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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
?? ??
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