Since cartilage contains no nerve endings, symptoms of osteoarthritis (OA) are indirect. Therapy of OA, to date, has been directed at the symptoms of pain, signs of inflammation and loss of function. A major advance has been surgical joint replacement. This benefit however, is often limited by the joint area involved and to the survival of the endoprosthesis. Orthopedic new approaches to therapy of OA include removal of abnormal tissue to stimulate repair (e.g., burring, abrasion) and grafting (e.g., osteochondral grafts, perichondrium, periosteum) to the subchondral bone. Controlled activity (e.g., passive motion) has been studied alone and with the above. Can a medication retard or reverse the degradative process of OA? Several medications are being examined for potential "chondroprotective" characteristics. Some of these agents are not new: oversulfated glycosaminoglycans (Arteparon) derived from cartilage and glycosaminoglycan peptides (Rumalon) derived from cartilage and bone marrow extracts may be prototypes of this approach to therapy. Other agents demonstrating potential benefit in retarding cartilage degradation may include non-steroidal anti-inflammatory agents, tiaprofenic acid, sodium pentosan sulfate and low dose corticosteroids. This concept of "chondroprotection" provides us a new approach to a disease in need of a new approach.
|Original language||English (US)|
|Number of pages||6|
|Journal||Scandinavian Journal of Rheumatology, Supplement|
|State||Published - 1988|
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