牵张成骨技术因其具有许多无可替代的优越性使其在颅颌面外科领域具有广阔的应用前景，但对严重的骨缺损、骨畸形且难以利用自身骨段制作输送盘的患者来说却难以奏效。我们提出"非血管化游离输送盘牵张成骨新模式，NTDO"为这一问题的解决提供了可能。我们在成功构建并验证"NTDO"动物模型的基础上，为进一步阐明其机制，本课题组拟用基因沉默的方法筛选促进EPCs增殖、分化、迁移最有效的TPRC分子，并检测其下游靶向基因的定位及表达，之后，转染筛选出的TRPC分子将其导入骨髓内皮祖细胞，促使被筛选出的TRPC分子在EPCs中过表达，并观察其调控血管新生的作用。研究TRPC通道在"非血管化游离输送盘牵张成骨新模式"新骨形成时调节血管形成的机理，从而进一步阐明"非血管化游离输送盘牵张成骨新模式"新骨形成机制，为进一步在临床上广泛应用"非血管化游离输送盘牵张成骨新模式"治疗各种严重骨缺损或骨畸形提供理论依据。

Transport Distraction Osteogenesis(TDO) technique has broad application prospects because of its many irreplaceable advantages in the field of cranial and maxillofacial surgery, but for those patients who has serious bone defects , bone deformities and can't use their bone segments ,TDO doesn't work. We put forward a new model of TDO that is Nonvascular Transport Distraction osteogenesis (NTDO) for the solution of this problem. On the basis of successful construction of NTDO animal models, in order to further elucidate the NTDO's mechanism ,we will employ the method of gene silencing to filtrate TPRC molecules, which can mostly facilitates EPCs proliferation, differentiation, migration and detect the location and expression of downstream target genes. We will transfect and import the filtrated TRPC molecules into the endothelial progenitor cells (EPCs) of bone marrow and make it overexpression on EPCs, and observe its effect in regulating angiogenesis. We will study the mechanisms of TRPC channels and its regulation of angiogenesis during NTDO. The study can further clarify new bone formation mechanism of NTDO and provides theoretical basis for NTDO's widely clinical application in treating all kinds of serious bone defects or bone deformities.