TREATMENT OF INFLAMATORY AND DEGENERATIVE DAMAGES OF THE SMOOTH PARODONT TISSUE WITH IMMUNE MODULATING DRUGS

The oxidative and immune status was assessed in a rat model of inflammatory and degenerative damages of the smooth parodont tissue due to administration of 2% formaldehyde water solution (0,3 ml) into the smooth parodont tissues. The lipid peroxidation indexes (malonic dialdehyde and dienic conjugates level) were в 3,6-5,8-fold higher in the blood serum and parodont tissue in 3 days after inflammation beginning. The inflammation was accompanied by inhibition of lymphokin-producing function of lymphocytes in reaction of inhibition of leucocytes migration with concanavalin A (Con A) by 39% and with phytohaemagglutinin (PGA) by 37%. The activity of oxygen-independent microbicide system of phagocytes was decreased by 13%, that was typical for subacute duration of inflammatory process. The phagocyte number was increased by 26% and the phagocytosis index by 22% with decrease of phagocytes participating in phagocytosis by 31%. The spontaneous NBT-test index was increased by 63%, and stimulating one by 35%. Trekrezan administered for 3 days decreased malonic dialdehyde level by 61%, dienic conjugates level by 68%, in 2,9-fold increased the concentration of recovered glutatione and superoxide dismutase activity by 79% Simultaneously, the elevation of lymphokin-producing function of lymphocytes in reaction of inhibition of leucocytes migration with Con A by 67% and with PGA by 73% was registered. Phagocyte activity of neutrophils was increased by 24% Phagocyte number equal to middle number of microorganisms phaged by one active neutrophil and phagocytosis index were decreased by 26% and 14% respectively. Trekrezan administered orally revealed the same but less significant action. Preliminary administration of lidocaine intragastrally for blockade of gastric afferents did not affect the trekrezan action. Therefore, trekrezan possesses both anti-inflammatory and immune stimulating action. Oral administration of trekrezan induced more weak effect than after intraperitoneal administration and did not depend on activation of gastric afferents.