TUMOR NECROSIS FACTOR (TNF)-α PLAYS A ROLE IN ORAL ULCERATION IN RATS

Abstract

<h3>Objectives</h3> Evaluate the role of tumor necrosis factor (TNF)-α in the healing process of oral traumatic ulcers (OTUs) in rats. <h3>Study Design</h3> The animals were randomly divided into 6 experimental groups: 1 treated intravascularly with saline solution and 5 treated with infliximab at Infliximab (INF)-1, INF-INF-3, INF-5, INF-7, or INF-10 mg/kg. The animals were euthanized on days 1, 3, 7, 14, and 21 after ulceration. The ulcers were clinically measured (wound area) and the mucosa samples were histologically (scores 0-4), histomorphometrically (cell counting polymorphonuclear cells), and immunohistochemically (scores 0-3 for TNF-α and alfa-smooth muscle actin (α-SMA)) analyzed. Evans blue assay was performed to measure vascular permeability. One- and two-way analyses of variance and Kruskal-Wallis tests were performed (GraphPad Prism 5.0, <i>P</i> < .05). <h3>Results</h3> There was a reduction in the OTU area of the infliximab-treated groups (INF-5, INF-7, and INF-10) on day 1 (<i>P</i> = .043) and Evan blue extravasation (<i>P</i> = .032), polymorphonuclear cell counts (<i>P</i> = .001), and TNF-α immunostaining (<i>P</i> = .025) were significantly reduced in the dose INF-5 group compared to the saline group on the same day. In day 3, all INF-treated groups showed lower scores than the saline group (<i>P</i> = .023), but α-SMA immunostaining was reduced in day 7 in the INF-treated groups (<i>P</i> = .006). <h3>Conclusions</h3> TNF-α blockade reduced acute inflammatory process and delay wound healing in OTU.