OBJECTIVE

Chronic pain may result both from a generalized hypersensitivity to acute pain, suggestive of central sensitization processes, and dysfunction of the endogenous pain regulatory system. One purpose of this study was to compare experimental pain sensitivity at several anatomic sites in temporomandibular disorder (TMD) patients and pain-free controls during baseline and after standardized mechanical load of the orofacial region. A second purpose was to compare the pain-modulating effects of cardiovascular responses in TMD patients and pain-free controls.

METHODS

Experimental pain was induced by electrocutaneous stimulation of the dorsal left hand and pressure algometry at the right masseter muscle and the sternum. The pain sensitivity of the orofacial region was manipulated by isometric contraction of the masseter muscles. Elevations of mean arterial pressure and heart rate were induced by a simulated job interview.

RESULTS

At baseline, the TMD patients exhibited a significantly higher electrocutaneous pain threshold. Relative to the healthy controls, the TMD patients reported increased electrocutaneous and pressure pain sensitivity after isometric contraction of the orofacial region. In addition, there were correlations between mean arterial pressure and pain sensitivity in the TMD group only.

DISCUSSION

Significant increases in generalized pain sensitivity occurred in the TMD group, but not in the control group, after isometric contraction of the orofacial muscles, suggestive of a central sensitization process in TMD. Moreover, only in the TMD group there were significant associations between cardiovascular responsesand pain sensitivity, challenging previous assumptions of this relationship occurring mainly in pain-free individuals.