Abstract
Patients with muscular temporomandibular disorder (TMD) present with abnormal oxygenation of the jaw muscles. Nonetheless, the deoxygenation pattern of jaw muscles of healthy subjects with frequent wake-time tooth-clenching episodes, who are at greater risk for TMD, has never been investigated. This case-control study compared the deoxygenation of the masseter during standardized tasks between TMD-free individuals with frequent self-reports of wake-time clenching and those with infrequent self-reports. University students (N = 255) filled out the Oral Behavior Checklist. Fourteen females with high versus low scores—high parafunctional (HP) group (n = 7, ≥80th percentile of score distribution) versus low parafunctional (LP) group (n = 7, ≤20th percentile)—completed 2 sessions during which they clenched at their maximum voluntary contraction (MVC) for 2 min and at 10% to 20% MVC for 20 min. Tissue oxygen saturation (StO2) and changes in oxygenated hemoglobin, deoxygenated hemoglobin, and total hemoglobin of the masseter were measured via near-infrared spectroscopy and analyzed with a generalized mixed effect model. A significant interaction effect (task × study group) was found on all outcome measures, indicating that the deoxygenation pattern of the HP group differed from the LP group (all P < 0.001). MVC of the masseter induced an almost 5-times-greater reduction of StO2 in the HP group as compared with the LP group (P = 0.023). However, the relative increase in StO2 at rest after the MVC was similar between groups (P > 0.05). At the end of the prolonged MVC task (10% to 20%), the blood flow (change in total hemoglobin) was almost 6 times higher in the LP group as compared with baseline. On the contrary, it increased minimally in the HP group (all P < 0.001). Healthy individuals at risk for TMD have abnormalities in masseter deoxygenation. Future prospective studies are needed to test whether this contributes to the onset of muscular TMD.
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