Bedenyuk O. Pathogenetic features of the development of generalized periodontitis on the background of atrophic gas-tritis: mechanisms of metabolic disorders and their complex correction

The thesis presents theoretical generalization and new experimental solution of the scientific problem, consisting in defining of the biochemical, immune and morphological mechanisms of the development of generalized lipopolysaccharide periodontitis in animals with chronic atrophic gastritis, as well as in the pathogenetic reasoning of the use of antioxidant and nitric oxide synthesis systems modulators for the correction of the combined pathology. In lipopolysaccharide periodontitis, the microbiocenosis of the oral cavity is disturbed (the number of coccal forms of microorganisms increases with a simultaneous decrease in the level of lacto- and bifidobacteria), oxidative and nitrooxidative stress is activated, the production of proinflammatory cytokines increases periodontium (increased depolymerization reactions of glycoproteins, proteoglycans, collagenolysis, increased content of C-reactive protein), there is a protein vascular-stromal dystrophy in periodontal tissues. The presence of concomitant atrophic gastritis significantly worsens the studied parameters in animals with periodontitis. The antioxidant lycopene and the iNOS inhibitor aminoguanidine partially prevent the activation of free radical reactions, NO overproduction, increased catabolism of connective tissue components, inhibit the formation of proinflammatory cytokines and improve the morphological structure of periodontal tissues in animals with periodontitis and ha. The use of the combination "lycopene + aminoguanidine" is significantly more effective than the use of each of the drugs separately.