Sun Yuqing, Fu Jingfei, Lin Feiran, Li Shengnan, Du Juan, Liu Yi, Bai Yuxing
Department of Orthodontics, School of Stomatology, Capital Medical University, China.
Laboratory of Tissue Regeneration and Immunology and Department of Periodontics, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, School of Stomatology, Capital Medical University, China.
Stem Cells Int. 2022 Sep 6;2022:4775445. doi: 10.1155/2022/4775445. eCollection 2022.
The aim of this study was to investigate the effect of nitric oxide (NO) on orthodontic tooth movement and the regulatory effect on bone formation.
A mouse orthodontic tooth movement model was established to measure the level of releasing NO. Besides, orthodontic tooth movement distance and the bone formation in the tension side of the orthodontic tooth were also analyzed. In vitro, human periodontal ligament stem cells (hPDLSCs) were cultured under tensile force stimulation. The production of NO and the expression level of nitric oxide synthase (NOS) were detected after mechanical stimulation. Furthermore, the downstream cellular signaling pathway regulated by NO was also explored.
The generation of NO steadily increased throughout the orthodontic tooth movement in mice. Orthodontic tooth movement was decreased in the NOS inhibitor group while it was accelerated in the NO precursor group. Force-induced NO promoted the osteogenic differentiation of human hPDLSCs under tensile force stimulation. And force-induced NO in hPDLSCs regulated the PI3K/Akt/-catenin signal pathway.
NO is involved in the regulation of orthodontic tooth movement and promotes bone formation on the tension side of the orthodontic tooth. The PI3K/Akt/-catenin pathway is one of the downstream cell signal transduction pathways of NO in the orthodontic process.
本研究旨在探讨一氧化氮（NO）对正畸牙齿移动的影响以及对骨形成的调节作用。
建立小鼠正畸牙齿移动模型以测量NO释放水平。此外，还分析了正畸牙齿移动距离以及正畸牙齿张力侧的骨形成情况。在体外，将人牙周膜干细胞（hPDLSCs）在拉伸力刺激下进行培养。机械刺激后检测NO的产生以及一氧化氮合酶（NOS）的表达水平。此外，还探索了由NO调节的下游细胞信号通路。
在小鼠正畸牙齿移动过程中，NO的生成稳步增加。NOS抑制剂组的正畸牙齿移动减少，而NO前体组的正畸牙齿移动加速。力诱导的NO在拉伸力刺激下促进了人hPDLSCs的成骨分化。并且hPDLSCs中力诱导的NO调节了PI3K/Akt/β-连环蛋白信号通路。
NO参与正畸牙齿移动的调节，并促进正畸牙齿张力侧的骨形成。PI3K/Akt/β-连环蛋白途径是正畸过程中NO的下游细胞信号转导途径之一。
