FEATURES OF EXPERIMENTAL OSTEOARTHROSIS CAUSED BY DEXAMETHASONE AND TALC

Author:

Osmanova S.O.1,Osmanov O.O.1,Alimkhanova A.A.1

Affiliation:

1. Dagestan State Medical University, pl. Lenina 1, Makhachkala, 367000, Russian Federation

Abstract

Introduction. An experimental study of the pathogenetic mechanisms of the development of inflammatory-destructive changes in the joints in animal models was carried out in order to develop new diagnostic strategies for further implementation of the results obtained in clinical practice, determination of morphometric and metabolic features of the skeletal connective tissue of the rat knee joints. Material and methods. The authors studied histological preparations of knee joints stained with Mayer’s hematoxylin and eosin, alcian blue (pH 1.0 and 2.5) according to Van Gieson, Masson and Mallory. The metabolic properties of cartilage and bone tissue were studied by determining the concentration of hyaluronic acid, osteocalcin, and type I collagen in the blood serum of laboratory animals. Results. In rats with osteoarthritis induced by the administration of dexamethasone and talc, a 50% decrease in the thickness of the articular cartilage in its loaded areas was noted. There was also a violation of the spatial distribution of chondrocytes, a decrease (p<0.01) in the nuclear-cytoplasmic ratio of chondrocytes to 0.3 and an increase in the serum concentration of hyaluronic acid (p<0.001) to 110.2 ng/ml, fragments of type I collagen (p<0.001) to 217.9 ng/ml and osteocalcin (p<0.001) to 231.1 ng/ml. Conclusion. The main pathogenetic features of experimental osteoarthritis induced by dexamethasone and talc are a violation of the density of distribution, morphological features and functional activity of chondrocytes. All this leads to inhibition of the synthesis of the components of the extracellular matrix of the articular cartilage, and is also accompanied by the activation of the destruction of proteoglycans containing non-sulfated glycosaminoglycans.

Publisher

Russian Vrach, Publishing House Ltd.

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