The Japanese Dental Science Review

Vol. 45 No. 2       2009

ISSN: 1882-7616      UBIC: 99

SUMMARY

Butyric acid, an extracellular metabolite from periodontopathic bacteria, induces apoptosis in murine thymocytes, splenic T-cells, as well as human Jurkat T-cells and peripheral blood mononuclear cells. Butyric acid-induced apoptosis is mediated by ceramide production, as well as reactive oxygen species (ROS) synthesis in mitochondria and subsequently JNK activation in MAP kinase cascades. Although the production of ROS and ceramide by themselves do not completely influence butyric acid-induced apoptosis, it can be concluded that ROS and ceramide production are the major contributors to butyric acid-induced apoptosis. Human gingival fibroblasts rescue butyric acid-induced T-cell apoptosis via pro inflammatory cytokines, which are produced by fibroblasts stimulated with butyric acid. Moreover, T-cell adherence to fibroblasts is enhanced by butyric acids and butyric acid-induced T-cell apoptosis is down-regulated by T-cell adhesion to gingival fibroblasts. Butyric acid significantly suppresses the viability of inflamed gingival fibroblasts and induces apoptosis in a dose-dependent manner, whereas intact gingival fibroblasts isolated from healthy humans are resistant to butyric acid. This review focuses on the effects of butyric acid and its possible contribution to destruction of gingival tissues and modulation of local immunity at gingival sites (175/max. 200). KEYWORDS: Periodontal diseases; Periodontopathic bacteria; Butyric acid; Short-chain fatty acids; Apoptosis

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