also very common, more so than the pres-ence. Of course, the absence does not indicate thelack of significant pathosis; most irreversiblepulpal and apical pathoses are asymptomatic atany age. Thus when pathosis is suspected, objec-

FIGURE 31-5Calcific metamorphosis. Although there usually is vital pulptissue, these teeth in older adults often do not respond topulp testing because of decreased nerve supply and an in-crease in insulating dentin. (From Walton RE: Dent Clin NorthAm 41:795,1997.)


551

tive tests are required whether or not there aresignificant signs and symptoms.

Objective Tests

These are primarily related to pulpal and periapi-cal tests. Oral examination and transilluminationare also commonly required.

1. Pulp testing: Although similar in older andyounger patients, there are some differ-ences. The pulp becomes less responsive tostimuli with age (Figure 31-5). Thus testingin older patients should be done slowlyand carefully, with the use of different stim-uli. It is common for a tooth with a vitalpulp to be nonresponsive to one form oftesting (e.g., electrical) but respond to an-other stimulus (e.g., cold). These resultsmust be correlated with other tests andfindings as well as with radiographs.

There is a question of whether electricpulp tests should be used in patients withpacemakers . 27 Although it is unlikely thatthese tests could cause a pacemaker to mal-function, there usually are other tests thatcan be used safely to give information onpulp status.

A test cavity is often indicated but may notbe as useful in the older patient because ofreduced dentin innervation. A false-negative(no response/vital pulp) response is not un-usual, even with a test cavity.

2. Periapical testing: Percussion (biting and tap-ping) and palpation tests indicate periapical

inflammation but are not particularly usefulunless the patient reports significant pain.These are most useful to confirm that suchsymptoms are indeed from a particular toothand determine the severity of response.


Current, good quality periapical films are alwaysnecessary; the same principles apply as in theyounger patient. The techniques of making radio-graphs are similar but with some differences.Bony growths such as tori and muscle attach-ments (frena) may affect film positioning. Also,the older patient may have difficulty in placingthe film; holders should be used. Generally, a par-allel film is preferred for diagnosis with occa-sional supplementation of mesially or distally an-gled cone positioning or a Panelipse or occlusalview. Often bitewing projections are helpful inshowing chamber size and location and relativedepths of caries and restorations.

Apically, there may be some differences in theolder patient. The incidence of nonendodonticpathosis of the jaws tends to increase with age;careful determination of pulp status is even moreimportant in these situations when the nature ofthe pathosis is uncertain. If the pulp is vital, a le-sion in the apical region is not endodontic.

Radiographs are studied for pulp size and forroot and pulp anatomy. Again, pulps tend to besmaller and may disappear radiographically (Fig-ure 31-6). Importantly, nonvisualization of a pulpspace does not mean that a pulp is not present. In

FIGURE 31-6A, Although the pulp is barely visible apically (arrow), a corresponding histologic section of this region (B) showsa sizable pulp space containing vital tissue. (From Walton RE: Dent Clin North Am 41:795, 1997.)

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fact, it has been demonstrated28 that there is al-ways a pulp space, even when it is not visible ra-diographically. Apical root and canal anatomytends to be somewhat different in elderly patientsbecause of continued cementum formation .29, 30

This may be further complicated by apical root re-sorption from pathosis. 31

Differential DiagnosisThis is the ultimate determination of whetherthere is an endodontic or another type of pathosisand, if endodontic, the specific details of the pulpor periapical lesion.

ENDODONTIC PATHOSIS

Signs and symptoms, test results, and other ob-servations in the older patient should follow afairly consistent pattern. There may be the com-plications of mind-altering medications as wellas occasional perceptive problems in elderly pa-tients. Vague symptoms that cannot be localizedor do not follow an identifiable pattern probablyare not endodontic in origin. Other pathosis ornonpathologic entities must then be considered.

OTHER PATHOSES

These include numerous entities, many of whichare more common in elderly patients. The lesion

that commonly mimics endodontic pathosis isperiodontal. Nonendodontic symptomatic disor-ders that may mimic endodontic pathosis includeheadaches, temporomandibular joint dysfunction,and neuritis and neuralgia. The incidence of thesetends to increase somewhat with age, particularlyin patients who have specific disorders such asarthritis that may affect the joints.

Differentiating periodontal from endodonticpathosis is a common problem because of the in-creasing incidence of both endodontic and peri-odontal disease. Usually the underlying problemis either periodontic or endodontic, with few truecombined lesions (see Chapter 26). Radiographicchanges, swellings, sinus tracts, and deep probingdefects may be either endodontic or periodonticin origin. Although all findings should be consid-ered, the ultimate indicator is pulp testing. If thepulp is indeed vital, the problem is periodontal. Ifthe pulp is necrotic, the likelihood is that theproblem is endodontic. Pulp tests are critical; atest cavity may be helpful.

Treatment Planningand Case SelectionAfter differential diagnosis, a definitive treatmentplan is determined-usually root canal treatment,but including additional procedures. Everythingshould be considered (restorability, periodontalstatus, and overall treatment plan). This would be

FIGURE 31-7

A, Castings are frequently misoriented due to tipping and rotation. B, Access is more challenging; observation be-fore and caution during access are critical to avoid perforation. (From Walton RE: Dent Clin North Am 41:795,1997.)

the time to consider referral of the patient to an en-dodontist if the situation is deemed too complex.

PROCEDURE

Whatever the treatment, procedures are generallymore technically complex in older patients. Ex-tensive restorations, a history of multiple cariousinsults, periodontal involvement, decreasing pulpsize, tipping (Figure 31-7) and rotation are all fac-tors. An original treatment plan often has to bemodified during the procedure because of unex-pected findings. For example, root canal treat-ment may be initiated only to find that a canalcannot be located or negotiated; periradicularsurgery then becomes a necessity (Figure 31-8).These possibilities should be explained to the pa-tient, preferably before treatment is begun.

PROGNOSIS

Although periradicular tissues will heal as readilyin elderly as in young patients, 32,33 there are manyfactors that reduce the rate of success. The samefactors that complicate treatment also may com-promise ultimate success. An extensively restoredtooth is more prone to coronal leakage. Canalsthat cannot be negotiated to length may containpersistent irritants. Tipped or rotated teeth re-stored with castings that are misaligned are moredifficult to access and therefore to clean, shape,and obturate.


