BMPR-IA/MAPK信号轴在UHMWPE诱导破骨细胞分化成熟中的作用及机制

近年研究发现，人工关节假体周围产生的磨损颗粒，诱导破骨细胞过度分化成熟，引起局部骨溶解是导致人工关节晚期松动的主要原因。因此如何抑制局部破骨细胞的骨吸收效应，是防治术后无菌松动的关键。最近研究发现骨形态发生蛋白（bone morphogenetic proteins, BMPs）及其BMP受体在破骨细胞分化成熟中起着重要作用。但目前为止，其具体的作用机制尚不明确，针对IA型BMP受体与MAPK信号轴在磨损颗粒诱导破骨细胞分化成熟中作用的研究，国内外至今未见相关报道。结合近年研究文献以及课题组已有的前期工作基础，本项目将研究BMPR-IA在磨损颗粒诱导破骨细胞分化成熟及骨溶解中的作用，同时探讨MAPK信号轴在其中是否起到信号传递的意义，为防治磨损颗粒诱导溶骨性疾病提供新的思路和实验依据。

Recent studies have found that wear particles around the artificial joint prostheses induce excessive osteoclast differentiation and maturation, causing local osteolysis and leading to the loosening of the artificial joint. Therefore, the key of prevention and treatment of postoperative aseptic loosening is how to inhibit the resorption of osteoclasts around the replacement. Recent studies have found that bone morphogenetic protein (BMPs) and BMP receptor plays an important role in the differentiation and maturation of osteoclasts. But so far, the specific mechanism of action is not clear,there are no reports about the role of BMPR-IA and MAPK signaling axis in wear debris induced osteoclast differentiation and maturation around the world. Combined with the research literature in recent years and the preliminary work of our research group, this project will study the effect of BMPR-IA on wear debris induced osteoclast differentiation and osteolysis, and the role of MAPK signaling axis in the process, provide new ideas and experimental evidence for the prevention of wear debris induced osteolytic disease.