Dessem Dean, Lovering Richard M
Department of Neural and Pain Sciences, University of Maryland, 650 West Baltimore Street, Baltimore, MD 21201, USA.
Pain Res Treat. 2011;2011:647967. doi: 10.1155/2011/647967. Epub 2011 Jun 12.
skeletal muscles sustain a significant loss of maximal contractile force after injury, but terminally damaged fibers can eventually be replaced by the growth of new muscle (regeneration), with full restoration of contractile force over time. After a second injury, limb muscles exhibit a smaller reduction in maximal force and reduced inflammation compared with that after the initial injury (i.e., repeated bout effect). In contrast, masticatory muscles exhibit diminished regeneration and persistent fibrosis, after a single injury; following a second injury, plasma extravasation is greater than after a single injury and maximal force is decreased more than after the initial injury. Thus, masticatory muscles do not exhibit a repeated bout effect and are instead increasingly damaged by repeated injury. We propose that the impaired ability of masticatory muscles to regenerate contributes to chronic muscle pain by leading to an accumulation of tissue damage, fibrosis, and a persistent elevation and prolonged membrane translocation of nociceptive channels such as P2X(3) as well as enhanced expression of neuropeptides including CGRP within primary afferent neurons. These transformations prime primary afferent neurons for enhanced responsiveness upon subsequent injury thus triggering and/or exacerbating chronic muscle pain.
骨骼肌在受伤后会显著丧失最大收缩力，但终末受损的纤维最终可被新肌肉的生长（再生）所替代，随着时间的推移收缩力会完全恢复。在第二次受伤后，与初次受伤相比，肢体肌肉的最大力量下降较小，炎症也有所减轻（即重复刺激效应）。相比之下，咀嚼肌在单次受伤后再生能力减弱且纤维化持续存在；在第二次受伤后，血浆外渗比单次受伤后更严重，最大力量下降也比初次受伤后更多。因此，咀嚼肌不表现出重复刺激效应，反而会因重复受伤而日益受损。我们认为，咀嚼肌再生能力受损会导致组织损伤、纤维化的积累，以及伤害性通道（如P2X(3)）的持续升高和长时间膜转位，同时初级传入神经元中包括降钙素基因相关肽在内的神经肽表达增强，从而导致慢性肌肉疼痛。这些变化使初级传入神经元在后续受伤时反应性增强，从而引发和/或加剧慢性肌肉疼痛。