553

Each patient should have a pretreatment andpost-treatment assessment of prognosis. Thepretreatment assessment is the anticipated out-come; the post-treatment assessment reviewswhat should happen according to modifiers de-termined during treatment. Many teeth are se-verely compromised and would be a problem toretain (Figure 31-9). Extraction is often the pre-ferred approach; a recent study34 on the out-come of not replacing a missing tooth showedthat the consequences generally were not signif-icant. Thus when extraction is discussed as anoption, the patient is informed that "filling thespace" may be unnecessary.


Whether to treat in a single visit or in multiplevisits has always been a subject of debate and con-jecture. Studies have shown that, overall, there areno advantages to multiple appointments relatingto post-treatment pain or prognosis. However,with pulp necrosis, treatment in multiple ap-pointments and the use of calcium hydroxide asan intracanal medicament may speed healing, 35and longer term better outcomes were conclu-sively demonstrated. 36

There are benefits to single appointment pro-cedures in elderly patients. Longer appointmentsmay be less of a problem than several shorterappointments if the patient must rely on othersfor transportation or requires assistance to reach

FIGURE 31-8A, Calcific metamorphosis and apical pathosis (arrows) after trauma. In this tooth, conventional access would bedifficult and would jeopardize retention of the bridge. B, A surgical approach was used with the hope of sealingi n irritants apically. (From Walton RE: Dent Clin North Am 41:795, 1997.)

554

31 I Geriatric Endodontics

FIGURE 31-9Recurrent caries have created challenges in retaining thismolar. Crown lengthening would be necessary both for res-toration and isolation during root canal treatment. Crownl engthening may infringe upon the furcation. Canals wouldbe difficult to locate and negotiate. The tooth probablyshould be extracted. (From Walton RE: Dent Clin North Am41:795, 1997.)

FIGURE 31-10Elderly patients often have postural problems. This patient ismade comfortable with a rolled-up towel, forming a braceunder his neck.

Root Canal TreatmentTREATMENT CONSIDERATIONS

Time Required

On average, longer appointments are necessary toaccomplish the same procedures in elderly pa-tients for the reasons discussed earlier.

Anesthesia

the office or to get in the chair. At times, the el-derly patient may require special positioning ofthe chair, support of the back or neck or limbs,or other such considerations (Figure 31-10).These problems may require shorter, multipleappointments.

ADDITIONAL CONSIDERATIONS

In treatment planning for elderly patients thereis a tendency to plan according to anticipatedlongevity.37 It is natural to assume that proce-dures need not be as permanent because the pa-tient may not live for very long. The concept thattreatment should not outlast the patient is not ac-cepted by most elderly patients, who desire healthcare equivalent to that rendered to younger pa-tients. Esthetic and functional concerns may beno different.

Primary injections. The need for anesthesia issomewhat less in the older patient. It is necessaryfor vital pulps but is often unnecessary for pulpnecrosis, obturation appointments, and retreat-ments. Older patients tend to be less sensitiveand are more likely to prefer procedures withoutanesthetic. Also, they tend to be less anxious andtherefore have a higher threshold of pain. Al-though there are no differences in effectivenessof anesthetic solutions, various systemic prob-lems or medications may preclude the use ofvasoconstrictors.

Supplemental injections. Intraosseous, perio-dontal ligament (PDL), and intrapulpal anes-thesia are effective adjuncts if the primary anes-thesia is not give adequate. Again, certaincardiac conditions may preclude the use ofepinephrine, particularly with the intraosseousand PDL techniques. Duration of anesthesiais considerably decreased without a vasocon-strictor; reinjection during the procedure maybe required.


555

FIGURE 31-12Aids in orientation during access. The preparation is initiatedwithout the rubber dam in place. A mark to guide the bur isplaced on the crown in the long axis of the root. (From Wal-ton RE: Dent Clin North Am 41:795, 1997.)

FIGURE 31-11Age, caries, and restorations have resulted in small chambers(arrows); either would be a challenge to access.

Procedures

I solation. Isolation is often difficult because ofsubgingival caries and/or defective restorations.However, placement of a rubber dam is imperative,often requiring ingenuity (see Chapter 8). A fluid-tight isolation reduces salivary contamination ofthe pulp space and prevents introduction of irrig-ants into the mouth. If there are questions aboutthe integrity of a restoration, it should be removedbefore rubber dam placement. Also, temporarycrowns, orthodontic bands, or temporary restora-tions should be removed in their entirety; improvedvisibility and good isolation are more predictable.

Access preparation. Achieving good access toenable locating and then negotiating canal orificesis challenging in old teeth because of internalanatomy (Figure 31-11). Radiographs are helpful. Aslightly larger rather than a too small access open-ing is preferred, particularly through large restora-tions such as crowns. Magnification is also helpful,either from a microscope or other vision aids.

A supra-erupted tooth, as a result of caries orrestoration, has a short clinical crown, requiring a

less deep access preparation. The distance fromthe reference cusp to the chamber roof should bemeasured on the bur radiographically. A verysmall or nonvisible chamber may be an indicationfor beginning the access without the rubber dam;this aids in staying in the long axis of the tooth(Figure 31-12). Once the canal is located, the rub-ber dam is immediately placed before workinglength radiographs are made.

Locating canal orifices is often fatiguing andfrustrating to both clinician and patient. Althougha reasonable period of time should be allocated,there is a limit. It may be best to stop and have thepatient return for another appointment. Often, thecanals are readily located at a subsequent visit. Thisalso is a time to consider a referral; another proce-dure, such as surgery, may be indicated.

Working length. There are some differences inthe older patient.38 Because the apical foramenvaries more widely (Figure 31-13) than in theyounger tooth and because of decreased diame-ter of the canal apically, it is more difficult todetermine the preferred length.29 In teeth of anyage, materials and instruments are best con-fined to the canal space. One to 2 mm short ofthe radiographic apex is the preferred workingand obturation length39; this should be decreasedif an apical stop is not detected.

Cleaning and shaping. A common challenge isa much smaller canal that requires more time

556


FIGURE 37-13Variability in apical foramen location. A, The foramen is not visible radiographically. B, Histologically, the distalroot shows the foramen to be well short of the apex. (From Walton RE: Dent Clin North Am 41:795, 1997.)

and effort to enlarge. A very small canal may bemore easily negotiated and initially preparedwith a lubricant, such as glycerin. This may beused through two or three smaller sizes of filesto facilitate enlarging as well as to reduce therisk of binding and separation. The same princi-ples of debridement and adequate shaping arefollowed.

