PULP & PERIAPICAL LESIONS

PULPITS

APICAL PERIODONTITIS

PERIAPICAL ABSCESS

PERIAPICAL GRANULOMA

PERIAPICAL CYST

OSTEOMYELITIS

PERIOSTEITIS

CELLULITIS

ABSCESS

Acute

Acute

Acute

Chronic

Chronic

Chronic

Focal

Diffuse

Acute

Chronic

Complications of Infected Pulp

Jaw Bone

Mucosa

Pulpitis

• A general term, describing all pulpal inflammation
• Pulp is connective tissue and the inflammation here is similar to inflammation of C.T. elsewhere in the body.

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Pulp is unique in that…..

• It is surrounded by rigid dentin
• Has no collateral circulation because the arteries are end arteries.
• Pain is the only sign that can determine severity
• Biopsy or direct application of medicine is not possible without causing necrosis

Further more…

• Referred pain makes it difficult to localize the problem
• Poor correlation between microscopic changes & clinical symptoms.

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Classification

• Depending on rapidity of progress
• Acute or chronic.
• Depending on extent of involvement - Partial/focal or total/generalized.
• Based on presence or absence of communication to oral environment
• Open( pulpitis aperta) or closed ( pulpitisclausa).

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• Exudative or suppurative.
• Reversible or irreversible

Causes of pulpitis/ Etiology

1. Microbial:

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Dental caries.

Traumatic exposure.

Marginal leakage.

Cracked tooth.

Coronal fracture.

Attrition/ Abrasion.

Traumatic restorative procedure.

Invaginated odontome.

Advanced periodontitis (periodontal-endodontic lesion).

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• Pulpitis starts before leading organisms in carious dentin reach pulp.

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2. Chemical Injury

• Use of acidic restorative materials

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• irritating filling materials in deep cavities substances.

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• May respond by reactionary dentin formation.

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3. Thermal injury:

• Cavity cutting / tooth preparation without sufficient coolant
• Polishing procedure
• Exothermic restorative materials
• Large metallic restoration without adequate insulation

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• 4. Mechanical injury

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• Trauma

• 5. Anachoretic pulpitis

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• Bacteria in circulating blood stream settle out or accumulate at sites of pulpal inflammation
• This may follow a chemical or mechanical injury to pulp
• Probable reason could be increased capillary permeability in the affected area

6. Galvanism

• When dissimilar matallic restorations are used

7. Barotrauma (aerodontalgia):

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• Flying at high altitude in unpressurized aircraft, or rapid decompression in divers.

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• Attributed to formation of nitrogen bubbles in pulp tissue or vessels.

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• Thought not to be a direct cause, but rather an exacerbating cause in presence of caries or recently restored tooth.

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• Pain with pulpitis is due to pressure from inflammation within a confined chamber.
• Progressive inflammatory changes in the pulp are:
• Hyperemia
• Acute Suppurative Pulpitis
• Acute Serous Pulpitis
• Chronic Pulpitis

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Focal reversible pulpitis / Pulpal hyperemia

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• This is an early transient form of pulpitis, localized chiefly pulpal end of irritant dentinal tubules.
• Characterized by vascular dilatation
• Called as reversible because the irritants are removed before pulp is severely damaged

Causes

• Caries: most common cause
• Large restoration with inadequate insulation
• Restoration with defective margins
• Lost temporary or permanent restoration.
• Heat: High speed drill; polishing cup.
• Traumatic injury: Mild blow to tooth
• Occlusal trauma
• Chemical irritants: Bases, liners.
• Galvanic shock: An electrical current caused from saliva and two different metals.

Clinical features

• Pain / sensitivity thermal changes.
• Sharp pain that lasts for a short period of time and disappears after removal of thermal irritant.
• Vitality Test:
• electric pulp tester: readings are lower than normal (indicating a greater sensitivity or lower pain threshold)

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• X-rays
• may show deep caries. Hyperemia is confined to the pulp
• PDL is normal;

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Histopathology

• Multiple dilated blood vessels filled with RBCs
• Edematous changes
• Extravasation of RBCs & few infl. cells

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Treatment

• Remove the cause.
• If pain persists, Possibility of Acute Serous Pulpitis should be suspected.

