Recent studies of the cellular mechanisms involved in chronic inflammatory periodontal disease (CIPD) have contributed significantly to our understanding of the pathogenesis of the disease process. Functional studies have demonstrated polymorphonuclear neutrophil (PMN) chemotactic defects in some 70% of subjects with localized juvenile periodontitis while chemiluminescence data have suggested that periphertal blood PMNs from young subjects with adult periodontitis (AP) may be in a metabolically active state. Further studies have shown that stimulation of PMNs with a number of periodontopathic bacteria resulted in the production of an IL‐1 inhibitor suggesting a possible regulatory role for PMNs in CIPD in addition to their established protective role. Most work on the immunoregulation of CIPD has, however, concentrated on T‐cells. Recent limit dilution analysis has demonstrated the presence of periodontopathic bacteria‐specific T cells in peripheral blood and the involvement and homing of these cells to the local lesions of CIPD is currently the focus of many studies. In animal studies, Actinobacillus actinomycetemcomitans (Aa)‐specific T‐cell clones home to the gingival tissues where they may exert a protective role. Homing and retention of lymphocytes to and in specific sites is dependent upon the expression of adhesion molecules. Recent data indicate however, that while there are increasing levels of ICAM‐1, LECAM‐1 and PECAM‐1 expression with increasing degrees of inflammation, there are no differences between gingivitis and periodontitis lesions. Cytokine profiles may be related to the role of T‐cell clones homing to the gingiva in CIPD. In subjects susceptible to periodontal breakdown there may be an increase in the type 2 IL‐4 producing T‐cells whereas in non‐susceptible subjects, type 1 IL‐2/IFN‐γ producing T‐cells may preferentially home to the gingiva. This hypothesis is generally supported by recent data obtained from human studies but data obtained from animal studies is only partly supportive and may suggest the opposite. Nevertheless, it is now possible to construct a testable framework or model of CIPD based on these cellular and molecular mechanisms.
|Original language||English (US)|
|Number of pages||9|
|Journal||Journal of Periodontal Research|
|State||Published - Nov 1993|
- periodontal disease
ASJC Scopus subject areas