Periapical pathology 22 (1)

PULP AND PERIAPICAL DISEASES

Submitted by Hina bhatia (521)

Contents Introduction

Pathobiology of periapex

Acute and chronic

Inflammation Vs Immunology

Classifications of pulpoperipaical pathoses

Clinical signs and symptoms

Healing mechanisms

Differential diagnosis

Ludwig’s angina , Cellulitis

Osteomyelitis , Periapical actinomycosis

Foreign body reactions

Conclusion

Contents

Introduction

Apical Pulp tissue less cellular more fibrous whitish in colour large conc of glycogen →anaerobic environment higher conc of sulfated glycosaminoglycans fibrous tissue ~ PDL

Apical dentin

Less tubular , more amorphous , irregular Sclerotic dentin increases with age Odontoblasts of the pulp are absent/flattened/cuboidal Optically transparent Less permeable

Pathways of infection

Opening in dental hard tissue wall

caries

clinical procedures

trauma induced fractures

microcracks

Bacteria from the gingival sulcus/ P.pocket

Endodontic reinfection

Anachoresis

HOST ALLERGEN

HOST ALLERGEN

Inflammation

Phagocyte system

Lymphatic system / T & B cells

Immune/complement system

Neural mechanism

chemotaxis

Endotoxins

Exotoxins

Enzymes

PUS / tissue damage

Stimulation of clast cells

Exudate (inflam edema)- pain

Acute (exudative)

Chronic (proliferative)

Classification by Franklin.s.weinePerapical pathosis of pulpal origin:

1.Painful pulpoperiapical pathoses

a. Incipient acute apical periodontitis

b. Advanced ’’ ’’ ’’

(i) acute periapical abscess

(ii) recrudescent / phoenix abscess

(iii) subacute peiapical abscess

2. Non painful periapical pathoses

a. Pulpopariapical osteosclerosis(condensing osteitis)

b. Incipient chronic apical periodontitis

c. Advanced ’’ ’’ ’’

(i) periapical granuloma

(ii) chronic periapical abscess

(iii) periapical cyst

Hirsch et al (1979) – surgically excised pulpoperiaical lesions

I. Periapical granuloma

II. Epithelial granuloma III. Radicular cyst with modern (chronic inflammation) IV. Radicular cyst with strong ( acute or subacute )

inflammation and epithelial necrosis V. Radicular cyst without inflammation (chronic or acute)

WHO(1995) CLASSIFICATION

Code number

CATEGORY

K04.4K04.5K04.6K04.60K04.61K04.62K04.63

K04.7

K04.8K04.80K04.81K04.82

Acute apical periodontitisChronic ’’ ’’ (periapicalgranuloma)Periapical abscess with sinusPeriapical abscess wth sinus to maxillary antrum ’’ ’’ ’’ to nasal cavity ’’ ’’ ’’ to oral cavity ’’ ’’ ’’ to skin

Periapical abscess without sinus

Radicular cyst(apical periodontal cyst, periapical cyst)Apical and lateral cystResidual cystInflammatory paradental cyst

Classification by Franklin.s.weinePerapical pathosis of pulpal origin:

1.Painful pulpoperiapical pathoses





(iii) subacute peiapical abscess

Painful pulpoperiapical pathoses

Early apical changeHealthy tooth





(iii) subacute periapical abscess

Abscess

Healthy tooth Early apical change

Abscess

Tooth becomes extremely tender

Vascular congestion

Regional anoxia

Cell breakdown(autolysis)

Neutrophils increase in number

Release osteolytic fragments

Pus core

Gumboil (parulis)

Breach the cortical bone (sinus opening)

“STOMA”

ACUTE

CHRONIC

parulis / gum boil

(acute/chronic)

stoma

(chronic)

Apical periodontitis

A draining sinus is evident on the labial aspect of the upper left lateral incisor. (A) A gutta percha (GP) point has been placed into the draining sinus in order

to trace its origin. (B) The radiograph taken with the GP point in the sinus shows that it tracks

from the periapical region of the upper left central incisor, which has a chronic apical abscess. The lateral incisor has chronic apical periodontitis but this tooth is not associated with the draining sinus.

