Articular cartilage plays an important role in joint health and mobility. It provides a near frictionless surface for bones to glide upon each other, which allows for joint movement, and it absorbs high impacts. Cartilage function can be greatly altered by changes in the structural or biochemical composition of the tissue, which can lead to joint complications. Osteoarthritis is the most common form of joint disease caused by degeneration of cartilage. In this thesis, a protocol was developed using a displacement control indentation method to detect spatial variances in permeability and shear modulus over a cartilage surface. Cartilage degeneration was generated by inducing focal defects on bovine tibial plateaus using trypsin. We hypothesized that cartilage degradation could be detected by changes in permeability more sensitively than changes in modulus.

Our findings from experimental testing suggested that areas of known cartilage damage can be detected by more rapid increase in permeability through the duration of the experiment compared to undamaged areas of the same surface. Investigation of the changes in shear modulus did not yield a substantial difference between treated and control plateaus, which is consistent with findings from previous work. The permeability and shear modulus were validated in a poroelastic finite element model of the indentation test in which cartilage properties from the experimental tests were used to simulate the stress relaxation behavior. The cartilage behavior was consistent with the physical tests;​ thus, successfully validating the method used to calculate the materials properties. Glycosaminoglycan content declined with cartilage degradation, likely the compositional factor causing the change in permeability. Thus, permeability can be used as the critical parameter to determine early signs of osteoarthritis.