Diseases of the pulp

DISEASES OF THE DENTAL PULP- Part IIDeepthi P.R.1st year MDSDept of Conservative Dentistry & Endodontics

CONTENTS Introduction Irritants Inflammatory process Immunologic responses Lesion progression Classification of diseases

INTRODUCTION Etiologic factors causing pulp

inflammation Mechanism of spread of inflammation Mediators of pulpal inflammation Classification & features of diseases

IRRITANTS

Living • Micro organisms

• Viruses

Non Living• Mechanical• Thermal• Chemical

Microbial irritants Main source Numerous species: S. mutans,

Lactobacilli, Actinomyces Toxins: deep penetration to pulp Local infiltration of pulp- chronic

inflammatory cells Progression: intensity & character

changes

Microbial irritants Actual exposure: PMN infiltration &

liquefaction necrosis Long periods of inflammation/ necrosis-• Virulence• Release of inflammatory fluid: avoiding intrapulpal pressure• Host resistance• Circulation• Lymphatic drainage

Microbial irritants Yamasaki et al : pulpal necrosis in rats Exposed pulp: bacteria & by products Temporary impeding of spread &

destruction Persistence: extensive destruction –

spread throughout pulp- periapical spread & inflammatory lesions

Microbial irritants Kakehashi et al : pulp exposures in

conventional & germ free rats Mӧller et al: sealed infected & non

infected canals in monkeys Sundqvist et al: traumatised teeth with

and without apical pathosis

Microbial irritants Viruses: symptomatic apical pathoses Periapical lesions: CMV & EBV-

symptomatic

Mechanical irritants Deep cavity preparations Removal of tooth structure without

proper cooling Impact trauma Occlusal trauma Deep periodontal curettage Orthodontic movement

Mechanical irritants Extensive restorative procedures: pulpal

inflammation Dentin permeability closer to pulp

Operative procedures without coolant- more pulpal irritation

Mechanical irritants Impact injuries : severity of trauma &

degree of apical closure – pulpal recovery

Orthodontic forces beyond physiologic tolerance: cellular atrophy, alteration of nerve axons, apical resorption

Deep scaling & curettage

48 hours after crown preparation through enamel & 1mm into dentin

Aspiration of odontoblasts into tubules & pulpal infiltration by PMNs & Lymphocytes

M Torabinejd. Endodontics

Chemical irritants Dentin sterilizing :

Silver nitrate, phenol, eugenol & desensitizing substances

Cleansers: Alcohol, chloroform, H2O2, various acids

Restorative materials & liners

Periapical extrusion of filling materials causing periapical

inflammation M Torabinejd. Endodontics

Pulpal pathosis Injury: cell death & inflammation Slight: little or no inflammation Incipient caries, shallow cavity

preparations More damaging: severe inflammation Deep caries, extensive operative

procedures, persistent irritants

Pulpal pathosis

Severity & duration of illness Host capacity

Reversible pulpitis

Irreversible pulpitis

Total necrosis

Inflammatory process Irritation of dental pulp – mediators:

Histamine, Bradykinin, Arachidonic acid metabolites

Lysosomal granule products: Elastase, Cathepsin G, Lactoferrin

Protease inhibitors: Antitrypsin, CGRP, Substance P

Inflammatory process Mast cells: Histamine, Leukotrienes, PAF Released: Physical injury to mast cells or

bridging of IgE

Bradykinin, Substance P, Neurokinin A

Plasma/ Tissue

kallikreinsKininogens Kinins

Inflammatory process iCGRP release : PGE2

Pulpal nerve fibers: SP, CGRP- protective Mild- moderate injuries: iCGRP Severe: iCGRP

Cellular damage

Arachidonic acid

Immunologic Responses Bacteria & by products: Antigen Immunocompetent cells – Normal pulp

Ig levels in inflamed pulps Arthus reaction Delayed hypersensitivity reactions Necrotic foci & pulpal necrosis

Healthy pulp Pulp : vital; free of inflammation Prosthetic reasons First hours after traumatic pulp

exposure

Pulpitis Vital & inflamed No info on:

