Strauss Eric J, Goodrich Laurie R, Chen Chih-Tung, Hidaka Chisa, Nixon Alan J
Laboratory for Soft Tissue Research, Hospital for Special Surgery, New York, New York 10021, USA.
Am J Sports Med. 2005 Nov;33(11):1647-53. doi: 10.1177/0363546505275487. Epub 2005 Aug 10.
Chondral defects may lead to degradative changes in the surrounding cartilage, predisposing patients to developing osteoarthritis.
To quantify changes in the biomechanical and biochemical properties of the articular cartilage adjacent to chondral defects after experimental defect repair.
Controlled laboratory study.
Specimens were harvested from tissue within (lesion), immediately adjacent to, and at a distance from (remote area) a full-thickness cartilage defect 8 months after cartilage repair with genetically modified chondrocytes expressing insulin-like growth factor-I or unmodified, control chondrocytes. Biomechanical properties, including instantaneous Young's and equilibrium aggregate moduli, were determined by confined compression testing. Biochemical properties, such as water and proteoglycan content, were also measured.
The instantaneous Young's modulus, equilibrium modulus, and proteoglycan content increased, whereas water content decreased with increasing distance from the repaired lesion. The instantaneous Young's and equilibrium moduli of the adjacent articular cartilage were 80% and 50% that of remote area samples, respectively, whereas water content increased 0.9% and proteoglycan content was decreased by 35%. No significant changes in biomechanical and biochemical properties were found either in the lesion tissue or in adjacent cartilage with genetic modification of the chondrocytes.
Articular cartilage adjacent to repaired chondral defects showed significant remodeling 8 months after chondral defect repair, regardless of whether genetically modified or unmodified cells were implanted.
Changes in the biochemical and biomechanical properties of articular cartilage adjacent to repaired chondral defects may represent remodeling as part of an adaptive process or degeneration secondary to an altered distribution of joint forces. Quantification of these changes could provide important parameters for assessing progress after operative chondral defect repair.
软骨损伤可能导致周围软骨发生降解性改变，使患者易患骨关节炎。
量化实验性缺损修复后软骨损伤周边关节软骨的生物力学和生物化学特性变化。
对照实验室研究。
在使用表达胰岛素样生长因子-I的转基因软骨细胞或未修饰的对照软骨细胞进行软骨修复8个月后，从全层软骨缺损处（损伤部位）、紧邻缺损处以及距缺损一定距离处（远隔区域）获取组织样本。通过受限压缩试验测定生物力学特性，包括瞬时杨氏模量和平衡聚集体模量。同时测量水和蛋白聚糖含量等生物化学特性。
随着与修复损伤处距离的增加，瞬时杨氏模量、平衡模量和蛋白聚糖含量增加，而水含量降低。紧邻关节软骨的瞬时杨氏模量和平衡模量分别为远隔区域样本的80%和50%，而水含量增加0.9%，蛋白聚糖含量降低35%。在损伤组织或经软骨细胞基因修饰的相邻软骨中，未发现生物力学和生物化学特性有显著变化。
软骨损伤修复后8个月，无论植入的是转基因细胞还是未修饰细胞，修复后的软骨损伤周边关节软骨均显示出显著重塑。
修复后的软骨损伤周边关节软骨的生物化学和生物力学特性变化可能代表重塑，是适应性过程的一部分，或因关节力分布改变继发退变。量化这些变化可为评估软骨损伤手术修复后的进展提供重要参数。
