Biomechanics of Healthy, Degraded and Photochemical Crosslinked Cartilage

Articular cartilage is a strong but flexible connective tissue that covers and protects the ends of long bones. Osteoarthritis (OA) is a degenerative joint disease which is the most prevalent type of arthritis. The progression and development of OA involves changes in cartilage composition and tissue degradation. As a result, the biomechanical and biotribological properties of the joint may be affected. It has not been determined how cartilage composition and mechanical properties affect its wear and friction, or if there are feasible strategies to improve cartilage performance. Photochemical crosslinking is one method to enhance the modulus and strength of collagenous tissues and improve their resistance to enzymatic degradation. In chapter 2, the effect of photochemical crosslinking on viscoelastic properties of cartilage using an indentation test were investigated. Results of the study indicated that chloro-aluminum pthalocyanine tetrasulfonic acid (CASPc) photo-initiator and 670 nm light increases the modulus of articular cartilage, though this effect is likely limited to the tissue surface. The objective of research described in chapter 3 was to assess correlations between tissue composition and modulus with friction and wear properties in healthy cartilage specimens. Viscoelastic properties of cartilage were obtained via indentation and then the coefficient of friction was measured during an accelerated in vitrowear test. The composition of adjacent cartilage tissue including collagen, glycosaminoglycans, and pyridinoline crosslinks were obtained by biochemical assays. Correlation analysis suggested that stiffer cartilage with higher glycosaminoglycans (GAGs) and collagen content leads to higher wear resistance of the cartilage. Enzymatic collagen crosslinks in type II collagen, pyridinoline (PYD), also enhances the wear resistance of the collagen network. The three parameters of wear, composition, and mechanical properties of cartilage were interrelated and were all correlated with one another. However, friction was independent of these in healthy cartilage tissue. In chapter 4, the hypothesis that mechanical wear is exacerbated in degraded cartilage tissue was tested. Fresh osteochondral specimens were treated with interleukin-1β, with chondroitinase ABC (ChABC) to specifically remove GAGs, or with collagenase to degrade the collagen network during culture. Viscoelastic properties of the tissues were characterized followed by an accelerated in vitrowear test. Results of this study suggest that although the degradation of cartilage was observed with exposure to IL-1β, ChABC and collagenase, wear was not uniform between the three. All three treatments lost GAGs across their superficial zone, and tissue loss due to wear appeared to be confined to the superficial zone. The passive loss of GAGs did not induce increased wear of the tissue. However, an increase in wear was observed with degradation of the collagen network. As the COF was not affected by the degradative treatments, the changes in wear were attributed to alterations in tissue structure and composition. Finally, in chapter 5, conclusions, and summary of all main three chapters were stated and directions for future studies were presented