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RESEARCH REPORT |
1 Department of Microbiology and Immunology, Nihon University School of Dentistry at Matsudo, Matsudo, Chiba 271-8587, Japan;
2 Department of Microbiology and
3 Department of Biochemistry, Nihon University School of Dentistry, Tokyo 101-8310, Japan; and
4 Department of Infectious Diseases, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka 431-3192, Japan
* corresponding author, ochiai.tomoko{at}nihon-u.ac.jp
Butyric acid, an extracellular metabolite from periodontopathic bacteria, induces apoptosis in murine and human T- and B-cells, whereas intact gingival fibroblasts isolated from healthy humans are resistant to butyric-acid-induced apoptosis. We examined the susceptibility of inflamed gingival fibroblasts isolated from adult persons with periodontitis to butyric-acid-induced apoptosis. Butyric acid significantly suppressed the viability of inflamed gingival fibroblasts and induced apoptosis in a dose-dependent manner. The incubation of inflamed gingival fibroblasts with butyric acid induced DNA fragmentation and apoptotic changes such as chromatin condensation, hypodiploid nuclei, and mitochondrial injury. Furthermore, butyric-acid-induced apoptosis in inflamed gingival fibroblasts was reduced by caspase-3/7, -6, -8, and -9 inhibitors. Thus, inflamed gingival fibroblasts from adult persons with periodontitis appear to be highly susceptible to mitochondria- and caspase-dependent apoptosis induced by butyric acid, compared with healthy gingival fibroblasts.
KEY WORDS: apoptosis • butyric acid • fibroblasts • periodontitis
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| IADR Journals | Advances in Dental Research ® |
| Journal of Dental Research ® | Critical Reviews (1990-2004) |
