The correlation between periodontitis and fatty liver and the improvement of NAFLD by periodontal treatment

Background: Emerging evidence highlights a pathophysiological interplay between periodontitis and non-alcoholic fatty liver disease yet the mechanistic underpinnings and therapeutic implications remain contentious. This review systematically elucidates molecular crosstalk through the "oral-gut-liver axis" and "oral-liver axis". Methods: A comprehensive literature review was conducted using PubMed, Scopus and Web of Science, employing keywords related to periodontal disease and non-alcoholic fatty liver disease. Results: Analysis of 16 original studies revealed that periodontitis and its associated pathogens promote the progression of non-alcoholic fatty liver disease through multiple pathways: (1) activation of hepatic inflammatory responses (elevated IL-6, IL-17, and TNF-α levels), (2) exacerbation of metabolic dysregulation (increased HOMA-IR, ALT, and AST), and (3) disruption of the oral-gut-liver axis. Notably, non-surgical periodontal therapy demonstrated therapeutic potential by simultaneously improving periodontal health and attenuating non-alcoholic fatty liver disease progression through reduction of hepatic pro-inflammatory cytokines and fibrogenic mediators. Conclusions: Periodontitis may exacerbate systemic inflammation via the oral-liver and oral-gut-liver axes, inducing insulin resistance and promoting non-alcoholic fatty liver disease. Non-surgical periodontal therapy can improve non-alcoholic fatty liver disease, but methodological heterogeneity in current studies necessitates further prospective research to clarify their relationship.