牵张成骨在颅颌面的临床应用越来越广泛，但目前对牵张成骨的生物学机制究还很少。骨细胞作为骨组织中含量最多的细胞，其在骨重建中的作用已被学者所认可，大量研究证据表明骨细胞可直接调控成骨细胞和破骨细胞完成骨改建。但目前关于DO的相关机理研究中，几乎没有文献涉及骨细胞在牵张成骨中的作用机理。另外，骨硬化蛋白作为骨细胞分泌的经典的Wnt信号通路负向调节因子，采用骨硬化蛋白单克隆抗体或者采用SOST基因敲除的方法可以抑制骨硬化蛋白的生物学作用，促进局部的成骨或者骨折愈合。因此本研究拟通过对DO过程中骨细胞的组织形态学、分子生物学变化进行观察，并通过SOST 基因敲除小鼠的DO模型及应用anti-sclerostin抗体对DO的成骨促进作用进行研究。深入探索骨细胞对DO骨改建过程的调控作用，并期望可以通过抑制骨细胞来源Sclerostin蛋白对颌面部DO成骨起到有效的促进作用，提高临床上DO成骨的效率。

Distraction osteogenesis (DO) is an endogenous bone engineering technique. It utilizes continous external forces to bone segments and promotes mesenchymal cells differentiation and proliferation. The osteoblasts between the bone segments will be activated. And newly formed bone could prolong the length of bone. At present, the clinical application of DO in craniomaxillofacial regions is more extensive, but there are few studies on the biological mechanism of distraction osteogenesis. Osteocytes comprise more than 95% of skeletal cells, they were long thought to be passive residents. More than 2 decades of intense study of osteocytes in vivo and in vitro overturned this paradigm, revealing that osteocytes modulate bone homeostasis and remodeling, act as mechanosensors, and direct endocrine regulation of mineral metabolism.However, there is almost no literature on the mechanism of osteocytes in distraction osteogenesis.Sclerostin is a specific osteocytes marker, secreted by osteocytes and negatively regulate the Wnt / β-catenin signaling pathway in bone remodeling. the use of anti-sclerostin monoclonal antibody or SOST gene knockout could inhibit the biological function of sclerostin, and promote local osteogenesis or fracture healing.Therefore, this study intends to observe the histomorphological and molecular biological changes of osteocytes during DO, and investigate the the osteogenic stimulation effects of SOST knockout and anti-sclerostin antibody application on DO animal model, and to explore the roles of osteocytes in the process of distraction osteogenesis and effects of sclerostin on the osteogenesis of craniomaxillofacial DO, and to improve the efficiency of DO osteogenesis in clinic.