Efeitos do consumo de álcool e nicotina no desenvolvimento da periodontite apical em ratos

Abstract

This study aimed to evaluate the effects of chronic alcohol and nicotine consumption, when used alone or simultaneously, on the development of induced periapical lesions in rats. Twenty-eight male Wistar rats, about 60 days old, were used in this study. Fourteen rats were exposed to consumption of alcoholic solution at 25%, while fourteen drunk only filtered water. After five weeks of adaptation to alcohol dosing, half of the animals in each group received daily intraperitoneal injection of saline solution, while the other half received daily intraperitoneal injection of nicotine solution. Seven days after the beginning of nicotine administration, the rats were anesthetized and the pulp of the left lower first molar was exposed to induce apical lesion. Twenty-eight days after pulp access the animals were euthanized and the mandible fragments were removed. Throughout the experiment, the animals were weighed, and food and water consumption were measured. The apical lesion size was measured from micro-computed tomography images, where the largest diameter, area and volume of the lesion were calculated. After histological preparation, the samples were submitted to hematoxylin and eosin staining for histopathological evaluation and immunohistochemical tests to evaluate the expression of the osteoclastic activity markers RANKL and PTHrP. Statistical analysis was submitted with a significance level of 5%. Nonparametric data were analyzed using the Kruskal-Wallis test followed by Dunn's test, while ANOVA followed by Tukey's test was performed for parametric data. The Alcohol + Nicotine group presented lesions with larger volume and area when compared to the other groups, while the Alcohol and Nicotine groups presented larger lesions than the Control group (p <0.05). There was no significant difference in the largest diameter of lesions between groups (p> 0.05). The groups that received alcohol had lower solid and liquid consumption and gained less weight when compared to the non-alcoholic groups (p <0.05). The Nicotine, Alcohol and Alcohol + Nicotine groups had higher inflammatory response scores than the control group (p <0.05). Similarly, the experimental groups showed higher immunoreaction against RANKL and PTHrP antibodies than the Control group. Acoording to the present results, alcohol or nicotine consume contributed to the exacerbation of the inflammatory response and a higher development of the perirradicular lesions. The association of both substances enhances their harmfull effects.