Objective: The study aimed to investigate the involvement of astrocytes in the medullary dorsal horn (MDH) in the orofacial hyperalgesia induced by experimental tooth movement (ETM) and related mechanism.
Materials and methods: Experimental tooth movement was produced with nickel-titanium alloy closed-coil spring fixed between the left maxillary first molar and the left upper incisor. Fluorocitrate was administrated through medullary subarachnoid at 3 days after ETM. Pressure pain threshold (PPT) in masseter cutaneous area was measured. The expression of glial fibrillary acidic protein (GFAP) and c-Fos in MDH was measured using immunofluoroscence staining. The expression of interleukin-1β (IL-1β) and phosphorylated N-methyl-D-aspartic acid (NMDA) receptor subunit NR1 (p-NR1) was measured with Western blotting.
Results: Experimental tooth movement-induced orofacial hyperalgesia from 1 to 9 days as the PPT was significantly reduced (P < .05). Immunofluoroscence staining showed that the expression of c-Fos in MDH was dramatically upregulated at 1 day and 3 days after ETM, while GFAP expression with both immunofluoroscence staining and Western blotting was significantly enhanced at 3 days and 7 days after ETM. Western blotting analysis indicated that the expression of IL-1β and p-NR1 in MDH was significantly enhanced at 3 days after ETM. Furthermore, we found that fluorocitrate administration at 3 days after ETM could markedly suppress the expression of c-Fos, GFAP, IL-1β and p-NR1 and attenuate the reduction of PPT induced by ETM.
Conclusion: Astrocyte activation in MDH is involved in the mechanical hyperalgesia, and the subsequent upregulated IL-1β and overexpression of p-NR1 may participate in this process.
Keywords: astrocytes; experimental tooth movement; fluorocitrate; medullary dorsal horn; orofacial hyperalgesia.
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