Background: 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). Methods: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). Results: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. Conclusion:Occlusal dental interference induced transitory orofacial discomfort by trigeminal inflammatory mediator overexpression, and TNF-α blockage attenuated these processes.

No abstract

Objective The objective of this study was to evaluate the role of nitric oxide synthase (NOS) isoforms influence during tooth movement with different forces. Settings and sample population 100 male Wistar rats (n = 10/group) were divided into a Sham group (animals not submitted to device installation nor Induced Toot Movement [ITM]), Negative Control Group (NCG) (animals submitted to device installation but not to ITM) and three experimental groups (F1, F2 and F3) (submitted to ITM with forces of 25, 50 and 100 gF respectively). Materials and methods A daily count of biting and scratching on the vibrissae and the Grimace scale were applied. After 4 (D4) and 11 (D11) days, the molar diastema was measured, and the animals were euthanized for histological (vascular parameters) and immunohistochemistry (iNOS, eNOS and nNOS) in the dental pulp. Results On D4, there was significant movement in the F3 group (P = .001) and on D11 in F1, F2 and F3 (P < .001). The number of bites (P < .001) and scratching (P = .006) was higher in F2‐F3, and F3 had higher Grimace scores (P < .001) and weight loss (P < .001). At D4, there was an increase in pulp ectasia in F2‐F3 (P = .021) and a reduction in the number of vessels in F3 (P = .005). In D4 and D11, there was a significant increase in immunostaining for iNOS and eNOS in F1 (P = .025 and P < .001 respectively) and F2 (P = .007 and P < .001 respectively). At D4, F2 and F3 showed higher immunostaining for nNOS (P = .027). Conclusion Thus, IDM induced inflammatory changes in the dental pulp reflecting in force‐dependent pain/suffering signs.