大量研究显示炎症因子引发的炎症反应在牙合创伤、不良正畸等力学刺激引起的牙周组织破坏吸收中具有重要作用，但力信号引起牙周炎症反应的机理尚不清楚。近年来炎症体、炎性caspases和细胞焦亡在炎症过程中的作用逐渐显露，研究显示牙周炎症组织细胞中表达炎症体，而包括申请者在内的研究者发现力刺激能诱导牙周细胞发生程序性死亡以及炎性caspase活化。因此，本课题拟对体外培养人牙周膜细胞施加牵张应变，检测炎症因子表达，程序性细胞死亡的发生情况，NLRP/caspase炎症复合体基因、蛋白表达及活化情况，明确NLRP/caspase炎症复合体在牵张诱导人牙周膜细胞发生炎症反应过程中的作用，并探索ROS在力激活牙周膜细胞炎症体机制中的作用，对于阐明机械力引起牙周组织破坏吸收的机理，指导口腔修复及正畸临床对牙齿合理施力，以及为控制牙周炎症中牙周组织的破坏吸收、防治牙周炎症寻找新的靶点，具有重要的科学意义。

Plenty of researches have proved that the inflammatory response induced by excessive force loading resulting from occlusal trauma or improper orthodontic treatment played an important role in periodontal tissue wound and injury.However,the mechanisms involved in this force-induced inflammatory process remains unclear. In recent years,the roles of inflammasome,inflammatory caspases and pyroptosis in tissue inflammatory response started to be uncovered.Researches confirmed the expression of inflammosomes in inflammatory periodontal tissue,and researchers including us previously reported force-induced programmed cell death and activation of inflammatory caspases in periondontal cells.In the present research, the in vitro cultured human periodontal ligament (PDL) cells will be stretched. After stretch loading, the expression of proinflammatory cytokines,the occurrence of programmed cell death and the expression of the genes and protein of NLRP/caspase inflammasome will be examined,to confirm the role of NLRP/caspase inflammasome in stretch-induced inflammatory response in human PDL cells,and to probe the possible role of ROS in the force-induced activation of inflammasome in PDL cells. The results of the present research may give important scientific supports to revealing the mechanisms involved in the force-induced periodontal tissue wound and injury,instructing the proper force loading in the prosthodontic and orthodontic treatments and finding new targets for controlling the tissue wound in periodontal inflammation and for prevention and treatment of periodontitis.