糖尿病牙周炎的治疗关键是炎症控制及牙周组织的修复再生，有研究表明C反应蛋白（CRP）是炎症反应的关键调控因子。以往CRP相关研究大多未区分亚型，且受技术所限均采用与人CRP同源性差的小鼠为动物模型，研究结果存争议。项目组前期发现高糖炎性环境促进单体型CRP（mCRP）的表达，CRP敲除大鼠（与人CRP同源性高）炎症诱导的牙槽骨吸收明显减轻，提示CRP可能参与糖尿病牙周炎的调控，但相关分子机制不明。牙周炎与Ⅱ型糖尿病均为中老年高发且互为危险因素。因此，项目拟通过CRP基因敲除大鼠结合体外实验，明确mCRP与II型糖尿病牙周炎的致病关系及调控牙周再生的可能机制；并构建加载CRP变构抑制剂（1，6双磷酸胆碱己烷）的静电纺丝材料，结合牙周膜干细胞形成缓释修复体系，验证其对大鼠II型糖尿病牙周炎缺损的修复效果。该研究预期进一步丰富II型糖尿病牙周炎发病机制，为其精准治疗提供参考靶点和综合治疗策略。

Inflammation control and periodontal tissue regeneration are key factors for periodontitis with diabetes mellitus (DM) therapy. It is known that C-reactive protein (CRP) is a pivotal regulation factor of inflammation. Most research on CRP hasn’t distinguish the different conformation due to the limiting of the technology. Besides, almost all of the study use mouse rather than rat for the animal model. However, the structure of mouse CRP is quite different from human’s, results of these studies remain controversial. Our group found that high glucose and inflammatory culture environment induces mono-CRP (mCRP) expression and CRP-/- periodontitis rats(high homology with human) got less alveolar bone resorption than control ones. It is suggested that CRP could be a regulation factor of periodontitis with DM, but the mechanism remains unclear. Periodontitis and type II DM are considered as an independent risk factor for each other and get high incidence among older people,. Our project will use CRP-/- rats with in vitro experiments to explore the relationship of mCRP and periodontitis with type II DM, and the mechanism how mCRP regulate the periodontal regeneration. In addition, electrostatic spinning material carrying CRP dissociation inhibitor (1,6 bisphosphocholine) and Periodontal Ligament Stem Cells will be established to explore its effects on periodontitis with type II DM. Our project will uncover the pathogenesis of periodontitis with type II DM and provides a referential target and a comprehensive treatment strategy for patients of periodontitis with type II DM.