Nociceptor mechanisms underlying pain and bone remodeling via orthodontic forces: toward no pain, big gain.

IF 2.5 Q2 CLINICAL NEUROLOGY
Frontiers in pain research (Lausanne, Switzerland) Pub Date : 2024-02-22 eCollection Date: 2024-01-01 DOI:10.3389/fpain.2024.1365194
Sheng Wang, Ching-Chang Ko, Man-Kyo Chung
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引用次数: 0

Abstract

Orthodontic forces are strongly associated with pain, the primary complaint among patients wearing orthodontic braces. Compared to other side effects of orthodontic treatment, orthodontic pain is often overlooked, with limited clinical management. Orthodontic forces lead to inflammatory responses in the periodontium, which triggers bone remodeling and eventually induces tooth movement. Mechanical forces and subsequent inflammation in the periodontium activate and sensitize periodontal nociceptors and produce orthodontic pain. Nociceptive afferents expressing transient receptor potential vanilloid subtype 1 (TRPV1) play central roles in transducing nociceptive signals, leading to transcriptional changes in the trigeminal ganglia. Nociceptive molecules, such as TRPV1, transient receptor potential ankyrin subtype 1, acid-sensing ion channel 3, and the P2X3 receptor, are believed to mediate orthodontic pain. Neuropeptides such as calcitonin gene-related peptides and substance P can also regulate orthodontic pain. While periodontal nociceptors transmit nociceptive signals to the brain, they are also known to modulate alveolar bone remodeling in periodontitis. Therefore, periodontal nociceptors and nociceptive molecules may contribute to the modulation of orthodontic tooth movement, which currently remains undetermined. Future studies are needed to better understand the fundamental mechanisms underlying neuroskeletal interactions in orthodontics to improve orthodontic treatment by developing novel methods to reduce pain and accelerate orthodontic tooth movement-thereby achieving "big gains with no pain" in clinical orthodontics.

痛觉感受器机制与正畸力导致的骨重塑:无痛苦,大收获。
正畸力与疼痛密切相关,这是佩戴正畸矫治器的患者的主要抱怨。与正畸治疗的其他副作用相比,正畸疼痛常常被忽视,临床治疗效果有限。正畸力会导致牙周炎症反应,引发骨质重塑,最终诱发牙齿移动。牙周的机械力和随后的炎症会激活牙周痛觉感受器并使其敏感,从而产生正畸疼痛。表达瞬时受体电位香草素亚型 1(TRPV1)的痛觉传入在传递痛觉信号方面发挥着核心作用,导致三叉神经节的转录变化。痛觉分子,如 TRPV1、瞬时受体电位碱亚型 1、酸感应离子通道 3 和 P2X3 受体,被认为是正畸痛的介导因素。降钙素基因相关肽和 P 物质等神经肽也可以调节正畸疼痛。牙周痛觉感受器向大脑传递痛觉信号的同时,还能调节牙周炎时牙槽骨的重塑。因此,牙周痛觉感受器和痛觉分子可能有助于调节正畸牙齿的移动,而这一点目前仍未确定。未来的研究需要更好地了解正畸中神经骨骼相互作用的基本机制,以便通过开发新型方法来减少疼痛和加速正畸牙齿移动,从而改善正畸治疗,实现临床正畸中的 "无痛大收益"。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
2.10
自引率
0.00%
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审稿时长
13 weeks
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