Issue 14, 2020

Nanoscale insight into the degradation mechanisms of the cartilage articulating surface preceding OA

Abstract

Osteoarthritis (OA) is a degenerative joint disease and a leading cause of disability globally. In OA, the articulating surface of cartilage is compromised by fissures and cracks, and sometimes even worn away completely. Due to its avascular nature, articular cartilage has a poor self-healing ability, and therefore, understanding the mechanisms underlying degradation is key for OA prevention and for optimal design of replacements. In this work, the articulating surface of bovine cartilage was investigated in an environment with enhanced calcium concentration -as often found in cartilage in relation to OA- by combining atomic force microscopy, spectroscopy and an extended surface forces apparatus for the first time. The experimental results reveal that increased calcium concentration irreversibly weakens the cartilage's surface layer, and promotes stiction and high friction. The synergistic effect of calcium on altering the cartilage surface's structural, mechanical and frictional properties is proposed to compromise cartilage integrity at the onset of OA. Furthermore, two mechanisms at the molecular level based on the influence of calcium on lubricin and on the aggregation of the cartilage's matrix, respectively, are identified. The results of this work might not only help prevent OA but also help design better cartilage replacements.

Graphical abstract: Nanoscale insight into the degradation mechanisms of the cartilage articulating surface preceding OA

Associated articles

Supplementary files

Article information

Article type
Paper
Submitted
26 мар 2020
Accepted
09 юни 2020
First published
10 юни 2020

Biomater. Sci., 2020,8, 3944-3955

Author version available

Nanoscale insight into the degradation mechanisms of the cartilage articulating surface preceding OA

T. Shoaib, C. Yuh, M. A. Wimmer, T. M. Schmid and R. M. Espinosa-Marzal, Biomater. Sci., 2020, 8, 3944 DOI: 10.1039/D0BM00496K

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