نبذة مختصرة : During tooth eruption, a complex cascade of cellular and molecular events occurs to promote the degradation of the lamina propria and bone located in the eruptive pathway. Tumor necrosis factor alpha (TNF-α) and interleukin-1 (IL-1) are cytokines involved in osteoclastogenesis and activation of matrix metalloproteinases (MMPs). The purpose of this study was to evaluate whether infliximab (TNF-α blocker) and diacerein (IL-1 synthesis inhibitor) interfere in the eruptive process, and in the osteoclastogenesis as well as in the degradation of the lamina propria during the tooth eruption in rat. One hundred and eight rats at 6 and 12 days of age were distributed in 4 groups (n = 27 rats per group): CG (control group) – physiological saline; DIAG -100 mg/kg/day diacerein (anti-IL-1 - Artrodar® - TRB Pharma Industry Chemical and Pharmaceutical Ltd.); INFG - 5mg/kg/day of infliximab (anti-TNF-α - Remicade® - Janssen Biotec.); INF+DIAG - 5mg/kg/day of infliximab + 100mg/kg/day of diacerein. Rats at 6 days of age received treatment for 3 and 5 days; rats at 12 days of age were treated for 4 days. After 24 hours of the last dose, the rats were sacrificed. Fragments of the oral mucosa were frozen for detection of TNF-α and IL-1β by western blot. Fragments of maxilla containing the first molar were fixed, decalcified and embedded in paraffin for light microscopy. Sections containing the eruptive pathway of first molar were stained with HE for morphological analysis. Some sections were submitted to immunohistochemical reactions for detection of TNF-α, IL-1, IL-6, receptor activator of nuclear factor kappa-Β ligand (RANKL), osteoprotegerin (OPG), MMP-1 and MMP-9. The number of immunolabelled cells for IL-1, IL-6, MMP-1 and MMP-9 in the lamina propria was computed while the number of RANKL- and OPG-positive cells was obtained on the bone surface. Some sections were submitted to the histochemical reaction for tartrate-resistant acid phosphatase (TRAP), and the number of TRAP-positive osteoclasts on the bone surface was ...
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