Gene expression of transcription factor NFATc1 in periodontal diseases

被引:15
作者
Belibasakis, Georgios N. [1 ]
Emingil, Gulnur [2 ]
Saygan, Buket [2 ]
Turkoglu, Oya [2 ]
Atilla, Gul [2 ]
Bostanci, Nagihan [1 ]
机构
[1] Univ Zurich, Fac Med, Ctr Dent Med, Inst Oral Biol, CH-8032 Zurich, Switzerland
[2] Ege Univ, Sch Dent, Dept Periodontol, Izmir, Turkey
关键词
NFATc1; RANKL; DC-STAMP; T-cells; periodontal diseases; GINGIVAL CREVICULAR FLUID; DIFFERENTIAL EXPRESSION; BONE-RESORPTION; RANKL; OSTEOPROTEGERIN; OSTEOCLASTS; ACTIVATION; INDUCTION; KEY;
D O I
10.1111/j.1600-0463.2010.02706.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Periodontitis is a disease of infectious aetiology that causes inflammatory destruction of the tooth-supporting tissues. Activated T cells are central to the pathogenesis of the disease, by producing receptor activator of nuclear factor kappa B (NF-kappa B) ligand (RANKL) that stimulates bone resorption. Antigenic activation of T cells is regulated by the induction of transcription factor nuclear factor of activated T cells, cytoplasmic 1 (NFATc1). There is as yet no information on the potential involvement of NFATc1 in periodontal diseases. This study aimed to investigate NFATc1 gene expression levels in periodontal diseases, and analyse the potential correlation with RANKL expression and clinical periodontal parameters. In this cross-sectional study, gingival tissue biopsies were obtained from healthy (n = 10) and periodontally diseased (n = 58) sites. NFATc1 and RANKL gene expression levels in these samples were analysed by quantitative real-time polymerase chain reaction. Compared with healthy subjects, patients with gingivitis, chronic and aggressive periodontitis, exhibited higher NFATc1 expression, which proved to be statistically significant in the periodontitis groups. NFATc1 and RANKL expression levels strongly correlated with each other, and with clinical periodontal parameters. The increased expression of NFATc1 in periodontitis denotes a role for this transcription factor in the pathogenesis of the disease.
引用
收藏
页码:167 / 172
页数:6
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