Duration Of Inflammatory Process Research Articles

Современные этиологические и патогенетические аспекты воспалительнодеструктивных процессов тканей пародонта

The article presents the overview of modern etiological and pathogenetic aspects of inflammatory diseases of periodontal tissues, which have multifactorial origin. At the same time, one of the major factors causing inflammatory process development is periodontium pathogenic microorganisms where with the greatest aggression actinobacillus actinomycetemcomitans, porphiromonas gingivalis, bacteroides forsythus, prevotella intermedia prevail. Meanwhile, one of the main nutritious assets for bacteria is the soft dental plaque that is usually connected with an unsatisfactory hygienic condition of the oral cavity. A microcirculation disorder in periodontal vessels which is followed by blood velocity reduction and development of periodontal tissue hypoxia, generally at the level of capillaries is the main cause from the pathogenetic point of view of chronic periodontal disease development. This situation causes further increase of pathological process in periodontal tissues which is followed by severe disturbances of angioarchitecture where a degree of its expressiveness depends on intensity and duration of inflammatory process. The wide range of etiological and pathogenetic factors of pathological processes of periodontal tissues of inflammatory and destructive character needs further researches to improve the treatment-and-prophylactic dental help taking into account their possible reasons and mechanisms of cause and development.

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.

Anti-inflammatory and immune stimulating effects of trekrezan in treatment of of inflammatory and degenerative damages of the smooth parodont tissue

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 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.

Pathological studies on experimental pulmonary fibrosis induced by soluble immune complex--especially on its electron microscopic observations.

Diffuse pulmonary fibrosis was induced experimentally in guinea pig by administration of heterologous immune complex with simultaneous inhalation of subtoxic oxygen. The capillary endothelium was affected primarily by soluble immune complex and this resulted in interstitial pulmonary edema. The most characteristic findings in this study were demonstrated in the basement membrane. Within several days, the basement membrane of both capillary endothelium and alveolar epithelium was diffusely thickened and increased in electron density. These pathological changes are supposed to cause persistence of edema fluid within interstitium and prolonged duration of inflammatory process.