Abstract
The purpose of the present review is to correlate recent knowledge of the role of peripheral ionotropic glutamate receptors in the temporomandibular joint and muscle pain from animal and human experimental pain models with findings in patients. Chronic pain is common, and many people suffer from chronic pain conditions involving deep craniofacial tissues such as temporomandibular disorders or fibromyalgia. Animal and human studies have indicated that the activation of peripheral ionotropic glutamate receptors in deep craniofacial tissues may contribute to muscle and temporomandibular joint pain and that sex differences in the activation of glutamate receptors may be involved in the female predominance in temporomandibular disorders and fibromyalgia. A peripheral mechanism involving autocrine and/or paracrine regulation of nociceptive neuronal excitability via injury or inflammation-induced release of glutamate into peripheral tissues that may contribute to the development of craniofacial pain is proposed.
Highlights
It is possible that under certain conditions, such as in the presence of temporomandibular disorders (TMD), an increase in peripheral levels of glutamate in craniofacial tissues activates peripheral excitatory amino acid (EAA) receptors, a process that can modify the excitability of trigeminal afferent fibres and evoke nociception
Animal and human studies have indicated that the activation of peripheral ionotropic glutamate receptors in deep craniofacial tissues may contribute to muscle and temporomandibular joint pain and that sex differences in the activation of glutamate receptors may be involved in the female predominance in temporomandibular disorders and fibromyalgia
We have found that activation of peripheral excitatory amino acid (EAA) receptors by injection of the EAA glutamate into the temporomandibular joint (TMJ) or craniofacial muscles excites nociceptive afferent fibres and evokes jaw muscle electromyographic (EMG) activity similar to that produced by the injection of inflammatory algesic chemicals, but does not result in any signs of inflammation in these tissues [14,15,16,17,18,19,20,21,22]
Summary
It is possible that under certain conditions, such as in the presence of TMD, an increase in peripheral levels of glutamate in craniofacial tissues activates peripheral EAA receptors, a process that can modify the excitability of trigeminal afferent fibres and evoke nociception. The authors first documented that capsaicin injected into the rat TMJ or craniofacial muscles produces an inflammatory response [92], evokes activity and peripheral sensitization in small-diameter, mechanosensitive fibres [21,22], induces a dose-dependent reflex increase in jaw muscle EMG activity [74] and evokes central sensitization in brainstem nociceptive neurons [86,93].
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