• 1 January 1982
    • journal article
    • research article
    • Vol. 41  (5) , 202-211
Abstract
In vitro studies confirmed that various corticosteroids and many nonsteroidal antirheumatic drugs exert inhibitory effects on anabolic processes in connective tissue cells. Depending on dose and at concentrations that in many cases correspond to therapeutic plasma levels, these drugs may lead to a pronounced reduction or complete blockade of synthesis of the proteoglycans and collagen of the cartilage matrix. In vivo animal experiments showed that single or repeated intraarticular applications of various antiinflammatory antirheumatics into the knee joint of hens or rats can induce progressive joint degeneration within 3-4 mo. The degenerative process was monitored by macroscopic, radiological, histological, biochemical and stereoelectron microscopic methods and corresponded very well with the pathology of human osteoarthrosis. This experimental osteoarthrosis, induced by metabolic lesions or inhibition of chondrocytes, can be influenced therapeutically by intraarticular or i.m. treatment with the biological GAG[glycosaminoglycan]-peptide complex (Rumalon) or with its high molecular fraction DAK-16. These compounds significantly reduce or even stop the degenerative progression in the osteoarthrotic knee joints. The chondroprotective and antiarthrotic properties of Rumalon or DAK-16 can be explained by its stimulation of connective tissue anabolism and by its inhibitory effect on catabolic enzymes responsible for cartilage breakdown. Catabolic reactions of corticosteroids on articular cartilage can be counteracted or reduced by concomitant administration of the chondroprotective agents. This effect might be desirable and beneficial during treatment of inflammatory phases of osteoarthrosis with intraarticular injections of corticosteroids.