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Acute Pulpitis

• Acute Pulpitis is extensive acute inflammation of dental pulp that develop as an immediate sequelae of focal reversible pupitis or as an acute exacerbation of chronic inflammatory process

• Etiology: Same as Hyperemia
• Caries: most common cause
• Large restoration with inadequate insulation
• Restoration with defective margins& recurrent caries

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Clinical features

• Pain elicited by thermal change particularly to cold:
• Severe
• Prolonged
• Pain may persists even after removal of stimulus.
• Poorly localized and felt in any tooth of affected quadrant( pulp of individual tooth are represented precisely on the sensory cortex)

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When inflammation spreads to involve greater portion of pulp

• Pain becomes more severe and described as lancinating or throbbing or excruciating pain
• Lasts for 15 mts or more and is more or less continuous
• Increases on lying down

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In cases of liquifaction of pulp has occurred cold may alleviate symptoms

Intensity of pain is more if it is closed type due to build up of pressure because of lack of escape of infl. exudate

In case of open cavity

pain is dull and throbbing type

Tooth is not sensitive to percussion

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• Vitality Test:
• EPT: Very sensitive and lower-than-normal readings.( later when necrosis occurs sensitivity is lost)
• Ice: A quick response of pain.
• Heat: No noticeable response.
• X-rays
• Everything appears normal other than deep caries.

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Histopathology

• Early changes include
• Continued vascular dilatation
• Accumulation of edema fluid
• Infiltration of PMNLs
• Degeneration of odontoblasts

Changes are confined to local area & rest of pulp appears relatively normal

• As inflammation progresses --- Increased pressure due to edema fluid –----- compression of vessels –---- Hypoxia---- localized destruction of pulp tissue –--- Formation of pulp abscess

• Within few days
• Inflammation spreads to entire pulp
• Infiltration of PMNLs in entire pulp
• Degeneration of odontoblast layer
• Multiple small abscess formation
• Liquifaction degeneration of entire pulp
• Presence of mixes organisms in pulp

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• Acute suppurative pulpitis

Treatment:

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• Pulpotomy/ RCT/ extraction

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CHRONIC PULPITIS

• Is an inflammatory reaction that results from long term, low grade injury or occasionally from quiescence of an acute process

• Considerably Mild symptoms / no symptoms because of death of pulp
• Mild Dull aching pain may be presenting symptom which is often intermittent and appear over an extended period but
• Patient may ignore this pain.

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• Vitality Test:
• EPT: high readings or no response at all due to degeneration of nerve tissue in affected pulp
• Hot/cold: no response
• Treatment:
• rct

Histopathology

• Infiltration of pulp with lymphocytes & plasma cells
• Microorganisms in the pulp
• Deposition of granulation tissue around inflamed area to ward off infection – ulcerative pulpitis

CHRONIC HYPERPLASTIC PULPITIS (Pulp Polyp)

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• Unique form of pulpitis wherein chronically inflamed dental pulp tissue, instead of perishing by continued suppuration, reacts by excessive proliferation

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• Seen in children & young adults.
• Primary molars and first permanent molar
• Related to high tissue resistance and good blood supply due to open apical foramen

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• Occurs in teeth with large, open carious lesions
• A red or pink nodule of tissue, filling the entire cavity of the tooth and protrudes from the pulp chamber.
• Insensitive to manipulation due to few nerve fibers
• May bleed easily on manipulation depending on vascularity

D/D

• Gingival polyp

Histopathology

• The tissue is granulation tissue covered by stratified squamous epithelium.
• Granulation tissue comprises of delicate connective tissue with proliferating endothelial cells, budding capillaries and chronic inflammatory cells
• Continuity to pulp is evident
• Pulp also shows infl. changes

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• Epithelium is
• implantation of desquamated cell in saliva
• Implantation from oral mucosa due to continuous rubbing

PULP

PULP

CONNECTION TO PULP

GRANULATION TISSUE

EPITHELLIUM

Treatment

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• Extraction or RCT.

