Pathogenesis of periodontitis.
Periodontitis is an inflammatory disease of the periodontium which is characterized by a progressive destruction of the tissues supporting the tooth. Its primary etiology is an ill-defined series of microbial infections which may be composed of only some of the more than 300 species of bacteria currently recognized in the oral cavity. The disease is currently considered to progress as periodic, relatively short episodes of rapid tissue destruction followed by some repair, and prolonged intervening periods of disease remission. Despite the apparent random distribution of episodes of disease activity, the resulting tissue breakdown exhibits a symmetrical pattern of alveolar bone loss and pocket formation which is common to several forms of periodontitis, although the distribution of the most affected teeth and surfaces may vary among diseases (e.g., juvenile periodontitis versus adult periodontitis or rapidly progressive periodontitis). Several reports have indicated that bacterial cells can be found in the pocket wall of periodontitis lesions. The translocation of bacteria into the tissues from the pocket environment is quite common, as evidenced by the common occurrence of bacteremias in patients with periodontitis following relatively minor events such as chewing and oral hygiene procedures. However, it is important to distinguish between the passive introduction of bacteria into periodontal tissues and frank invasion as might occur in an acute infection, since the pathological implications may be quite different.
D000328:Adult; D001419:Bacteria / Q000302:isolation & purification; D018407:Bacterial Physiological Phenomena; D003773:Dental Plaque / Q000382:microbiology / Q000503:physiopathology; D006801:Humans; D008214:Lymphocytes / Q000502:physiology; D010513:Periodontal Ligament / Q000503:physiopathology; D010518:Periodontitis / Q000145:classification / Q000209:etiology* / Q000382:microbiology / Q000503:physiopathology