Periodontitis May Drive NAFLD via Systemic Inflammation: Study
A new study has found that periodontal disease may act as a modifiable contributor to the development and progression of non-alcoholic fatty liver disease (NAFLD) by influencing oral–gut–liver interactions, immune signaling, and metabolic regulation.Chronic periodontitis and NAFLD appear to be biologically connected through systemic inflammation, microbial dysbiosis, and metabolic disruption. This could be due to the increasing prevalence of both conditions globally and also their frequent coexistence; this has raised interest in shared disease pathways beyond traditional metabolic risk factors. The study was published in the International Journal of General Medicine by Zhe Lyu and colleagues.
Chronic periodontitis is a common inflammatory disease characterized by progressive loss of attachment and destruction of alveolar bone, whereas NAFLD encompasses a spectrum of liver conditions extending from simple steatosis to fibrosis and cirrhosis.
This narrative review synthesized evidence from observational, interventional, and mechanistic studies investigating the association of periodontal status or periodontal treatment with NAFLD-related outcomes. Included were studies that assessed oral and gut dysbiosis, inflammatory mediators, microbial metabolites, oxidative stress, microRNA regulation, and gut barrier function. Evidence was integrated across human epidemiological research, animal models, and mechanistic experiments.
Key Findings
Various epidemiological studies have determined that periodontitis is associated with an increased risk and severity of NAFLD as compared to individuals without periodontal disease.
Oral dysbiosis, mainly the enrichment of periodontal pathobionts, is repeatedly associated with hepatic steatosis and the progression of fibrosis.
Mechanistic data show microbial translocation from the oral cavity and gut induced pro-inflammatory cytokine release, disruption of gut barrier integrity, and hepatocellular injury.
Changes in microbial metabolites, including SCFAs and TMAO, were associated with insulin resistance and metabolic dysregulation. Oxidative stress amplifies inflammatory signaling.
Emerging evidence also identified microRNAs as epigenetic regulators that connect periodontal inflammation and bone remodeling to immune-metabolic pathways relevant to NAFLD.
Limited direct interventional evidence is available on the improvement in NAFLD following periodontal treatment.
Chronic periodontitis and NAFLD are associated through similar pathways of systemic inflammation, microbial dysbiosis, oxidative stress, and metabolic disturbance. The cumulative evidence supports periodontitis as a potentially modifiable factor in the NAFLD progression and stresses the importance of integrated management of oral health and liver health in the prevention and treatment of these commonly comorbid conditions.
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