缺血缺氧局部环境是导致口腔颌面部骨缺损和种植体周骨缺损成骨不全或骨移植失败的重要原因。如何使细胞耐受恶劣环境并尽快建立血供是解决此难题的关键。由于软骨细胞对缺血缺氧环境有较强的抵抗力，多年前软骨块移植治疗颌骨缺损曾被寄予厚望，但因其效果不佳被否决。有学者认为软骨成骨的策略并不适用于膜内成骨来源的颌骨。但是，Martin组和本课题组都发现预诱导处理的肥大软骨细胞形成的组织工程软骨可在体内异位成骨，而且我们又发现它在膜内成骨来源的牙槽骨和颅骨内同样有效。这一现象背后的机制不明。因此，本项目提出预诱导软骨分化促进颌骨成骨的两个可能机制：肥大软骨细胞募集间充质干细胞、内皮祖细胞和单核巨噬细胞等迁移到缺损部位，并相互作用最终促进成骨；同时软骨块中的肥大软骨细胞向成骨细胞分化，进一步加强成骨。本课题建立在大量前期研究基础上，预诱导软骨块移植有望为颌骨和牙周骨再生、种植体周骨缺损治疗提供新思路和新方法。

Maxillofacial bone defects or inflammatory stimuli often cause local environmental ischemia and hypoxia, leading to osteogenesis imperfecta or bone graft failure. Cell survival and the establishment of the blood supply has become the key to solve the problem. Due to its strong resistance to ischemia and hypoxia, chondrocytes has been suggested to be applied in maxillofacial bone defects, but the poor clinical outcome restricted its application, some researchers believed that cartilage transplantation does not apply to the membrane bone. Our group and other research group found that the hypertrophic cartilage derived from pre-induction treatment benefit in vivo bone formation, even in the membrane bone, while the mechanism is still unknown. Combined with the concept of development engineering, we proposed that pre-induction strategy of chondrogenic differentiation could be applied in maxillofacial defects, and the possible mechanisms to promote pre-differentiated cartilage into bone are: after implantation of pre-differentiated cartilage into the bone defect, cartilage could chemotactic mesenchymal stem cells, endothelial progenitor cell and other cells migrate to the defect site, interacts with each other, and ultimately improve bone formation; meanwhile hypertrophic chondrocytes in the cartilage block could differentiate into osteoblasts, then strengthen osteogenesis. Preliminary experiments showed that this approach could be the key to resolve the osteogenesis imperfecta or bone grafts failure coursed by critical ischemia and hypoxia, and provide new ideas and new methods for maxillofacial bone regeneration.