Rolauffs Bernd, Muehleman Carol, Li Jun, Kurz Bodo, Kuettner Klaus E, Frank Eliot, Grodzinsky Alan J
Massachusetts Institute of Technology, Cambridge, Rush University Medical Center, Chicago, Illinois, USA.
Arthritis Rheum. 2010 Oct;62(10):3016-27. doi: 10.1002/art.27610.
The zonal composition and functioning of adult articular cartilage causes depth-dependent responses to compressive injury. In immature cartilage, shear and compressive moduli as well as collagen and sulfated glycosaminoglycan (sGAG) content also vary with depth. However, there is little understanding of the depth-dependent damage caused by injury. Since injury to immature knee joints most often causes articular cartilage lesions, this study was undertaken to characterize the zonal dependence of biomechanical, biochemical, and matrix-associated changes caused by compressive injury.
Disks from the superficial and deeper zones of bovine calves were biomechanically characterized. Injury to the disks was achieved by applying a final strain of 50% compression at 100%/second, followed by biomechanical recharacterization. Tissue compaction upon injury as well as sGAG density, sGAG loss, and biosynthesis were measured. Collagen fiber orientation and matrix damage were assessed using histology, diffraction-enhanced x-ray imaging, and texture analysis.
Injured superficial zone disks showed surface disruption, tissue compaction by 20.3 ± 4.3% (mean ± SEM), and immediate biomechanical impairment that was revealed by a mean ± SEM decrease in dynamic stiffness to 7.1 ± 3.3% of the value before injury and equilibrium moduli that were below the level of detection. Tissue areas that appeared intact on histology showed clear textural alterations. Injured deeper zone disks showed collagen crimping but remained undamaged and biomechanically intact. Superficial zone disks did not lose sGAG immediately after injury, but lost 17.8 ± 1.4% of sGAG after 48 hours; deeper zone disks lost only 2.8 ± 0.3% of sGAG content. Biomechanical impairment was associated primarily with structural damage.
The soft superficial zone of immature cartilage is vulnerable to compressive injury, causing superficial matrix disruption, extensive compaction, and textural alteration, which results in immediate loss of biomechanical function. In conjunction with delayed superficial sGAG loss, these changes may predispose the articular surface to further softening and tissue damage, thus increasing the risk of development of secondary osteoarthritis.
成年关节软骨的分层结构和功能导致其对压缩损伤产生深度依赖性反应。在未成熟软骨中，剪切模量和压缩模量以及胶原蛋白和硫酸化糖胺聚糖（sGAG）含量也随深度而变化。然而，对于损伤引起的深度依赖性损伤了解甚少。由于未成熟膝关节损伤最常导致关节软骨损伤，因此本研究旨在描述压缩损伤引起的生物力学、生化和基质相关变化的分层依赖性。
对牛犊浅层和深层区域的椎间盘进行生物力学特性分析。通过以100%/秒的速度施加50%压缩的最终应变来损伤椎间盘，随后进行生物力学重新表征。测量损伤时的组织压实以及sGAG密度、sGAG损失和生物合成。使用组织学、衍射增强X射线成像和纹理分析评估胶原纤维取向和基质损伤。
损伤的浅层区域椎间盘显示表面破坏、组织压实20.3±4.3%（平均值±标准误），以及即时生物力学损伤，表现为动态刚度平均±标准误降至损伤前值的7.1±3.3%，平衡模量低于检测水平。组织学上看似完整的组织区域显示出明显的纹理改变。损伤的深层区域椎间盘显示胶原卷曲，但仍未受损且生物力学完整。浅层区域椎间盘损伤后未立即丢失sGAG，但48小时后丢失了17.8±1.4%的sGAG；深层区域椎间盘仅丢失了2.8±0.3%的sGAG含量。生物力学损伤主要与结构损伤有关。
未成熟软骨的柔软浅层区域易受压缩损伤，导致浅层基质破坏、广泛压实和纹理改变，从而导致生物力学功能立即丧失。结合浅层sGAG延迟丢失，这些变化可能使关节表面更容易进一步软化和组织损伤，从而增加继发性骨关节炎发展的风险。
