Epithelial mesenchymal transition (EMT) is a process comprising cellular and molecular events which result in cells shifting from an epithelial to a mesenchymal phenotype. Periodontitis is a destructive chronic disease of the periodontium initiated in response to a dysbiotic microbiome, and dominated by Gram-negative bacteria in the subgingival niches accompanied by an aberrant immune response in susceptible subjects. Both EMT and periodontitis share common risk factors and drivers, including Gram-negative bacteria, excess inflammatory cytokine production, smoking, oxidative stress and diabetes mellitus. In addition, periodontitis is characterized by down-regulation of key epithelial markers such as E-cadherin together with up-regulation of transcriptional factors and mesenchymal proteins, including Snail1, vimentin and N-cadherin, which also occur in the EMT program. Clinically, these phenotypic changes may be reflected by increases in microulceration of the pocket epithelial lining, granulation tissue formation, and fibrosis. Both in vitro and in vivo data now support the potential involvement of EMT as a pathogenic mechanism in periodontal diseases which may facilitate bacterial invasion into the underlying gingival tissues and propagation of inflammation. This review surveys the available literature and provides evidence linking EMT to periodontitis pathogenesis.

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.

Sequencing technologies have reshaped the study of the subgingival microbiome, but selecting the appropriate method remains challenging because of differences in resolution, cost, host DNA contamination, and computational complexity. This review compares 16S rRNA sequencing, full-length 16S, shotgun metagenomics, and metatranscriptomics with respect to taxonomic resolution, functional output, sample requirements, and analytical limitations. Key practical issues, including low microbial biomass, contamination control, and the choice of appropriate bioinformatic tools, are emphasized to help researchers avoid common pitfalls. A decision-making framework is provided to link study goals to suitable sequencing methods while outlining realistic budget and sample-handling constraints. The review concludes with recommendations for integrating sequencing with complementary techniques to improve the accuracy, reproducibility, and clinical relevance of periodontal microbiome studies.

Periodontitis is a chronic inflammatory disease initiated by dysbiotic biofilms and sustained by an altered host response, resulting in progressive destruction of the tooth-supporting tissues. Alongside immune-mediated damage, epithelial–mesenchymal transition has been proposed as a contributing mechanism in gingival barrier disruption and periodontal tissue remodeling. This narrative review examines the roles of the EMT-related transcription factors Snail1 and Twist1 in periodontitis, with particular focus on their involvement in epithelial junction loss, mesenchymal activation, and disease-associated tissue change. Relevant literature was identified through targeted searches of PubMed/MEDLINE and Google Scholar using terms related to periodontitis, gingival epithelium, EMT, Snail, and Twist, while selected non-periodontal studies were used only for mechanistic context where direct evidence was limited. Current findings suggest that periodontal disease is commonly associated with reduced epithelial adhesion markers and increased mesenchymal-associated markers, with Snail1 appearing more closely linked to epithelial repression and Twist1 to motility and matrix remodeling. However, the evidence remains largely preclinical or associative. Overall, Snail1 and Twist1 may participate in EMT-like remodeling in periodontitis, but periodontal-specific mechanistic and functional studies are still needed to clarify causality and clinical relevance.

Introduction: Adipose tissue releases pro- and anti-inflammatory cytokines and hormones such as irisin, visfatin, and interleukin-6, which may be linked to periodontal diseases. Objectives: Our study aimed to determine salivary irisin, visfatin, and interleukin-6 levels in gingivitis and periodontitis patients, compare them with healthy periodontal patients, and evaluate the association between these biomarkers. Materials and methods: Ninety participants were involved in this case-control study: 30 patients diagnosed with periodontitis (P), 30 patients with gingivitis (G), and 30 periodontally healthy subjects (control; C). The periodontal clinical parameters were documented. The ELISA test examined irisin, visfatin, and interleukin-6 saliva levels. Data were analyzed using SPSS (V.29). Results: Irisin significantly decreased in gingivitis and periodontitis compared to the control group ( p < 0.05). In contrast, gingivitis and periodontitis reported elevated levels of visfatin and interleukin-6 compared to the control group ( p < 0.05). Visfatin levels did not significantly change between gingivitis and periodontitis ( p > 0.05). All periodontal clinical measures showed a significant negative association with irisin ( p < 0.05), except plaque index in the gingivitis group. At the same time, visfatin and interleukin-6 showed significant positive relationships with all clinical periodontal markers ( p < 0.05). Conclusions: Salivary irisin levels were reduced in individuals with gingivitis and periodontitis, whereas visfatin and interleukin-6 levels were elevated. These biomarkers may predict susceptibility to periodontal disease.