Wnt信号通路在成骨细胞发生及骨形成过程中起着关键作用，LPR5是Wnt信号通路中的受体之一，与Wnt蛋白及Frizzled蛋白的结合可启动信号通路的传导。研究证明它的缺失可导致Wnt信号途径传导出现障碍。本项目从基因水平出发来探讨LRP5基因在BMSCs成骨分化中的所起的作用，并以此为基础，通过构建慢病毒干扰/过表达型载体将LRP5基因转染进入BMSCs，进一步明确其作用及与其他成骨信号之间的联系；然后在透明基板上通过细胞薄层技术获得LRP5转染的BMSCs细胞膜层，并将该细胞膜层在钛片表面进行培养，体外和体内实验来评价该细胞膜层在种植体骨结合中作用及机制。本实验探讨LRP5在BMSCs成骨分化中的作用及LRP5转染BMSCs膜层在种植体骨结合中的作用及相关机制，为促进种植体骨结合提供新的治疗思路和治疗靶点，从而为快速建立并长期维持种植体骨结合提供科学而合理的实验依据和理论支持。

The Wnt signaling pathway plays an important role in the control of osteoblastogenesis and bone formation. LRP5 is a kind of transmembrane protein that belong to the LDLR family, it acts as co-receptor of Frizzleds to induce the canonical Wnt signaling pathway. Loss-of-function mutation in LRP5 leads to the blocking of the Wnt signaling pathway. This study investigated the role of LRP5 through the process of osteogenic differentiation of BMSCs on the surface of titanium .As a result of microarray assay the dual expression lentivirus vector carrying siRNA of LRP5 was constructed and transduced into BMSCs, then BMSCs were dealt with cell sheet technology on the surface of transparent carrier.Subsequently, BMSCs layers were cultured on the surface of titamium. We evaluated the function of BMSCs layers through the process of osseointergration both in vivo and in vitro. This study focus on the role of LRP5 through the process of BMSCs differentiation into osteoblasts and the function of BMSCs layers transfetcted with LRP5 lentivirus in the control of osseointergration. It will enriches new therapy thoughts for implant surgery and provides scientific reasonable experimental proof for osseointergration theory.