The exact pathophysiology of TMD pain is not known, given the fact that multiple factors related to anatomical, psychological-psychosocial, and neurobiological components seem to be involved.22 Thus, on a population basis, TMD may still be viewed as multifactorial conditions, which in the individual patient actually means an idiopathic pain condition.11,23

One of the most prominent features of painful TMDs is the report of pain on palpation of jaw muscles or TMJ. Several studies have, indeed, reported lower pressure pain thresholds in the jaw muscles of patients with TMD pain compared to normal subjects.24,25,26,27 The pathophy-siological mechanism responsible for lower pain thresholds in deep tissues could be a sensitization of peripheral nociceptors. Animal data have documented that deep noxious inputs cause sensitization of the peripheral receptors.28,29 Thus, endogenous substances released by tissue trauma such as bradykinin, serotonin, pros-taglandins, adrenaline, and hypoxia, in addition to the excitatory amino acid glutamate, lower the mechanical threshold of nociceptors into the innocuous range making weak stimuli able to excite nociceptors and elicit

pain. 31^2

Patients with myofascial TMD pain have also been found to have hyperalgesic responses to segmental, as well as extrasegmental, application of thermal heat, although this may less often be a clinical problem.27 Temporal summation mechanisms and wind-up phenomena in central neurons could be strongly related to the development of central hyperexcitability.33,34 This indicates that patients with persistent TMD pain are in a state of generalized central hyperexcitability. Dysfunction of the nociceptive system is also implicated by the finding of suppression of cortical responses and brain stem reflexes elicited by painful laser stimulation of the skin in TMD patients.35 Furthermore, ischemic pain models have been used to demonstrate a less effective activation of endogenous pain-inhibitory systems in TMD patients.36 In particular, female TMD patients appear unable to effectively engage the normal pain-inhibitory systems37 and it has been suggested that opioid receptor desensitization and/or down-regulation could be involved.38 Catechol-O-methyl transferase (COMT) activity has been linked to experimental pain sensitivity, and it appears that the three major haplotypes which determine COMT activity in humans are inversely correlated with pain sensitivity and the risk of developing TMD.39,40 Recently, variations in the adrenergic receptor beta (2) (ADRB2) has also been suggested to be a genetic risk factor for the development of TMD pain.41,42 Taken together, the pain studies cited above suggest that a more generalized state of neuronal hyperexcitability is likely to play an important role in TMD patients.43 Thus, peripheral sensitization of deep craniofacial tissues alone may not be adequate to explain persistent TMD pain.

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