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正畸力作用下大鼠牙根表面微裂纹的产生、扩展模拟及蛋白质组学研究。

Microcracks on the Rat Root Surface Induced by Orthodontic Force, Crack Extension Simulation, and Proteomics Study.

机构信息

Beijing Advanced Innovation Centre for Biomedical Engineering, Key Laboratory for Biomechanics and Mechanobiology of Chinese Education Ministry, School of Biological Science and Medical Engineering, Beihang University, Beijing, 100083, China.

College of Stomatology, Chongqing Medical University, Chongqing, 401147, China.

出版信息

Ann Biomed Eng. 2021 Sep;49(9):2228-2242. doi: 10.1007/s10439-021-02733-y. Epub 2021 Mar 8.

Abstract

Root resorption is a common complication during orthodontic treatment. Microcracks occur on the root surface after an orthodontic force is applied and may be related to the root resorption caused by the orthodontic process. However, the mechanisms underlying root resorption induced by microcracks remain unclear. In this study, a rat orthodontic model was used to investigate the biological mechanisms of root resorption caused by microcracks. First, the first molar was loaded with 0.5-N orthodontic force for 7 days, and microcracks were observed on the root apex surface using a scanning electron microscope. Second, to describe the mechanical principle resulting in microcracks, a finite element model of rat orthodontics was established, which showed that a maximum stress on the root apex can cause microcrack extension. Third, after 7 days of loading in vivo, histological observation revealed that root resorption occurred in the stress concentration area and cementoclasts appeared in the resorption cavity. Finally, proteomics analysis of the root apex area, excluding the periodontal ligament, revealed that the NOX2, Aifm1, and MAPK signaling pathways were involved in the root resorption process. Microcrack extension on the root surface increases calcium ion concentrations, alters the proteins related to root resorption, and promotes cementoclast formation.

摘要

牙根吸收是正畸治疗中的常见并发症。正畸力作用后,根表面会出现微裂纹,可能与正畸过程引起的牙根吸收有关。然而,微裂纹引起牙根吸收的机制尚不清楚。本研究采用大鼠正畸模型探讨微裂纹引起牙根吸收的生物学机制。首先,对第一磨牙施加 0.5-N 的正畸力 7 天,并用扫描电子显微镜观察根尖表面的微裂纹。其次,为描述导致微裂纹的力学原理,建立了大鼠正畸的有限元模型,结果表明根尖的最大应力会导致微裂纹扩展。第三,在体内加载 7 天后,组织学观察发现,在应力集中区发生了牙根吸收,并且在吸收腔中出现了破牙骨质细胞。最后,对根尖区(不包括牙周膜)进行蛋白质组学分析,发现 NOX2、Aifm1 和 MAPK 信号通路参与了牙根吸收过程。根表面微裂纹的扩展会增加钙离子浓度,改变与牙根吸收相关的蛋白质,促进破牙骨质细胞的形成。

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