Articular cartilage is the load-bearing connective tissue that covers the ends of long-bones in diarthoidal joints and provides low friction, wear resistant sliding during joint articulation. Cartilage has complex mechanical and surface properties that greatly complicate the biomechanics of contact between opposing cartilage surfaces. Focal damage to articular cartilage is common, and once initiated, shows limited capacity for repair. Furthermore, changes in the mechanical environment at a site of damage may make the tissue more susceptible to continued degeneration. The goal of this dissertation work was to contribute to the understanding of changes in the mechanical environment due to focal articular defects and to quantify the extent to which normal mechanical properties are restored following in vivo cartilage defect repair.

Experimental methods were developed to allow in vitro mechanical testing of two contacting cartilage surfaces while tissue deformation was imaged;​ image analysis methods were introduced to automatically track fiducial markers within the tissue, and a mathematical framework was developed to describe the dynamic deformation and sliding between opposing surfaces from the movement of these discrete tissue markers.

In vitro experiments on both bovine and human cartilage showed elevated axial compressive strains in the cartilage adjacent to a defect and sharp increases in shear and lateral strains in the region opposing the defect rim. Changes in intra-tissue strains arose early during compressive loading and were maintained following stress relaxation in the loaded state. Increased sliding was also observed between surfaces near a focal defect and was related to characteristics of the defect edge.

Assessment of samples retrieved following in vivo defect repair showed that currently available cell-based therapies may result in greater integration strength than has previously been reported (~1/2 normal tensile strength), but that the tensile modulus of the repair tissue remains orders of magnitude lower than that of normal articular cartilage after 9 months in vivo.

Understanding the changes in mechanical environment near a focal defect that are likely to lead to continued degeneration, and the ability for repair strategies to restore normal biomechanical tissue function, may help to guide treatments to arrest or reverse the degenerative process.