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Plaque and chronic inflammatory Periodontal disease A question of ecology
Author(s) -
Newman H. N.
Publication year - 1990
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1111/j.1600-051x.1990.tb01102.x
Subject(s) - fusobacterium nucleatum , actinobacillus , dental plaque , periodontitis , gingivitis , bacteroides , periodontal disease , spirochaete , chronic periodontitis , biology , microbiology and biotechnology , disease , host (biology) , ecology , medicine , dentistry , porphyromonas gingivalis , pathology , bacteria , genetics
The nature of the relationship between dental plaque and chronic inflammatory periodontal disease (CIPD) remains unclear, although there is no doubt that plaque is the direct cause. Non–specific, specific and exogenous hypotheses have been proposed to explain plaque‐host relationships. Current evidence indicates that plaque is part of the natural human microflora, one of many such in nature, and that disruption of oral microbial ecology, due primarily to diet texture changes, leads to gingivitis and periodontitis. These result in increased plaque accumulation, and particularly in increased interdental effective plaque thickness. The latter leads to alterations in plaque ecology, particularly increasing anaerobiosis, with resultant shifts in proportions of its constituent species. These shifts are responsible for the increased counts of, for example, Bacteroides gingivalis, Actinobacillus actinomycetemcomitans, Fusobacterium nucleatum, Wolinella recta , spirochaetes and others, associated with chronic periodontitis in its various forms. Measures to prevent or control chronic periodontitis should aim, not to eliminate plaque, which ignores ecology and would compromise host defence, but to restore the species distribution in plaque to that compatible with health.