SUMMARY
The aim of the study was to investigate in experiment the biochemical mechanisms of periodontal tissues lipopolysaccharide inflammation on the background of gastric mucosa chronic inflammatory injury. Periodontitis was initiated in white rats by the injection of E. Coli lipopolysaccharide (40 µl, 1 mg/ml) into gingival tissues. For the modeling of chronic gastritis 2 % sodium salicylate was administered intragastrically for 6 weeks. Lipopolysaccharide periodontitis was accompanied with the increase of TBA-active products and oxidative-modified proteins as well as with the decrease of superoxide dismutase activity and reduced glutathione content in periodontal tissues and blood serum. The total NO synthase activity and NOx content increased significantly in rats with periodontitis. In animals with both pathologies, periodontitis and chronic gastritis, oxidative and nitrooxidative stress was much more pronounced than in rats without gastritis. It was concluded that chronic gastritis markedly enhances oxidative and nitrooxidative stress in periodontal tissues injured by the bacterial endotoxin lipopolysaccharide.