In-vitro studies have confirmed that various corticosteroids and also 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. Our in-vivo animal experiments have shown 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 months. The degenerative process was monitored by macroscopic, radiological, histological, biochemical, and stereoelectronmicroscopic methods and corresponded very well with the pathology of human osteoarthrosis. Our experimental osteoarthrosis, induced by metabolic lesions or inhibition of chondrocytes, can be influenced therapeutically by intraarticular or intramuscular treatment with the biological GAG-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 anti-arthritic properties of Rumalon or DAK-16 can be explained by its stimulation of connective tissue anabolism as well as by its inhibitory effect on catabolic enzymes responsible for cartilage breakdown. Our experiments also indicate that 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.