Induction of advanced glycation end products and alterations of the tensile properties of articular cartilage
Article first published online: 12 DEC 2002
Copyright © 2002 by the American College of Rheumatology
Arthritis & Rheumatism
Volume 46, Issue 12, pages 3212–3217, December 2002
How to Cite
Chen, A. C., Temple, M. M., Ng, D. M., Verzijl, N., DeGroot, J., TeKoppele, J. M. and Sah, R. L. (2002), Induction of advanced glycation end products and alterations of the tensile properties of articular cartilage. Arthritis & Rheumatism, 46: 3212–3217. doi: 10.1002/art.10627
- Issue published online: 12 DEC 2002
- Article first published online: 12 DEC 2002
- Manuscript Accepted: 2 AUG 2002
- Manuscript Received: 22 FEB 2002
- Arthritis Foundation
- Dutch Arthritis Association
- The Netherlands Organization for Scientific Research
To determine whether increasing advanced glycation end products (AGEs) in bovine articular cartilage to levels present in aged human cartilage modulates the tensile biomechanical properties of the tissue.
Adult bovine articular cartilage samples were incubated in a buffer solution with ribose to induce the formation of AGEs or in a control solution. Portions of cartilage samples were assayed for biochemical indices of AGEs and tested to assess their tensile biomechanical properties, including stiffness, strength, and elongation at failure.
Ribose treatment of cartilage induced increases in tissue fluorescence, absorbance, and pentosidine content (P < 0.001 for each comparison) by amounts similar to those that occur during aging in humans. Ribose treatment of cartilage also induced an increase in dynamic modulus (60% increase) and strength (35% increase), and a decrease (25% decrease) in strain (P < 0.001 for each comparison).
The concomitant increase in AGEs and alteration of tensile properties of cartilage after ribose treatment suggest that aging-associated changes in AGEs have functional consequences for this tissue. The AGE-associated increases in strength and stiffness of cartilage may be beneficial by counteracting the decreases in these properties that are associated with degeneration. Conversely, the AGE-associated decrease in failure length, or increase in brittleness, together with increased stiffness may predispose cartilage to increased stress concentration, fracture, and aging-associated biomechanical dysfunction.