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Proprioceptive mechanisms in occlusion‐stimulated masseter hypercontraction
Author(s) -
Liu Xin,
Zhang Chunkui,
Wang Dongmei,
Zhang Hongyun,
Liu Xiaodong,
Li Jinlian,
Wang Meiqing
Publication year - 2017
Publication title -
european journal of oral sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.802
H-Index - 93
eISSN - 1600-0722
pISSN - 0909-8836
DOI - 10.1111/eos.12331
Subject(s) - masseter muscle , spinal trigeminal nucleus , medicine , trigeminal nerve , periodontal fiber , proprioception , inferior alveolar nerve , axon , neuroscience , anatomy , biology , nociception , dentistry , receptor , physical medicine and rehabilitation , molar
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 ( CT b) 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 ( VGLUT 1) 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 CT b‐treated rats, many CT b‐labeled cell bodies and endings were identified in the Vme and in the Vmo, respectively. In UAC rats, VGLUT 1 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.