牵张成骨技术因其本身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，但对于那些骨质缺损过大、剩余骨量不多难以利用自身骨段制作输送盘的患者来说却难以奏效。我们提出的"非血管化游离输送盘牵张成骨新模式"为这一问题的解决提供了可能。我们在成功构建并验证"非血管化游离输送盘牵张成骨新模式"动物模型的基础上，为进一步探明其机制，本课题拟用Notch1 ICN作为细胞诱导因子，利用基因转染的方法将其导入骨髓内皮祖细胞，构建骨髓内皮祖细胞内的Notch 信号转导通路，检测激活血管内皮祖细胞Notch 信号通路后靶向基因的表达情况，研究Notch 信号通路在"非血管化游离输送盘牵张成骨新模式"新骨形成中调节血管新生的机理，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 a broad clinical application in craniomaxillofacial surgery because of its irreplaceable advantages. But TDO does not work for those patients who can't make an appropriate bone transport disc for TDO by their own bone segment because of the large bone defect or residual bone, so we put forward a new pattern of TDO that is Nonvascular Transport Distraction Osteogenesis (NTDO) and it provides a new possibility to solve the problem. Based on the successful construction and test of the NTDO animal model, in order to further our research on NTDO's mechanism, we will integrate the new induced factor Notch1 ICN into the bone marrow endothelial progenitor cells by gene transfection, construct the notch signaling in the bone marrow endothelial progenitor cells and detect the expression of the target gene after activating the Vascular endothelial progenitor cells ( EPCs ). We will also study the mechanisms of Notch's signaling and its regulation of Angiogenesis during NTDO. The study can further clarify the mechanism of new bone formation in NTDO and provide a theoretical basis for NTDO's clinical application in treating serious bone defect or bone deformities.