Degree of inflammation Reversible/ irreversible

Two clinical diagnoses for inflamed pulp Symptomatic pulpitis

Asymptomatic pulpitis

Pulpitis Symptomatic Vital, inflamed Symptoms of

pulpitis Exacerbation of

chronic pulpitis Acute

Asymptomatic Vital, inflamed &

no symptoms Knowledge of

etiology of pulpitis & reaction pattern of pulp

Lesion Progression Moderate to severe injuries: localized

inflammation & mediators Increase in protease inhibitors: natural

modifiers Increased vascular permeability,

vascular stasis, migration of WBCs- injury site

CGRP: increased blood flow during inflammation

Accumulation of inflammatory cells within the pulp horn

Beer. Pocket Atlas of Endodontics

Neutrophilic granulocytes in Predentin layer & Dentin tubules

Beer. Pocket Atlas of Endodontics

Lesion Progression capillary pressure & permeability

Exudation tissue pressure: passive compression & complete collapse of venules Increased pressure Inablity to expand Lack of collateral circulation

Pulpal necrosis

Lesion ProgressionInflammatory

mediators

IndirectDirect

PULPITIS Acute/ Chronic: Clinical differentiation Partial/ Total Infected/ Sterile: smear or culture Acute: Precipitous short course Violently painful Chronic: Practically symptomless Slightly painful Longer durationExposed

pulp: caries/ trauma

Hyperplastic pulpitis

Ulcerative pulpitis

CLASSIFICATION OF PULPAL DISEASES

CONTENTS Introduction Different classifications Normal pulp Reversible pulpitis Irreversible pulpitis Chronic hyperplastic pulpitis Necrotic pulp Pulp degeneration Previously treated pulp Previously initiated therapy

CLASSIFICATION OF PULPAL DISEASES *No correlation between histologic

findings & symptoms Clinical classification: Signs & symptoms Helps: appropriate treatment, prognosis,

restorative needs Indistinct demarcation between the

classes

Garfunkel et al: direct correlation -49%, partial correlation- 46%.

Wegner & Knorr: Correlation- 40%

CLASSIFICATION OF PULPAL DISEASES Grossman Baume Seltzer & Bender Wiliam T. Johnson American Board of Endodontics (ABE)- 2007 Reit, Petersson & Molven Walton & Torabionejad Torabinejad & Shabahang Tronstad Ingle & Beveridge Castelucci Beer & Baumann Abbott WHO- 1995

Grossman1. Inflammatory diseases of the dental

pulpa. Reversible pulpitis (i) Symptomatic (acute) (ii) Asymptomatic (chronic)b. Irreversible pulpitis (i) Acute - Abnormally responsive to cold - Abnormally responsive to heat

Grossman(ii) Chronic - Asymptomatic with pulp exposure - Hyperplastic pulpitis - Internal resorption2. Pulp degenerationa. Calcific (radiographic diagnosis)b. Others (histopathologic diagnosis)

3.Necrosis

Baume Symptomless vital pulp: Deep caries-

pulp capping done History of pain: Amenable to

pharmacotherapy & restorative rehabilitation

Infected pulps: Extirpation & immediate RCT

Infected & necrosed pulps: Intracanal serous drainage- medicament prior to RCT

Seltzer & Bender(a) Treatable without

pulp extirpation and RCT:

Intact, uninflamed pulp

Transitional stage Atrophic pulp Acute pulpitis Chronic partial pulpitis

without necrosis

(b) Untreatable without pulp extirpation and RCT:

Chronic partial pulpitis with necrosis

Chronic total pulpitis Total pulp necrosis

William T.Johnson Normal Reversible pulpitis Irreversible pulpitis

American Board of Endodontics (ABE)- 2007 Normal pulp Reversible pulpitis Irreversible pulpitis Symtomatic Asymptomatic Pulp necrosis Previously treated Previously initiated therapy

Reit, Petersson & Molven Pulpa sana Pulpitis Necrosis pulpae Periodontitis apicalis chronica/ acuta

Walton & Torabinejad Normal Reversible pulpitis Irreversible pulpitis Hyperplastic pulpitis Necrosis

Torabinejad & Shabahang Normal pulp Reversible pulpitis Irreversible pulpitis Hyperplastic pulpitis Necrosis Previously treated pulp

