Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, British Columbia, Canada.
J Oral Rehabil. 2022 Nov;49(11):1115-1126. doi: 10.1111/joor.13370. Epub 2022 Sep 23.
Temporomandibular disorders (TMD) are diagnosed based on symptom presentation and, like other functional pain disorders, often lack definitive pathology. There is a strong association between elevated stress levels and the severity of TMD-related pain, which suggests that alterations in autonomic tone may contribute to this pain condition.
This narrative review examines the association between altered autonomic function and pain in TMD.
Relevant articles were identified by searching PubMed and through the reference list of those studies.
TMD sufferers report an increased incidence of orthostatic hypotension. As in other chronic musculoskeletal pain conditions, TMD is associated with increased sympathetic tone, diminished baroreceptor reflex sensitivity and decreased parasympathetic tone. It remains to be determined whether ongoing pain drives these autonomic changes and/or is exacerbated by them. To examine whether increased sympathetic tone contributes to TMD-related pain through β adrenergic receptor activation, clinical trials with the beta blocker propranolol have been undertaken. Although evidence from small studies suggested propranolol reduced TMD-related pain, a larger clinical trial did not find a significant effect of propranolol treatment. This is consistent with human experimental pain studies that were unable to demonstrate an effect of β adrenergic receptor activation or inhibition on masticatory muscle pain. In preclinical models of temporomandibular joint arthritis, β adrenergic receptor activation appears to contribute to inflammation and nociception, whereas in masticatory muscle, α adrenergic receptor activation has been found to induce mechanical sensitisation. Some agents used to treat TMD, such as botulinum neurotoxin A, antidepressants and α adrenergic receptor agonists, may interact with the autonomic nervous system as part of their analgesic mechanism.
Even if dysautonomia turns out to be a consequence rather than a causative factor of painful TMD, the study of its role has opened up a greater understanding of the pathogenesis of this condition.
颞下颌关节紊乱（TMD）是根据症状表现来诊断的，与其他功能性疼痛疾病一样，通常缺乏明确的病理。压力水平升高与 TMD 相关疼痛的严重程度之间存在很强的关联，这表明自主神经张力的改变可能导致这种疼痛状况。
本文综述了自主神经功能改变与 TMD 相关疼痛之间的关系。
通过在 PubMed 上搜索和参考这些研究的参考文献，确定了相关文章。
TMD 患者报告直立性低血压的发生率增加。与其他慢性肌肉骨骼疼痛疾病一样，TMD 与交感神经张力增加、压力感受器反射敏感性降低和副交感神经张力降低有关。目前尚不清楚持续疼痛是否会导致这些自主神经变化，或者它们是否会加剧疼痛。为了研究增加的交感神经张力是否通过β肾上腺素能受体激活导致 TMD 相关疼痛，已经进行了使用β受体阻滞剂普萘洛尔的临床试验。尽管来自小型研究的证据表明普萘洛尔减轻了 TMD 相关疼痛，但一项更大的临床试验并未发现普萘洛尔治疗的显著效果。这与人类实验性疼痛研究一致，这些研究未能证明β肾上腺素能受体激活或抑制对咀嚼肌疼痛的影响。在颞下颌关节关节炎的临床前模型中，β肾上腺素能受体激活似乎会导致炎症和伤害感受，而在咀嚼肌中，α肾上腺素能受体激活已被发现会引起机械敏感化。一些用于治疗 TMD 的药物，如肉毒杆菌神经毒素 A、抗抑郁药和α肾上腺素能受体激动剂，可能会作为其镇痛机制的一部分与自主神经系统相互作用。
即使自主神经功能紊乱最终被证明是 TMD 疼痛的后果而不是原因，对其作用的研究也使人们对这种疾病的发病机制有了更深入的了解。
