期刊
JOURNAL OF DENTAL RESEARCH
卷 86, 期 9, 页码 888-892出版社
INT AMER ASSOC DENTAL RESEARCHI A D R/A A D R
DOI: 10.1177/154405910708600916
关键词
gingival overgrowth; fibrosis; fibroblast; apoptosis; FOXO1
资金
- NCRR NIH HHS [M01 RR00533, M01 RR000533] Funding Source: Medline
- NIDCR NIH HHS [R01 DE011004, DE11004, R29 DE011004, R01 DE017732, R01 DE017732-01A1, DE07559, R01 DE007559] Funding Source: Medline
Variations in the balance between cell proliferation and apoptosis could contribute to the etiology of gingival overgrowth. The aim of this study was to test the hypothesis that, in fibrotic gingival lesions, fibroblast proliferation is stimulated and apoptosis is decreased. Apoptotic index, caspase 3 expression, the proliferative index, FOXO1 expression, and histological inflammation were measured in situ. Analysis of data showed that apoptosis decreased in all forms of gingival overgrowth examined ( p < 0.05), and inflammation caused a small but significant increase compared with non-inflamed tissues ( p < 0.05). The greatest decrease of apoptosis occurred in the most fibrotic tissues. Cell proliferation was elevated in all forms of gingival overgrowth tested, independent of inflammation ( p < 0.05). To identify potential mechanisms of transcriptional regulation of apoptosis, we assessed FOXO1 and caspase 3 expression levels and found them to correlate well with diminished apoptosis. Analysis of data suggests that increased fibroblast proliferation and a simultaneous decrease in apoptosis contribute to gingival overgrowth.
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