Park Seonghun, Krishnan Ramaswamy, Nicoll Steven B, Ateshian Gerard A
Department of Mechanical Engineering, Columbia University, SW Mudd, Mail Code 4703, 500 West, 120th Street, New York, NY, USA.
J Biomech. 2003 Dec;36(12):1785-96. doi: 10.1016/s0021-9290(03)00231-8.
Under physiological conditions of loading, articular cartilage is subjected to both compressive strains, normal to the articular surface, and tensile strains, tangential to the articular surface. Previous studies have shown that articular cartilage exhibits a much higher modulus in tension than in compression, and theoretical analyses have suggested that this tension-compression nonlinearity enhances the magnitude of interstitial fluid pressurization during loading in unconfined compression, above a theoretical threshold of 33% of the average applied stress. The first hypothesis of this experimental study is that the peak fluid load support in unconfined compression is significantly greater than the 33% theoretical limit predicted for porous permeable tissues modeled with equal moduli in tension and compression. The second hypothesis is that the peak fluid load support is higher at the articular surface side of the tissue samples than near the deep zone, because the disparity between the tensile and compressive moduli is greater at the surface zone. Ten human cartilage samples from six patellofemoral joints, and 10 bovine cartilage specimens from three calf patellofemoral joints were tested in unconfined compression. The peak fluid load support was measured at 79 +/- 11% and 69 +/- 15% at the articular surface and deep zone of human cartilage, respectively, and at 94 +/- 4% and 71 +/- 8% at the articular surface and deep zone of bovine calf cartilage, respectively. Statistical analyses confirmed both hypotheses of this study. These experimental results suggest that the tension-compression nonlinearity of cartilage is an essential functional property of the tissue which makes interstitial fluid pressurization the dominant mechanism of load support in articular cartilage.
在生理加载条件下,关节软骨会受到垂直于关节表面的压缩应变以及切向于关节表面的拉伸应变。先前的研究表明,关节软骨在拉伸时的模量远高于压缩时,理论分析表明,这种拉伸 - 压缩非线性在无侧限压缩加载过程中,当超过平均施加应力的33%这一理论阈值时,会增强组织间隙流体增压的幅度。本实验研究的第一个假设是,在无侧限压缩中,峰值流体负载支撑显著大于对拉伸和压缩模量相等的多孔可渗透组织预测的33%理论极限。第二个假设是,在组织样本的关节表面侧,峰值流体负载支撑高于深部区域,因为表面区域的拉伸和压缩模量之间的差异更大。对来自六个髌股关节的十个人类软骨样本以及来自三个小牛髌股关节的十个牛软骨标本进行了无侧限压缩测试。在人类软骨的关节表面和深部区域,峰值流体负载支撑分别测得为79±11%和69±15%,在小牛软骨的关节表面和深部区域分别测得为94±4%和71±8%。统计分析证实了本研究的两个假设。这些实验结果表明,软骨的拉伸 - 压缩非线性是该组织的一种基本功能特性,它使组织间隙流体增压成为关节软骨负载支撑的主要机制。