Periapical disease

periapical immune responsesto infection

Dr. Mohammed Alshehri BDS, AEGD, SSC-Resto, SF-DI

• The ultimate biological aim of endodontic treatment is either to prevent or cure apical periodontitis

Tissue response to pulpal inflammation caused by microorganism invasion from:– Caries

– Trauma

– Microleakage from restorations

– Others.

An intent to localize the infection within the confines of the root canal system.

• There is no evidence that necrotic pulp tissue per se can elicit periapical inflammation, in the absence of bacteria.

78 monkey teethwithaseptically necrotized pulps

78 monkey teethwithaseptically necrotized pulps

26 bacteria-free 26 bacteria-free

52 bacteria infected52 bacteria infected

7 months

Apical periodontitisApical periodontitis

No apical inflammationNo apical inflammation

Moller & Fabricius 1981Moller & Fabricius 1981

• In traumatized necrotic teeth with ‘intact’ crowns, microorganisms can reach the pulp through:

• Microcracks• Accessory canals• Exposed dentinal tubules

Anachoresis

• Odontoblastic process (Nagoka 1995, Bacterial invasion into dentinal tubules of human vital and non vital teeth. J. Endodon.)

• Dentinal fluid

– Effects on the tubular diameter– Antibodies

Physical barriers to bacterial invasion in vital teeth

• In contrast to pulp, periradicular tissues have an :

• Unlimited source of undifferentiated cells

• Rich collateral blood supply

• Lymph drainage system

Peri-radicular tissues

• Resorption of the bone provides a separation between the irritants and the bone, thereby preventing osteomyelitis. Depending on the :

• severity of irritation

• duration

• host response

periradicular pathoses may range from slight inflammation to extensive tissue destruction

Periapical bone destruction

• Neuropeptides

• Fibrinolytic peptides

• Kinins

• Lysosomal enzymes

Non specific mediators of inflammation

• Antigen-presenting cells

• Immunoglobulin E

• Mast cells

• Macrophage-like cells

• T cells

• B cells are extremely rare

• Plasma cells are absent in normal pulp

Specific mediators of inflammation

MacrophageMacrophage

BacteriaBacteria

Phagocyte Response to Infection

•Vascular adherence

•Diapedesis

•Chemotaxis

•Activation

•Phagocytosis and killing

Pulpal and Periapical Responses

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Early pulpal response to infection

Bacteria or bacterial antigens

Infiltration of PMNs and monocytes.

Bacteria or bacterial antigens

Infiltration of PMNs and monocytes.

Progress of infection

PMNs, monocytes

T-helper, T-cytotoxic/supressor, B cells,

plasma cells, antibodies.

PMNs, monocytes

T-helper, T-cytotoxic/supressor, B cells,

plasma cells, antibodies.

Increased number and

diameter of

capillaries

Increased number and

diameter of

capillaries

http://www.usc.edu/hsc/dental/opfs/CP/indexCP.html

Pulp hyperemia

Lymphocytes and

plasma cells Neutrophils

Lymphocytes and

plasma cells Neutrophils

Chronic pulpitis

Many neutrophils in a

fibrin network.

Many neutrophils in a

fibrin network.

Acute pulpitis

• Normal periapical tissues

• Symptomatic apical periodontitis

• Asymptomatic apical periodontitis

• Acute apical abscess

• Chronic apical abscess

• Condensing Osteitis

CLASSIFICATION OF PERIAPICAL LESIONS

• No pain

• Not abnormally sensitive to palpation and percussion

• Normal intact lamina dura

• Normal periodontal ligament

NORMAL PERIAPICAL TISSUES

• Defined as painful inflammation of periodontium as a

result of trauma, irritation or infection through root canal,

regardless of whether tooth is vital or non-vital.

