Song Yongnam, Carter Dennis R, Giori Nicholas J
J Biomech Eng. 2014 Jun;136(6):064503. doi: 10.1115/1.4027298.
Postmeniscectomy osteoarthritis (OA) is hypothesized to be the consequence of abnormal mechanical conditions, but the relationship between postsurgical alterations in articular cartilage strain and in vivo biomechanical/biochemical changes in articular cartilage is unclear. We hypothesized that spatial variations in cartilage nominal strain (percentile thickness change) would correlate with previously reported in vivo articular cartilage property changes following meniscectomy. Cadevaric sheep knees were loaded in cyclic compression which was previously developed to mimic normal sheep gait, while a 4.7 T magnetic resonance imaging (MRI) imaged the whole joint. 3D cartilage strain maps were compared with in vivo sheep studies that described postmeniscectomy changes in shear modulus, phase lag, proteoglycan content and collagen organization/content in the articular cartilage. The area of articular cartilage experiencing high (overloaded) and low (underloaded) strain was significantly increased in the meniscectomized tibial compartment by 10% and 25%, respectively, while no significant changes were found in the nonmeniscectomized compartment. The overloaded and underloaded regions of articular cartilage in our in vitro specimens correlated with regions of in vivo shear modulus reduction. Glycosaminoglycans (GAG) content only increased at the underloaded articular cartilage but decreased at the overloaded articular cartilage. No significant correlation was found in phase lag and collagen organization/content changes with the strain variation. Comparisons between postsurgical nominal strain and in vivo cartilage property changes suggest that both overloading and underloading after meniscectomy may directly damage the cartilage matrix stiffness (shear modulus). Disruption of superficial cartilage by overloading might be responsible for the proteoglycan (GAG) loss in the early stage of postmeniscectomy OA.
半月板切除术后骨关节炎(OA)被认为是异常机械条件的结果,但关节软骨应变的术后改变与关节软骨体内生物力学/生物化学变化之间的关系尚不清楚。我们假设软骨名义应变(百分厚度变化)的空间变化与先前报道的半月板切除术后体内关节软骨特性变化相关。对尸体羊膝关节进行循环压缩加载,该加载方式先前已被开发用于模拟正常羊的步态,同时用4.7T磁共振成像(MRI)对整个关节进行成像。将三维软骨应变图与描述半月板切除术后关节软骨剪切模量、相位滞后、蛋白聚糖含量和胶原组织/含量变化的体内羊研究进行比较。在半月板切除的胫骨间室中,经历高(过载)应变和低(欠载)应变的关节软骨面积分别显著增加了10%和25%,而在未进行半月板切除的间室中未发现显著变化。我们体外标本中关节软骨的过载和欠载区域与体内剪切模量降低的区域相关。糖胺聚糖(GAG)含量仅在欠载的关节软骨处增加,但在过载的关节软骨处减少。在相位滞后以及胶原组织/含量变化与应变变化之间未发现显著相关性。术后名义应变与体内软骨特性变化之间的比较表明,半月板切除术后的过载和欠载都可能直接损害软骨基质刚度(剪切模量)。过载对表层软骨的破坏可能是半月板切除术后OA早期蛋白聚糖(GAG)丢失的原因。