I ntracanal medicaments. These are contraindi-cated, with the exception of calcium hydroxide.This chemical is antimicrobial, inhibits bacterialgrowth between appointments, and may reduceperiradicular inflammation." It is indicated if thepulp is necrotic and the canal preparation is es-sentially complete.

Obturation. There is no demonstrated preferredapproach, although cold-lateral and warm-verticalgutta-percha obturations are the most commonlyused and the best documented.

crown and (2) blockage of access and poor in-ternal visibility.

The porcelain-fused-to-metal crown is morecommon than a full metal crown and createsadditional problems. Porcelain may fracture orcraze. This problem is minimized by using bursspecifically designed to prepare through por-celain" combined with slow cutting and copi-ous use of water spray. Occlusal access is wide(Figure 31-14). Metal should not be removedafter the chamber is opened to prevent metalshavings from entering and blocking canals. Anaccess through a PFM or a gold crown (eitheranterior or posterior) that is to be retained, isbest permanently repaired with amalgam. Ante-rior nonmetallic crowns may be repaired withcomposite.

Retreatment

Impact of RestorationGenerally the larger and deeper the restoration,the more complicated the root canal treatment.The old tooth is more likely to have a fullcrown. There are two concerns: (1) potentialdamage to retention or components of the

Factors that lead to failure tend to increase withage; thus retreatment is more common in olderpatients. Retreatment at any age is often compli-cated and should be approached with caution;these patients should be considered for referral.Retreatment procedures and outcomes are similarin both older and younger teeth.


557

FIGURE 31-14Access through a porcelain-fused-to-metal crown. The out-l i ne is large for visibility. Also, the preparation does not ex-tend to the porcelain to avoid fracturing it. (From Walton RE:Dent Clin North Am 41:795, 1997.)

Endodontic SurgeryConsiderations and indications for surgery are sim-ilar in elderly and younger patients. These includeincision for drainage, periradicular procedures, cor-rective surgery, root removal, and intentional re-plantation. Overall, the incidence of most of thesewill increase with age. Small non-negotiable canals,resorptions, and canal blockages occur more oftenwith age. Perforation during access or preparation,ledging, and instrument separation are related torestorative and anatomic problems.

apy should preferably not be altered and that hem-orrhage was controllable by local hemostatic agents.

BIOLOGIC AND ANATOMIC FACTORS

Bony and soft tissues are similar and respond thesame in older and younger patients. There maybe somewhat less thickness of overlying soft tis-sue; however, alveolar mucosa and gingiva seem tobe structurally similar. Anatomic structures suchas the sinuses, floor of the nose, and location ofneurovascular bundles are essentially unchanged.Often, periodontal and endodontic surgery mustbe combined. Also, crown-to-root ratios may becompromised because of periodontal disease orroot resorption.

HEALING AFTER SURGERY

Hard and soft tissues will heal as predictably al-though somewhat more slowly.47.49 Postsurgicalinstructions should be given both verbally andin writing to minimize complications. If the pa-tient has cognitive problems, instructions are re-peated to the person accompanying the patient.Even very elderly patients will have good healing,provided they follow post-treatment protocols. Iceand pressure (in particular) applied over the surgi-cal area reduces bleeding and edema and mini-mizes swelling. Overall, older patients experienceno more significant adverse affects from surgerythan do younger patients; outcomes are more de-pendent on oral hygiene than on age per se, as hasbeen shown in periodontal surgery patients.50

One problem that seems to be more prevalentin older patients is ecchymosis after surgery. Thisis hemorrhage that often spreads widely throughunderlying tissue and commonly presents as dis-coloration (Figure 31-15). Patients are informedthat this may occur and that it is not of concern.Normal color may take 1 to 2 weeks or longer toreturn. In addition, the discoloration may gothrough different color phases (purple, red, yel-low, green) before disappearing.

MEDICAL CONSIDERATIONS

These may require consultation and are of concernbut generally do not contraindicate a surgical ap-proach . 42 This is particularly true when extractionis the alternative; surgery is often less traumatic . 43

Excessive hemorrhage during or after surgery isof concern; many elderly patients are receiving anti-coagulant therapy. Interestingly, recent studies ex-amined bleeding patterns in oral surgery patientstaking low-dose aspirin44 and prescribed anticoagu-lants .46.45 The findings were that anticoagulant ther-

Bleaching

Both internal and external tooth discoloration oc-curs in older patients. 13 Internal discoloration isrelated to dental (restorative or endodontic) pro-cedures or to an increase in dentin formation witha loss of translucency. External discoloration oc-curs from stains and restorative procedures aswell (see Figure 31-1). Overall, teeth tend to dis-color with time and with age. Both external and

558


Teeth that are discolored because of increasedamounts of dentin formation and loss of translu-cency generally should not be considered for in-ternal bleaching, which would require root canaltreatment first. External bleaching may lightenthe teeth somewhat.

Restorative ConsiderationsOVERDENTURE ABUTMENTS

This involves the reduction of a root to permitthe resting' of a removable partial or completedenture on a restored or natural root face.

An important consideration is that, although apulp space may not be evident on a radiograph(Figure 31-16), usually small components of thepulp chamber extend into the crown.28 Reductionwould create an clinically undetectable exposure.If untreated, this will result in pulp necrosis.Teeth to be reduced for overdenture abutmentsshould have root canal treatment followed by anappropriate restoration to seal the access. Amal-gam, composite resin, and glass ionomer are ade-quate materials.-'

CORONALSEAL

In the elderly (as in the younger) patient, the coro-nal surface must be sealed from oral fluids foreverto prevent failure. A concern for elderly patientsis that the dentist will be less careful with the de-sign and placement of a restoration or select lessdurable materials. In addition, the older patient islikely to be more susceptible to recurrent caries orabrasion, particularly on cervical root surfaces.These lesions do not have to penetrate as deeplyto expose the obturating material. Subsequent tothis exposure will be contamination of the obtu-rating material by saliva and bacteria with resul-tant periapical pathosis. Again, this is probablythe number one cause of treatment failure andreason for retreatment.

Trauma

Traumatic injuries occur in elderly patients morecommonly with recreational activity and becauseof postural instability and loss of coordination.Generally, the older patient who experiences fa-cial trauma will have different concerns and re-quire some differing approaches than the youngerpatient."

A major issue is that there may be cranial in-juries that are masked by the obvious superficialfacial trauma. Evidence of such injuries, as shown

FIGURE 31-15Postsurgical ecchymosis. Root-end surgery of a maxillary lat-eral incisor resulted in widespread migration of hemorrhagei nto the tissues, with resultant discoloration. This is not anuncommon occurrence in elderly patients. No treatment is in-dicated, and the problem resolves in 1 to 2 weeks.

internal bleaching procedures can be successful inthese patients.

