Ethanol binge drinking exposure affects alveolar bone quality and aggravates bone loss in experimentally-induced periodontitis

Abstract

Background Periodontitis is a multifactorial inflammatory disease of tooth supporting tissues caused by oral biofilms, influenced by environmental and genetic factors, among others. Ethanol consumption has been considered a factor that enhances alveolar bone loss, especially in high doses. The present study aims to investigate the changes promoted by ethanol binge drinking per se or associated with ligature-induced periodontal breakdown on alveolar bone loss. Materials and methods Thirty-two Wistar rats were randomly allocated into four groups: control (C), ethanol (3g/kg/day; 3 days On-4 days Off protocol by gavage for 28 days, EtOH), experimental periodontitis (EP) and experimental periodontitis plus ethanol administration (EP+EtOH). On day 14 th , periodontitis was induced by ligatures that were placed around the lower first molars. On day 28 th , the animals were euthanized and mandibles were submitted to stereomicroscopy for exposed root area analysis and micro-computed tomography (micro-CT) for the evaluation of alveolar bone loss and microstructural parameters. Results The results revealed that ligature-induced alveolar bone loss is aggravated by ethanol binge drinking compared to controls (1.06 ± 0.10 vs 0.77 ± 0.04; p<0.0001). In addition, binge drinking per se altered the alveolar bone quality and density demonstrating a reduction in trabecular thickness, trabecular number parameter and bone density percentual. Periodontal disorder plus ethanol binge drinking group also demonstrated reduction of the quality of bone measured by trabecular thickness. Conclusions In conclusion, intense and episodic ethanol intake decreased alveolar bone quality in all microstructural parameters analyzed which may be considered a modifying factor of periodontitis, intensifying the already installed disease.

Binge‐Like Exposure During Adolescence Induces Detrimental Effects in Alveolar Bone that Persist in Adulthood

“…Since the susceptibility of alveolar bone to the detrimental effect caused by EtOH seems to be particularly exacerbated during adolescence and upon repeated exposure, previous studies with different age ranges and different protocols of EtOH exposure were not able to highlight this relationship (De Souza et al, 2018; Liberman et al, 2011; Oballe et al, 2014). In fact, our previous research with a similar binge‐like protocol did not reveal additional alveolar bone loss in adult rats; however, reduced alveolar bone quality was present (Frazão et al, 2020). The findings of this study suggest that the imbalance of bone metabolism mediators induced by EtOH during adolescence was spontaneously counterbalanced only after long‐term abstinence.…”

“…Although this binge‐like EtOH protocol was used in adult subjects, with reduced alveolar bone quality, alveolar bone loss was not observed (Frazão et al, 2020). Early microstructure changes already have been reported by our group, as reduced trabecular thickness, increased trabecular separation and decreased bone volume in the alveolar bone of rats exposed to 4 cycles of binge‐like EtOH exposure (Maia et al, 2020).…”

Еxperimental justification of the efficacy of cocarnite for correction of disorders in rat periodont tissues under alcohol neuropathy

“…Точний патогенний механізм, який лежить в основі шкідливого впливу етанолу недостатньо досліджений, однак було припущено, що запальне та окислювальне ушкодження є двома важливими ланками пошкодження тканин, пов'язаних із вживанням алкоголю та ці обидві патогенетичні ланки є спільними для пародонтиту [31].…”

“…Experimental and clinical physiology and biochemistry, ECPB 2022, 1/2(94):[31][32][33][34][35][36][37] …”

Imbalance of Antioxidant-Prooxidant System in Rat's Jaw Bone Tissue Under Long-Term Introduction of Ethanol

“…Ці висновки підтверджують дослідження D. R. Frazão еt al. [7], а також de J. M. Almeida еt al. [5], які вказують на стимуляцію алкоголем остеокластогенезу за рахунок збільшення експресії ліганду рецептора ядерного фактора kB (RANK), що опосередковується виробництвом активних форм кисню.…”