IMMUNE REGULATION OF HEMOSTASIS IN INFLAMMATORY PERIODONTAL DISEASES CADETS OF UFA LAW INSTITUTE OF THE MINISTRY OF INTERNAL AFFAIRS OF THE RUSSIAN FEDERATION
Abstract and keywords
Abstract (English):
Subject. Inflammatory periodontal diseases are accompanied by violations of the body's reactivity to the introduction of the pathogen. At various stages of the immune response, Pro-inflammatory cytokines are produced, such as interleukins 1, 6 (IL-1, IL-6), tumor necrosis factor-alpha (TNF-α), and chemokines in particular IL-8. Cytokines serve as an organizing system that forms and regulates the entire complex of protective reactions of the body, provides activation of various types of cells, including white blood cells, dendritic, endothelial, epithelial cells, fibroblasts, macrophages, lymphocytes, and others. They cause endothelial activation, leading to increased permeability, increased expression of adhesive molecules, and increased procoagulant activity. The appearance of interleukins in the focus of inflammation causes the production of tissue factor, Willebrand factor, plasminogen activators, etc., which stimulate the reactions of vascular-platelet hemostasis, which activate the Pro-enzyme-enzyme cascade of blood clotting and fibrinolysis. The aim — to study the effect of cytokines on the hemostatic system in individuals with healthy periodontitis, chronic gingivitis, and chronic generalized periodontitis. Methodology. 60 cadets aged 18 to 25 years participated in the clinical study at the dental office of the medical unit No. 1 of the medical and sanitary unit of the Ministry of Internal Affairs of the Russian Federation (Ufa). The study group consisted of 45 people: 15 patients with intact periodontitis, 15 patients with moderate chronic gingivitis, and 15 patients with moderate chronic generalized periodontitis. Results. Correlations between IL-1β, IL-6, TNF-α, and IL-8 in gingival sulcus flushes, pockets, and hemostasis parameters were revealed. Conclusions. In inflammatory periodontal diseases, interleukins can inhibit fibrinolysis, leading to hypercoagulation. Increased thrombosis contributes to the progression of gingivitis to periodontitis.

Keywords:
gingivitis, periodontitis, cytokines, hemostasis, cadets
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