EXTERNAL STAINS

These are on, or close to, the enamel surface andare best managed by conventional night guard/oxidizing gel techniques.

INTERNAL STAINS

Stains that are most amenable to internal bleach-ing are related to discoloration after root canaltreatment or pulp necrosis. The considerations re-lated to diagnosis, etiology, treatment planning,and prognosis for successful short-term and long-term internal bleaching are detailed in Chapter23. Often discolorations in these teeth can be sig-nificantly resolved, much to the satisfaction of theolder patient.

by in-office tests (see Chapter 25), would require animmediate hospital emergency room visit. Otherconcerns would be similar to those discussedearlier in this chapter: medical status, cognitivefactors, and patient expectations. In conjunctionwith these considerations, the actual managementof the hard and soft tissues would be similar to andhave an expected outcome much like that of ayounger patient.

Many of these elderly trauma patients mayhave initial injury management by a generalistand then be referred to an oral surgeon for fa-cial injury assessment. Follow-up, long-term den-tition care may then be best managed by theendodontist.

REFERENCES

1. Meskin L, Berg R: Impact of older adults on privatedental practices, 1988-1998J Am DentAssoc 131:1188,2000.

2. Berkey D, Berg R, Ettinger R, et al: The old-old dentalpatient, JAm Dent Assoc 127:321, 1996.

3. Marcus S, Drury T, Brown L, Zion G: Tooth retentionand tooth loss in the permanent dentition of adults:United States, 1988-1991, J Dent Res 75 (special issue):684, 1996.

4. Lloyd P: Oral and dental problems. In Yoshikawa T,Coobbs E, Brummel-Smith K, editors: Practical ambula-tory geriatrics, ed 2, St Louis, 1998, Mosby.


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FIGURE 31-16A, This central incisor was cross-sectioned at the level of the arrow, where no pulp space is visible. B, Histologi-cally, a small pulp space is apparent. Reducing such a tooth for overdentures would result in pulp exposure. (FromWalton RE: Dent Clin North Am 41:795,1997.)

5. Lloyd P: Fixed prosthodontics and esthetic considera-tions for the older adult, JProsthetDent 72:525, 1994.

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Pulpal Anatomyand Access Preparations

The illustrations in this section depict the size,shape, and location of the pulp space withineach tooth, as well as the more common mor-phologic variations. Based on this knowledge ofthe shape of the pulp and its spatial relationshipto the crown and root, the correct outline formfor access preparation is presented from boththe occlusal-lingual and proximal views. Fromthese illustrations, the following features can beobserved:

1. The location of access on posterior teeth rela-tive to occlusal landmarks such as marginalridges and cusp tips.

In addition, the percentages of the more com-mon morphologic variations of the roots andcanals are given. With many of the tooth groups,the percentages do not total 100 percent. The re-maining percentage represents the less commonvariations not illustrated. Percentages are approx-

2. The size and appearance of the access on ante-rior teeth as viewed from the incisal surface.

3. The approximate size of the access opening.4. The location of canal orifices and their positions

relative to occlusal landmarks and to eachother.

5. The canal curvatures and the location of theapical,formamens.

6. The configuration of the chamber and cervicalportion of the canals following straight-lineaccess preparation.

7. The root curvatures that are most common.Each illustration gives the following information:

imate to give general information, primarily todemonstrate relative occurrences. The more com-mon root and canal curvatures are included.These are curvatures not readily identified on ra-diographs, that is, toward the facial and lingualaspects.

561

562 Appendix

Maxillary Right Central Incisor

Maxillary Right Lateral Incisor

Maxillary Right Canine

Appendix 563

Maxillary Right First Premolar

564 Appendix

Maxillary Right Second Premolar

Appendix 565

Maxillary Right First Molar

566 Appendix

Maxillary Right Second Molar

Maxillary Right Second Molar

Appendix 567

Mandibular Right Central and Lateral Incisor

Mandibular Right Canine

568

Mandibular Right First Premolar

Appendix 569

570 Appendix

Mandibular Right Second Premolar

Mandibular Right First Molar

Appendix 571

572 Appendix

Mandibular Right Second Molar

Appendix 573

Mandibular Right Second Molar

574 Appendix

Examples of access openings prepared in ex-tracted teeth are given here. It is important to rec-ognize: (1) the location of the access relative to oc-clusal or lingual landmarks (marginal ridge andcusp tips) and (2) the size and shape of the accessrelative to the size and shape of the occlusal or lin-gual surface.

1. Maxillary lateral2. Mandibular canine3. Maxillary premolar4. Four-canal maxillary molar (arrow indicates

dentin shelf covering mesiolingual orifice)5. Three-canal mandibular molar6. Four-canal mandibular molar

AAbrasion, 384Access preparation

anterior teeth, 195-196, 197fburs, 191, 192f-193fcaries considerations, 187-188difficult-to-locate canals, 191errors in, 221-222misorientation during, 196-198, 198fperforation during, 198, 199f, 203,

311-319permanent restoration considera-

tions, 188posterior teeth, 196preparations for, 183-187straight-line, 183-185, 184f, 195techniques for, 191-196temporary restoration considera

tions, 188-189tooth surface conservation, 185-186

Acid etching, 377Acid-pumice technique, of bleaching,

419, 419fAlveolar bone, 22f, 24Alveolar fractures, 464Alveolar process, 24Amalgam, 272-273,381-382, 409Amelogenesis imperfecta, 409Amoxicillin, 541Anachoresis, 284Analgesics, 536-537Anesthesia

description of, 73difficulties, 104-105factors that affect, 100-101history of, 96fincision for drainage, 426initial management, 101-102mandibular, 103-104maxillary, 104profound, 301referrals for, 73selective, 63success of, 102-103supplemental, 105-112

Anterior teethaccess preparation of, 195-196, 197Eretention and core systems for,

275-276Antibiotics, 291-292, 539-541Anxiolytics, 541-542Apexogenesis, 389Apical abscess

acute, 43, 44f, 65t, 66-67, 290, 305f,307f

chronic, 43-44, 65t, 67Apical canal zipping, 224Apical clearing, 216, 216f-217f, 253

Apical constriction, 201-203Apical curvature, 222, 222fApical cyst, 41Apical delta, 7Apical foramen, 7, 8, 9f, 22f, 173-174,

