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Review
. 2009 Mar;15(1):43-53.
doi: 10.1089/ten.teb.2008.0435.

Hydrostatic pressure in articular cartilage tissue engineering: from chondrocytes to tissue regeneration

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Review

Hydrostatic pressure in articular cartilage tissue engineering: from chondrocytes to tissue regeneration

Benjamin D Elder et al. Tissue Eng Part B Rev. 2009 Mar.

Abstract

Cartilage has a poor intrinsic healing response, and neither the innate healing response nor current clinical treatments can restore its function. Therefore, articular cartilage tissue engineering is a promising approach for the regeneration of damaged tissue. Because cartilage is exposed to mechanical forces during joint loading, many tissue engineering strategies use exogenous stimuli to enhance the biochemical or biomechanical properties of the engineered tissue. Hydrostatic pressure (HP) is emerging as arguably one of the most important mechanical stimuli for cartilage, although no optimal treatment has been established across all culture systems. Therefore, this review evaluates prior studies on articular cartilage involving the use of HP, with a particular emphasis on the treatments that appear promising for use in future studies. Additionally, this review addresses HP bioreactor design, chondroprotective effects of HP, the use of HP for chondrogenic differentiation, the effects of high pressures, and HP mechanotransduction.

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Figures

FIG. 1.
FIG. 1.
Illustration of a chondrocyte exposed to hydrostatic pressure. The cell experiences a uniform normal stress, without any measurable tissue strain.
FIG. 2.
FIG. 2.
Representative hydrostatic pressure (HP) bioreactor design. (a) Computer controls (Instron), which compress piston and generate pressure within chamber. Chamber is placed in water bath to maintain temperature at 37°C. (b) HP chamber, with pressure sensor to verify pressures applied within the chamber. Color images available online at www.liebertonline.com/ten.
FIG. 3.
FIG. 3.
Hydrostatic pressure mechanotransduction. Pressurization inhibits sodium/potassium (Na/K) and Na/K/chloride channels, whereas it activates Na/hydrogen and stretch-activated calcium (Ca) channels, and triggers release of intracellular Ca stores.

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