α1 adrenergic receptor activation has a dynamic effect on masticatory muscle afferent fibers

Benbow, Tarique; Ekbatan, Maryam Ranjbar; Cairns, Brian E.

doi:10.1016/j.neuropharm.2020.108197

Cited by 5 publications

(14 citation statements)

References 39 publications

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“…45,67 However, activation of α 1 receptors expressed by slowly conducting (Aδ and C fibres), putatively nociceptive afferent fibres results in mechanical sensitisation. 45 Approximately 40% of trigeminal ganglion neurons are thought to express α 2a or α 2c adrenergic receptors. 68,69 In vitro, application of clonidine, an α 2 adrenergic receptor agonist, to trigeminal ganglion neurons results in their hyperpolarisation.…”

Section: It Has Been Shown That the Duration Of Nocifensive Behaviour...mentioning

confidence: 99%

“…In theory, spillover of noradrenaline could act on white blood cells through the β 2 receptor to alter release of inflammatory mediators, or directly through activation of α 1 adrenergic receptors found on the endings of the sensory afferent fibres to induce sensitisation. 45,70 These mechanisms may allow an interaction between the sensory and autonomic nervous systems that modulate pain input. IL, interleukin; TNFα, tumour necrosis alpha; WBC, white blood cell noradrenaline, adrenaline, dopamine, and serotonin both in the central nervous system and in the periphery.…”

Section: Biogenic Amine Metabolism and Nociceptionmentioning

confidence: 99%

“…In the temporomandibular joint, both sympathetic and parasympathetic fibres are most often found near blood vessels where many sensory afferent fibres are also located 42 . In the masseter muscle, sensory afferent fibres from the trigeminal ganglia, and in the case of spindle afferents, the mesencephalic ganglia, innervate the masseter and temporalis muscles 44–47 . Sympathetic efferent fibres from the superior cervical ganglion and parasympathetic efferent fibres from the otic ganglion primarily innervate muscle blood vessels 48–50 .…”

Section: Pharmacological Evidencementioning

confidence: 99%

“…Activation of α 1 receptors on dorsal root ganglion neurons results in neuronal depolarisation 66 . Masseter muscle spindle afferent fibres and faster conducting mechanoreceptors exhibit decreased mechanical sensitivity in response to activation of α 1 receptors 45,67 . However, activation of α 1 receptors expressed by slowly conducting (Aδ and C fibres), putatively nociceptive afferent fibres results in mechanical sensitisation 45 .…”

Section: Pharmacological Evidencementioning

confidence: 99%

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

Cairns

2022

J of Oral Rehabilitation

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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.

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Section: It Has Been Shown That the Duration Of Nocifensive Behaviour...mentioning

confidence: 99%

Section: Biogenic Amine Metabolism and Nociceptionmentioning

confidence: 99%

Section: Pharmacological Evidencementioning

confidence: 99%

Section: Pharmacological Evidencementioning

confidence: 99%

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

Cairns

2022

J of Oral Rehabilitation

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“…That is, sympathetic nervous system innervation of muscle spindles has been reported in humans (Radovanovic et al 2015) and animals (Bombardi et al 2006). Animal models have shown sympathetic activity can modulate jaw muscle spindle and LTMR sensitivity (Roatta et al 2002; Benbow et al 2020) and potentiate the excitatory effects of glutaminergic neurotransmission to enhance the gain of trigeminal motor output (Schwarz et al 2014). In humans, nocturnal ultradian cycling of ANS activity was correlated with jaw muscle duty factors (Iwasaki et al 2019).…”

Section: Discussionmentioning

confidence: 99%

Chronic Pain–Related Jaw Muscle Motor Load and Sensory Processing

Nickel

Gonzalez

et al. 2022

J Dent Res

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Chronic pain associated with temporomandibular disorders (TMDs) may reflect muscle mechanoreceptor afferent barrage and dysregulated sensory processing. This observational study tested for associations between Characteristic Pain Intensity (CPI), physical symptoms (Patient Health Questionnaire–15 [PHQ-15]), and cumulative jaw muscle motor load (mV*s). In accordance with institutional review board oversight and Strengthening the Reporting of Observational Studies in Epidemiology guidelines, adult subjects gave informed consent and were identified via Diagnostic Criteria for TMD (DC-TMD) examination and research protocols. Subjects were assigned to ±Pain groups using DC-TMD criteria for myalgia. CPI scores characterized pain intensity. PHQ-15 scores were surrogate measures of dysregulated sensory processing. Laboratory tests were performed to quantify masseter and temporalis muscle activities (mV) per bite force (N) for each subject. In their natural environments, subjects recorded day- and nighttime electromyography from which cumulative jaw muscle motor loads (mV*s) were determined for activities consistent with bite forces of >1 to ≤2 and >2 to ≤5 N. Data were assessed using univariate analysis of variance, simple effects tests, K-means cluster classification, and 3-dimensional regression analyses. Of 242 individuals screened, 144 enrolled, and 125 with complete data from study protocols, there were 35 females and 15 males for +Pain and 35 females and 40 males for −Pain. Subjects produced 324 daytime and 341 nighttime recordings of average duration 6.9 ± 1.7 and 7.6 ± 1.7 h, respectively. Overall, +Pain compared to −Pain subjects had significantly higher (all P ≤ 0.002) CPI and PHQ-15 scores. Cumulative jaw muscle motor loads showed significant between-subject effects for time, diagnostic group, and sex (all P < 0.003), where motor loads tended to be higher for daytime versus nighttime, +Pain versus −Pain groups, and males versus females. Two clusters were identified, and regression relations showed associations of low-magnitude daytime masseter motor load, PHQ-15, and CPI scores for cluster 1 ( n = 105, R2 = 0.44) and cluster 2 ( n = 18, R2 = 0.80). Furthermore, these regression relations showed thresholds of motor load and PHQ-15 scores, above which there were nonlinear increases in reported pain.

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