176f, 469Apical fracture, 429Apical perforation, 184, 203, 320, 322Apical periodontitis

acute, 40, 41f, 65t, 66, 289, 301chronic, 40-42, 65t, 66, 289

Apical plug, 394Apical preparation, 211, 213-214Apical ramifications, 217fApical seal, 241-242Apical stop, 211, 211fAppointments, 64-66, 94, 553-554Arachidonic acid, 32Arterioles, 15, 15f, 18f, 23Attrition, 384Avulsion, 461-464Axons, 18, 19fAzithromycin, 541

BBacteria

colonization of, 283, 378culturing of, 291-292ecosystem, 287pathoses and, 288-290portals of entry, 283-284pulpal reaction to, 284terminology associated with, 283types of, 285tvirulence factors of, 287-288

Balanced forces method, 230Bands, 189Bicuspidization, 438, 440-442, 441fBitewing projections, 144, 144fBiting test, 56fBleaching

complications of, 414-415description of, 163elderly use of, 558-559external techniques, 415-420final restoration, 411, 413-414internal, 410-414laser, 421materials for, 410mouthguard, 420-421thermocatalyic technique, 411trauma-related, 414f-416fwalking bleach technique, 411,

412f-414fwhen to bleach, 414, 416f-417f

Blood dyscrasias, 409Blow-out lesion, 474-475, 475fBody language, 89

Bradykinin, 31-32Broaches, 156, 158, 212Burs, 191, 192f-193f, 198, 200E

CC fibers, 18Calcific metamorphosis, 36, 36f, 62f,

69f, 75-76, 76-77f, 349f,407-408, 548f

Calcifications, 14f, 14-15, 170, 170ECalcitonin gene-related peptide, 16, 32Calcium hydroxide, 233-234, 250-251,

291, 384, 397, 400f, 414Canal. See Root canal(s).Capillary bed, 15, 16ECapping of pulp, 384-385Carbamide peroxide bleaching,

410-411Carbon dioxide ice testing, 57, 57fCaries

access preparation considerations,187-188

depth of penetration assessments,61,63

microorganisms in, 28periapical repair after treatment of,

385pulpal disease and, 284, 383removal of, 61, 63rubber dam considerations, 127

Cavity preparation, 374-378Cementodentinal junction, 9, 23, 468Cementum, 6, 7f, 9, 22-23, 468Chelators, 219-220Chemical burns, 415Chemical irritants, 31, 169-170Chief complaint, 51Clamps, 122-124Clarithromycin, 541Cleaning and shaping

accidents during, 319-326apical clearing, 216, 216f-217fapical preparation, 211, 213-214balanced forces method, 230debridement, 207-209dentin softening, 220-221energized vibratory systems, 230-232extirpation, 212instrumentation, 163, 225-229, 232intracanal medicaments, 232-234irrigants, 218-220ledge formation during, 184,

222f-223f, 222-223, 319-320, 321flubricants, 221master apical file determination, 210objectives of, 207preparation errors, 221-225preparations

575

576 I ndex

Cleaning and shaping-continued

flaring, 212-214standardized, 212, 213fstep-down, 212-216, 213f, 215f

shaping principles, 209-210Clindamycin, 541Clinical tests, 58-56Cold testing, 57-58Collagen fibers, 5, 14Condensing osteitis, 42-43,43f, 61f, 143fCone-image shift, 132, 136-141Coronal fracture, 415Coronal leakage, 342fCoronal root perforation, 322-323Coronal seal, 241, 269-270, 400, 559Cracked tooth, 80-81, 500, 5Olt, 502f,

505-510Craze lines, 501-502, 503f, 507Crown

cementation of, 378formation of, 5fracture of, 449-456indications, 273-274lengthening of, 79, 80f, 120,

493-494, 494flongitudinal fractures of, 63perforation of, 83placement of, 93fpreparation of, 374-378removal of, 351, 353, 354ftemporary, 121, 189, 279, 378

Crown-down technique, 214Crown-root fracture, 270f, 454-486Culture, 291-292Cusp fracture, 501t, 502f, 502-505,

504f-505fCytokines, 39

DDam. See Rubber dam.Debridement, 207-209, 290, 302Decalcifiers, 220-221Dendritic cells, 13, 33, 33fDens evaginatus, 176, 177fDens invaginatus, 174, 176, 177fDental follicle, 7Dental history, 52, 298-299Dentin

age-related changes, 22cementum junction with. See Cemen-

todentinal junction.desiccation of, 382drying of, 376excess removal of, 196-198formation of, 5, 5f, 9, 10f, 21histology of, 11hypersensitivity of, 20-21, 21finjury-induced formation of, 10innervation of, 17-18, 20irritant effects, 190odontoblasts role in formation of,

4,10permeability of, 374-375resorption of, 36, 37fsecondary formation of, 21softening of, 220-221stimulation of, for pulp vitality

testing, 57structural changes in, 270tertiary, 10, 372, 372f-373f

Dentinal tubules, 467-468Dentinoenamel junction, 11Dentinogenesis, 10-11Dentinogenesis imperfecta, 409Dentin-pulp complex, 370Dentition. See Tooth.Dentogingival junction, 22Desiccants, 221Desmosomes, 11-12Diagnosis, 50-53, 63-64, 64f, 65t, 73Dilaceration, 176, 179Discolorations

aging and, 408, 558-559bleaching for. See Bleaching.causes of, 406-409coronal restorations, 409-410endemic fluorosis and, 408extrinsic, 418-420in elderly patients, 558-5S9intrapulpal hemorrhage, 407intrinsic, 416-418obturation materials, 409tetracycline-induced, 408, 416-417tooth formation defects as cause of,

408-409Disinfection, 12S, 163Doctor

listening by, 88-89patient interactions with, 89-98questions frequently asked, 90-97

Drainageincision for, 114, 425-426infection treatment by, 291

Drains, 304fDrills, 157-158

EEctomesenchymal cells, 4Elderly

bleaching, 558-559diagnostic approach, 850-551differential diagnosis, 552endodontic surgery in, 557-558healing, 549periradicular response, 549pulpal response changes, 546-549radiographic imaging, 851-552restoration considerations in, 556,

559retreatment in, 556root canal treatment in, 554-556systemic problems in, 549-550trauma in, 559-560treatment planning in, 552-554

Electronic apex locators, 201-203Emergencies. See also specific emergency

or condition.challenges associated with, 297-298definition of, 297description of, 296-297diagnostic approach, 298-299interappointment, 297, 305-307postobturation, 297, 307-308pretreatment, 297, 300-305referral for, 83-84treatment planning, 300

