Investigation of diabetes-associated periodontitis pathogenesis from a point of relevance for advanced glycation end-product and redox regulation.

本研究的目的是从氧化应激的角度探讨糖尿病牙周炎的发病机制，并利用抗氧化应激机制作为新的治疗手段。晚期糖基化终产物（AGE）和牙周病因子（P-LPS）可增加人牙龈成纤维细胞AGE受体、氧化应激标志物、抗氧化酶和炎性细胞因子的表达。MAPK通路抑制剂抑制AGE诱导的细胞因子表达。KGF增加抗氧化酶的表达。提示AGE和P-LPS通过产生氧化应激和炎性细胞因子，加重糖尿病牙周炎的发病。KGF可能增强抗氧化应激机制。

The aim of this study is investigation of diabetes-associated periodontitis pathogenesis from a point of oxidative stress, and utilization of antioxidative stress mechanism as new treatment. Advanced glycation end-product (AGE) and periodontopathic factor (P-LPS) increased expressions of AGE receptor, oxidative stress markers, antioxidative enzyme and inflammatory cytokine in human gingival fibroblasts. Inhibitors of MAPK pathway inhibited AGE-induced cytokine expression. KGF increased expression of antioxidative enzyme . These findigs suggest that AGE and P-LPS make a diabetes-associated periodontitis pathogenesis worse by production oxidative stress and inflammatory cytokine. KGF may enhance antioxidative stress mechanism.