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INTERRELATION BETWEEN INFLAMMA- TORY PERIODONTAL DISEASES AND FATTY LIVER DYSTROPHY: MODERN CONCEPTS AND PATHOGENETIC MECHANISMS

Affiliations
a Toshkent davlat tibbiyot universiteti image/svg+xml
b Toshkent davlat tibbiyot universiteti image/svg+xml

Annotatsiya

The present review summarizes current knowledge about the relationship between inflammatory periodontal diseases (IPD) and fatty liver dystrophy (FLD). According to the World Health Organization (WHO), periodontal diseases remain one of the most common chronic inflammatory conditions affecting the quality of life through pain, bleeding, halitosis, and premature tooth loss. At the same time, fatty liver dystrophy, a nonalcoholic metabolic liver disorder characterized by excessive fat accumulation in hepatocytes, is increasingly recognized as part of systemic inflammatory and metabolic syndromes. This review discusses the mutual pathogenetic mechanisms linking periodontal inflammation and hepatic lipid metabolism disorders, highlighting the roles of oxidative stress, cytokine imbalance, immune dysregulation, and oral microbiota. Modern diagnostic approaches and therapeutic perspectives are also considered. The interrelation between oral and systemic health emphasizes the importance of an integrated approach to early diagnosis, prevention, and management of both conditions.

References

  1. WHO. Global data on oral health. World Health Organization, 2022
  2. Kinane DF, Stathopoulou PG, Papapanou PN. Periodontal diseases. Nat Rev Dis Primers. 2017;3:17038
  3. Tonetti MS, Jepsen S, Jin L, Otomo-Corgel J. Impact of the global burden of periodontal diseases. Clin Periodontol. 2017;44(5):456–462
  4. Hajishengallis G. Periodontitis: from microbial immune subversion to systemic inflammation. Nat Rev Immunol. 2015;15:30–44
  5. Cekici A, Kantarci A, Hasturk H, Van Dyke TE. Inflammatory and immune pathways in the pathogenesis of periodontal disease. Periodontol 2000. 2014;64(1):57–80
  6. Sanz M, Ceriello A, Buysschaert M, et al. Scientific evidence on the links between periodontal diseases and systemic diseases. J Clin Periodontol. 2018;45(Suppl 20):S138–S148
  7. Loos BG, Van Dyke TE. The role of inflammation and genetics in periodontal disease. Periodontol 2000. 2020;83(1):26–39
  8. Bartold PM, Van Dyke TE. Periodontitis: a host-mediated disruption of microbial homeostasis. Unlearning learned concepts. Periodontol 2000. 2013;62(1):203–217
  9. Preshaw PM, Alba AL, Herrera D, et al. Periodontitis and diabetes: a two-way relationship. Dia- betologia. 2012;55(1):21–31
  10. Van Dyke TE, Dave S. Risk factors for periodontitis. J Int Acad Periodontol. 2005;7(1):3–7
  11. Lamont RJ, Koo H, Hajishengallis G. The oral microbiota: dynamic communities and host in- teractions. Nat Rev Microbiol. 2018;16(12):745–759
  12. Younossi ZM, et al. Nonalcoholic fatty liver disease: global epidemiology and perspectives. Nat Rev Gastroenterol Hepatol. 2018;15(1):11–20
  13. Chalasani N, et al. The diagnosis and management of nonalcoholic fatty liver disease: Practice guidance. Hepatology. 2018;67(1):328–357
  14. Tilg H, Moschen AR. Evolution of inflammation in NAFLD: the multiple parallel hits hypothe- sis. Hepatology. 2010;52(5):1836–1846
  15. Byrne CD, Targher G. NAFLD: a multisystem disease. J Hepatol. 2015;62(1):S47–S64
  16. Buzzetti E, Pinzani M, Tsochatzis EA. The multiple-hit pathogenesis of NAFLD. Metabolism. 2016;65(8):1038–1048
  17. Sies H, Jones DP. Reactive oxygen species and antioxidant defense. Redox Biol. 2020;29:101675
  18. Qin N, et al. Alterations of the human gut microbiome in liver cirrhosis. Nature. 2014;513(7516):59–64
  19. Arab JP, et al. Inflammation, immunity, and oxidative stress in NAFLD. Dig Dis Sci. 2018;63(10):2712–2723
  20. Feldstein AE, et al. Cytokine imbalance in the progression of NAFLD. Hepatology. 2003;38(3):734–742
  21. Donnelly KL, et al. Sources of fatty acids in liver triglyceride accumulation in NAFLD. J Clin Invest. 2005;115(5):1343–1351
  22. Seki E, Schwabe RF. Hepatic inflammation and fibrosis: functional links and key pathways. Hepatology. 2015;61(3):1066–1079
  23. Polimeni L, et al. Oxidative stress and NAFLD: pathophysiology and therapeutic implications. Free Radic Res. 2018;52(9):1106–1114
  24. Peverill W, Powell LW, Skoien R. Evolving concepts in NAFLD pathogenesis. Hepatol Int. 2014;8(4):472–486
  25. Wu J, et al. Oxidative stress biomarkers in patients with NAFLD and periodontitis. Clin Oral Investig. 2022;26(2):1391–1400
  26. Byrne CD, Targher G. Interaction of NAFLD and metabolic syndrome. Diabetes Obes Metab. 2020;22(6):1203–1215
  27. Podimova SD. Fatty liver dystrophy in adults and children: epidemiology and clinical features. Clin Med (Moscow). 2021;99(4):312–319
  28. Nobili V, et al. Pediatric NAFLD: a growing problem. J Hepatol. 2019;70(2):472–484
  29. Anderson EL, et al. Gender differences in NAFLD. J Gastroenterol Hepatol. 2019;34(3):568– 575
  30. Albillos A, et al. Systemic inflammation and immune dysfunction in liver disease. J Hepatol. 2020;73(2):409–423
  31. Schwimmer JB, et al. Prevalence of fatty liver in children and adolescents. Pediatrics. 2006;118(4):1388–1393
  32. Welsh JA, et al. Risk factors for fatty liver in youth. J Pediatr Gastroenterol Nutr. 2018;67(1):41– 47
  33. Loomba R, et al. Advances in NAFLD pathogenesis and treatment. Hepatology. 2021;74(6):3412–3429

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