Tracing with gutta percha in:
A- symptomatic periradicular periodontitis
B- acute exacerbation of chronic periapical abscess***
In primary endodontic lesions, there is an acute exacerbation of a chronic apical lesion. Patients tend to experience varying degrees of pain. When tested, the pulp is necrotic. Drainage can be seen through the PDL into the gingival sulcus or as a swelling in B/L attached gingiva. A sinus tract may be present and is usually associated with deep pocket depths. Radiographic bone loss will vary, depending on the avenue of fistulation. A radiolucency may be present and is consistent with the origin of the lesion. It is imperative to trace the sinus tract with gutta percha and take a radiograph to determine the origin of the lesion. Typically, lesions will heal with endodontic therapy.
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CHRONIC ALVEOLAR ABSCESS:
Synonyms:
- chronic alveolar abscess (Grossman)
- chronic apical abscess (Siqueira)
- suppurative periodontitis (Coolidge and Kesel);
- chronic rarefacient periradiculitis (Kuttler);
- chronic periodontitis (Maisto);
- chronic periapical osteitis (Paiva and Álvarez);
- suppurative apical periodontitis (Ingle and Beveridge);
- chronic alveolar process ((Holland and Sommer);
- suppurative asymptomatic irreversible apical periodontitis (Canalda)
- suppurative chronic apical periodontitis (Siqueira)
Definition:
Chronic alveolar abscess is an infection of low virulence and long span in the periapical alveolar bone and of pulp origin.
It is a variation of the apical periodontits.
Cause:
It is a natural consequence of pulp death with extension of the infectious process periapically or it may result from a pre-existing acute abscess or inadequate endodontic therapy.
Chronic apical abscess results from a gradual discharge of irritants from the root canal to the periradicular tissues, with the consequent formation of purulent exudate within the granuloma or it may be a chronicity of an acute abscess.
Bacteriology:
The most commonly collected microorganisms are low-virulence alpha hemolytic streptococci.
Chronic infections are usually associated with low virulence of the bacterial community, which, however, generally represents a persistent source of tissue aggression. The persistence of chronic infections usually occurs because bacterial communities are organized in biofilms and inaccessible to host defenses due to their anatomical location.
The juxtaposition of bacterial biofilms to non-customary tissues and adapted to their presence, triggers destructive inflammatory and immunological responses. Bacteria in the necrotic root canal produce chronic infection due to the production of protected biofilms in the duct walls and maintaining intimate contact with the apical periodontal ligament, which reacts with persistent inflammation. The disease is ordinarily mediated by factors derived from the host in an effort to eliminate these settled communities.
Histopathology:
Chronic apical abscess is a granulomatous lesion containing areas of liquefaction necrosis with disintegrated polymorphonuclear surrounded by macrophages and active polymorphonuclear leukocytes. The fistulous tract is covered by epithelium or inflamed connective tissue and communicates these areas of liquefaction necrosis with the periphery.
There is loss of ligament fibers at the apex. Lymphocytes and plasma cells with polymorphonuclear leukocytes in the center. Mononuclear cells may occur.
----------------------
CHRONIC ALVEOLAR ABSCESS:
Synonyms:
- chronic alveolar abscess (Grossman)
- chronic apical abscess (Siqueira)
- suppurative periodontitis (Coolidge and Kesel);
- chronic rarefacient periradiculitis (Kuttler);
- chronic periodontitis (Maisto);
- chronic periapical osteitis (Paiva and Álvarez);
- suppurative apical periodontitis (Ingle and Beveridge);
- chronic alveolar process ((Holland and Sommer);
- suppurative asymptomatic irreversible apical periodontitis (Canalda)
- suppurative chronic apical periodontitis (Siqueira)
Definition:
Chronic alveolar abscess is an infection of low virulence and long span in the periapical alveolar bone and of pulp origin.
It is a variation of the apical periodontits.
Cause:
It is a natural consequence of pulp death with extension of the infectious process periapically or it may result from a pre-existing acute abscess or inadequate endodontic therapy.
Chronic apical abscess results from a gradual discharge of irritants from the root canal to the periradicular tissues, with the consequent formation of purulent exudate within the granuloma or it may be a chronicity of an acute abscess.
Bacteriology:
The most commonly collected microorganisms are low-virulence alpha hemolytic streptococci.
Chronic infections are usually associated with low virulence of the bacterial community, which, however, generally represents a persistent source of tissue aggression. The persistence of chronic infections usually occurs because bacterial communities are organized in biofilms and inaccessible to host defenses due to their anatomical location.
The juxtaposition of bacterial biofilms to non-customary tissues and adapted to their presence, triggers destructive inflammatory and immunological responses. Bacteria in the necrotic root canal produce chronic infection due to the production of protected biofilms in the duct walls and maintaining intimate contact with the apical periodontal ligament, which reacts with persistent inflammation. The disease is ordinarily mediated by factors derived from the host in an effort to eliminate these settled communities.
Histopathology:
Chronic apical abscess is a granulomatous lesion containing areas of liquefaction necrosis with disintegrated polymorphonuclear surrounded by macrophages and active polymorphonuclear leukocytes. The fistulous tract is covered by epithelium or inflamed connective tissue and communicates these areas of liquefaction necrosis with the periphery.
There is loss of ligament fibers at the apex. Lymphocytes and plasma cells with polymorphonuclear leukocytes in the center. Mononuclear cells may occur.