Toxic components from pulp irritants / necrosis Occlusal disharmony – persistant periapical tissue

compression Related to root canal procedures

ETIOLOGY of Painful pulpoperiapical pathoses

Etiologic factors related to rot canal procedures

Note the space between the gutta-percha filling and the root canal walls clearly visible

JOSE´ F. SIQUEIRA

Common problems that may cause post-treatment disease

at least seven problems

1. Inadequate RCT without iatrogenically altered root canal morphology

2. Inadequate RCT with iatrogenically altered root canal morphology

3. Infection remaining in inaccessible areas in the apical portion of the

root

4. Extraradicular infection including extruded dentin debris with bacteria

present in

the dentinal tubules

5. True radicular cysts and tumors

6. Foreign body reaction to cholesterol crystals or extruded materials

such as talc-

contaminated guttapercha, particles of paper points, and particles of

sealer

7. Vertical root fractures

The quality of the root canal obturation as visualized on a buccal–lingual radiograph is in no way indicative that the root canal was well sealed, particularly when canals are oval or ribbon-shaped in transverse section. Note the discrepancy of the image taken in abuccal–lingual direction as compared to that taken in a mesio-distal direction.

Endodontic Topics 2005, 10, 123–147

Diagnosis

Slight tenderness to intense continuous throbbing pain

Sense of fullness Readily localised – tenderness on percussion Palpable fluctuant swelling Vitality test (if viable Cfibers ) Radiographs

2 . Non-Painful pulpoperiapical pathoses







2 . Non-Painful pulpoperiapical pathoses







Pulpoperiapical osteosclerosis (Condensing osteitis)

Occur most frequently in the mandible, around teeth with a periapical granuloma or radicular cyst, RCT,or restorations.

exudate from the pulp (low toxicity and long standing) the resulting mild irritation

circumscribed proliferation of the periapical bone.

“condensing osteitis or focal sclerosing osteomyelitis”

Incipient Chronic apical periodontitis Initially chronic periapical connective response to pulpal

irritants characterized by :

slightly widened apical periodontal space (containing dilated blood

vessels, a mild inflammatory exudate)

a dense accumulation of chronic inflammatory cells(plasma cells and

lymphocytes)

If the pulpal contaminants are not removed the response will intensify to one of the acute or chronic forms







Periapical granuloma

This is advanced form of chronic apical periodontitis; characterized by growth of granulation tissue and the presence of chronic inflammatory cells (granulomatous) in response to continued pulpal irritation.

Zones of periapical granuloma

Exudative

Granulomatous

Granulofibrotic

Fibrotic granulomas O3 OR,Endo 1996:81:93-102

Periapical cyst

“A periapical cyst is chronic inflammatory response of the periapex that develops from chronic lesions with preexisting granulomatous tissue.”

characterized by:

Central fluid filled epithelium lined cavity surrounded by

granulomatous tissue and peripheral fibrous encapsulation.

Periapical / Radicular cyst Direct sequel to chronic AP Incidence: 6-55% Two types : true and pocket Typical radiographic appearance-round/pear shaped radiolucent unilocular lesion less than 1cm in diameter Process of formation

Dormant cell rests of malassez proliferate

Epithelium lined cavity comes into existence

Cyst grows in size

Do periapical cysts heal ?