Tronstad Healthy pulp Asymptomatic pulpitis Symptomatic pulpitis Necrotic pulp

Ingle & Beveridge Incipient acute pulpalgia Moderate & advanced acute pulpalgia Chronic pulpalgia Hyperplastic pulposis Necrosis

Castelucci Healthy pulp Hyperemia Pulpitis Necrosis

Beer & Baumann Asymptomatic pulp pathology Reversible pulpitis Irreversible pulpitis Pulpal necrosis

Abbott a.Clinically normal pulpb.Reversible pulpitisTypes: Acute, Chronicc. Irreversible pulpitisTypes: Acute Chronic, Necrobiosisd. Pulp necrosisTypes: Necrosis without infection, Necrosis with infection

Abbott e. Pulpless CanalsTypes: Pulpless and no signs of infection Pulpless and infectedf. Degenerative ChangesTypes: Atrophy, Pulp canal obliteration(calcification)- Partial, Total Hyperplasia Internal resorption- Inflammatory, Replacement

Abbott g. Previous Root Canal TreatmentTypes : Satisfactory – No signs of infection - InfectedTechnically inadequate - No signs of infection - Infectedh. Endodontic- Periodontal Lesions

Abbott h. Endodontic- Periodontal LesionsClassification based on the origin of the periodontal defect: - Lesion of endodontic origin- Lesion of Periodontal origin- Combined Endo- Perio Lesions Types: Separate endo & perio lesions that do NOT communicate endodontic and periodontal lesions that DO communicate

Application of the International Classification of Diseases to Dentistry and Stomatology (3rd ed), World Health Organization (WHO), Geneva, 1995

K04 DISEASES OF PULP AND PERIAPICAL TISSUES K04.0 Pulpitis K04.00 Initial (hyperaemia) K04.01 Acute K04.02 Suppurative [pulpal abscess] K04.03 Chronic K04.04 Chronic, ulcerative K04.05 Chronic, hyperplastic [pulpal polyp] K04.08 Other specified pulpitis K04.09 Pulpitis, unspecified

Gutmann et al. JOE — Volume 35, Number 12, December 2009

Application of the International Classification of diseases to Dentistry and Stomatology (3rd ed), World Health Organization (WHO), Geneva, 1995

K04.1 Necrosis of pulp Pulpal gangrene K04.2 Pulp degeneration Denticles Pulpal calcification Pulpal stones K04.3 Abnormal hard tissue formation in pulp K04.3X Secondary or irregular dentineExcludes: pulpal calcifications (K04.2)pulpal stones (K04.2


Application of the International Classification of diseases to Dentistry and Stomatology (3rd ed), World Health Organization (WHO), Geneva, 1995

K04.4 Acute apical periodontitis of pulpal origin Acute apical periodontitis K04.5 Chronic apical periodontitis Apical granuloma K04.6 Periapical abscess with sinusIncludes: dental abscess with sinus dentoalveolar abscess with sinus periodontal abscess of pulpal origin K04.60 Sinus to maxillary antrum K04.61 Sinus to nasal cavity K04.62 Sinus to oral cavity K04.63 Sinus to skin K04.69 Periapical abscess with sinus, unspecified


K04.7 Periapical abscess without sinus Dental abscess } Dentoalveolar abscess } without sinus Periodontal abscess of pulpal origin } K04.8 Radicular cystIncludes: cyst apical periodontal periapical K04.80 Apical and lateral K04.81 Residual K04.82 Inflammatory paradentalExcludes: developmental lateral periodontal cyst (K09.04) K04.89 Radicular cyst, unspecified K04.9 Other and unspecified diseases of pulp and periapicaltissues


Normal pulp A clinical diagnostic category in which

the pulp is symptom-free and normally responsive to pulp testing*.

Asymptomatic Mild to moderate response: stimuli Subside immediately on removal

AAE Consensus Conference.JOE — Volume 35, Number 12, December 2009

No painful response: palpation & percussion

Radiographs: clearly delineated canal- tapers to apex, intact lamina dura, no calcification/ resorption.

