Matthew Szarko1, Yang Xia2. 1. Division of Biomedical Sciences, St. George's, University of London, Cranmer Terrace, London, SW17 0RE, Telephone: +44 (0)20 8725 2831, , mszarko@sgul.ac.uk. 2. Department of Physics, Oakland University, Rochester MI, USA 48309, Tel: 001-248-370-3420, , xia@oakland.edu.
Abstract
OBJECTIVE: The structural anisotropy of articular cartilage controls its deformation response. As proteoglycans and collagen vary with depth, simple uniaxial compression results in inhomogeneous deformation with distinct depth-dependent mechanical properties. Investigations into depth-dependent mechanical properties of articular cartilage have previously required tissue modification after specimen isolation. Such modifications include histological processes, freezing, subchondral bone removal, and fluorescent staining that may alter the tissue, limiting in vivo applicability. DESIGN: Using a custom tissue-sectioning device, 0.1 mm thick unfixed, unstained, osetochondral samples were obtained. A customized apparatus loaded samples to 12.5, 24, and 29% compression in under a microscope with 10× magnification. Equilibrium load was measured after stress relaxation. Intra-tissue displacement was measured by tracing groups of cells between the different compression levels using a digital imaging program. Cell distance from the subchondral bone was measured to identify intra-tissue displacement and calculate strain. RESULTS: The results reveal that stress levels and intra-tissue displacement increased with greater tissue compression (p <0.05). Intra-tissue displacement decreased as depth from the articular surface increased (p<0.01). This occurred for each level of tissue compression. Overall compressive resistance is seen to increase with depth from the articular surface. CONCLUSIONS: The current study identifies a method directly visualising and assessing the depth-dependent structural response to compression. The ability to avoid tissue modification after specimen isolation, allows this procedure to more closely approximate in vivo conditions and may provide an important method for analyzing the coordinated changes in cartilage composition and function due to ageing and disease.
OBJECTIVE: The structural anisotropy of articular cartilage controls its deformation response. As proteoglycans and collagen vary with depth, simple uniaxial compression results in inhomogeneous deformation with distinct depth-dependent mechanical properties. Investigations into depth-dependent mechanical properties of articular cartilage have previously required tissue modification after specimen isolation. Such modifications include histological processes, freezing, subchondral bone removal, and fluorescent staining that may alter the tissue, limiting in vivo applicability. DESIGN: Using a custom tissue-sectioning device, 0.1 mm thick unfixed, unstained, osetochondral samples were obtained. A customized apparatus loaded samples to 12.5, 24, and 29% compression in under a microscope with 10× magnification. Equilibrium load was measured after stress relaxation. Intra-tissue displacement was measured by tracing groups of cells between the different compression levels using a digital imaging program. Cell distance from the subchondral bone was measured to identify intra-tissue displacement and calculate strain. RESULTS: The results reveal that stress levels and intra-tissue displacement increased with greater tissue compression (p <0.05). Intra-tissue displacement decreased as depth from the articular surface increased (p<0.01). This occurred for each level of tissue compression. Overall compressive resistance is seen to increase with depth from the articular surface. CONCLUSIONS: The current study identifies a method directly visualising and assessing the depth-dependent structural response to compression. The ability to avoid tissue modification after specimen isolation, allows this procedure to more closely approximate in vivo conditions and may provide an important method for analyzing the coordinated changes in cartilage composition and function due to ageing and disease.
Authors: Albert C Chen; Stephen M Klisch; Won C Bae; Michele M Temple; Kevin B McGowan; Kenneth R Gratz; Barbara L Schumacher; Robert L Sah Journal: Methods Mol Med Date: 2004
Authors: David Kahn; Daniel Mittelstaedt; John Matyas; Xiangui Qu; Ji Hyun Lee; Farid Badar; Clifford Les; Zhiguo Zhuang; Yang Xia Journal: Open Orthop J Date: 2016-11-30
Authors: Sheetal R Inamdar; Ettore Barbieri; Nicholas J Terrill; Martin M Knight; Himadri S Gupta Journal: Acta Biomater Date: 2019-07-30 Impact factor: 8.947