近年来，越来越多的糖尿病患者寻求成人正畸治疗，而异常的高糖状态和晚期糖基化终末产物会导致全身骨代谢紊乱，严重影响了正畸的疗效。项目申请人课题组在前期工作中论证了二甲双胍能够明显改善Ⅱ型糖尿病大鼠牙齿正畸的效果，并对该过程中二甲双胍应用所引起的牙槽骨骨细胞标志蛋白硬骨素和牙本质基质蛋白1的表达变化产生了浓厚的兴趣。文献报道二甲双胍在治疗糖尿病时会引起miR222显著减少以及miR222在维持骨骼稳态方面具有重要作用。申请人对miR222进行了靶基因预测，然后对靶基因进行了功能富集分析，包括GO与KEGG信号通路分析，结果显示miR222与流体剪切应力以及涉及骨细胞的多种生物学效应和信号通路密切相关。申请人拟在前期工作基础上，通过该课题对miR222参与二甲双胍调控骨细胞的相关机制进行深入探讨。预期成果将为Ⅱ型糖尿病患者的正畸治疗提供有效的靶点和理论依据，具有积极的科学意义。

Adult orthodontic treatment is attracting more and more diabetic patients. Yet, the abnormal high glucose status and advanced glycation endproducts caused by diabetes will lead to bone metabolism disorder and impair orthodontic tooth movement effect. The applicant’s team has reported that metformin could improves the efficacy of orthodontic tooth movement in rats with type 2 diabetes. Specially, the expression change of sclerostin and dentin matrix protein 1 inspires our interests. It has been proved that miR222 plays an important role in regulating bone metabolism and metformin could reduce the expression of miR222 in the course of diabetes treatment. So the applicant researched further by analyzing the function of the enriched target gene based on miR222 target gene prediction, which includes GO and KEGG signal pathway analysis. The result suggests that miR222 closely involved in fluid shear stress, various biological effects and signal pathways in osteocytes. Based upon our previous works, the applicant purpose to further explore the mechanism of miR222 during metformin improves the efficacy of orthodontic tooth movement in SD rat with type 2 diabetes by regulating alveolar osteocytes. The expected outcomes will provide an effective targets and a theoretical basis for orthodontic treatment in patients with type 2 diabetes mellitus.