Enamelformation of, 5, 9fracture of, 449hypocalcification of, 408

Enamel-continuedhypoplasia of, 418spurs, 480

Endemic fluorosis, 408Endodontiss. See also Root canal treat-

ment.definition of, 1i mplants, 496-497longevity of treated teeth, 269pain secondary to, 534-535periodontium health and, 470pulpal effects, 471surgery, 94, 95fundergraduate curriculum, 1-2

Endodontist, 85-86Enostosis, 143fEnzymes, 288Epithelial cell rests of Malassez, 6, 23,

24fErosion, 384Examination

extraoral, 54for emergencies, 299intraoral, 84-55open apex, 391-393pain assessments, 53periapical tests, 56periodontal, 59, 299present illness, 52-53, 447pulp vitality tests, 57-59radiographic, 59-61, 75soft tissue, 54-55teeth, 55, 55f

Explorer. See Mirror and explorer.Extirpation, 212Extracellular vesicles, 288

FFatty acids, 288Fibrinopeptides, 38Fibroblasts, 12-13File(s)

characteristics of, 154f, 155cleaning and shaping use of, 226,

226fcore material use of, 247gutta-percha removal using, 357, 360intracanal use of, 15S-159K-type, 154f, 155nickel-titanium, 228separation of, 324f

Flaps, 430-434Flare-ups, 305-307Focal sclerosing osteomyelitis. See Con-

densing osteitis.Follicle, 7Fractures

alveolar, 464categories of, 500-501, 501tcrown, 449-456enamel, 449root, 244, 456-458

Frictional heat, 375-376, 382Furcation perforation, 314-315, 317f

GGates-Glidden drills, 157-158, 192f,

194f, 215Geriatrics. See Elderly.Gingivectomy, 120

I ndex 57 7

Glass ionomer cements, 381Gram stain, 292Ground substance, 14Gutta-percha, obturation using

carrier systems, 262lateral condensation, 252-257removal of, 274-275, 275f, 357, 360,

360f-361fsolvent-softened custom cones,

257-259techniques for, 251-252vertical condensation, 259-262

HHageman factor, 38Headaches, 528-529Healing, 44-45, 435-436, 549, 558Health history, 51-52, 73Hertwig's epithelium, 5-6, 6fHyaline layer of Hopewell-Smith, 6-7Hydrodynamic theory, of dentin

hypersensitivity, 20-21Hydrogen peroxide bleaching, 410Hyperalgesia, 101, 105, 535bHyperplastic pulpitis, 35-36

II mmune system

activation of, 371cells of, 13responses to pulpal injury, 32-33

I mmunoglobulins, 32,32f, 39I mplants, endodontic, 496-497Infections

control measures for, 290drainage of, 291site of, 348treatment of, 290-292

Inflammationcauses of, 91, 91fcells involved in, 31changes caused by, 36neurogenic, 17process of, 16-17, 28f, 31-32signs and symptoms of, 91, 92f

Informed consent, 89-90, 90b, 90fInfraorbital block, 104Injections, 101-102Instruments

aspiration of, 324-325cleaning and shaping use of, 163,

225-227diagnostic, 161disinfection of, 163endodontic-specific types of,

161-162engine-driven, 157-158extraction of, 362, 365f-366ffabrication of, 153failure of, 340hand-operated, 153f-154f, 153-154ingestion of, 324-325intracanal use of, 158-159, 208nickel-titanium, 156-157, 159, 160f,

227-229nomenclature for, 152physical properties of, 154-155rotary, 157-158separated, 323f-324f, 323-324, 340,

349f, 360, 362

Instruments-continuedsizing of, 155sonic, 231-232standardization of, 155-156sterilization of, 162-163ultrasonic, 230-231variations in, 156-157

Intentional replantation, 486-488, 487fIntracanal medications, 232-234,

291,409Intraosseous anesthesia, 105-107Intrapulpal hemorrhage, 407Intrapulpal injection, 111-112, 112fIrreversible pulpitis, 34, 61, 65t, 66,

112-113Irrigants, 218-220, 303, 325-326, 326fIrritants

chemical, 28-31, 169-170, 190obturation failure caused by, 241

Isolation methods. See Rubber dam.

KKininogens, 31Kinins, 31

LLaser bleaching, 421Lateral canals, 244, 468, 469fLateral channels, 6-7, 8fLateral condensation, 160-161,

252-256, 514Lateral perforation, 322, 329fLedge formation, 184, 222f-223f,

222-223, 319-320, 321f, 427fLiners, 382Lingual groove, 176, 178fLipopolysaccharides, 287Listening, 88-89Local anesthesia

blood flow reductions associatedwith, 371

description of, 73difficulties, 104-105factors that affect, 100-101mandibular, 103-104maxillary, 104pain management, 538-539success of, 102-103supplemental, 105-112

Lubricants, 221Luxation injuries, 459-461Lymphatic system, 17, 18f

MMandibular anesthesia, 103-104Mandibular molars, 197fMantle dentin, 5-6Mast cells, 31, 32f, 38-39Master apical file determination, 210Master cone, 253-254Maxillary anesthesia, 104Maxillary molars, 197, 198fMcInnes technique, 419Medical history, 51-52, 73, 298-299Mental foramen, 45, 45fMetronidazole, 541Microleakage, 379-380Mineral trioxide aggregate, 389,

401-402,402fMirror and explorer, 56

Mobility tests, 59Mouthguard bleaching, 420-421Myofascial pain, 53

NNeuritis, 529Neurogenic inflammation, 17Neuropeptides, 32, 38Nickel-titanium instruments, 156-157,

159, 160f, 227-229Nonsteroidal antiinflammatory drugs,

537-538

OObturation

accidents during, 326-328, 341apical seal, 241coronal seal, 241discoloration caused by, 409emergencies after, 297, 307-308evaluation of, 262-263failures in, 240-242files, 247gutta-percha. See Gutta-percha.instruments for, 160-161, 163, 255flateral seal, 241length of, 241-242, 242f-243fmaterials, 245-248objectives of, 240overextended, 340pastes, 248sealers. See Sealers.sectional, 260silver points, 247, 247fti ming of, 244-245

Odontalgia, 534Odontoblasts

cell body of, 11-12, 13fdentin formation by, 4, 10differentiation of, 5displacement of, 376, 376finjury to, 376morphology of, 11number of, 11secretory production of, 12structure of, 11-12

