The Influence of NSAIDs on Morphology of Articular Cartilage

Abstract

A large number of experimental data have given evidence that many NSAIDs can inhibit the synthetic processes of connective tissue in-vitro and ex-vivo (For review see Trnavsky, 1974) (1). During the past 18 years we have investigated the in-vivo effect of antirheumatic drugs on knee joint cartilage using rats and hens. Single or once-weekly intraarticular injections of salicylates, indomethacin, phenylbutazone, naproxen, ibuprofen, clofezone, fufenamic acid, niflumic acid, or dexamethasone induced morphological alterations in the joint cartilage and subchondral bone, which were demonstrable by means of histology, stereoelectron-microscopy, biochemistry and X-ray. The cartilage of these laboratory animals had a faster turnover compared to man, and the degenerative and destructive processes occurred within 8–12 weeks and were identical or very similar to osteoarthritis in man. In contrast to the general opinion that all NSAIDs possess more or less the same pharmacological properties, the influence of these drugs on articular cartilage was, surprisingly, quite different. In our animal experiments we found that comparable doses between NSAIDs, such as fenbufen, ketoprofen, diclofenac, and tiaprofenic acid, did not induce any degenerative processes in cartilage and subchondral bone in-vivo. A documentation of our radiographical, macroscopical and histomorphological results demonstrated the pronounced differences between NSAIDs on joint tissue. Our experimental data suggested that in the pharmacotherapy of osteoarthritis a specific selection of NSAIDs between those with catabolic and those with non-catabolic characteristics in regard to connective tissue metabolism was important and beneficial.

Key Words:

• Antirheumatic drugs
• articular cartilage
• degenerative joint disease
• osteoarthritis
• catabolic effect