Proprioceptive mechanisms in occlusion‐stimulated masseter hypercontraction

Abstract

Neurons in the trigeminal mesencephalic nucleus (Vme) have an axon that branches peripherally to innervate the orofacial region and projects centrally to the trigeminal motor nucleus (Vmo). They function as the primary neurons conveying proprioceptive messages. The present study aimed to demonstrate the presence of a periodontal-Vme-Vmo circuit and to provide evidence for its involvement in an experimental unilateral anterior crossbite (UAC) model, which can induce osteoarthritis in the temporomandibular joint. Cholera toxin B subunit (CTb) was injected into the inferior alveolar nerve of rats to help identify the central axon terminals of Vme neurons in the Vmo. The levels of vesicular glutamate transporter 1 (VGLUT1) expressed in the periodontal region, Vme, Vmo, and masseter, and the level of acetylcholinesterase (AChE) expressed in the masseter, were assessed in UAC rats and controls. In CTb-treated rats, many CTb-labeled cell bodies and endings were identified in the Vme and in the Vmo, respectively. In UAC rats, VGLUT1 was expressed at a statistically significantly higher level in the periodontal ligament, Vme, Vmo, and masseter than it was in control rats. The level of AChE protein was 1.97 times higher in UAC rat masseter compared with control rat masseter. These findings reveal a trigeminal mechanism underlying masseter hyperactivity induced by an altered occlusion.

Dental malocclusion stimulates neuromuscular circuits associated with temporomandibular disorders

“…To explore the effect of occlusion on the TMJ and on neuromuscular function, we designed a rodent model for acute malocclusion involving UAC. Using this animal model we confirmed previous observations of an effect of dental malocclusion on the TMJ and on the multi‐motor nuclei via Vme . In our previous study , we injected cholera toxin B subunit (CTb) into the inferior alveolar nerve, which innervates the mandibular teeth.…”

“…The remaining 24 rats were randomly assigned to a control or a UAC experimental group and analyzed at 2 time points in the study (8 wk and 12 wk, n = 6/group). The UAC model was achieved using a pair of metal tubes adhering to the left incisors to create a crossbite, as reported previously . Briefly, a section of a metal tube (length 2.5 mm; inside diameter 3 mm) was bonded to the left maxillary incisor, and a curved section of a metal tube (length 4.5 mm; inside diameter 3.5 mm) was bonded to the left mandibular incisor.…”

“…No prosthesis fell off during the experimental period. The UAC was kept on until sampling scarification at the end of weeks 8 and 12, at which time‐points osteoarthritic lesions in TMJ and hyperactivation of the masseter were elicited .…”

“…Recently, we developed an animal model of dental malocclusion by creating unilateral anterior crossbite (UAC) in rats . We observed masseter hyperactivity in rats with UAC and demonstrated mechanisms involving the periodontal trigeminal mesencephalic nucleus (Vme)–trigeminal motor nucleus (Vmo) jaw closing muscles circuit . The cell bodies of the primary sensory neurons in Vme reside in the brainstem.…”

Prevalence of gingival recession after orthodontic treatment of infraversion and open bite

“…However, changes in gingival tissue are less well described [16–18]. Questions remain regarding the factors associated with an increase of gingival recession rate after orthodontic treatment.…”