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Effect of Mechanical Forces on the Metabolic Responses of Articular Cartilage

As for the interactions between the biomechanics and the biology of articular cartilage, the TCL has been investigating the relationship between the mechanical loading and the biological response of articular cartilage in order to understand the mechanisms of mechanical stress-induced degeneration (i.e., the fibrillation or degradation of the tissue matrix) and hypertrophy (i.e., the excessive production of the tissue matrix) of articular cartilage, which are often seen during the early stage of osteoarthritis. The mechanical stress is also known to play an important role in maintaining a homeostasis of normal articular cartilage, a balance between the anabolic and catabolic processes of chondrocytes.

We have recently discovered that during a cyclic compressive joint loading an intermittent negative pressure (vacuum) can be created within the extracellular matrix of articular cartilage, and that this intermittent negative pressure has a stimulative effect on the metabolism of chondrocytes. An in vitro experiment conducted in our laboratory has found that even a small dose of an intermittent negative pressure can stimulate chondrocytes to increase the production of cartilage-specific molecules by up to 40%.

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Abstract From Selected Publications

Intermittent Sub-Ambient Interstitial Hydrostatic Pressure As A Potential Mechanical Stimulator For Chondrocyte Metabolism
Osteoarthritis & Cartilage, 7:71-80, 1999.

Experimental findings have suggested that the metabolic activities of articular cartilage can be influenced by mechanical stimuli. Our mathematical analysis predicted that cyclic compressive loading may create periods of intermittent negative hydrostatic pressure within the cartilage extracellular matrix. Based on this mathematical analysis, we hypothesize that intermittent negative hydrostatic pressure, created in the cartilage extracellular matrix during cyclic compression, has a stimulative effect on the biosynthesis of chondrocytes. In order to test this hypothesis, the present study developed a custom-designed negative pressure generator to subject a monolayer culture of chondrocytes to an intermittent negative pressure. It was found that the intermittent negative pressure produced a 40% increase in proteoglycan and a 17% increase in non-collagenous protein synthesis during the pressurization period (p<0.05). The collagenous protein synthesis was not affected by the intermittent negative pressure regimen used in this study. After the intermittent negative pressurization, the metabolic activities of the chondrocytes returned to normal (control level). The intermittent negative pressure also produced an increase in the mRNA signals for aggrecan. Therefore, we conclude that intermittent negative pressure may be one of the potential mechanical stimulators of chondrocytes in articular cartilage during dynamic compression.

See our Publications for the further details about our projects on mechanical regulations of metabolic responses of articular cartilage.

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