Apoptosis in gingival overgrowth tissues

Kantarci A., Augustin P., Firatli E., Sheff M. C., Hasturk H., Graves D. T., ...Daha Fazla

JOURNAL OF DENTAL RESEARCH, cilt.86, sa.9, ss.888-892, 2007 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 86 Sayı: 9
  • Basım Tarihi: 2007
  • Doi Numarası: 10.1177/154405910708600916
  • Dergi Adı: JOURNAL OF DENTAL RESEARCH
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.888-892
  • Anahtar Kelimeler: gingival overgrowth, fibrosis, fibroblast, apoptosis, FOXO1, FORKHEAD TRANSCRIPTION FACTORS, CELL-CYCLE, FIBROBLAST APOPTOSIS, GROWTH-FACTOR, EXPRESSION, INHIBITION, PERIODONTITIS, INFLAMMATION, ACTIVATION, KINASE
  • İstanbul Üniversitesi Adresli: Evet

Özet

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.