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Periapical lesions

Apical periodontitis

• Inflammation of periodontal lig. Around the apical portion of tooth
• May be acute or chronic
• Caused by
• Spread of infection following pulp death
• Occlusal trauma
• Inadvertant endodontic treatment( over instrumentation, pushing of infected materials,chemicals used)

Acute Apical periodontitis

• History of previous pulpitis
• No pain or sensitivity to thermal changes
• Tooth appears slightly elevated in the socket due to collection of edema fluids
• Tenderness on biting & on percussion
• Radiographically – widening of periodontal lig. Space around root apex

Histology

• Dilated blood vessels filled with RBCs
• Edematous changes
• Extravasation of RBCs & few infl. Cells
• Initially changes are restricted to root apex
• Later bone resorption and abscess formation may develop

Treatment

• Extraction / endodontic treatment

Periapical Abscess/ Dento-alveolar abscess

• Acute or chronic suppurative process of periapical region
• May develop from apical periodontitis or from periapical granuloma
• Acute exacerbation of a chronic periapical lesion is called PHOENIX ABSCESS

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causes

• Infection following caries & pulpal infection
• Traumatic injury & following death of pulp
• Irritaton of periapical tissue either by mechanical manipulation or chemicals in endo. Procedures

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Clinical features

• Initial stages
• Tenderness which is releived on application of pressure

Later tooth becomes extremely painfuland is slightly extruded from socket

Regional lymphadenitis & fever may be present

Infection rapidly spread through bone & cause osteomyelitis

• Chronic periapical abscess presents no clinical symptoms
• Mild circumscribed area of suppuration and show little tendency to spread

Radiographic features

• Acute – since it is a rapid process, no features other than widening of periodontal lig.
• Chronic – ill defined radiolucncy

Histopathology

• Central area of disintegrating PMNLs surrounded by viable leukocytes, occasional lymphocytes, cellular debris, necrotic material & bacterial colonies
• Adjacent marrow space and perio lig shows inflammatory changes

Treatment

• Establish the drainage by opening the pulp chamber & RCT or extraction

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• Complications
• Osteomyelitis
• Cellulitis
• Bacteremia
• Cavernous sinus thrombosis
• Formation of fistula & drainage

Periapical granuloma/ Chronic apical periodontitis

• Is a low grade infection & develop as a sequelae of pulpitis or acute apical periodontitis.
• Chronic inflammation is proliferative reaction
• Is characterized by localized mass of chronic granulation tissue attached to the root apex
• Lateral granuloma

Clinical features

• Tooth is nonvital
• Tender on percussion
• Dull sound on percussion
• Mild pain on biting or chewing solid food
• Tooth may be elevated in socket
• May be entirely asymptomatic

Radiographic features

• Early finding is widening of pero. Lig. Space
• Later as granuloma grows & bone resorbs – well circumscribed radiolucency( less than 2mm)
• Surrounding sclerotic zone may be seen

Histologic features

• Early changes

Hyperemia , edema& inflammatory cell infiltration of perio lig

As bone resorption progresses

proliferation of fibroblasts and endothelial cells & formation of more vascular channels as well as delicate connective tissue fibrils

infiltrated with lymphocytes & plasma cells and few macrophages – immune granuloma

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GRANULOMA ATTACHED TO ROOT APEX

GRANULOMA ATTACHED TO ROOT APEX

Root apex

• 80% T- lymphocytes forming OAF, cytotoxic lymphokines, collagenase, enzymes etc
• 20% B- lymphocytes producing IgG, IgA, IgM etc.
• B cells are modulators of disease process
• Russel bodies are seen

• In some granulomas, large number of macrophages with injested materials forms sheets and are called as foam cells
• Deposition of cholesterol & hemosiderin from break down of RBCs
• Cholesterol is seen as clear needle like or cleft like spaces surrounded by multinucleated giant cells

