正畸牙齿移动过程中，牙周膜细胞将力学刺激转化为生物学信号引起牙周组织改建，该过程涉及多种信号转导分子和细胞因子，项目申请人课题组在前期工作中发现骨膜蛋白（PN）和高迁移率族蛋白1（HMGB1）参与调控正畸应力介导的牙齿移动过程，并通过构建骨膜蛋白基因敲除（PN-/-）小鼠的牙齿移动模型阐明PN对HMGB1具有调控作用，但具体机制尚不十分明确。结合细胞焦亡是HMGB1释放的重要途径、正畸应力能够通过产生活性氧（ROS）促进牙周膜细胞的焦亡，以及研究证实TNF-α等炎症介质能够显著降低牙周膜成纤维细胞的PN表达，我们推测PN和HMGB1在牙齿正畸所导致的牙周组织改建过程中存在较为精细的相互调控机制，并通过相互调控协同参与牙周组织改建。为此，本课题拟在前期工作基础上，通过构建相应的动物模型和细胞模型，针对上述假说展开深入探究工作。预期成果将为口腔正畸临床提供有益的理论依据，具有积极的科学意义。

During orthodontic tooth movement, periodontal ligament cells stimulate periodontal tissues remodeling through transforming mechanical stimuli into biological signals under the stimulation of orthodontic stress. Various signal transduction molecules and cytokines were involved in this process. In previous work, the applicant's team has reported that periostin (PN) and high-mobility group box 1 (HMGB1) participate in the regulation of orthodontic stress-mediated tooth movement and has clarified that PN has a regulatory effect on HMGB1 by constructing a periostin gene knockout (PN-/-) mouse tooth movement model. While the specific mechanism is not yet clear. Studies have shown that pyroptosis is a vital method to release HMGB1 and orthodontic stress promotes the pyroptosis of periodontal ligament cells by producing reactive oxygen species (ROS). Also, inflammatory mediators such as TNF-α can significantly reduce PN expression in periodontal ligament fibroblasts. Due to the results above, We speculate that PN and HMGB1 have a relatively fine mutual regulation mechanism during periodontal tissue remodeling caused by orthodontics and they participate in periodontal tissue remodeling through mutual regulation. Therefore, in-depth researches on the above hypotheses was designed to conduct through building corresponding animal models and cell models based on previous work. The expected results will provide a useful theoretical basis for clinical orthodontics and will have a positive scientific significance.