Current understanding of the aetiology and progression of periodontal disease.
There is overwhelming evidence that bacteria cause periodontitis and that they do so by extending apically along the surfaces of the tooth roots and creating pockets. A very complex mixture of microbial species, mostly although not exclusively gram-negative, anaerobic, and motile, is involved. Infection probably occurs in a progressive and sequential manner. The bacteria involved include various species of Bacteroides, Actinobacillus, Eikenella, Fusobacterium, Capnocytophaga, and Eubacterium. Local oral conditions such as tooth position play an aetiologic role by affecting plaque accumulation and retention. Host defence factors, particularly the phagocytic cells and the immune system, play a determinative role in the aetiology by monitoring, controlling, and regulating microbial colonization and infection. These diseases begin as an acute inflammation of the marginal gingiva, and they progress through orderly stages to the formation of a gingival pocket. Transition from gingivitis to periodontitis is not well-understood, but it probably involves colonization by additional microbial species or invasion of the periodontal tissue by species already present. Progression of periodontal destruction is episodic, possibly as a consequence of successful host defence. In most patients, periodontal destruction occurs more infrequently than previously suspected. In both treated and untreated patients, a small subgroup accounts for most of the disease activity. The most important problem we now face is to develop diagnostic methods to identify individuals in this subgroup and devise ways to prevent and control their diseases.
D001419:Bacteria / Q000302:isolation & purification; D005891:Gingivitis / Q000209:etiology* / Q000382:microbiology / Q000503:physiopathology; D006801:Humans; D010518:Periodontitis / Q000209:etiology* / Q000382:microbiology / Q000503:physiopathology