111614
论文已发表
注册即可获取德孚的最新动态
IF 收录期刊
- 3.4 Breast Cancer (Dove Med Press)
- 3.2 Clin Epidemiol
- 2.6 Cancer Manag Res
- 2.9 Infect Drug Resist
- 3.7 Clin Interv Aging
- 5.1 Drug Des Dev Ther
- 3.1 Int J Chronic Obstr
- 6.6 Int J Nanomed
- 2.6 Int J Women's Health
- 2.9 Neuropsych Dis Treat
- 2.8 OncoTargets Ther
- 2.0 Patient Prefer Adher
- 2.2 Ther Clin Risk Manag
- 2.5 J Pain Res
- 3.0 Diabet Metab Synd Ob
- 3.2 Psychol Res Behav Ma
- 3.4 Nat Sci Sleep
- 1.8 Pharmgenomics Pers Med
- 2.0 Risk Manag Healthc Policy
- 4.1 J Inflamm Res
- 2.0 Int J Gen Med
- 3.4 J Hepatocell Carcinoma
- 3.0 J Asthma Allergy
- 2.2 Clin Cosmet Investig Dermatol
- 2.4 J Multidiscip Healthc
已发表论文
慢性牙周炎与非酒精性脂肪肝疾病：关联机制的最新进展
Received 19 July 2025
Accepted for publication 30 October 2025
Published 7 December 2025 Volume 2025:18 Pages 7357—7369
DOI https://doi.org/10.2147/IJGM.S554833
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Vinay Kumar
Zhe Lyu,1 Jieying Zhu,2 Deying Chen3
1Department of Stomatology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, People’s Republic of China; 2Department of Stomatology, The First Affiliated Hospital, College of Medicine, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, People’s Republic of China; 3State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, People’s Republic of China
Correspondence: Deying Chen, Email deyingchen@zju.edu.cn
Background: Chronic periodontitis (CP) and non-alcoholic fatty liver disease (NAFLD) are increasingly prevalent worldwide. Although mechanisms remain incompletely defined, recent studies suggest a close association between these two diseases. This review systematically outlines potential links between periodontitis and NAFLD, emphasizing their pathological mechanisms and interactions within an oral–gut–liver framework.
Methods: We reviewed observational, interventional, and mechanistic studies evaluating associations between periodontal status/treatment and NAFLD-related outcomes, integrating evidence on dysbiosis, inflammatory mediators, microbial metabolites, oxidative stress, microRNA regulation, and gut barrier function.
Results: Across epidemiological studies, periodontitis is associated with higher risk and greater severity of NAFLD. Mechanistically, oral dysbiosis, especially enrichment of oral pathobionts, is linked to hepatic steatosis and fibrosis. Translocation of microbial products and the resulting cytokine release drive systemic inflammation, impair gut barrier integrity, and induce hepatocellular injury. Microbial metabolites (such as short-chain fatty acids (SCFAs) and trimethylamine N-oxide (TMAO)) and oxidative stress contribute to metabolic dysregulation. Emerging evidence suggests that microRNAs (miRNAs) function as epigenetic regulators linking periodontal inflammation and bone remodeling to immune-metabolic pathways relevant to non-alcoholic fatty liver disease (NAFLD). However, direct evidence on whether treating periodontitis can improve NAFLD outcomes remains limited. Despite heterogeneity in study designs and diagnostic criteria, cumulative evidence supports periodontitis as a modifiable risk factor for the progression of NAFLD.
Conclusion: CP and NAFLD appear to be linked through systemic inflammation, dysbiosis, and metabolic disturbances. Future research should prioritize microbiome modulation, advance interdisciplinary care models, and develop personalized prevention and treatment strategies. Integrating oral and liver health within comprehensive management may provide new options for preventing and treating these frequently coexisting diseases.
Keywords: periodontitis, non-alcoholic fatty liver disease, NAFLD, oral-gut-liver axis, dysbiosis, inflammatory mediators
1Department of Stomatology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, People’s Republic of China; 2Department of Stomatology, The First Affiliated Hospital, College of Medicine, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, People’s Republic of China; 3State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, People’s Republic of China
Correspondence: Deying Chen, Email deyingchen@zju.edu.cn
Background: Chronic periodontitis (CP) and non-alcoholic fatty liver disease (NAFLD) are increasingly prevalent worldwide. Although mechanisms remain incompletely defined, recent studies suggest a close association between these two diseases. This review systematically outlines potential links between periodontitis and NAFLD, emphasizing their pathological mechanisms and interactions within an oral–gut–liver framework.
Methods: We reviewed observational, interventional, and mechanistic studies evaluating associations between periodontal status/treatment and NAFLD-related outcomes, integrating evidence on dysbiosis, inflammatory mediators, microbial metabolites, oxidative stress, microRNA regulation, and gut barrier function.
Results: Across epidemiological studies, periodontitis is associated with higher risk and greater severity of NAFLD. Mechanistically, oral dysbiosis, especially enrichment of oral pathobionts, is linked to hepatic steatosis and fibrosis. Translocation of microbial products and the resulting cytokine release drive systemic inflammation, impair gut barrier integrity, and induce hepatocellular injury. Microbial metabolites (such as short-chain fatty acids (SCFAs) and trimethylamine N-oxide (TMAO)) and oxidative stress contribute to metabolic dysregulation. Emerging evidence suggests that microRNAs (miRNAs) function as epigenetic regulators linking periodontal inflammation and bone remodeling to immune-metabolic pathways relevant to non-alcoholic fatty liver disease (NAFLD). However, direct evidence on whether treating periodontitis can improve NAFLD outcomes remains limited. Despite heterogeneity in study designs and diagnostic criteria, cumulative evidence supports periodontitis as a modifiable risk factor for the progression of NAFLD.
Conclusion: CP and NAFLD appear to be linked through systemic inflammation, dysbiosis, and metabolic disturbances. Future research should prioritize microbiome modulation, advance interdisciplinary care models, and develop personalized prevention and treatment strategies. Integrating oral and liver health within comprehensive management may provide new options for preventing and treating these frequently coexisting diseases.
Keywords: periodontitis, non-alcoholic fatty liver disease, NAFLD, oral-gut-liver axis, dysbiosis, inflammatory mediators