磷酸钙骨水泥体内血管通路构建及其诱导成骨研究

Injectable Calcium phosphate bone Cement (CPC) as a new generation of bone repair materials has received widespread attention. It is composed of kinds of phosphates, containing self curing ability and degradation activity in the physiological condition. It also has high biocompatibility, plasticity, isothermal property. But the compact structure induces it show the slow degradation behavior compared with new bone formation in vivo. And the low strength of tissue engineering based on CPC material greatly limits its clinical application. The project is a basic theoretical research, aimed at the study of revascularization of a novel injectable calcium phosphate bone repair material after setting in the body. The stimulation of osteogenic factors and response mechanism will be explored from the material point. The special biodegradable vascular channel (PLGA fiber-apatite deposition-gelatin second attachment) with bone growth factor will be built within CPC. The hydration reaction of cement matrix contains a gradient hydration process, which provides the ideal intensity of support. The revascularization theory of calcium and phosphorus hydration system will be built on, and the finite element model will be used to analyze the response mechanism between tissue and material. This project will be focused on developing a novel injectable bone repair material.

注射型磷酸钙骨水泥（Calcium phosphate Cement）作为新一代骨修复材料已经受到了广泛的关注与研究。它是一类以各种磷酸盐为主要成份, 在生理条件下具有自固化能力及降解活性、成骨活性的无机材料。它还具有高度的生物相容性,可任意塑型, 固化过程等温性等特点, 是目前唯一既能自行固化又能产生骨传导效果的骨修复材料。但因为其致密的结构使其在体内的降解相对新骨生成缓慢。而基于骨水泥制备的组织工程支架，也因强度偏低大大限制了其在临床的应用。本项目旨在对注射型磷酸钙骨修复材料体内固化后，内部的血管通路构建过程进行研究，并复合成骨活性因子探究材料诱导成骨的刺激与响应机理。具体在磷酸钙基体内部构建独特的可降解连通血管通道（PLGA纤维主线-磷灰石沉积-明胶二次附着），同时附着成骨生长因子，达到体内缓释目的。深入研究材料与组织的界面相互作用机理，在上述基础上构建钙磷水化体系的血运重建理论。

磷酸钙骨水泥（Calcium phosphate Cement）作为新一代骨修复材料已经受到了广泛的关注与研究。它是目前唯一既能自行固化又能产生骨传导效果的骨修复材料。但因为其致密的结构使其在体内的降解相对新骨生成缓慢。本项目旨在保留磷酸钙骨水泥自固化能力，调控其降解活性、成骨活性。根据其可任意塑型, 固化过程等温性等特点, 在对磷酸钙骨修复材料体内固化后，内部的血管通路构建过程进行研究；研究制备可原位形成血管通道的磷酸钙基骨支架，构建具备血运重建功能的骨组织修复材料。根据目前的研究成果，基本实现了预期目标，同时我们进一步对血管化的发生机制进行了研究，明确了缺氧诱导因子在血管长入过程中的诱导作用；进一步证实了无机铁离子对血管化的促进作用。同时通过该项目的开展建立了鹿茸为动物模型的长效研究方向，为后续的研究延伸奠定了良好基础。