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Volume 54, Issue 12, Pages 1143-1150 (December 2009)


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

Xiao-Dong Liua1, Jing-Jie Wangb1, Lei Suna, Liang-Wei Chenc, Zhi-Ren Raoc, Li Duanc, Rong Caoc, Mei-Qing WangaCorresponding Author Informationemail address

Accepted 26 September 2009.

Abstract 

Objective

To investigate 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).

Design

Five groups of adult Sprague–Dawley rats (n=60) were divided into control (CON), minocycline (MIN), ETM, and 10mg/kg or 30mg/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 (30mg/kg) and METM (10mg/kg or 30mg/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 30mg/kg METM groups.

Results

Baseline 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 30mg/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.

Conclusions

These 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.

a Department of Oral Anatomy & Physiology and TMD, School of Stomatology, The Fourth Military Medical University, 145 West Changle Road, Xi’an, Shaanxi 710032, PR China

b Department of Gastroenterology, Tangdu Hospital, The Fourth Military Medical University, Xi’an, PR China

c Institute of Neurosciences, The Fourth Military Medical University, Xi’an, PR China

Corresponding Author InformationCorresponding author. Tel.: +86 29 84776144; fax: +86 29 83286858.

1 These authors contributed equally to this work.

PII: S0003-9969(09)00245-3

doi:10.1016/j.archoralbio.2009.09.006


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