Issue title: Selected papers of the 5th International Symposium on Mechanobiology of Cartilage and Chondrocyte, Athens, May 2007
Article type: Research Article
Authors: Gratz, Kenneth R. | Wong, Benjamin L. | Bae, Won C. | Sah, Robert L.; ; ;
Affiliations: Department of Bioengineering, University of California, San Diego, La Jolla, CA, USA | Department of Radiology, University of California, San Diego, La Jolla, CA, USA | Stein Institute for Research on Aging, University of California, San Diego, La Jolla, CA, USA | Whitaker Institute of Biomedical Engineering, University of California, San Diego, La Jolla, CA, USA
Note: [] Address for correspondence: Dr. Robert L. Sah, Department of Bioengineering, 9500 Gilman Drive, Mail Code 0412, University of California, San Diego, La Jolla, CA 92093-0412, USA. Tel.: +1 858 534 0821; Fax: +1 858 822 1614; E-mail: [email protected].
Abstract: Focal damage to articular cartilage is commonly found in symptomatic knees and may contribute to patient discomfort and progressive cartilage degeneration. The objective of this study was to quantify changes in cartilage intra-tissue strain and sliding occurring near a focal defect. Pairs of human osteochondral blocks were compressed by 20% of the total cartilage thicknesses, and tissue deformation was recorded by video microscopy. Then, a single, full-thickness defect was created in one block from each pair, blocks were allowed to re-swell, and the pairs were retested. Stained nuclei, acting as fiducial markers, were tracked by digital image correlation and used to calculate cartilage strains and surface displacement. With intact samples, axial strain decreased with depth, as is typical of cartilage, and relatively little sliding occurred between surfaces. With defect samples, axial compression of cartilage at the defect rim rose by ~30%, shear in the opposing tissue increased 10-fold to ~0.15, and local sliding was elevated to >50 μm. In vivo, tissue near a defect likely experiences increased overall compression, magnifying these observed in vitro effects. Excessive strains may contribute to cell death, matrix damage, or accelerated wear, and repair efficacy may depend on the ability to alleviate adverse mechanical conditions.
Keywords: Osteoarthritis, biomechanics, cartilage damage, cartilage deformation
DOI: 10.3233/BIR-2008-0475
Journal: Biorheology, vol. 45, no. 3-4, pp. 193-207, 2008
