牙周炎造成牙周组织破坏且与糖尿病存在密切联系。组蛋白赖氨酸甲基转移酶SET7可使组蛋白H3K4发生单甲基化(H3K4me1)激活基因转录；也可通过对非组蛋白的甲基化修饰发挥调节作用影响细胞行为。本项目拟将SET7作为研究牙周炎和糖尿病相联系的关键分子，探讨高糖通过上调SET7，对牙龈卟啉单胞菌P.g破坏牙龈上皮屏障和引发宿主牙周组织细胞炎症反应的促进作用。检测高糖及P.g分别及共同作用于牙龈上皮细胞后，细胞内SET7水平、细胞间粘合连接成分β-catenin甲基化、β-catenin降解的差异；检测高糖及P.g分别及共同作用于牙周膜细胞后，细胞内SET7水平、p65基因H3K4me1水平、p65表达激活、炎症介质IL-1β、TNF-α表达释放的差异。检测SET7shRNA和SET7抑制剂对上述过程的抑制作用。并通过动物模型予以观察验证。探讨牙周炎与糖尿病相联系的机制，为二者防治寻找新靶点。

Periodontitis has been the most prevalent oral disease which results in periodontal destruction, as well as has a close relationship with diabetes mellitus.SET domain containing lysine methyltransferase 7 (SET7) induces the transcription activity of genes by histone 3 lysine 4 monomethylation (H3K4me1),or regulates cell behavior by the methylation of non-histone proteins. Our project will focus on SET7 as the key regulator in the relationship between periodontitis and diabetes, investigate the enhancement of gingival barrier destruction and periodontal tissue inflammation induced by Porphyromonas gingivalis through up-regulation of SET7 by high dose glucose. After exposure to high dose glucose and/or P.gingivalis challenge, SET7 up-regulation, methylation of cell adhesion junction component β-catenin and degradation of β-catenin in gingival epithelial cells will be observed and SET7 up-regulation, H3K4me1 of NF-κb subunit p65 gene promoter region, up-regulation and activation of p65, secretion of inflammatory mediators IL-1β and TNF-α will be also observed in periodontal ligament cells. The inhibitory role of SET7shRNA and SET7 inhibitor will be investigated next. Animal models will be used to test our hypothesis in the end. The project is aimed to study the mechanism in the relationship between periodontitis and diabetes, and to search new approaches for the treatment and prevention of both diseases.