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Research Article Free access | 10.1172/JCI106660

The Glycosaminoglycans of Normal and Arthritic Cartilage

Henry J. Mankin and Louis Lippiello

Hospital for Joint Diseases, New York 10035

Mount Sinai School of Medicine of the City University of New York, New York 10035

Find articles by Mankin, H. in: PubMed | Google Scholar

Hospital for Joint Diseases, New York 10035

Mount Sinai School of Medicine of the City University of New York, New York 10035

Find articles by Lippiello, L. in: PubMed | Google Scholar

Published August 1, 1971 - More info

Published in Volume 50, Issue 8 on August 1, 1971
J Clin Invest. 1971;50(8):1712–1719. https://doi.org/10.1172/JCI106660.
© 1971 The American Society for Clinical Investigation
Published August 1, 1971 - Version history
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Abstract

The cartilages from the hip joints of 13 normal and 15 osteoarthritic humans were analyzed for glycosaminoglycan content and distribution. The GAGs were separated by elution with CPC on a short cellulose column by the technique of Svejcar and Robertson after digestion of the tissue with pronase and papain. The eluates were identified by a variety of methods including determination of molar ratios, N-acetyl-hexosamine determinations after hyaluronidase treatment and thin-layer chromatography of unhydrolyzed and hydrolyzed GAGs.

From the data obtained, it was demonstrated that cartilage from arthritic patients showed a significant increase in the concentration of chondroitin 4-sulfate and a significant decrease in keratan sulfate, with only slight changes in the total amount of GAG present. Calculations of the molar ratios showed variation in the sulfation with chondroitin 4-sulfate appearing in the “supersulfated” state in the arthritic cartilage.

The data lead to speculation regarding the process of osteoarthritis, and it is concluded that the changes seen are more likely to represent an altered pattern of synthesis rather than selective degradation. Since the changes suggest a younger cartilage, a theory is advanced that the chondrocyte responds to the chronic stress of osteoarthritis by modulation to a chondroblastic phase.

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