牙周炎患者牙周支持组织的破坏与长期慢性炎症密切相关。课题组前期研究了牙周膜干细胞分化的IGF-1R下游通路机制，但其上游分子机制仍不明确。预试验发现lncRNA ANRIL在炎性牙周膜干细胞中显著低表达，生物信息学预测lncRNA ANRIL与miR-7-5p、miR-7-5p与IGF-1R之间存在结合位点，因此我们假设lncRNA ANRIL通过miR-7-5p/IGF-1R轴调控炎性牙周膜干细胞衰老和骨向分化。本课题拟从验证炎性牙周膜干细胞lncRNA ANRIL、miR-7-5p、IGF-1R三者间的相互作用入手，探讨lncRNA ANRIL/miR-7-5p/IGF-1R轴对炎性牙周膜干细胞的衰老、成骨及下游mTOR/NF-κB/MAPK信号通路的调控作用，以期阐明该调控轴在炎性牙周膜干细胞衰老和成骨过程中的作用机制。研究成果为改善炎性牙周膜干细胞的定向分化和组织再生能力奠定基础。

The destruction of periodontal tissues in patients with periodontitis is closely related to the prolonged chronic inflammation. Our previous study has investigated the downstream signal mechanism of the insulin-like growth factor 1 receptor (IGF-1R) in the committed differentiation of periodontal ligament stem cells (PDLSCs). However, the upstream molecular regulation mechanism of IGF-1R is still unclear. Our preliminary studies have revealed that lncRNA ANRIL is significantly downregulated in inflamed PDLSCs (iPDLSCs) as compared with normal PDLSCs, while the bioinformatics analysis has predicted the binding sites between lncRNA ANRIL and miR-7-5p, miR-7-5p and IGF-1R. Thus, we presume that the lncRNA ANRIL/miR-7-5p/IGF-1R axis can regulate the osteogenic differentiation and senescence process of iPDLSCs. In this study, normal and inflamed PDLSCs were respectively obtained to detect the expression of lncRNA, miR-7-5p and IGF-1R, as well as the interactions among them. Meanwhile, we will evaluate the effects of the lncRNA ANRIL/miR-7-5p/IGF-1R axis on senescence indicators, osteogenic markers, mTOR/NF-κB/MAPK-related signals and in vivo osteogenesis in order to elucidate the modulatory action of this axis on the osteogenesis and senescence of iPDLSCs. These upcoming results can help reveal the molecular mechanisms during the osteogenic differentiation and senescence process of iPDLSCs, which will provide the theoretical foundation for improving the committed differentiation of iPDLSCs and regeneration of periodontium in the inflammatory state.