牙槽骨病理性吸收是牙周炎的标志性特征，最终导致牙齿松动甚至脱落。干细胞修复缺损牙槽骨打破了以往治疗的瓶颈。间充质干细胞（MSCs）通过分泌转化生长因子β1（TGF-β1）诱导调节性T细胞（Treg）形成在炎症和免疫应答中发挥重要作用，然而TGF-β1和Treg相关细胞因子介导的免疫调控对MSCs骨向分化作用机制尚不清楚。我们前期研究证实炎症环境下骨髓间充质干细胞（BMMSCs）抗炎能力较强，TGF-β1和IL-10表达增高，本项目拟通过①中和抗体和抑制剂实验阻断TGF-β1受体；②构建TGF-β1和转录因子Foxp3过表达及siRNA的慢病毒载体，转染BMMSCs；③体外调控基础上观察BMMSCs体内修复牙槽骨缺损；证实炎性微环境下TGF-β1和Treg相关细胞因子介导的免疫调节对BMMSCs骨向分化有重要的调控作用，为建立基于干细胞和组织工程技术的骨组织再生研究提供理论依据。

Pathological alveolar bone resorption is the hallmark feature of periodontitis. Eventually lead to teeth loose or falling off. Recently, stem cells has used to repair the alveolar bone defect and restoring the physiological function of the natural tooth. Previous studies shown that mesenchymal stem cells (MSC) promote the formation of regulatory T cell (Treg), which is mediated directly by transforming growth factor beta 1 (TFG-β1). However, the mechanism of TGF-β1/Treg-related cytokines mediated immune regulation on osteogenic differentiation of bone marrow mesenchymal stem cells under inflammatory microenviroments is not fully identified. Bone marrow mesenchymal stem cells (BMMSCs ) displayed anti-inflammatory capacities in our previous studies. And the expression of TGF-β1 and IL-10 upregulated. This study intends to verify that the TGF-β1 and Treg-related cytokines play an important role in the regulation of BMMSCs osteogenic differentiation. The experiment consists of three parts as follows: (1) neutralizing antibodies against the TGF-β1 receptor and the inhibitor of the TGF-β1 receptor; (2) overexpression or siRNA of TGF-β1 and Foxp3 in BMMSCs transduced with lentiviral vectors; and (3) observation of the ability of BMMSCs in restoring alveolar bone defects in vivo based on in vitro regulation. These researches provide a theoretical basis for the study of bone regeneration based on stem cells and tissue engineering.