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Toxicological evidence that methylmercury exposure amplifies bone destruction and systemic impact associated with apical periodontitis in rats

Daiane Claydes Baia-da-Silva; Paulo Fernando Santos Mendes; Vinicius Ruan Neves dos Santos; Deiweson Souza-Monteiro; Rayssa Maitê Farias Nazário; Leonardo Oliveira Bittencourt; Charles Miller de Souza Borges; Kelly das Graças Fernandes Dantas; Douglas Magno Guimarães; Fabricio Mezzomo Collares; Rogerio Castilho Jacinto; Rafael Rodrigues Lima
BioMetals · 2026

Abstract

This study investigated whether long-term methylmercury exposure aggravates apical periodontitis in Wistar rats. Thirty-two male rats (90 days old) were randomized into four groups (n = 8): control, methylmercury, apical periodontitis, and methylmercury + apical periodontitis. Methylmercury was administered daily by intragastric gavage (0.04 mg/kg/day) for 60 days, while apical periodontitis was induced on day 32 by pulp exposure to the oral cavity for 28 days. After euthanasia, total mercury levels and systemic oxidative stress markers were analyzed in blood; additionally, mandibles were evaluated for lesion volume and alveolar bone quality using micro-computed tomography and histological analysis. Data were analyzed using the Shapiro–Wilk test, followed by two-way ANOVA and Tukey’s post hoc test (p < 0.05). The methylmercury + apical periodontitis group showed significantly larger periapical lesions and reduced alveolar bone quality compared to non-exposed animals (p < 0.05), with decreased trabecular thickness, lower bone volume/tissue volume ratio, and increased tissue destruction. Moreover, this group exhibited more intense oxidative alterations, including reduced antioxidant defenses (reduced glutathione and total antioxidant capacity equivalent to Trolox) and increased lipid peroxidation. Therefore, under the conditions of the present experimental model, long-term methylmercury exposure preceding and overlapping with apical periodontitis development resulted in increased lesion volume, impaired alveolar bone quality, and more pronounced systemic oxidative alterations, indicating an aggravation of apical periodontitis.

Bibliographic Information

JournalBioMetals
PublisherSpringer
Publication Date2026-09-05
Publication Year2026
Document TypeJournal Article
Print ISSN0966-0844
eISSN1572-8773
DOI10.1007/s10534-026-00883-x

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NARA Access Coverage1988-01-01~Current
Journal Homepagehttps://www.springer.com/journal/10534
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