Tumor necrosis factor alpha mediates orofacial discomfort in an occlusal dental interference model in rats: The role of trigeminal ganglion inflammation.

<bold>Background: </bold>Tumor necrosis factor alpha (TNF-α) is a proinflammatory cytokine that plays an important role in the early stages of inflammation. In this study, we investigated its role in orofacial discomfort in rats subjected to occlusal dental interference (ODI).<bold>Methods: </bold>Female Wistar rats (180-200 g) were divided in three groups (n = 30/group): sham group, without ODI, and two experimental groups with ODI pre-treated with 0.1 mL/kg saline (ODI + SAL) or 5 mg/kg infliximab (ODI + INF) and treated every 3 days. The animals were euthanized after 1, 3, and 7 days. The number of bites and scratches and grimace scale scores were determined daily, and the bilateral trigeminal ganglion was histomorphometrically (neuronal body area) analyzed and submitted for immunohistochemistry for TNF-α, nitric oxide synthesis (NOS) neuronal (nNOS) and inducible (iNOS), peroxisome proliferator-activated receptors (PPAR) y (PPARy) and δ/β (PPARδ/β), and glial fibrillary acidic protein (GFAP). One-way/two-way ANOVA/Bonferroni tests were used (P < .05, GraphPad Prism 5.0).<bold>Results: </bold>ODI + SAL showed a large number of bites (P = .002), scratches (P = .002), and grimace scores (P < .001) in the firsts days, and ODI + INF partially reduced these parameters. The contralateral and ipsilateral neuronal body area was significantly reduced on day 1 in ODI + SAL, but returned to the basal size on days 3 and 7, by increase in TNF-α, nNOS, PPARy, PPARδ/β, and GFAP immunostaining. The infliximab treatment attenuated these alterations (P < .05). There was no iNOS immunostaining.<bold>Conclusion: </bold>Occlusal dental interference induced transitory orofacial discomfort by trigeminal inflammatory mediator overexpression, and TNF-α blockage attenuated these processes. [ABSTRACT FROM AUTHOR]