Abstract
Objectives Epithelial–mesenchymal transition (EMT) is a process that shifts cellular phenotype. It is linked to several different inflammatory diseases including periodontitis. This study was conducted to investigate the involvement of the EMT process in an experimental periodontitis (EP) model.
Materials and Methods Second upper molars of Wistar albino male rats were ligated to induce periodontitis, while controls were not ligated. The animals were sacrificed after 0, 3, 7, 14, and 21 days (n = 6 for each time point). The maxillae were resected, posterior to the incisor teeth, and the gingival tissue surrounding teeth were analyzed. Alveolar bone loss (ABL), epithelial thickness, and the number of inflammatory cells were measured at each time point. Expressions of EMT-related biomarkers (E-cadherin, N-cadherin, Snail1, Twist1, and vimentin) were assessed using the immunohistochemical technique. All experiments were performed in triplicate.
Statistical Analysis Inferential comparisons were performed by the kruskall-wallis test. To determine the correlation between the dependent and independent variables ,Spearman's correlation test was used.
Results ABL, epithelial thickness, and inflammatory cell count were gradually increased throughout the EP study period. Switching of E-cadherin/N-cadherin was evident and associated with increased nuclear expression of Snail1 and Twist1. Additionally, positive cytoplasmic expression of vimentin was detected from day 7 and increased at subsequent time points. Histoscore of E-cadherin was negatively and significantly correlated with N-cadherin and Snail1. Furthermore, Snail1 and Twist1 histoscores were significantly and positively correlated.
Conclusion The results demonstrated induction of an EMT phenotype in the EP model. This was supported by cadherin switching and positive vimentin expression along with nuclear translocation of Snail1 and Twist.