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Review
. 2014 Oct;16(10):451.
doi: 10.1007/s11926-014-0451-6.

The mechanobiology of articular cartilage: bearing the burden of osteoarthritis

Johannah Sanchez-Adams  1 , Holly A Leddy, Amy L McNulty, Christopher J O'Conor, Farshid Guilak
Affiliations
Review

The mechanobiology of articular cartilage: bearing the burden of osteoarthritis

Johannah Sanchez-Adams et al. Curr Rheumatol Rep. 2014 Oct.

Abstract

Articular cartilage injuries and degenerative joint diseases are responsible for progressive pain and disability in millions of people worldwide, yet there is currently no treatment available to restore full joint functionality. As the tissue functions under mechanical load, an understanding of the physiologic or pathologic effects of biomechanical factors on cartilage physiology is of particular interest. Here, we highlight studies that have measured cartilage deformation at scales ranging from the macroscale to the microscale, as well as the responses of the resident cartilage cells, chondrocytes, to mechanical loading using in vitro and in vivo approaches. From these studies, it is clear that there exists a complex interplay among mechanical, inflammatory, and biochemical factors that can either support or inhibit cartilage matrix homeostasis under normal or pathologic conditions. Understanding these interactions is an important step toward developing tissue engineering approaches and therapeutic interventions for cartilage pathologies, such as osteoarthritis.

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Figures

Figure 1
Figure 1
A. Physiologic strain magnitudes measured in articular cartilage. During normal activities, diurnal strains range from 0–10% [9, 10], post activity strains range from 5–15% [–14, 102], and dynamic strains during activity range from 15–35% [15, 16]. At higher nominal strain magnitudes (50–70%), mechanical compression can cause injury [–39, 41], eventually inducing cell death via necrosis and apoptosis at strains of the highest levels (70–90%) [40, 47, 48]. B. Effects of different loading conditions on chondrocyte function. Static loading decreases cartilage metabolic activity [46], physiologic levels of dynamic loading can be anabolic or anti-inflammatory [42, 45, 85, 91, 95, 96], while hyperphysiologic levels of dynamic loading and injurious loading can induce catabolic or pro-inflammatory response [41, 49, 50, 91].
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