Differential diagnosis

Granuloma vs Cyst vs Abscess

Chronic

non painful

Definite outline

Smaller in size

Chronic

non painful

Sclerotic opaque border

Bigger in size

Contain more protein and albumins

Acute /Chronic

Pain/non painful

Swelling/parulis

Sinus opening(chronic)

Diffuse outline

Mobility of the tooth

historyConformative histology

Condensing osteitis

Hypercementosis …. Vital , lying within intact lamina dura

and PDL space

Periapical cemental dysplasia ….lesion is seperated from

the surrounding normal bone by a

radioluscent border , vital

Osteosclerosis …. idiopathic

Odontogenic pain

Dentinal hypersensitivity

Reversible pulpitis

Irreversible pulpitis

Acute apical periodontitis

Acute apical abscess

Non odontogenic pain –musculoskeletal Myofacial pain TMD bruxism

Non odontogenic pain– neuropathic Trigeminal neuralgia Atypical odontalgia Glossopharyng neuralgia

Non odontogenic pain– neurovascular migraine cluster headache

Non odontogenic pain – inflammatory allergic rhinitis bacterial sinusitis

Non odontogenic pain – systemic disorders Cardiac pain Herpes zoster Sickle cell anaemia Neoplastic disease

Ludwig’s angina

“potentially life-threatening, rapidly expanding, diffuse inflammation of the submandibular and sublingual spaces that occurs most often in young adults with dental infections.”

Symptoms: severe neck pain Swelling Fever Malaise Dysphagia

Stridor suggests an impending airway crisis. Causative bacteria include many gram-negative and anaerobic organisms, streptococci and staphylococci

Ludwig’s angina

The submandibular space is composed of two spaces separated anteriorly by the mylohyoid muscle: the sublingual space, which is superior, and the submaxillary space, which is inferior. The spread of infection is halted anteriorly by the mandible and inferiorly by the mylohyoid muscle. The infectious process expands superiorly and posteriorly, elevating the floor of the mouth and the tongue. The hyoid bone limits the process inferiorly, and swelling spreads to the anterior aspect of the neck, causing distortion and a "bull neck" appearance. This then evolves to an infectious compartment syndrome of the submandibular and sublingual spaces.

Cellulitis (Phlegmon)

Cellulitis is a diffuse inflammation of the soft tissues which is not circumscribed or confined to one area,but which,in contradistinction to the abscess,tends to spread through tissue spaces along facial planes.

Cellulitis –etiology (of face and neck)

Dental infection as a sequelae of an abscess or osteomyelitis,or following periodontal infection.

Pericoronitis (operculitis)

Infection following tooth extraction ( injection either thro an infected needle or infected area)

Cellulitis -pathogenesis

Microorganisms

Hyaluronidase / fibrinolysins

Breakdown or dissolve intercellular cement substance

(hyaluronic acid and fibrin)

Streptococci are particularly potent producers of hyaluronidase

Staphylococci – less potent – also pathogenic – freq give rise to cellulitis

Cellulitis – clinical features (of face and neck)

Painful swelling of the involved soft tissues Skin overlying is firm and brawny,inflamed,sometimes even

purplish (when spread is in deeper planes –normal) Moderatily ill-elevated temperature Leukocytosis Regional lymphadenitis

Infections arising in the maxilla – perforate the outer cortical layer of bone above buccinator attachment –swelling of upper half of face

In mandible –below buccinatorattachment – lower half of faceTreatment – analgesics + antibiotics + removal of cause

Osteomyelitis If the periapical infection and inflammation extend through the marrow spaces of the jaw, the result is osteomyelitis.

Odontogenic infection

Infection thro PDL space

Extraction wound

Trauma-fracture

Metastasis from remote area

of infection In this case, you can identify the offending tooth causing the diffuse and irregular bone

destruction

Osteomyelitis – predisposing conditions

Malnutrition Diabetes h/o Alchoholism Leukemia Various anaemias Conditions that are characterized by the formation of avascular

bone that precludes an effective defensive response • Osteopetrosis

• Paget’s disease

• Florid osseous dysplasia

• Post-irradiation states

• Flourosis

Classification - Osteomyelitis

Suppurative

> acute suppurative

> chronic suppurative

* primary

* secondary

> infantile

Non suppurative

> diffuse sclerosing

> focal sclerosing

> proliferative periosteitis

> osteoradionecrosis

Acute osteomyelitis

Develops in a matter of days Does not show any early radiographic changes Most commonly arises from a periapical abscess Ther is no swelling or redness until later-penetrated cortex and

involved periosteum WBC count and Temp Reflex spasm of muscles attached to the involved area of bone Local signs and symptoms:

severe pain,soreness of the involved teeth,which are also loose,regional lymphadenopathy,parasthesia/anaesthesia of lip.

