Involvement of medullary dorsal horn glial cell activation in mediation of masseter mechanical allodynia induced by experimental tooth movement

Objective estigate the involvement of microglial and astrocytic activation in the medullary dorsal horn (MDH) during the mediation of masseter area allodynia induced by experimental tooth movement (ETM). roups of adult Sprague–Dawley rats (n = 60) were divided into control (CON), minocycline (MIN), ETM, and 10 mg/kg or 30 mg/kg MIN plus ETM (METM) groups. The upper-first-molar was moved mesially for rats in ETM and METM groups. Rats were pre-injected with minocycline in the MIN (30 mg/kg) and METM (10 mg/kg or 30 mg/kg) groups. Pressure pain threshold (PPT) in masseter area was tested from day 0 to 14 for all 5 groups. Immunohistochemistry against OX42 (microglial marker) or GFAP (astrocytic maker) in the MDH was examined at days 1, 3, 7 and 14 for CON, MIN and 30 mg/kg METM groups. s ne PPT was expectedly seen in either CON or MIN groups, masseter mechanical allodynia was detected in the ETM group from day 4 to 13 (P < 0.05). OX42 expression level at days 1, 3 and 7, and GFAP expression level at days 3, 7 and 14 were higher in ETM (P < 0.05), but not in 30 mg/kg METM, than in CON group. Minocycline reduced activation of microglia and astrocytes, and significantly attenuated the development of masseter mechanical allodynia in this model. sions results indicate that mechanical allodynia in the masseter area induced by ETM can be attenuated by minocycline. Activation of microglia, possibly together with subsequent activation of astrocytes, seems to contribute to masseter mechanical allodynia.