Activation of the Mesencephalic Trigeminal Nucleus Contributes to Masseter Hyperactivity Induced by Chronic Restraint Stress.

Psychological stress is commonly accepted to be closely associated with masticatory muscle disorder, which is the main symptom of temporomandibular disorder (TMD). Previous studies have confirmed that exposure to stress may cause masticatory muscle hyperactivity. However, the central mechanism underlying this process remains unclear. The mesencephalic trigeminal nucleus (Vme), which resides in the brainstem, is the primary afferent center for masticatory proprioception and plays a key role in oral-motor movements by projecting to the trigeminal motor nucleus (Vmo). Therefore, the present study was designed to examine the role of Vme neurons in masseter overactivity induced by chronic stress. We found that subjecting mice to restraint stress (6 h/day) for 14 days caused significant anxiety-like behavior, obvious masseter overactivity, and markedly enhanced electrophysiological excitability of Vme neurons. By using anterograde tract tracing combined with immunofluorescence staining methods, we observed vesicular glutamate transporter 1 (VGLUT1)-positive glutamatergic projections from the Vme to the Vmo. Moreover, chronic restraint stress (CRS) elevated the expression of VGLUT1 and choline acetyltransferase (ChAT) in Vmo. Furthermore, administration of VGLUT1-targeted short hairpin RNA (shRNA) into the bilateral Vme significantly suppressed the enhanced overexcitability of Vme neurons, downregulated the overexpression of VGLUT1 and ChAT in the Vmo, and attenuated the elevated overactivity of the masseter caused by CRS. Taken together, we showed that CRS can excite neurons in the Vme, enhancing glutamatergic excitatory projections from the Vme to the Vmo and resulting in masseter muscle overactivity. These findings provide us with a novel central mechanism underlying the correlation between psychological factors and TMD.

Mandibular distraction osteogenesis reconstructed the upper airway in a case of Melnick-Needles syndrome.

INTRODUCTION: We report a 16-year-old female with Melnick-Needles syndrome complicated with severe obstructive sleep apnea-hypoxia syndrome. CLINICAL REPORT: An overnight sleep study demonstrated that the patient had severe obstructive sleep apnea with an apnea-hypopnea index of 95/h. The lowest oxygen saturation was only 34%. The distraction osteogenesis technique was used to lengthen her mandible for the reconstruction of her upper airway. RESULT AND DISCUSSION: Postoperative panorex showed that the bilateral body of her mandible had been distracted about 16 mm singulorumly in the end of our distraction. Lateral radiograph revealed that the diameter of oral pharynx widen nearly 5 mm. The patient recovered after the upper airway reconstruction.