Radiograph – solitary/multiple small radioluscent areas

Trabeculae-decreased density,outlines become blurred or fuzzy.

Acute suppurative osteomyelitis

The clinical manifestations in this case are severe and debilitating.

Radiograph- Almost the entire body of the mandible is involved and shows diffuse mottled resorption. The decayed first molar is the guilty tooth.

Chronic osteomyelitis

is persistent abscess of bone charact by inflammatory processes , including necrosis of mineralised and marrow tissues,suppuration,resorption,sclerosis, and hyperplasia.

o Symptoms are milder,

o pain is less ,

o bone destruction is slower,

o sinus tracts develop intermittently and then cease draining and close.

Chronic sclerosing osteomyelitis

Here is an extensive chronic osteomyelitis characterized by bone formation only (chronic diffuse sclerosing osteomyelitis).

Garres osteomyelitis(COPP) Children/young adults Mandibular molars-inferior border of mandible Hard bony nontender swelling Size:1-2cm;cortex becomes 2-3cm thick R/f: onion skin appearance-alt radioluscent,opaque layers

Sequestrum In many cases of osteomyelitis there are bone sequestra. This necrotic piece of bone is being actively resorbed and is surrounded by intense inflammation and granulation tissue.

Treatment guideline for acute or chronic osteomyelitis

Disrupt the infectious foci. Debride any foreign bodies necrotic tissue, or sequestra. Culture and identify specific pathogens for eventual definitive antibiotic treatment. Drain and irrigate the region. Begin empiric antibiotics based on Gram stain. Stabilize calcified tissue regionally. Consider adjunctive treatments to enhance microvascular reperfusion (usually reserved for refractory forms only).

Trephination Decortication;sequestrectomy Vascular flaps Hyperbaric oxygen therapy

Reconstruction as necessary following resolution of the infection.

Extra radicular infections

Found in following situations:

1. Acute apical periodontitis lesions

2. Periapical actinomycosis

3. In ass with pieces of infected root dentin that may be displaced

into the periapex during RC instrumentation or have been cut

off from the rest of root by massive apical resorption

4. Infected periapical cysts, particularly in periapical pocket cysts

with cavities open to the root canal.

Actinomycosis is a chronic, granulomatous, infectious disease in humans and animals caused by the genera Actinomyces and Propionibacterium (McGhee et al.1982).

Etiological agent : Actinomyces bovis- first species to be identified(Harz 1879). in cattle - ‘lumpy jaw’ or ‘big head disease’ characterized by>extensive bone rarefaction, >swelling of the jaw, >suppuration > fistulation.

Actinomycosis

Causative agents nonacid fast, non-motile, Gram-positive ‘sulphur granules’ - yellow specks in exudates.a ‘starburst appearance’ ‘ray fungus’.

Actinomycosis

Human actinomycosis is clinically divided into Cervicofacial(60%) Thoracic(15%) Abdominal forms(20%) (Kapsimalis &Garrington 1968, Oppenheimer et al. 1978).

The most common species isolated from humans is A. israeliiwhich is followed by Propionibacterium propionicum (Buchanan & Pine 1962) (Wolff &

Israel 1891), Actinomyces naeslundii (Thompson & Lovestedt 1951),Actinomyces viscosus and Actinomyces odontolyticus in descending order (Batty 1958)

Foreign body reactions

Oral pulse granuloma Cellulose granuloma Gutta percha Other materials- amalgam,endo sealants, and calcium salts derived from periapically extruded

Ca(OH)2

CONCLUSION

It is essential that we understand the progressive nature of the periapical disease process as well as how and why the various stages occur so they can be diagnosed and managed appropriately.

Thank you

Health & Medicine

Periapical pathology 22 (1)