On how degenerative changes influence the microstructural response of articular cartilage to mechanical loading

Abstract

The general objective of this PhD project was to understand how degenerative changes associated with collagen network de-structuring in articular cartilage (AC) influence its microstructural response to loading. Two main testing methods were employed: Firstly, cartilage-on-bone blocks were compressed using an indenter incorporating a central relief channel to allow the AC to bulge into this channel during creep compression to an extent governed by its inherent matrix constraints. Secondly, transverse stretching and swelling experiments were conducted using isolated cartilage samples consisting exclusively of radial zone matrix. Three channel indentation studies are described. In the first study, a single radial incision was made in the AC to varying depths with respect to its zonal structure. This resulted in an altered pattern of matrix shear following compression whose intensity varied with incision depth. The second study showed that a reduced water-binding potential in otherwise intact cartilage matrix did not lead to altered patterns of shear, but led to surface rupture and abnormal matrix collapse. The important role of the osteochondral junction in the development of internal matrix shear was demonstrated in the third study. De-structured isolated cartilage samples had a decreased transverse stiffness compared to structurally intact samples, despite their similar glycosaminoglycan content. It was shown that this resulted from the reduced level of fibrillar interconnectivity in the former, which also led to a loss of functional coupling between the collagen network and the proteoglycans. The proteoglycans in the degenerate matrix did, however, still contribute significantly to tissue stiffness. Further, it was shown that tissue swelling and the maximum tensile stiffness in isolated cartilage samples are more reliable indicators of its degenerative state than could be obtained from a measurement of its lower isostrain modulus. The results of the studies described in this thesis have increased our understanding of the mechano-structural mechanism underlying the degenerative cascade and provide important implications for the development of cartilage replacements and computational models. An intact collagen network incorporating a functional zonal distribution, sufficient fibrillar interconnectivity, and proper attachment to the subchondral bone are all critical for the containment of matrix water and development of internal shear.