Cartilage disease is a significant health issue that affects millions of patients of all ages, yet there are few interventions to prevent or slow the disease. As mechanical wear is an important component of cartilage disease, the primary objective of this project was to investigate the wear characteristics of articular cartilage and factors that may improve the tissue’s wear resistance.

In developing test parameters for cartilage wear, two different cartilage surface geometries were compared:​ smaller flat specimen and larger curved specimens that made contact in the center but not at the edge. The cartilage wear of the two geometries was compared using three different techniques. A modified wear factor was considered to be the most accurate assessment of cartilage wear, but surface damage measurement with india ink was an effective, inexpensive and quick technique to evaluate potential implant materials. Finite element models showed that flat specimens showed excessive wear at the edges due to a non-physiologic stress concentration, while the larger specimens wore more uniformly across the surface.

To identify mechanical changes due to cartilage treatments, a semiautomated indentation protocol for repeatable material characterization of the tissue was developed. The technique incorporated a small preload to detect the tissue surface, followed by a stress relaxation test at a defined indentation depth.

The effect of artificially crosslinking collagen with genipin, a naturally occurring crosslinking agent, on the modulus, coefficient of friction and wear factor of cartilage was quantified. It was found that the concentration and the duration of exposure to genipin could both be varied to alter the cartilage modulus. Artificially crosslinking bovine cartilage in genipin solutions decreased the wear factor in a dose dependent manner. Crosslinking in 2 and 10 mM genipin for 15 minutes increased the stiffness by 16 and 62% and decreased the wear factor by 43 and 71%, respectively.

Finally, it was found that a single traumatic impact decreased the elastic modulus of cartilage by 23%. Immunohistochemistry demonstrated that this may be due to damage in the collagen matrix. Crosslinking the impacted cartilage reversed the loss of the modulus and left the tissue 37% stiffer than initially.