How do oral pathogenic bacteria potentially contribute to inflammatory processes in autoimmune liver disease? Results from a systematic review

Background: Emerging evidence suggests that the oral–gut–liver axis may play a role in the immunopathogenesis of autoimmune liver diseases (AILDs), particularly autoimmune hepatitis (AIH) and primary biliary cholangitis (PBC). Alterations in the oral microbiota may influence hepatic immune responses; however, this relationship remains poorly defined. Objective: This systematic review aimed to evaluate current evidence on the association between oral microbiota dysbiosis and AILDs, with a focus on microbial alterations, inflammatory profiles, and potential diagnostic implications. Methods: A systematic search of PubMed, Web of Science, and Scopus was conducted up to January 2026 in accordance with PRISMA guidelines. Eligible studies investigated oral microbiota composition in patients with AILDs compared with healthy controls. Data extraction was performed independently, and study quality was assessed using the Newcastle–Ottawa Scale (NOS). Results: Six studies published between 2015 and 2021 met the inclusion criteria, comprising 252 patients with AILDs and 345 healthy controls. All included studies reported significant oral microbiota dysbiosis in AILD patients. The most consistent findings were an increased abundance of Veillonella in AILDs and Eubacterium in the PBC subgroup, along with a reduced presence of Streptococcus and Fusobacterium. These microbial alterations were associated with elevated salivary inflammatory markers, and showed correlations with disease activity. Some studies also suggested interactions between oral and gut microbiota, potentially mediated by increased intestinal permeability and bacterial translocation. Conclusions: Current evidence supports an association between oral microbiota dysbiosis and inflammatory mechanisms. Although causality cannot be established, the oral–gut–liver axis may represent a promising source of biomarkers and therapeutic targets.