ABSTRACT
Osteoarthritis (OA) is the most common arthropathy worldwide and a significant cause of morbidity and disability, especially in the elderly.[1] Both biomechanical forces and biochemical processes are important in its pathogenesis, which is characterized by progressive deterioration of articular cartilage causing debilitating pain and loss of normal joint motion. Standard therapies can alleviate the symptoms of OA to some extent but have no ability to prevent disease progression. A number of alternative substances, collectively referred to as nutraceuticals, have been touted in the lay press as being beneficial for OA, with particular interest focused on glucosamine and chondroitin sulfate.[2,3]
Chondroitin sulfate is a key component of normal cartilage that is substantially reduced in the cartilage of individuals with OA. This observation stimulated interest in its potential role as a therapeutic agent, and continuing investigations have now identified a number of apparent biologic actions. No consensus exists, however, as to its clinical efficacy or utility. While it has gained a measure of acceptance in Europe, physicians in the United States appear to be less convinced by the available clinical data. Nonetheless, the interest of the general population has been piqued, and owing to its universal availability as an overthe-counter supplement, present use of chondroitin sulfate, either with or without standard OA therapy, is not uncommon.[4]
STRUCTURE, BIOCHEMISTRY, AND PHYSIOLOGY
Chondroitin sulfate is classified as a glycosaminoglycan (GAG) and is present abundantly in articular cartilage as well as in many other tissues, including bone, tendon, intervertebral disk, aorta, cornea, and skin. It is composed of alternating N-acetylgalactosamine and D-glucuronic acid residues, which form a long, unbranched chain. While the length of the chain is variable, it seldom exceeds 200-250 disaccharide units. Sulfation occurs at the 4 or 6 position of the N-acetylgalactosamine residue to produce chondroitin4-sulfate (chondroitin sulfate A) and chondroitin6-sulfate (chondroitin sulfate C), respectively, whereas the substitution of L-iduronic acid for D-glucuronic acid produces dermatan sulfate, formerly known as chondroitin sulfate B (Fig. 1).
