Дослідження цитокінового спектру ротової рідини хворих із генералізованим пародонтитом на тлі метаболічного синдрому

Abstract

The purpose of the study was to study the state of cytokine regulation of oral fluid in patients with generalized periodontitis and metabolic syndrome. Materials and methods. For this study, 3 groups of surveys were formed. The main group included 30 people with generalized periodontitis on the background of metabolic syndrome; 30 people with generalized periodontitis, without somatic pathology, formed a comparison group. The obtained results were compared with the data of 20 practically healthy individuals with intact periodontium who were included in the control group. The content of pro-inflammatory cytokines IL-1β, IL-6, TNF-α and anti-inflammatory cytokines IL-4, TGF-β1 in the oral fluid of the study groups was determined by solid-phase enzyme-linked immunosorbent assay. Results and discussion. According to the research, on average, the highest levels of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) were observed in patients with periodontal disease on the background of metabolic syndrome. We investigated increase in the concentration of proinflammatory IL-1β. The average value of IL-6 in the oral fluid of patients with metabolic syndrome exceeded this figure in persons not burdened with somatic pathology by 1.3 times, the difference with healthy individuals was more significant: the indicators differed by 2 times. That can be considered an immune response to the inflammatory process in periodontal tissues. The next stage is the beginning of the cytokine cascade, which is characterized by increased production of IL-6 and TNF-α – inducers of acute phase protein synthesis. TNF-α causes an increase in the number of free radicals and can lead to intensification of apoptosis. Due to the fact that anti-inflammatory IL-4 blocks the induced expression of pro-inflammatory IL-6 and TNF-α, a decrease in its level in oral fluid can be considered an unfavorable factor in the course of inflammatory-dystrophic periodontal lesions in patients with syndrome X. Given that TGF-β1 is an immunosuppressive factor, a decrease in its concentration indicates a deficiency of local factors of immune protection in patients with periodontal disease on the background of metabolic syndrome. Conclusion. Patients with metabolic syndrome and periodontal disease have significant disorders of cytokine regulation, which are complicated by age: expression of proinflammatory IL-1β, IL-6, TNF-α on the background of reduced anti-inflammatory cytokines IL-4 and TGF-β1. Such changes in cytokine homeostasis indicate chronic inflammation, insufficient efficiency of regenerative processes in tooth-retaining tissues, and, as a consequence, lead to a more severe course of periodontal disease in people with metabolic syndrome