Macro-, micro- and ultrastructural investigation of how degeneration influences the response of cartilage to loading.

J Mech Behav Biomed Mater

Tissue Mechanics Laboratory, Department of Chemical and Materials Engineering, University of Auckland, New Zealand.

Published: January 2012

Articular cartilage functions as a load-bearing tissue by virtue of a functional coupling between its hydrated proteoglycan component and its zonally differentiated fibrillar network. How degeneration influences this relationship at the macro-, micro-, and ultrastructural levels is investigated in this study. Healthy bovine patellae (N=9) and patellae exhibiting varying degrees of degeneration (N=16) formed the basis of the study. Cartilage-on-bone blocks obtained from each patella were subjected to creep loading under a nominal stress of 4.5 MPa via a rectangular planar indenter which incorporated a narrow channel relief space to create a defined region where the cartilage would not be directly loaded. Following the attainment of creep equilibrium each sample was chemically fixed while under load so as to preserve the deformed state of the cartilage matrix. The structural response of the matrix was then analysed using differential interference contrast (DIC) optical microscopy and scanning electron microscopy (SEM). The morphology of the cartilage matrix extruded into the channel relief region was dramatically influenced by the severity of degeneration. The microscopic and ultrastructural characteristics of the extruded matrix showed that the load response of bulk cartilage is determined primarily by the microstructural integrity of the strain-limiting tangential layer and the nano-level interconnectivity of the fibrillar network. In conclusion, this study showed that three mechanically significant structural features of cartilage are important: (1) the strain limiting surface layer; (2) the micro-level boundaries in its zonally differentiated structure, and (3) the extent of fibrillar interconnectivity. Degeneration degrades or destroys the articular surface and 'destructures' the fibrillar network such that the latter functions less effectively as a proteoglycan entrapment system.

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http://dx.doi.org/10.1016/j.jmbbm.2011.08.024DOI Listing

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