Efeito do consumo crônico de álcool na lesão periapical induzida em ratos
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Data
2017-07-10
Autores
Dal Fabbro, Renan [UNESP]
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Universidade Estadual Paulista (Unesp)
Resumo
Objetivo: analisar o efeito do consumo crônico de álcool no desenvolvimento da lesão periapical. Material e métodos: Trinta e dois ratos foram divididos em 4 grupos: Controle (C): sem periodontite apical (PA) e dieta não alcoólica (DNA); (AL): sem PA e dieta alcoólica (DA); (AP): com PA e DNA; (AP+AL): com PA e DA. Solução alcoólica à 20% foi fornecida aos grupos AL e AP+AL como única fonte de hidratação por todo experimento. A PA foi induzida nos primeiros molares inferiores esquerdos ao final da 4a semana de administração da dieta alcoólica. Alterações de peso, e quantidade de alimentos sólidos e líquidos foram tabulados ao longo das 8 semanas. Ao final deste período, os animais foram eutanaziados e as mandíbulas removidas para análise da densidade óssea seguida do processamento histológico para histomorfometria, bem como análise por imunohistoquímica da expressão das proteínas RANKL, OPG, TRAP, HIF-1α e ALP. As comparações múltiplas dos resultados foram realizadas por análise de variância seguida pelo teste de Tukey. Para dados não paramétricos foi utilizado o teste de Mann-Whitney nas comparações CvsAL e APvsAP+AL. O nível de significância utilizado foi de p<0,05. Resultados: animais que receberam a dieta alcoólica tiveram um ganho de peso inferior aos dos outros grupos p<0,05. A área da região periapical não foi influenciada pela administração da solução alcoólica, entretanto, o infiltrado inflamatório foi mais intenso em AP+AL comparado à AP p<0,05. Análise radiográfica mostrou diferença apenas entre os grupos com e sem PA. O grupo AP+AL mostrou os maiores valores para indicadores de osteoclastogênese TRAP, HIF-1α e RANKL p<0,05. Conclusão: A dieta alcoólica exerceu efeito significativo na severidade da periodontite apical, exacerbando a resposta inflamatória e a osteoclastogênese.
Aim: evaluate the effect of chronic alcohol consumption on the periapical lesion. Material and methods: Thirty-two rats were divided into 4 groups: Control (C): without apical periodontitis (AP) and non-alcoholic diet (NDA); (AL): without AP and alcoholic diet (AD); (AP): with AP and NDA; (AP + AL): with AP and AD. Alcoholic solution at 20% was given to the AL and AP+AL groups as the sole source of hydration throughout the experiment. AP was induced in the lower left first molars at the end of the 4th week. Changes in weight, and amount of solid and liquid foods were recorded over 8 weeks. At the end of this period, the animals were euthanized and the jaws removed for of x-ray bone density analysis followed by histological processing for histomorphometry, as well as immunohistochemical analysis for RANKL, OPG, TRAP, HIF-1α and alkaline phosphatase. Multiple comparisons of results were performed by analysis of variance followed by the Tukey test. For non-parametric data the Mann-Whitney test was used in the comparisons CvsAL and APvsAP+AL. The level of significance was set at p <0.05. Results: animals that received alcoholic diet had a weight gain lower than the other groups p <0.05. The periapical region area was not influenced by the administration of the alcohol solution, however, the inflammatory infiltrate was higher in AP+AL compared to the AP p <0.05. Radiographic analysis showed difference only in the comparisons between the groups with and without apical periodontitis. The AP+AL group showed the highest values for osteoclastogenesis markers TRAP, HIF-1α and RANKL p <0.05. Conclusion: Alcoholic diet had a significant effect on the severity of apical periodontitis, exacerbating the inflammatory response and osteoclastogenesis.
Aim: evaluate the effect of chronic alcohol consumption on the periapical lesion. Material and methods: Thirty-two rats were divided into 4 groups: Control (C): without apical periodontitis (AP) and non-alcoholic diet (NDA); (AL): without AP and alcoholic diet (AD); (AP): with AP and NDA; (AP + AL): with AP and AD. Alcoholic solution at 20% was given to the AL and AP+AL groups as the sole source of hydration throughout the experiment. AP was induced in the lower left first molars at the end of the 4th week. Changes in weight, and amount of solid and liquid foods were recorded over 8 weeks. At the end of this period, the animals were euthanized and the jaws removed for of x-ray bone density analysis followed by histological processing for histomorphometry, as well as immunohistochemical analysis for RANKL, OPG, TRAP, HIF-1α and alkaline phosphatase. Multiple comparisons of results were performed by analysis of variance followed by the Tukey test. For non-parametric data the Mann-Whitney test was used in the comparisons CvsAL and APvsAP+AL. The level of significance was set at p <0.05. Results: animals that received alcoholic diet had a weight gain lower than the other groups p <0.05. The periapical region area was not influenced by the administration of the alcohol solution, however, the inflammatory infiltrate was higher in AP+AL compared to the AP p <0.05. Radiographic analysis showed difference only in the comparisons between the groups with and without apical periodontitis. The AP+AL group showed the highest values for osteoclastogenesis markers TRAP, HIF-1α and RANKL p <0.05. Conclusion: Alcoholic diet had a significant effect on the severity of apical periodontitis, exacerbating the inflammatory response and osteoclastogenesis.
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Palavras-chave
Periodontite periapical, Alcoolismo, Endodontia, Apical periodontitis, Alcoholism, Endodontics