Abstract
Objective — to identificate of the quantitative composition of some representatives of II order periodontopathogens in patients with NAFLD.
 Materials and methods. 108 people were selected, including 44 patients with non‑alcoholic fatty liver disease (main group), 44 people — their spouses (comparison group). The control group consisted of 20 somatically healthy volunteers. A standard dental examination was performed using hygiene and periodontal indices, and some physical parameters of saliva (salivary salinity and viscosity, oral fluid endotoxin level in volume per unit time by enzyme‑linked immunosorbent assay) were determined. Quantitative composition of Fusobacterium nucleatum, Treponema denticola, Prevotela intermedia and Porphyromonas endodontalis in periodontal pockets was performed by real‑time PCR using paper endodontic absorbents. Statistical processing was performed using SPSS statistical programs using the nonparametric method.
 Results. In NAFLD, negative changes in the physical parameters of saliva were observed (decreased salivary flow rate, increased viscosity, pH shift to the acidic side), increased levels of oral endotoxin and increased quantitative content of periodontal pathogens of the second order (increase in Porphyromonas endodontalis compared to the control group by more than 4.5 times and increase in Prevotela intermedia by 2.5 times). A positive correlation was found between the presence of halitosis and the quantitative content of Fusobacterium nucleatum (r=0.40; p=0.065) and the quantitative content of Porphyromonas endodontalis (r=0.36; p=0.022). We also found a negative correlation between the level of Fusobacterium nucleatum and salivary flow rate (r=– 0.51; p=0.000) and a positive correlation with saliva viscosity (r=0.49; p=0.001).
 Conclusions. The combination of exogenous and endogenous risk factors forms a dysbiotic shift of conditionally pathogenic microflora (periodontal pathogens of the second order) in the oral cavity biotope, which creates conditions for the invasion of more aggressive microorganisms and the maintenance of chronic systemic inflammation. This fact requires increased attention from both the dentist and the internist, and the patient.
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