Open apexdefinition of, 389diagnosis of, 391-393electrical pulp testing for, 393illustration of, 390ftreatment planning, 393-394

Orofacial pain. See Pain.Orthodontic extrusion, 491-493Orthograde treatment. See

Retreatment.Overfills, 241-242, 242f, 258f,

327-328, 341

PPain

anesthesia for. See Anesthesia.antibiotic prophylaxis, 539-541anxiolytics for, 541-542causes of, 33-34characteristics of, 524, 530tcontinuous, 53deep vs. superficial, 524dentinal, 20diagnostic procedures, 529-531

578 I ndex

Pain-continuedflare-ups of, 84headache-related, 528-529hypersensitivity theories, 20-21intensity of, 53management of, 535-539mechanisms of, 522-524myofascial, 53perception of, 298percussion, 56periodontal, 525physiology of, 33-34posttreatment, 65post-treatment, 534-535procedural, 94-96psychogenic, 528pulpal, 10, 525reaction to, 298referred, 75, 525-527significance of, 521-522spontaneous, 53spreading, 527-528terminology associated with, 522btypes of, 522b

Palpation, 56, 56fPassive step-back technique, 214-216Pastes, 248Patient, 88-97Penicillin, 541Percolation, 241Percussion, 56Perforations

during access preparation, 198, 199f,203, 311-319

furcation, 315-316, 317fprognosis, 318-319retreatment considerations, 348root, 83, 314, 320-323stripping, 184-185, 224-225, 315,

316fPeriodontal abscess, 300fPeriodontal ligament

anatomy of, 23, 24fanesthesia injection, 107-110function of, 23mobility tests for evaluating, 59perforations into, 314vasculature, 23

Periodontitisacute apical, 40, 41f, 65t, 66, 289chronic apical, 40-42, 65t, 66, 289suppurative apical. See Apical ab-

scess, chronic.Periodontium

anatomy of, 22blood supply to, 7-8endodontically involved teeth effects,

470-471examination of, 59, 299formation of, 7-8tissues of, 7vasculature of, 23

Perio-endo lesion, 473, 474f, 481f-482fPeriradicular lesions. See also specific

lesion.bacterial role in, 29-30cytokines in, 39description of, 37-38healing of, 44-45

Periradicular lesions-continuedillustration of, 339fi mmunoglobulins in, 39malignant lesions that simulate, 46mediators of, 38-39nonendodontic, 45-46root canal treatment success and, 333

Periradicularsurgerycontraindications, 429-430description of, 114indications, 426-429procedure sequence, 430-435

Periradicular tests, 299Permanent restorations, 188-190Phenolics, 233Phospholipase A 2 , 32Pins, 277, 382-383, 409Plexus of Raschkow, 5Polyamines, 288Polycarboxylate cement, 381Polymicrobial infections, 284-287Polymorphonuclear leukocytes, 28f,

28-29,31Porcelain, 79, 128Post

for anterior teeth, 275-276for posterior teeth, 276removal of, 353, 355f-356f, 356-357selection of, 274space preparations for, 274-275,

328-330temporary, 279

Posterior superior alveolar block, 104Posterior teeth, 276-277Predentin, 5Preodontoblasts, 5, 12Present illness, 52-53, 447Probing, periodontal, 59, 472-473,

475f-476f, 482fProfound anesthesia, 301Prognosis, 69, 332-333Prostaglandin E2 , 39Psychogenic pain, 528Pulp

abscess, 378fage-related changes in, 21-22, 169,

546-548anatomy of, 12f, 68f, 167-168apical region, 173-174bacteria effects, 283-284, 378-379blood flow assessments, 59calcifications, 14f, 14-15, 36, 62f, 69f,

170, 170f, 547capping of, 384-385, 396-398caries effects, 284, 383cells of. See Odontoblasts.characteristics of, 370-371collagen fibers, 14coronal, 8electrical testing of, 58-59, 59fembryology of, 4-5extirpation of, 212frictional heat effects, 382functions of, 4, 10-11, 373, 373fground substance, 14immune responses of, 32-33inflammation of. See inflammation.injury, 16, 31-34innervation of, 17-21, 30

Pulp-continuedintrapulpal pressure, 371irritants of, 28-31, 169-170, 190lingual groove, 176, 178flocal anesthesia-induced reductions

i n blood flow, 371lymphatic system of, 17, 18fmorphologic changes in, 21necrosis of, 29, 36-37, 65t, 66,

113-114, 242f, 244-245, 277f,287, 301-304, 306, 371, 383,407, 458b, 469-470

neuropeptides, 32, 38pain of, 525pathosis of, 374, 375fperiodontal disease effects, 471protective measures for, 382radiographic evaluations of, 61repair potential of, 373restorative materials effect on,

378-383sensations transmitted by, 10-11size of, 4stimuli transmission, 19-20stones, 14f, 14-15, 170tissue pressure, 16trauma, 30, 448-449vasculature of, 15f-18f, 15-18, 21,

30,59vitality tests of, 57-59, 299, 472, 551

Pulp chamberanatomy of, 8f, 75, 76f, 172, 179, 179funroofing of, 186-187

Pulp hornanatomy of, 8, 8f, 172, 176discoloration caused by, 409exposure of, 187removal of, 195-196

Pulp space, 9, 9fPulp-dentin complex, 370Pulpectomy, 212Pulpitis

hyperplastic, 35-36irreversible, 34, 61, 65t, 66, 112-113,

277, 301, 393reversible, 34, 35f, 65t, 66

Pulpotomy, 212, 385, 396-398, 451,452f, 453b

RRadiographs and radiography

bitewing, 144,144fcone-image shift, 132, 136-141description of, 59-60diagnostic, 132, 134, 472difficulties in obtaining, 75elderly considerations, 551-552endodontic uses of, 141-144exploratory use of, 191exposure considerations, 136film-cone placement, 144-148for emergencies, 299limitations of, 60obturation evaluations, 262-263periapical lesions evaluated using,

60-61rapid processing, 148recall, 132-133, 135-136sequence of, 134-136

I ndex 579

Radiographs and radiography-continuedsuccess evaluations, 333, 335ftreatment uses of, 132viewers, 148working films, 132-135

Radiolucent lesions, 142, 142f,475-476, 477f

Radiopaque lesions, 142-143Reamers, 157-158Reaming, 216Recapitulation, 225, 225fReferrals, 74-86Referred pain, 75Resin composites, 273, 381, 410Restorations. See also Permanent restora-

tions; Temporary restorations.access through, 277design principles, 272direct, 272-273hypersensitivity after, 383in elderly, 556, 559indirect, 273-274microleakage of, 379-380patient questions regarding, 96removal of, 189-190structural and biochemical consider-

ations, 270-271timing of, 271-272

Retreatmentcase selection for, 347-351clinician considerations, 348, 351communication with patient,

