Periodontitis is a dysbiosis-driven inflammatory disease in which a pathogenic subgingival biofilm disrupts the host–microbe equilibrium and promotes progressive loss of tooth-supporting tissues. While periodontal destruction has traditionally been explained mainly through the host immune response, increasing experimental and clinical evidence suggests that epithelial–mesenchymal transition (EMT)-like changes in the gingival epithelium may contribute to barrier failure and tissue remodeling during disease progression. EMT is characterized by reduced epithelial adhesion and polarity, alongside a shift toward a mesenchymal-like phenotype with enhanced motility and impaired epithelial barrier function. This narrative review focuses on how periodontal pathogens, particularly red complex organisms and keystone species, may trigger gingival EMT through virulence factors such as gingipains, fimbriae, lipopolysaccharide, and outer membrane vesicles. These microbial signals can hijack host pathways including TGF-β/Smad, Wnt/β-catenin, and Notch to drive EMT-associated transcriptional changes and downstream functional consequences. Collectively, pathogen-induced gingival EMT may facilitate deeper microbial invasion, perpetuate chronic inflammation, impair wound healing, and contribute to fibrotic remodeling, ultimately linking microbial dysbiosis to connective tissue destruction. Understanding these mechanisms may support the development of EMT-related biomarkers and targeted interventions aimed at preserving epithelial barrier stability in periodontitis.
Akram et al. (Wed,) studied this question.