正畸牙移动中由于应力或炎症因素造成牙槽骨高度丢失一直是临床中亟待解决的常见并发症。破骨活动亢进是牙槽骨吸收发生的主要原因，至今的研究一般认为:破骨细胞的成熟与分化只要具备巨噬细胞集落刺激因子与破骨细胞分化因子这两个关键性因子启动就足够。但最新研究及申请者前期研究结果显示不同浓度IL-20(白介素-20)在破骨细胞的成熟与分化中扮演极重要的角色，并同时引起大鼠脑部ACC区星形胶质细胞活化显著，提示需以神经—免疫通信的新视角来重新审视正畸应力作用下破骨细胞活化的调控机制。本项目以具有重要生理功能且极可能在破骨细胞活化功能调控中处于反应上游地位的IL-20为切入点，应用体外应力及体内牙移动模型，在多个层面探讨验证应力刺激下靶向抑制和促进IL-20的表达及其通过神经-免疫通信调控破骨细胞活化的作用机制；为口腔正畸及牙周抑制骨吸收治疗的靶向精准药物干预提供可靠实验依据，具有积极的科学意义及临床价值。

Orthodontic tooth movement due to stress factors or inflammation caused by alveolar bone height loss has been a common clinical urgent solution to complications, osteoclast hyperactivity is the main reason for alveolar bone resorption, and the current study generally agreed that osteoclast The maturation and differentiation of macrophages colony stimulating factor (M-CSF) and osteoclast differentiation factor (RANKL) these two key factors to start enough. However, the latest research and applicant's preliminary results suggest that IL-20 (interleukin-20) plays an important role in the osteoclast maturation and differentiation. At the same time, it is found that alveolar bone resorption induces rat astrocyte Activated, suggesting that the need for neuro-immune communication such a new perspective to re-examine the role of orthodontic stress regulation of osteoclasts. The project intends to use in vitro stress and in vivo tooth movement model, the use of histomorphology and molecular biology techniques to explore stress stimulation by short interfering RNA (siRNA) inhibition of IL-20 expression to verify the IL-20 by neural-immune communication pairs Osteoclast regulation role and mechanism for the exploration of new oral orthodontics and periodontal treatment of targeted regulatory intervention provide experimental evidence, with a positive scientific significance and application value.