炎性环境下，牙周膜干细胞（PDLSCs）再生能力下降是导致牙周组织再生异常的重要原因。我们前期证明，炎性环境下PDLSCs中miR-17表达下降是导致其再生能力下降的重要原因。研究表明，表观遗传受环境因素影响且能够调控microRNA的转录。然而表观遗传是否影响炎性环境下PDLSCs中miR-17的表达仍不明确。我们发现，炎性环境中组蛋白去乙酰化酶(HDAC)表达增加，且其抑制剂能够上调pri-miR-17的表达。因此，我们推测HDAC通过调控miR-17-92的转录从而影响PDLSCs的再生能力。本课题拟从炎性环境下变化的特异性HDAC筛选、特异性HDAC与PDLSCs生物学特性的关系、HDAC调控miR-17-92的分子机制，以及动物体内验证四个方面探讨表观遗传、microRNA及干细胞再生能力之间的关系。本课题从新的角度阐明牙周炎再生能力下降的分子机制，并为牙周炎的治疗提供新的思路。

The regeneration capacity of periodontal ligament stem cells (PDLSCs) was reduced significantly in inflammation microenvironment. It is the main cause of decreased periodontium regeneration. Our previous research demonstrated that the osteogenic differentiation of PDLSCs was inhibited significantly in inflammation microenvironment. It was because that the inflammatory cytokines affected the expression of miR-17. Recently, researchers suggested that the environment could lead to the epigenetic changes. Moreover, the epigenetic could regulate the transcription of microRNA. Interestingly, we also found that the expression pattern of histone deacetylase (HDAC) was changed in inflammatory microenvironment. In addition, the HDAC inhibitors could up-regulate the expression of primary-miR-17 and rescue the osteogenic differentiation of PDLSCs in inflammatory microenvironment. Therefore, we infer that HDAC could affect the regeneration capacity of PDLSCs via modulating the expression of miR-17-92 cluster directly. In this study, we design four part experiments to demonstrated the intrinsic relationship among epigenetic, microRNA and bio-characteristic of stem cells. The experiments include choosing the specific HDAC related with inflammation, the relationship between specific HDAC and bio-characteristics of PDLSCs, the mechanism of specific HDAC regulates the expression of miR-17-92 cluster and the treatment effect of HDAC on periodontitis model in vivo. This study will elucidate the mechanism of the regeneration capacity of PDLSCs decreased in inflammation microenvironment from a new perspective. It will not only explain the regeneration capacity of PDLSCs reduced in inflammation microenvironment, but also provide a new therapeutic target for curing periodontitis.