抑制NF-κB信号通路在骨质疏松症种植体骨结合中的效应及相关机制研究

Osteoporosis is a systemic disease characterized by low bone mass and destroy of bone micro-structure, which can affect the early osseointegration. However the internal mechanism is not clear. There is no good method to improve the osseointegration for OP. Studies have found that NF-κB signaling pathway plays an important role in the development of OP, inhibition which can promote bone formation. This study used gene chip to screen out NF-κB up-regulated genes, and through further tests by gene silence and gene overexpression technologies, the genetically modified SD rat without up-regulated genes was obtained . The hydroxyapatite coatings containing S1627 were built by biomimetical method, which formed a local delivery system. Through in vitro and in vivo experiments, the mechanisms of the inhibition of NF-κB pathway were discussed on cellular,protein and mRNA dimansions and therefore the solution to promote bone formation were found. The proposal and completion of this project, can clarify the osseointegration mechanism for OP.

骨质疏松症（OP）是一种以低骨量和骨组织微结构破坏为特征的全身性疾病，可影响牙种植体早期的骨结合,但其内在机制尚不明确；目前尚缺乏促进骨质疏松情况下种植体骨结合的方法。有研究发现NF-κB信号通路在骨质疏松的发生发展中起着重要作用，抑制该通道可促进成骨。本研究使用基因芯片技术筛选出NF-κB的上调基因，通过基因沉默和基因过表达技术进一步验证，并获得沉默上调基因的转基因大鼠；同时采用仿生法在种植体表面构建含S1627的钙磷涂层，形成局部缓释系统；对这两种方法通过体内体外实验，在细胞、蛋白及mRNA水平上探讨抑制NF-κB通路对OP状态下提高骨结合作用的机理。本项目的提出和完成，可阐明OP状态下的种植体骨结合机制，为提高OP状态下的种植体骨结合提供理论基础。

骨质疏松症（OP）是一种以低骨量和骨组织微结构破坏为特征的全身性疾病，可影响牙种植体早期的骨结合,但其内在机制尚不明确；目前尚缺乏促进骨质疏松情况下种植体骨结合的方法。有研究发现NF-κB信号通路在骨质疏松的发生发展中起着重要作用，抑制该通道可促进成骨。本项目通过成功建立大鼠骨质疏松症模型，提取其BMSCs细胞，利用基因芯片技术筛选出NF-κB上调基因，并使用PCR技术得到验证；同时采用层层静电自组装技术在种植体表面构建含NBD多肽的涂层，形成局部缓释系统；通过体内体外实验，在细胞、蛋白及mRNA水平上探讨抑制NF-κB通路对OP状态下提高骨结合作用的机理。本项目的提出和完成，可阐明OP状态下的种植体骨结合机制，为提高OP状态下的种植体骨结合提供理论基础。