钙敏感受体、Asporin/BMP-2的相互作用在力刺激降低移植牙骨性粘连发生中的作用机制

自体移植牙术后骨性粘连是临床棘手问题，我们前期研究显示，术后早期施加正畸轻力，可减少骨性粘连的发生，但具体机制不清。机械刺激可通过几种途径将力学刺激转化为细胞内生物信号，钙离子信号是重要途径之一。钙敏感受体(CaSR)可引起细胞内钙离子的变化。我们研究发现，加载机械力后，牙周组织Asporin表达量增加，且与BMP-2的表达相关。据此我们提出假设：加力后，“CaSR表达变化，通过细胞内的钙离子浓度变化传递信息，继而引起Asporin/BMP-2反馈调节平衡状态改变，成骨效应减弱”是降低骨性粘连发生的机制。我们将体外培养牙周膜细胞和建立大鼠自体牙移植加力模型，通过阻滞或激动CaSR，siRNA技术，免疫共沉淀技术，从整体和细胞两个层次证明假说。旨在研究CaSR通路，Asporin/BMP-2的相互作用在骨性粘连中的调控机制，为防止自体牙移植术后骨性粘连提供新的思路。

Ankylosis is the most frequent PDL healing complication of autotransplanted tooth. Prevention of ankylosis may assist the PDL to regenerate periodontal tissues and lead to a successful prognosis. The conventional procedure needs high technical expertise based on extensive clinical experience. However, there are very few reports about the mechanism of ankylosis of teeth after autotransplantion. In this study, we are applying force to the autotransplanted teeth and periodontal ligament (PDL) cells to investigate the role of CaSR and Asporin/BMP-2 on the stimulated osteogenesis. the Asporin Gene, which encodes a new found protein PLAP-1, is considered to be one of the most highly expressed gene in periodontal tissue. It had been convinced that the mechanism of Asporin is to inactivate the BMP-2 signaling pathway. Its LRR (leucine-rich repeat) motif plays an important role in the Asporin-BMP-2 interaction and inhibits the cell proliferation induced by BMP-2. The force can activate Asporin/BMP-2 interaction, which was related to the activation of calcium-sensing receptor (CaSR) pathway. These research may provided valuable insights into the mechanism of ankylosis, and a strategy to optimize the periodontal healing of autotransplanted teeth.