SYMPTOMATIC APICAL PERIODONTITIS

• Extension of pulpal inflammation into periapical tissues

• In vital tooth its associated with occlusal trauma, high

points in restorations

• In non-vital tooth is associated with sequelae of pulpal

infections

• Over instrumentation

• Extrusion of necrotic pulp or obturating materials

Etiology

• Dull throbbing constant pain

• Pain on biting or percussion

• Negative or delayed vitality test response

• Not associated with apical radiolucency

• Widening of PDL space

• Cold may relieve pain

• Heat exacerbate pain

Signs and symptoms

• PMN leukocytes, Macrophages in localized area of apical

region

• Bone and root resorption

Histological

• If tooth in hyper occlusion, relieve occlusion

• If tooth infected, initiate endodontic therapy

Treatment

• Defined as a clinical asymptomatic condition of pulpal origin

with inflammation and destruction of periapical tissues.

ASYMPTOMATIC APICAL PERIODONTITIS

• Results from pulp necrosis and a sequelae of SAP

Etiology

• Does not respond to vitality test

• Percussion no pain

• Slight sensitivity to palpation

• Radio graphically interruption in lamina dura

• Destruction of periapical tissues

SIGNS AND SYMPTOMS

• AAP lesions are classified as granuloma or cyst

• Periapical granuloma consists of granulomatous

inflammatory tissue infiltrated by mast cells, macrophages,

lymphocytes

• Periapical cysts has a central cavity filled with semisolid

fluid lined by stratified squamous epithelium

Histological

• Removal Of necrotic pulp

• Complete obturation

Treatment

• Defined as a localized collection of pus in the alveolar bone

at the root apex of the tooth

• Following the death of pulp and extension of infection

through apical foramen into periapical tissues.

ACUTE APICAL ABSCESS

• Liquefaction necrosis of pulp

• Severe inflammatory response of microbial and non-

microbial irritants

Etiology

• Rapid onset

• Spontaneous pain

• Moderate to severe discomfort with swelling

• No response to vitality test

• Pain on percussion and palpation

• Radio graphically widening of PDL to periapical lesion.

Signs and symptoms

• PMN leucocytes

• Debris

• Cell remnants

• Accumulation of exudates

Histological

• Removal of cause

• Release of pressure ,drainage

• Root canal treatment

Treatment

• It’s an inflammatory lesion of pulpal origin characterized

by presence of long standing lesion with drainage into

mucosal or skin (sinus tract).

CHRONIC APICAL ABSCESS

• Abscess has burrowed through bone and soft tissue to form

sinus tract

Etiology

• Asymptomatic

• Pain

• Presence of sins tract

Signs and symptoms

• Drainage

• Endodontic treatment

Treatment

• A variant of asymptomatic apical periodontitis

• Irritant from canal to periapical tissues is the cause

• Mainly in mandibular posterior teeth

• Occurs in association with apex of any tooth

CONDENSING OSTEITIS

• Asymptomatic or associated with pain.

• Not respond to electric or thermal stimuli

• May or may not be sensitive to percussion

• Radio graphically ,radioopacity around root of tooth

Signs and symptoms

• Root canal treatment (when indicated)

Treatment

Regeneration is a process by which altered periapical tissues are

completely replaced by new tissues for their function

Extend of healing

• Level of healing is proportional to extend of tissue injury and

nature of tissue destruction

HEALING OF PERIAPICAL TISSUES AFTER ROOT CANAL TREATMENT

• After removal of irritants, inflammatory response tissue

organization and maturation occur.

• Bone that is resorbed is replaced by new bone, resorbed

cementum and dentin are repaired by cellular cementum

• PDL that is first affected is restored in the last to normal

Process of healing

Factors affecting healing

• Leukopenia

• Impaired blood supply systemic disorders

• Differential diagnosis

• Radiolucent and radiopaque lesions of non-endodontic lesion

mimic the radiographic appearance of endodontic lesion

• Pulp vitality test is important aid.

• Dentigerous cycst

• Lateral periodontal cyst

• Ameloblastoma etc.

NON-ENDODONTIC PERIRADICULAR PATHOSIS