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Updated: Jun 28, 2026

Addressing Practical Issues in Atomic Force Microscopy-Based Micro-Indentation on Human Articular Cartilage Explants
Published on: October 28, 2022
The effects of focal articular defects on cartilage contact mechanics
Kenneth R Gratz1, Benjamin L Wong, Won C Bae
1Department of Bioengineering, University of California-San Diego, 9500 Gilman Drive, Mail Code 0412, La Jolla, California 92093-0412, USA.
Abstract:
Focal damage to articular cartilage is common in arthroscopy patients, and may contribute to progressive tissue degeneration by altering the local mechanical environment. The effects of a focal defect, which may be oriented at various orientations relative to the subchondral bone, on the dynamics of cartilage contact and deformation are unclear. The objective of this study was to elucidate the effect of experimental full thickness focal defects, oriented at 80 degrees or 100 degrees relative to the subchondral bone, on intratissue strain and surface sliding of opposing cartilage surfaces during compression and stress relaxation. Pairs of intact bovine osteochondral blocks were compressed uniaxially by 20%, and allowed to stress relax. Tissue deformation was recorded by video microscopy. A full-thickness defect (with either 80 degrees or 100 degrees edges) was created in one block from each pair. Blocks were allowed to reswell and retested. Defect edges were then recut with the opposite orientation, allowed to reswell, and retested again. Stained nuclei were tracked by digital image correlation and used to quantify cartilage strains and surface sliding. The results indicated that loading of intact samples caused axial strain magnitudes that decreased with depth and relatively little sliding. With loading of samples containing defects, strain magnitudes were elevated in cartilage adjacent to, and opposing, defects. For samples with edge orientations of 100 degrees, sliding magnitudes were increased over surfaces adjacent to defects. These local mechanical changes due to full-thickness articular cartilage defects may contribute to altered chondrocyte metabolism, tissue damage, or accelerated wear.