Reversible Pulpitis Mild to moderate inflammatory

condition of the pulp caused by noxious stimuli in which the pulp is capable of returning to the uninflamed state following removal of the stimuli

*Pulpal inflammation which should resolve once the etiology is removed (defective restorations or caries).

Dabuleanu M. J Can Dent Assoc 2013;79:d90

Reversible Pulpitis Clinical condition associated with

subjective & objective findings indicating presence of mild inflammation in pulp tissue

A clinical diagnosis based on subjective and objective findings indicating that the

inflammation should resolve and the pulp return to normal*.*AAE Consensus Conference.JOE — Volume 35, Number 12, December

2009

Reversible Pulpitis - Causes Incipient caries Cervical erosion Occlusal attrition Thermal shock: Operative procedures Deep periodontal curettage Enamel fracture

Causes Trauma: Occlusal / Blow Fresh amalgam filling: contact with cast

restoration Circulatory disturbances Local vascular congestion

Reversible Pulpitis- Histopathology Reparative dentin Disruption of odontoblast layer Dilated blood vessels Extravasation of oedema fluid Immunologically competent chronic

inflammatory cells & occasional acute cells

Reversible Pulpitis- Symptoms Thermal stimuli: quick, sharp

hypersensitive response- subsides on removal of stimulus

More often by cold than hot Asymptomatic- incipient caries No spontaneous pain

Diagnosis Patient’s symptoms Momentary sharp

pain, disappearing on removal of stimulus

Cold, sweet, sour Chronic pain-

paroxysm of short or long duration

Complete recovery or shorter relief

Clinical tests Application of cold Normal reaction to

percussion, palpation, mobility

Normal on radiographic examination

Treatment Prevention Early restoration Desensitization – marked gingival

recession Cavity varnish/ cement base Care in cavity preparation & polishing Sedative dressing- ZOE dressing Vitality tests

Treatment & Prognosis Sealing & insulating exposed dentin/

vital pulpContinuous / increased irritation- moderate to severe inflammation

Irreversible pulpitis Pulpal necrosis

Favorable: irritant removed early enough

Persistence: irreversible pulpitis

Irreversible Pulpitis Persistent, inflammatory condition of

the pulp, symptomatic or asymptomatic, caused by a noxious stimulus

Clinical condition associated with subjective and objective findings indicating presence of severe inflammation in the pulp tissue

*Pulpal inflammation which will not resolve once the etiology is removed

*Dabuleanu M. J Can Dent Assoc 2013;79:d90

Irreversible Pulpitis Acute/ Subacute/ Chronic Partial/ Total Infected/ Sterile Acute: pain by hot/ cold stimulus or

spontaneous Lingering pain Chronic quiescent to Acute symptomatic-

hours/ years Exudate: vented- quiescent, confined- painful

Irreversible Pulpitis- Histopathology Chronic & acute inflammatory features Congestion of postcapillary venules Affect pulpal circulation : necrosis PMNs: acute inflammatory reaction Lysosomal enzymes + cellular debris of

PMNs: pus

Areas of microabscesses: necrotic tissue + micro organisms+ lymphocyte, plasma cells, macrophages

Walled off by fibrous connective tissue No micro organisms in the centre of

abscess On pulpal penetration: area of ulceration Necrotic tissue+ PMN zone+ proliferating

fibroblasts: calcific masses

Symptomatic Irreversible Pulpitis A clinical diagnosis based on subjective

and objective findings indicating that the vital inflamed pulp is incapable of healing. Additional descriptors: lingering thermal pain, spontaneous pain, referred pain*.

Spontaneous intermittent or continuous paroxysms of pain.

