Etiopathogenetic Mechanisms of Periodontal Diseases Against the Background of Viral Liver Disseases

Abstract

The article presents a review and analysis of relevant available literature sources on etiopathogenetic mechanisms of periodontal disease and liver diseases of viral aetiology, and, in particular, hepatitis B and C viruses. Significant prevalence, pronounced polymorphism of clinical hepatic and extrahepatic manifestations, the incidence rate of liver cirrhosis and hepatocellular carcinoma allows us to consider hepatitis of viral aetiology as a medical and social challenge. Multi-vector liver dysfunctions can cause oral presentations in this group of patients, and in particular, in their periodontal tissues. Viral liver damage is associated with significant impairment of the microbiocenosis in gingival sulcus and periodontal pockets. Dysbiotic changes are characterized by an increase in the number of opportunistic pathogens and anaerobic periodontal pathogens. Exacerbation of dysbiosis along with deterioration of oral hygiene occurs as a consequence of reduced local resistance and hyposalivation due to the sialotropic properties of hepatitis C virus. Significant pathogenetic role in the development of periodontal disease is played by disorders of metabolic and synthetic functions of the liver, as well as hormonal imbalance, metabolic disorders, immune-mediated damage, induction of autoimmune mechanisms and cytokine imbalance. The formation of hepatogenic osteopenia and osteoporosis enhances the loss of bone mass of the alveolar processes in the jaws and, accordingly, the resorption of bone tissue with the further progression of more aggressive forms of generalized periodontitis.