Khudan R. Pathogenetic features of the generalized periodontitis course associated with chronic hyperhomocysteinemia

In the dissertation work for the first time on the basis of complex researches and an assessment of metabolism disorders of bone and connective tissues, cytokinogenesis, the severity of inflammation, functional and metabolic activity of blood neutrophils, energy supply oxidation, realization of programmed blood neutrophil death, peroxide oxidation of lipids and proteins, antioxidant protection, the severity of endogenous intoxication, a comparative study of the course of experimental lipopolysaccharide (LPS)-induced periodontitis without concomitant pathology and periodontitis in case of chronic thiolactone hyperhomocysteinemia (HHcy) is conducted. A correlation between the level of Hcys in blood serum and the severity of inflammatory and destructive processes in periodontal tissues was established both in LPS-induced periodontitis without concomitant pathology and in periodontitis in case of chronic thiolactone HHcy. It has been shown that concomitant chronic HHcy significantly enhances the synthesis of acute inflammatory reactants and cytokine imbalance, which plays an important role in the progression of periodontitis and the initiation of metabolic cascade reactions. It has been shown that concomitant chronic HHcy significantly increases the intensity of free radical oxidation of lipids and proteins processes in periodontal tissues in case of decreased functional activity of antioxidant protection, accompanied by an increase of endogenous intoxication. It has been determined that concomitant chronic thiolactone HHcy adversely affects the functional and metabolic activity of blood neutrophils in case of LPS-induced periodontitis, which is confirmed by a violation of phagocytosis, a more pronounced decrease of the absorption capacity of blood neutrophils and depletion of the reserves of these cells compared to animals without concomitant pathology. It has been shown that concomitant chronic thiolactone HHcy enhances the initiation of programmed blood neutrophil death by triggering the mitochondrial pathway of apoptotic cell death. It has been shown that concomitant chronic thiolactone HHcy intensifies connective tissue destruction in case of LPS-induced periodontitis and inhibits synthetic processes in bone tissue in case of activation of osteoresorption reactions.