The contribution of autonomic mechanisms to pain in temporomandibular disorders: A narrative review

J Oral Rehabil. 2022 Nov;49(11):1115-1126. doi: 10.1111/joor.13370. Epub 2022 Sep 23.

Abstract

Background: 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.

Objectives: This narrative review examines the association between altered autonomic function and pain in TMD.

Methods: Relevant articles were identified by searching PubMed and through the reference list of those studies.

Results: 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 β2 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 β2 adrenergic receptor activation or inhibition on masticatory muscle pain. In preclinical models of temporomandibular joint arthritis, β2 adrenergic receptor activation appears to contribute to inflammation and nociception, whereas in masticatory muscle, α1 adrenergic receptor activation has been found to induce mechanical sensitisation. Some agents used to treat TMD, such as botulinum neurotoxin A, antidepressants and α2 adrenergic receptor agonists, may interact with the autonomic nervous system as part of their analgesic mechanism.

Conclusion: 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.

Keywords: adrenergic receptor; autonomic nervous system; masticatory muscle; noradrenaline; sympathetic; temporomandibular joint.

Publication types

  • Review

MeSH terms

  • Adrenergic Agonists / therapeutic use
  • Analgesics / therapeutic use
  • Antidepressive Agents / therapeutic use
  • Autonomic Nervous System
  • Botulinum Toxins, Type A* / therapeutic use
  • Clinical Trials as Topic
  • Humans
  • Pain / complications
  • Pain / drug therapy
  • Propranolol / therapeutic use
  • Receptors, Adrenergic / therapeutic use
  • Temporomandibular Joint Disorders*

Substances

  • Adrenergic Agonists
  • Analgesics
  • Antidepressive Agents
  • Receptors, Adrenergic
  • Propranolol
  • Botulinum Toxins, Type A