Irina-Georgeta Sufaru, Ioana Martu, Liliana Pasarin, Maria-Alexandra Martu, Diana Tatarciuc, Ilinca Luca, Silvia Martu, Sorina-Mihaela Solomon
Abstract
Metabolic dysfunction–associated steatotic liver disease (MASLD) and metabolic dysfunction–associated steatohepatitis (MASH) are now defined by clear metabolic criteria, with current approaches emphasizing fibrosis risk due to its impact on liver-related outcomes. Periodontitis is a common chronic inflammatory disease caused by dysbiotic subgingival biofilms and sustained by an exaggerated host response. This narrative review consolidates clinical and experimental evidence connecting periodontitis to MASLD/MASH through the oral–gut–liver axis.
Epidemiologic studies frequently observe the co-occurrence of periodontitis and steatotic liver disease, and several cohorts indicate dose–response patterns when periodontal severity correlates with fibrosis-related liver outcomes like elastography or validated non-invasive fibrosis scores. However, these associations are inconsistent and tend to diminish when adjusting for strongly related factors such as obesity, diabetes, smoking intensity, diet, socioeconomic status, and healthcare utilization. Interpretation is also constrained by differing case definitions, various liver outcomes (such as imaging-detected steatosis, aminotransferases, fibrosis scores, elastography, biopsy), and possible reverse causality.
Mechanistic plausibility is supported by several converging pathways: intermittent systemic spread of bacteria and microbial products (including LPS) from periodontal pockets; oral-to-gut microbial transmission causing ecological changes in the intestinal microbiome; intestinal barrier dysfunction leading to increased portal delivery of endotoxin and metabolites; and activation of hepatic innate immunity that enhances lipotoxic stress, oxidative injury, inflammasome signaling, and stellate-cell–mediated fibrogenesis. In obesity-prone models, induced periodontitis worsens steatotic liver phenotypes and highlights manageable targets such as TLR pathways and microbiota-dependent tryptophan–AHR signaling.
Clinically, the most justified implication is integrated risk recognition rather than definitive causal claims. Dental teams can start metabolic evaluation and fibrosis risk assessment for high-risk patients, while hepatology and metabolic clinics can include brief oral screenings and periodontal referrals. Future priorities include standardizing phenotyping, conducting repeated-measure cohort studies, and running periodontal intervention trials with fibrosis-related endpoints. Using multi-omics and causal frameworks will be crucial for translating research into clinical practice.
DOI : 10.62610/RJOR.2025.4.17.11
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