Guilak F, Ratcliffe A, Mow V C
Department of Surgery, Duke University Medical Center, Durham, North Carolina 27710, USA.
J Orthop Res. 1995 May;13(3):410-21. doi: 10.1002/jor.1100130315.
It is well accepted that mechanical forces can modulate the metabolic activity of chondrocytes, although the specific mechanisms of mechanical signal transduction in articular cartilage are still unknown. One proposed pathway through which chondrocytes may perceive changes in their mechanical environment is directly through cellular deformation. An important step toward understanding the role of chondrocyte deformation in signal transduction is to determine the changes in the shape and volume of chondrocytes during applied compression of the tissue. Recently, a technique was developed for quantitative morphometry of viable chondrocytes within the extracellular matrix using three-dimensional confocal scanning laser microscopy. In the present study, this method was used to quantify changes in chondrocyte morphology and local tissue deformation in the surface, middle, and deep zones in explants of canine articular cartilage subjected to physiological levels of matrix deformation. The results indicated that at 15% surface-to-surface equilibrium strain in the tissue, a similar magnitude of local tissue strain occurs in the middle and deep zones. In the surface zone, local strains of 19% were observed, indicating that the compressive stiffness of the surface zone is significantly less than that of the middle and deep zones. With this degree of tissue deformation, significant decreases in cellular height of 26, 19, and 20% and in cell volume of 22, 16, and 17% were observed in the surface, middle, and deep zones, respectively. The deformation of chondrocytes in the surface zone was anisotropic, with significant lateral expansion occurring in the direction perpendicular to the local split-line pattern. When compression was removed, there was complete recovery of cellular morphology in all cases. These observations support the hypothesis that deformation of chondrocytes or a change in their volume may occur during in vivo joint loading and may have a role in the mechanical signal transduction pathway of articular cartilage.
机械力可调节软骨细胞的代谢活性，这一点已得到广泛认可，尽管关节软骨中机械信号转导的具体机制仍不清楚。软骨细胞感知其机械环境变化的一种可能途径是直接通过细胞变形。理解软骨细胞变形在信号转导中的作用的重要一步是确定在组织施加压缩时软骨细胞的形状和体积变化。最近，开发了一种使用三维共聚焦扫描激光显微镜对细胞外基质内活软骨细胞进行定量形态测量的技术。在本研究中，该方法用于量化犬关节软骨外植体表面、中间和深部区域在生理水平的基质变形下软骨细胞形态和局部组织变形的变化。结果表明，在组织达到15%的表面对表面平衡应变时，中间和深部区域出现了类似程度的局部组织应变。在表面区域，观察到局部应变达到19%，表明表面区域的压缩刚度明显低于中间和深部区域。在这种程度的组织变形下，表面、中间和深部区域的细胞高度分别显著降低了26%、19%和20%，细胞体积分别显著降低了22%、16%和17%。表面区域软骨细胞的变形是各向异性的，在垂直于局部分裂线模式的方向上发生了显著的横向扩张。当去除压缩时，所有情况下细胞形态都完全恢复。这些观察结果支持了这样的假设，即在体内关节加载过程中软骨细胞可能会发生变形或其体积发生变化，并且可能在关节软骨的机械信号转导途径中起作用。
