Publications of Faculty of Medicine:Role of Articular Chondrocyte Changes and Mononuclear Apoptosis in the Pathogenesis and Strategy of Therapy in Juvenile Rheumatoid Arthritis: Abstract

Title:
Role of Articular Chondrocyte Changes and Mononuclear Apoptosis in the Pathogenesis and Strategy of Therapy in Juvenile Rheumatoid Arthritis
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Abstract:

The objective of this research work is to study the changes in articular cartilage and chondrocytes in juvenile rheumatoid arthritis (JRA) and the implication of mononuclear cells apoptosis, proinflammatory cytokines, keratan sulfate (KS) and Transforming Growth Factor B (TGFB) in the pathogenesis of the joints changes. The study included 42 children diagnosed as polyarticular JRA, according to the criteria of the American College of Rheumatology, and 50 normal children as control. The following investigations were carried out: histopathology of articular cartilage specimens and chondrocyte culture, assay of IL-1 a, IL-10, TNF-a, IL-1R, 'TNFp55, TNFp75 in synovial fluid (SF) and peripheral blood serum (ser), estimation of concentration of keratan sulfate (KS), transforming growth factor B (TGFB), CD95, and assessment of apoptotic index of mononuclear cells, in the synovial fluid and peripheral blood (PB). The results could be summarized as follows: morphological and immunohistochemical changes in the matrix and chondrocytes, increased levels of proinflammatory cytokines and KS, and decreased CD95, TGFB, apoptotic index of momonuclear cells, in synovial fluid and peripheral blood. The changes are more significant in SF. In conclusion, the delayed mononuclear cell apoptosis and increased secretion of proinflammatory cytokines lead to the morphological and immunchistochemical changes in articular castilage and chondrocytes, high KS and low TGFB. So far, we can recommend to add to the strategy of therapy, anti-proinflammatory cytokines and injections of TGFB for amelioration of the disease