Symptomatic Irreversible Pulpitis Prolonged painful response to cold:

relieved by heat Prolonged painful response to heat :

relieved by cold. Painful response to both Moderate/ severe Sharp/ dull

Localized/ referred Continuous/ intermittent Later: ‘boring, gnawing, throbbing’ Triggered by change in posture Cavity with no outlet: intense pain Kept awake at night

Asymptomatic Irreversible Pulpitis A clinical diagnosis based on subjective

and objective findings indicating that the vital inflamed pulp is incapable of healing. Additional descriptors: no clinical symptoms but inflammation produced by caries, caries excavation, trauma*

Progress to symptomatic/ necrotic Treatment as soon as possible

*AAE Consensus Conference.JOE — Volume 35, Number 12, December 2009

Diagnosis Grayish scum like layer: exposed pulp Odor of decomposition Probing painful & hemorrhage : deeper

areas of pulp Drop of pus: gaining access

Diagnosis Radiographs Little use Helps identification of suspect teeth Advanced stages: thickening of PDL Mobility, percussion & palpation:

Negative

Diagnosis Thermal tests Early: Persistent pain after removal of

stimulus Late: normal response, feeble EPT: marked variation from normal

Differential diagnosis Reversible

Pain disappears on removal of thermal stimulus

EPT: responds with less current than on control

Irreversible Lingering/

spontaneous pain Asymptomatic:

little/ no pain EPT: more current

required

Differential diagnosis Irreversible

Early symptomatic: less current with EPT

Abnormal response to cold- sharp, piercing

Later stage: diffuse dull constant pain

Abnormal severe response to heat

Acute alveolar abscess

Swelling Tenderness on

palpation, percussion

Mobility Lack of response

to vitality tests

Differential diagnosis Pain of non-odontogenic origin: Musculoskeletal pain Neurovascular pain Neuropathic pain Pain caused by a distant pathology

(cardiovascular, cranial, throat, neck) Psychogenic pain

*Dabuleanu M. J Can Dent Assoc 2013;79:d90

Treatment & Prognosis Pulpectomy Pulpotomy: emergency procedure Surgical removal: not restorable Favorable prognosis: Proper endodontic

therapy & post endodontic restoration

Chronic Hyperplastic Pulpitis ‘Pulp polyp’ Productive pulpal inflammation due to an

extensive carious exposure of a young pulp

A form of irreversible pulpitis that originates from overgrowth of a chronically inflamed young pulp onto the occlusal surface

Granulation tissue – epithelial covering Long standing, low grade irritation

Causes & Symptoms Slow progressive carious exposure Large open cavity Young resistant pulp Chronic low grade stimulus Symptomless: discomfort during

mastication

Chronic Hyperplastic Pulpitis- Histopathology Surface covering: Stratified squamous

epithelium (deciduous) Gingiva/ mucosa/ tongue Young vascular connective tissue+

PMNs+ lymphocytes+ plasma cells Nerve fibers

Diagnosis Fleshy, reddish pulpal mass filling

chamber & beyond confines of the tooth Size of a pin or upto interfering with

comfortable closure Sensitivity : < pulp, > gingiva No pain, easy bleeding Stalk traced back to pulp chamber

Diagnosis Radiographs: Large, open cavity:

direct access to the pulp chamber Thermal test: no or feeble response EPT: more current than normal Distinguished from proliferating gingival

tissue

Treatment & Prognosis Elimination of polypoid tissue; pulp

extirpation Bleeding controlled after tissue removal Temporary dressing after pulpotomy Radicular pulp extirpation later Favorable after adequate endodontic

treatment & restoration

Necrotic pulp Clinical condition associated with subjective

and objective fndings indicating death of the dental pulp

A clinical diagnostic category indicating death of the dental pulp. The pulp is usually nonresponsive to pulp testing*.

Exudate: absorbed / drained- necrosis delayed & radicular pulp vital for long periods

Closure/ sealing of inflamed pulp- rapid & total necrosis & periradicular pathosis


Necrotic pulp Non vital/ necrotic Suspected on negative reaction to

sensitivity tests Confirmed on inspection of root canal

space only Total/ Partial Sequel to inflammation/ trauma- before

inflammation: Dry gangrenous necrotic pulp

Necrosis- Types Coagulation : soluble portion precipitated/

converted to solid material Caseation : form of coagulation necrosis-

tissue converted to cheesy mass: coagulated proteins+ fat+ water

Liquefaction : softened mass/ liquid/ amorphous debris by proteolytic enzymes. Follows irrevrsible pulpitis

Ischemic : traumatic injury, disruption of blood supply

Necrotic pulpIntermediate products- unpleasant odor Indole Skatole Putrecine Cadaverine

