THE BIPHASIC POROVISCOELASTIC BEHAVIOR OF ARTICULAR-CARTILAGE - ROLE OF THE SURFACE ZONE IN GOVERNING THE COMPRESSIVE BEHAVIOR
THE BIPHASIC POROVISCOELASTIC BEHAVIOR OF ARTICULAR-CARTILAGE - ROLE OF THE SURFACE ZONE IN GOVERNING THE COMPRESSIVE BEHAVIOR
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DOI：
10.1016/0021-9290(93)90019-b
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发表时间：
1993-04-01
影响因子：
2.4
通讯作者：
MOW, VC
中科院分区：
文献类型：
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作者：
SETTON, LA;ZHU, WB;MOW, VC
关节软骨的表面纤维化是骨关节炎发展过程中退行性变化的早期迹象。为了评估表面区对压缩载荷下软骨粘弹性的影响，我们从成年阉牛制备了骨软骨栓，有和没有关节软骨的表面区，用于有限压缩蠕变实验的研究。两种粘弹性机制的相对贡献，即不依赖于流动的机制[Hayes和Bodine，J. Biomechanics 11，407-419（1978）]和依赖于流动的机制[Mow等人，J. biomech. Engng 102，73-84（1980）]，对这两类试样的压缩蠕变响应的影响，用Mak. [J.生物力学20，703-714（1986）]。从实验结果和双相多孔粘弹性理论，我们发现，摩擦阻力与间质流体流动和流体加压的负载支持在完整的标本的主导机制，即流量依赖的机制本身就足以描述正常的关节软骨压缩蠕变行为。对于去除表面的标本，我们发现一个增加的蠕变速率，这是来自一个增加的组织渗透性，以及显着变化的粘弹性固体基质的流动无关的参数。根据这些组织特性和双相多孔粘弹性理论，我们确定，在没有关节面的软骨中，负荷支持的流动依赖性机制（即摩擦阻力和流体加压）大大减少。基于这些材料参数的计算表明，对于去除表面区域的样本，软骨固体基质在蠕变的早期阶段变得更高负荷。这表明关节面的一个重要功能是提供低液体渗透性，从而限制液体渗出并增加间质液加压。因此，很可能随着关节面损伤严重程度的增加，压缩下软骨中的载荷支撑从流体阻力和加压的流动依赖性模式转变为增加的固体基质应力。这表明保持关节面的完整性对于保持组织的正常压缩行为和关节内的正常载荷承载非常重要。
Surface fibrillation of articular cartilage is an early sign of degenerative changes in the development of osteoarthritis. To assess the influence of the surface zone on the viscoelastic properties of cartilage under compressive loading, we prepared osteochondral plugs from skeletally mature steers, with and without the surface zone of articular cartilage, for study in the confined compression creep experiment. The relative contributions of two viscoelastic mechanisms, i.e. a flow-independent mechanism [Hayes and Bodine, J. Biomechanics 11, 407-419 (1978)], and a flow-dependent mechanism [Mow et al. J. biomech. Engng 102, 73-84 (1980)], to the compressive creep response of these two types of specimens were determined using the biphasic poroviscoelastic theory proposed by Mak. [J. Biomechanics 20, 703-714 (1986)]. From the experimental results and the biphasic poroviscoelastic theory, we found that frictional drag associated with interstitial fluid flow and fluid pressurization are the dominant mechanisms of load support in the intact specimens, i.e. the flow-dependent mechanisms alone were sufficient to describe normal articular cartilage compressive creep behavior. For specimens with the surface removed, we found an increased creep rate which was derived from an increased tissue permeability, as well as significant changes in the flow-independent parameters of the viscoelastic solid matrix. From these tissue properties and the biphasic poroviscoelastic theory, we determined that the flow-dependent mechanisms of load support, i.e. frictional drag and fluid pressurization, were greatly diminished in cartilage without the articular surface. Calculations based upon these material parameters show that for specimens with the surface zone removed, the cartilage solid matrix became more highly loaded during the early stages of creep. This suggests that an important function of the articular surface is to provide for a low fluid permeability, and thereby serve to restrict fluid exudation and increase interstitial fluid pressurization. Thus, it is likely that with increasing severity of damage to the articular surface, load support in cartilage under compression shifts from the flow-dependent modes of fluid drag and pressurization to increased solid matrix stress. This suggests that it is important to maintain the integrity of the articular surface in preserving normal compressive behavior of the tissue and normal load carriage in the joint.