Effect of methotrexate on alveolar bone loss in experimental periodontitis in Wistar rats

Authors

  • Giliano Nicolini Verzeletti Lutheran University of Brazil, Post-graduate Program in Dentistry, Canoas, Rio Grande do Sul, Brazil
  • Eduardo José Gaio Department of Conservative Dentistry, Federal University of Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil
  • Cassiano Kuchenbecker Rösing Lutheran University of Brazil, Post-graduate Program in Dentistry, Canoas, Rio Grande do Sul, Brazil; Department of Conservative Dentistry, Federal University of Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil

DOI:

https://doi.org/10.1080/00016350701742364

Keywords:

Cytokines, interleukin-1, periodontal disease, tumor necrosis factor

Abstract

Objective. Interleukin-1 (IL-1) and tumor necrosis factor (TNF) are pro-inflammatory cytokines directly related with tissue destruction in the pathogenesis of periodontitis. Inhibitory effects on IL-1 and TNF production have been attributed to the folate analog methotrexate. The purpose of this study was to evaluate the effect of methotrexate on the pathogenesis of alveolar bone loss in experimental periodontitis in rats. Methods. Ligature-induced experimental periodontitis was created in 44 Wistar rats. The animals were randomly divided into four groups and treated with methotrexate (0.1, 0.5, and 1.0 mg·kg−1) or saline. Morphometrical registration of alveolar bone loss was carried out after 28 days of ligature placement to determine the effect of methotrexate on the progression of experimental periodontitis. Results. Intra-group comparisons showed significantly higher alveolar bone loss mean values in maxillary sides with ligature (paired sample t-test; p<0.05). Mean alveolar bone loss was not different between groups and was independent of the dosage (range 0.63–0.67 mm, one-way ANOVA; p>0.05). Conclusion. Although methotrexate has important cytokine-inhibitory properties, its possible use in modulating the host immune-inflammatory response in periodontal disease was not confirmed.

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Published

2007-01-01