End products H2S NH3 Fatty substances Indican Protamines Water CO2

Necrotic pulpHistopathology Necrotic pulp

tissue Cellular debris Microorganisms Normal/ slight

evidence of inflammation: peripaically

Cause Bacteria Trauma Chemical irritation

Necrotic pulp- Symptoms No painful symptoms if otherwise

normal Discoloration: first symptom Dull/ Opaque: lack of normal

translucency Grayish/ Brownish discoloration By chance discovery

Symptoms Usually asymptomatic Episodes of spontaneous pain/ discomfort,

pain on pressurePartial necrosis: Vital nerve fibers- positive thermal tests

Pain on heat application- thermal expansion of gases present in RC space

Unlikely Cold, heat, electric stimuli: no response

Diagnosis Non responsive to vitality testing Presence of various degrees of

inflammatory response- teeth with multiple canals: confusion

Minimal response-EPT: conduction through moisture

Diagnosis Spread of inflammatory reactions to

periradicular tissues: sensitive to percussion & palpation

Radiographs: large cavity/ filling , open approach to RC, thickening of PDL

Treatment & Prognosis RCT Surgical removal Favorable: proper endodontic therapy

Pulp Degeneration Seldom recognized clinically Generally: old; persistent mild irritation:

young Not infected/ restored always Early: no definite symptoms Late: discolored, no response to

stimulation Types: Calcific, Atrophic, Fibrous

Calcific Degeneration/Hard tissue changes Pulp calcification Resorption

Pulp CalcificationExtensive- pulp stones/ diffuse Trauma Caries Periodontal disease Other irritants Sources: Thrombi in vessels & collagen

sheaths around vessel walls

Pulp stones Pulp chamber generally Laminated structure: Skin of an onion Source: True/ False Position: canal wall- Free - Attached/ Adherent - Embedded/ Interstitial

Pulp CalcificationCalcific Metamorphosis: Extensive formation of hard tissue on

dentin walls Irritation/ death & replacement of

odontoblasts Partial/ complete radiographic

obliteration of pulp chamber & root canal

Yellowish discoloration of the crown

Pulp Calcification Increased pain threshold to stimuli;

often unresponsive Palpation & percussion : WNL Various degrees of pulp space

obliteration- radiographic Reduction in coronal pulp space &

gradual narrowing of root canal Not pathologic, no treatment

Internal/ Intracanal resorption Idiopathic slow or fast progressive

resorptive process occurring in the dentin of the pulp chamber or root canals of teeth

Resorption of dentin walls, advancing from centre to periphery

Asymptomatic mostly Advanced cases: pink spots in the crown

Internal resorption- Histopathology Osteoclastic activity Lacunae- filled by osteoid tissue Granulation tissue MNGCs/ Dentinoclasts Chronic inflammation Metaplasia of pulp: Bone/ Cementum

Internal/ Intracanal resorption Pulpal & periapical tests: WNL Radiographs: Radiolucency with

irregular enlargement of root canal compartment; round/ ovoid radiolucent area

Immediate removal of inflamed tissue, RCT

Progression & perforation to lateral periodontium-

necrosis & treatment difficult

Treatment & Prognosis Routine endodontic therapy Obturation: Plasticized GP method Root perforation: MTA repair Prognosis: Best before perforation Guarded: perforation Surgical repair

Atrophic Degenration Histopathological diagnosis Older people Fewer stellate cells, increased

intracellular fluid Less sensitive pulp tissue ‘Reticular atrophy’- delay of fixative

agent reaching pulp: artifact

Fibrous degeneration Cellular elements replaced by fibrous

connective tissue Leathery fiber appearance on

extirpation No clinical diagnosis

Kouros et al Eur J Dent 2013;7 Suppl 1:s26-32

Pulp artifacts Unsatisfactory

fixation: Fatty degeneration

of pulp Vacoulization

Tumor metastasis

Rare Terminal stages Direct local

extension from jaw

PREVIOUSLY TREATED PULP A clinical diagnostic category in which

the tooth had had either partial or complete endodontic therapy

A clinical diagnostic category indicating that the tooth has been endodontically treated and the canals are obturated with various filling materials other than intracanal medicaments*