• At the periphery of granuloma, collagen bundles ar condensed to form a capsule
• Epithelial cells may be seen

• Giant cell hyaline angiopathy

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• Pulse granuloma

Bacteriologic features

• Streptococcus viridans, hemolyticus, nonhemolytic streptococci,staphilococcus aureus, staph albus,E. coli, and pneumococci

Treatment

• Extraction
• RCT with or without apicoectomy

Vitality test

• cold test: ethyl chloride

• electrical pulp test

• (test cavity)

DENTAL GRANULOMA (Periapical Granuloma)

• Well-Defined RADIOLUCENT Area at Apex of Non-Vital Tooth
• Filled with Granulation Tissue
• May or May Not be Symptomatic
• Requires Root Canal or Extraction
• Specific Diagnosis Requires Biopsy

PERIAPICAL CYST

• Well-Defined RADIOLUCENT Area at Apex of Non-Vital Tooth
• Fluid-Filled Cavity Lined by Epithelium
• May or May Not be Symptomatic
• Requires Root Canal or Extraction
• Specific Diagnosis Requires Biopsy

CONDENSING OSTEITIS

• Increased Bone Density in Response to Inflammation - RADIOPAQUE
• Variable Symptoms
• Usually no biopsy - Treat offending tooth
• May remain as residual sclerosis

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Classification of pulpal diseases�(according to symptoms and treatment)

1. Reversible pulpitis
2. Irreversible pulpitis
• Hyperplastic pulpitis
3. Pulpal necrosis

1. Reversible pulpitis

• Anamnesis:
• pain stimulated by cold and sweet, tooth can be fixed
• Clinical examination:
• vitality test: positive, „short” respond
• Treatment:
• removing of the exciting agent
• making a filling (or pulp capping)

2. Irreversible pulpitis

• Anamnesis:
• generally asymptomatic
• or mild or severe spontaneous pain
• difficult to localise
• Clinical examination:
• vitality test: „long”, sharp respond
• Treatment:
• root canal treatment

Hyperplastic pulpitis�- in young people, chronically inflammed pulp

• Anamnesis:
• asymptomatic
• Clinical examination:
• vitality test: positive
• open pulp chamber within polypous tissue
• Treatment:
• root canal treatment

3. Pulpal necrosis

• Anamnesis:
• asymptomatic
• Clinical examination
• vitality test: negative
• Treatment:
• root canal treatment

Periapical pathosis

Aetiology

• non-treated pulpal disease
• trauma (hyperocclusion)
• irrigants
• instrumentation

Symptoms of periapical pathosis generally

• Anamnesis:
• acute: pain, swelling
• chronic: mild or no symptoms
• Clinical examination:
• vitality test: usually negative
• Radiological symptoms

Classification of periapical pathosis

1. Acute apicalis periodontitis
2. Chronic apical periodontitis
• Condensing osteitis
3. Acute apical abscess („closed”)
4. Suppurative apical periodontitis („open”)

Acute apical periodontitis

• Anamnesis:
• symptoms of pulpitis or necrosis + pain on bite
• Clinical examination:
• pain on percussion
• X-ray:
• thickening of periodontal ligament space
• Treatment:
• root canal treatment, (adjustment of occlusion)

Chronic apical periodontitis

• Anamnesis:
• asymptomatic or slight discomfort
• Clinical examintaion:
• little or no pain on percussion
• X-ray:
• interruption of lamina dura or apical radiolucency
• Treatment:
• root canal treatment

Radiogram of healthy periodontium and chronic apical periodontitis

Acute apical abscess („closed”)

• Anamnesis:
• severe discomfort, swelling, fever
• Clinical examination:
• swelling, localisation?
• X-ray:
• radiolucent lesion (localisation)
• Treatment:
• root canal treatment, drainage, (antibiotics)

Suppurative apical periodontitis („open”)

• Anamnesis:
• asymptomatic (drain), swelling
• Clinical examination:
• fistula, swelling
• X-ray:
• radiolucent lesion (localisation with guttapercha)
• Treatment:
• root canal treatment