Contribution of Sympathetic Sensory Coupling to Craniofacial Nociception

Stress and anxiety are associated with increased pain intensity in temporomandibular disorders (TMDs) patients. It is possible that this association is due to a direct interaction between the sympathetic and sensory nervous systems. This narrative review examines evidence for a potential sympathetic sensory interaction in deep craniofacial tissues and the trigeminal ganglion. Research articles were identified using PubMed with the mesh terms adrenergic, ganglion neuron, masseter, sensory, signaling, temporomandibular and trigeminal and, subsequently, from the reference lists of those articles identified. The masticatory muscles and temporomandibular joint are innervated by sympathetic efferent fibres from the superior cervical ganglion, which primarily innervates blood vessels. As trigeminal sensory afferent fibres are often found near blood vessels, the anatomical relationship for potential sympathetic sensory coupling is present in the temporomandibular joint and masticatory muscles. Trigeminal afferent fibres express α1, α2, β1 and β2 adrenergic receptors as well as two of the four neuropeptide Y receptors. Stimulation of α1 receptors in the masticatory muscle mechanically sensitises nociceptors through a direct effect, but desensitises proprioceptors and spindle afferent fibres through an indirect effect on mechanosensitive organelles. Stimulation of β2 adrenergic receptors increases the mechanical activation threshold of masticatory muscle afferent fibres. There is also evidence that stimulation of β adrenergic receptors on immune cells contributes to nociception in temporomandibular joint arthritis. In contrast, α1 adrenergic receptor activation underlies nociception in masticatory muscle myositis. Taken together, the current research provides support for the concept that sympathetic sensory coupling could play a role in the pathogenesis of TMD-related pain.