PREVIOUSLY TREATED PULP Symptomatic/ asymptomatic Completion of partial RCT Retreatment of failed RCT Endodontic surgery Extraction

Previously Initiated Therapy A clinical diagnostic category indicating that

the tooth has been previously treated by partial endodontic therapy (eg, pulpotomy, pulpectomy)*

Pulpotomy/ Pulpectomy performed before presenting for RCT

Emergency procedure: Irreversible pupitis Vital pulp therapy Traumatic injuries Accurate pulpal diagnosis: Impossible


Dental pulp in Systemic diseases Systemic viral infections Genetic & developmental disorders Endocrine disorders Cancer

Genetic disorders Hypophosphatemic rickets Taurodontism Dens invaginatus Dentinogenesis imperfecta amelogenesis imperfecta Gaucher’s disease

Systemic viral infections

Glick et al

HIV: dental pulp & periradicular tissues- reinforcing universal precautions

HSV-I &II: pain, pulpal necrosis & internal resorption

Gregory et al- 1975Solomon et al- 1986Sigurdsson & Jacoway- 1995

Systemic viral infections Rubella:

cytopathic effects on ameoblasts

1st trimester

Paget’s disease: Measles virus –

Paramyxovirus family Pulpal obliteration Internal resorption Dystrophic

calcification Apical ending: difficult

to localize in treatment

Diabetes mellitus Presence of large-vessel and small-

vessel angiopathies and a thickened basement membrane*

Extensive amorphous calcifications** Larger & more prevalent periradicular

lesions of endodontic origin***

*Russel B.Acta Pathol Microbiol Scand 1967; 70: 319-320

**Bissada et al. Egypt Dent J 1970; 283-296***falk et al. Scand J Dent Res 1989; 97:198-206

Diabetes mellitus Limited dental collateral circulation Impaired immune response Increased risk of acquiring pulp

infection/ necrosis Hyperglycaemia- bone resorption,

inhibiting osteoblastic differentiation and reducing bone recovery.

Lima et al .International Endodontic Journal, 46, 700–709, 2013

New investigation EphA7 genetic expression: marked in

inflamed human dental pulp Pathogenesis, diagnosis & therapy of

tumors: lymphoma & GITDong Y et al. JOE — Volume 39, Number 2, February 2013

References Chandra BS, Gopi Krishna V. Grossman’s

Endodontic Practice. 12th Edition Beer R, Baumann MA, Kielbassa AM.

Pocket Atlas of Endodontics Tronstad L. Cinical Endodontics. A

textbook. 2nd revised edition Abbott PV. Endodontics and Dental

Traumatology. An overview of Modern Endodontics

References Castelucci A. Endodontics. Volume 1 Hargreaves KM, Cohen S. Cohen’s Pathways of

the Pulp. 10th Edition Ingle JI, Bakland LK. Ingle’s Endodontics. 5th

Edition Hargreaves KM, Goodis HE. Seltzer and

Bender’s Dental Pulp. AAE Consensus Conference on Diagnostic

Terminology: Background and Perspectives. J Endod .2009;35(12):1634

References Gutmann JL, Baumgartner GC, Gluskin AH,

Hartwell GR, Walton RE. Identify and Define All Diagnostic Terms for Periapical/

Periradicular Health and Disease States. J Endod 2009;35:1658–1674 Dabuleanu M. Pulpitis (Reversible/ Irreversible).

Can Dent Assoc 2013;79:d90 Lima SMF, Grisi DC, Kogawa EM. et al. Diabetes

mellitus and inflammatory pulpal and periapical disease: a review. Int End J. 46, 700–709, 2013

Fernandes M, de Ataide I, Wagle R. Tooth resorption part I - pathogenesis and case series of internal resorption. J Conserv Dent 2013;16:4-8

Kouros P, Koliniotou-Koumpia E, Koulaouzidou E, Helvatjoglu-Antoniades M, Tziafas D. Pulp response to dentine adhesives: A study on mature human pulps. Eur J Dent 2013;7 Suppl 1:s26-32

Thank You…..

Health & Medicine

Diseases of the pulp