High-intensity ethanol binge drinking accentuates bone damage in induced apical periodontitis in rats.

This study aimed to evaluate the effects of excessive and episodic consumption of ethanol (EtOH, a high-intensity drinking manner) on induced apical periodontitis in rats. Thirty-two animals were divided into the following four groups: control, EtOH, apical periodontitis, and EtOH + apical periodontitis. Ethanol exposure (3 g/kg 20 % w/v EtOH) was performed by orogastric gavage for 3 consecutive days, followed by 4 days of withdrawal for 4 weeks. Lesions were induced by exposing the dental pulp of the lower first molar and by the absence of any treatment/curative for 28 days. Finally, the animals were euthanized, and mandibles were collected. The mandible was divided medially, with one hemimandible being used for micro-computed tomography analysis of the volume of the periapical lesion and bone quality parameters, such as bone volume and trabecular bone assessments; the other hemimandible was used for histological analysis, with a descriptive histopathological analysis of the tissue and the pattern of bone loss presented, as well as an assessment of the collagen content present. The data were subjected to statistical analysis (one-way analysis of variance with Tukey's post-hoc test). Our results showed that the EtOH + apical periodontitis group had a larger volume of periapical lesions than animals that were not exposed to ethanol. Additionally, bone quality parameters showed a reduction in bone volume and thickening of the trabeculae, associated with increased tissue destruction and reduced collagen content in the remnant region of the alveolar bone. These results suggest that exposure to EtOH in a pattern of excessive alcohol consumption is an aggravating factor in apical periodontitis and, consequently, in its progression, the quality and quantity of the alveolar bone remaining in the region of the periapical lesion are the modulating aspects.