European journal of oral sciences
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This study tested the effect of short-term tooth-clenching on corticomotor excitability of the masseter muscle using transcranial magnetic stimulation (TMS). Fifteen subjects with normal stomatognathic function participated. All subjects performed a tooth-clenching task (TCT) on five consecutive days. ⋯ Masseter muscle MEPs were dependent on stimulus intensity and on session, whereas FDI muscle MEPs were only dependent on stimulus intensity. Post-hoc Tukey tests demonstrated significantly higher masseter muscle MEPs post-task on day 5 with 80 and 90% stimulus intensity and above when compared with pre- and post-task day 1 values. Our results suggest that the performance of repeated TCTs can trigger neuroplastic changes in the corticomotor control of the jaw-closing muscles and that such neuroplastic changes may contribute to the mechanism underlying the clinical manifestations of tooth clenching.
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Comparative Study
Chemokine CCL2 up-regulated in the medullary dorsal horn astrocytes contributes to nocifensive behaviors induced by experimental tooth movement.
To test the hypothesis that the astrocytic chemokine (C-C motif) ligand 2 (CCL2) plays an important role in nocifensive behaviors after experimental tooth movement (ETM), the expression and cellular localization of CCL2 and astrocyte activation in the medullary dorsal horn (MDH) were determined by immunohistochemistry in rats. The dose-dependent effects of intrathecal C-C chemokine receptor type 2 (CCR2) antagonists on these changes in nocifensive behaviors were evaluated. Exogenous CCL2 was added to medullary dorsal horn slices to evaluate its contributory role in the induction of extracellular signal-regulated kinase (ERK) activation ex vivo. ⋯ In addition, application of recombinant CCL2 led to ERK activation, which could be attenuated effectively by pretreatment with CCL2-neutralizing antibody ex vivo. The magnitude of the nocifensive behavior could be reduced by medullary CCR2 antagonists in a dose-dependent manner. Therefore, the astrocytic CCL2 is actively involved in the development and maintenance of tooth-movement pain and thus may be a potential target for analgesics in orthodontic nocifensive responses control.