Periodontitis and metabolic dysfunction-associated steatotic liver disease.
Publisher DOI
PubMed ID
42642906
Abstract
OBJECTIVE: Periodontitis is a chronic inflammatory disease with systemic effects that extend beyond the oral cavity and contribute to systemic immune and metabolic dysregulation. Chronic liver diseases, particularly metabolic dysfunction-associated steatotic liver disease (MASLD) and its progressive phenotypes, have emerged as major global health challenges. Increasing evidence suggests that these two conditions could be biologically and clinically interconnected, yet their relationship has not been comprehensively analyzed. This review critically appraises and integrates clinical, translational, and experimental evidence linking periodontitis and liver disease, with a particular focus on MASLD and related outcomes.
MATERIALS AND METHODS: A comprehensive narrative review of the literature was conducted to synthesize evidence from epidemiological, clinical, translational, genetic, microbiological, and experimental studies investigating the relationship between periodontitis and chronic liver disease. Particular attention was given to studies examining the oral-gut-liver axis, shared immunometabolic mechanisms, and the effects of periodontal therapy on liver-related outcomes.
RESULTS: Epidemiological studies consistently demonstrate a higher prevalence and severity of periodontitis among individuals with chronic liver disease. Population-based and longitudinal studies further support bidirectional associations between periodontal inflammation and hepatic steatosis, fibrosis, cirrhosis, and liver-related mortality. Interventional studies provide preliminary evidence that periodontal therapy may improve hepatic biochemical, imaging, and inflammatory parameters. Genetic and Mendelian randomization studies indicate partially shared genetic susceptibility and overlapping immunometabolic pathways. Clinical microbiological and experimental studies demonstrate that periodontal dysbiosis, microbial translocation, systemic inflammation, and alterations in gut barrier integrity contribute to hepatic immune activation, oxidative stress, and fibrogenesis, supporting the biological plausibility of an oral-gut-liver axis. Conversely, liver disease-associated metabolic and immune dysfunction may further aggravate periodontal tissue destruction.
CONCLUSIONS: Current evidence supports a biologically plausible bidirectional relationship between periodontitis and chronic liver disease, particularly MASLD. Integration of epidemiological observations with mechanistic findings suggests that periodontal inflammation may contribute to liver disease progression through interconnected microbial, inflammatory, immunological, and metabolic pathways. Although causality remains to be established, these findings support greater integration of periodontal care into the multidisciplinary management of chronic liver disease and highlight the need for well-designed prospective studies and interventional trials to clarify causal mechanisms and therapeutic implications.
CLINICAL RELEVANCE: The emerging evidence linking periodontitis and chronic liver disease has important implications for clinical practice and interdisciplinary care. Given the high global prevalence of both conditions and their shared inflammatory and metabolic underpinnings, periodontal inflammation should be considered a clinically relevant comorbidity in patients with steatotic liver disease and other chronic hepatic disorders. Individuals with severe or treatment-refractory periodontitis may benefit from assessment of hepatic metabolic risk, fostering bidirectional collaboration between dental and medical professionals. Incorporating oral health into liver disease management strategies may represent a low-risk, cost-effective adjunct to existing therapies, with the potential to mitigate systemic inflammatory burden and improve long-term outcomes. Ultimately, translating this growing body of knowledge into integrated preventive and therapeutic strategies holds promise for meaningfully improving disease control, quality of life, and overall health outcomes in patients living with MASLD and periodontitis.
MATERIALS AND METHODS: A comprehensive narrative review of the literature was conducted to synthesize evidence from epidemiological, clinical, translational, genetic, microbiological, and experimental studies investigating the relationship between periodontitis and chronic liver disease. Particular attention was given to studies examining the oral-gut-liver axis, shared immunometabolic mechanisms, and the effects of periodontal therapy on liver-related outcomes.
RESULTS: Epidemiological studies consistently demonstrate a higher prevalence and severity of periodontitis among individuals with chronic liver disease. Population-based and longitudinal studies further support bidirectional associations between periodontal inflammation and hepatic steatosis, fibrosis, cirrhosis, and liver-related mortality. Interventional studies provide preliminary evidence that periodontal therapy may improve hepatic biochemical, imaging, and inflammatory parameters. Genetic and Mendelian randomization studies indicate partially shared genetic susceptibility and overlapping immunometabolic pathways. Clinical microbiological and experimental studies demonstrate that periodontal dysbiosis, microbial translocation, systemic inflammation, and alterations in gut barrier integrity contribute to hepatic immune activation, oxidative stress, and fibrogenesis, supporting the biological plausibility of an oral-gut-liver axis. Conversely, liver disease-associated metabolic and immune dysfunction may further aggravate periodontal tissue destruction.
CONCLUSIONS: Current evidence supports a biologically plausible bidirectional relationship between periodontitis and chronic liver disease, particularly MASLD. Integration of epidemiological observations with mechanistic findings suggests that periodontal inflammation may contribute to liver disease progression through interconnected microbial, inflammatory, immunological, and metabolic pathways. Although causality remains to be established, these findings support greater integration of periodontal care into the multidisciplinary management of chronic liver disease and highlight the need for well-designed prospective studies and interventional trials to clarify causal mechanisms and therapeutic implications.
CLINICAL RELEVANCE: The emerging evidence linking periodontitis and chronic liver disease has important implications for clinical practice and interdisciplinary care. Given the high global prevalence of both conditions and their shared inflammatory and metabolic underpinnings, periodontal inflammation should be considered a clinically relevant comorbidity in patients with steatotic liver disease and other chronic hepatic disorders. Individuals with severe or treatment-refractory periodontitis may benefit from assessment of hepatic metabolic risk, fostering bidirectional collaboration between dental and medical professionals. Incorporating oral health into liver disease management strategies may represent a low-risk, cost-effective adjunct to existing therapies, with the potential to mitigate systemic inflammatory burden and improve long-term outcomes. Ultimately, translating this growing body of knowledge into integrated preventive and therapeutic strategies holds promise for meaningfully improving disease control, quality of life, and overall health outcomes in patients living with MASLD and periodontitis.
Date Issued
2026-08-25
Publication Type
Article
Subject(s)
Subjects
chronic liver disease
•
inflammation
•
metabolic dysfunction‐associated steatotic liver disease
•
oral–gut–liver axis
•
periodontal disease
•
periodontitis
Language(s)
en
Author(s)
de Molon, Rafael Scaf | |
de Avila, Erica Dorigatti | |
da Silva Barbirato, Davi | |
Fogacci, Mariana Fampa | |
Shibli, Jamil Awad | |
Kantarci, Alpdogan |
Additional Credits
Journal
Periodontology 2000
Publisher
Wiley
ISSN
1600-0757
0906-6713
Access(Rights)
open.access