365 1 367completion of, 362, 365considerations for, 346-347crown removal for, 351, 353, 354fdegree of difficulty, 365description of, 342disease prevention, 351, 352f-353fpost and core removal for, 353,

355f--356f, 356-357referrals, 367root canal obstructions, 357-362short- and long-term outcomes, 365tooth considerations, 348

Reversible pulpitis, 34, 35f, 65t, 66Root

amputation of, 436-439, 438,439f, 442

curvature of, 76, 78f-79fformation of, 5-6fractures of, 244, 456-458hemisection of, 438-439, 440f, 442identification of, 168-169length of, 9, 76perforation of, 83, 314, 320-323, 436resorption of, 81, 171, 171f, 202f,

261f, 414-415, 436, 548fsheath proliferation, 5submersion of, 494-496, 495fvertical fracture of, 244, 328, 480,

501t, 513-518, 516f--517fRoot canal(s)

aberrations of, 216-218accessory canals, 173, 244, 468, 469fanatomy of, 8f, 9, 172-173artificial, 320bacteria in, 285t, 285-286cone-image shift radiography, 138, 140

Root canal (s) -continuedC-shaped, 179, 179fidentification of, 168-169inability to locate, 84, 191ledge formation. See Ledge

formation.multiple, 76, 77f-78fnumber of, 76, 77f-78fobstruction of, 357-362overenlargement of, 222, 227f

Root canal(s)-continuedseparation of, 198, 200fshape of, 172-173, 209-210working length of. See Working

length.Root canal treatment

costs of, 96evaluation of, 334-337failure of, 95f, 334, 335f, 337-342,

437fin elderly, 554-556pain associated with, 94-96previously started, 189procedure, 91f-96fsuccess of, 333-334

Root planing, 471Root-end closure

case selection, 394definition of, 389, 398failure of, 402-403indications and contraindications, 396planning of, 394success of, 402, 402ftechnique, 399-401, 401fwith mineral trioxide aggregate,

401-402,402fRoot-end resection, 432-433Rotary instruments

characteristics of, 157-158gutta-percha removal using, 357intracanal use of, 159nickel-titanium, 228-229passive step-back technique and, 230stainless steel, 232

Rubber damapplication of, 124-125equipment for, 121-124leaking of, 126modifications for difficult situations,

126-128placement of, 120-121, 124-125positioning of, 125reasons for using, 119-120, 313referrals, 129

SSealers, 248-251Selective anesthesia, 63Separated instruments, 323f-324f,

323-324, 340, 349f, 360, 362Shaping. See Cleaning and shaping.Sharpey's fibers, 7Silver points, 247, 247f, 360, 363fSinus tract type probing, 476-480, 479fSmear layer, 376-377Sodium hypochlorite, 290-291, 410Sodium perborate bleaching, 410Soft tissue examination, 54-55, 447-448Solvent-softened custom cones, 257-259

Sonic instrumentation, 231-232Specialist referral, 84-85Split dam, 313, 313fSpoon excavator, 161Step-back technique, 212-216, 213f,

215f, 225, 230Sterilization of instruments, 162-163Steroids, 539Stoma parulis, 55Stones, pulpal, 14f, 14-15, 170Straight-line access, 183-185, 184fStripping perforation, 184-185,

224-225, 315, 316fSubodontoblastic plexus of Raschkow,

18, 20f, 20-21Substance P, 16Suppurative apical periodontitis. See

Apical abscess, chronic.Surgery

amputation, 436-439, 438, 439f, 442corrective, 436healing after, 435-436in elderly, 557-558incision for drainage, 425-426periradicular. See Periradicular

surgery.referrals, 442-443, 443f

TT cells, 13, 32, 40fTemporary restorations

access preparation considerations,188-189

crowns, 279description of, 278long-term, 280objectives of, 278placement of, 278, 279fremoval of, 189-190semipermanent, 271-272

Tertiary dentin, 372, 372f-373fTetracycline-induced discoloration,

408, 416-417Thermal tests, 57-58Thermocatalyic technique, 411Tooth

access considerations, 185-187anatomic regions of, 8-9avulsed, 461-464canals of, 76, 77f-78fcontrol, 56cracked, 80-81, 500, 501t, 502f,

505-510examination of, 55, 55fextraction of, 394fractured, 80-81isolation of, 79location of, 79, 80fluxation injuries of, 459-461malpositioning of, 79, 80fmobility testing of, 59palpation of, 56, 56fpercussion of, 56selective anesthesia, 63split, 501t, 502f, 510-513, 511fstructure of, 270, 272surface conservation, 185-187trauma, 82, 446-464

Transplantation, 488-491, 489f-490f

580 I ndex

Traumaexamination of, 447-449history-taking, 446-447in elderly, 559-560periodontal defect after, 480pulpal, 30, 448-449

Treatment and treatment planningadjunctive procedures, 68-69appointments, 64-66, 94complications that affect, 67, 68f-69fdescription of, 63diagnosis-specific approach, 64emergencies, 300form for, 64fmodifiers of, 67-69referral during, 84selection of, 67signs and symptoms persisting after,

83-84Trigeminal nerve, 17,19-20Trigeminal neuralgia, 529

UUltrasonic condensation, 256Ultrasonic instrumentation, 230-231Underfill, 242, 243f, 326-327, 341

VVarnishes, 382Vasoactive intestinal peptide, 16Venules, pulpal, 15, 15f, 17f-18fVertical condensation, 161, 259-262,

514Vertical root fracture, 244, 328, 480,

501t, 513-518, 516E 517fVibratory systems, 230-232Vital pulp therapy

complications of, 396definition of, 389-390failure of, 398, 402-403indications and contraindications, 395planning of, 394prognosis, 396pulpotomy. See Pulpotomy.

Vital pulp therapy-continued

success of, 402, 403ftechniques, 396-398

Vitality testing, of pulp, 57-59

WWalking bleach technique, 411,

412f-414f

Working lengthapical constriction, 201-203description of, 200, 201electronic apex locators, 201-203estimated, 201in elderly, 555-556patient response, 204reference point for, 200-201variations in, 201, 202f

ZZinc oxide-eugenol, 248, 380-381Zinc phosphate cement, 381

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