Department of Orthopaedics and Traumatology, The Chinese University of Hong Kong, Hong Kong SAR, China.
J Orthop Res. 2012 Jan;30(1):37-46. doi: 10.1002/jor.21495. Epub 2011 Jul 14.
The acquisition of chondro-osteogenic phenotypes and erroneous matrix deposition may account for poor tissue quality after acute tendon injury. We investigated the presence of chondrocyte phenotype, ossification, and the changes in the expression of major collagens and proteoglycans in the window wound in a rat patellar tendon window injury model using histology, von Kossa staining and immunohistochemistry of Sox 9, major collagens, and proteoglycans. Our results showed that the repair tissue did not restore to normal after acute injury. Ectopic chondrogenesis was observed in 33% of samples inside wound at week 4 while ectopic ossification surrounded by chondrocyte-like cells were observed in the window wound in 50% of samples at week 12. There was sustained expression of biglycan and reduced expression of aggrecan and decorin in the tendon matrix in the repair tissue. The erroneous deposition of extracellular matrix and ectopic chondro-ossification in the repair tissue, both might influence each other, might account for the poor tissue quality after acute injury. Higher expression of biglycan and aggrecan were observed in the ectopic chondro-ossification sites in the repair tissue, suggesting that they might have roles in ectopic chondro-osteogenesis.
软骨 - 成骨表型的获得和错误的基质沉积可能是急性肌腱损伤后组织质量差的原因。我们使用组织学、Sox9、主要胶原蛋白和蛋白聚糖的 von Kossa 染色和免疫组织化学,研究了大鼠髌腱窗损伤模型中窗口伤口中软骨细胞表型、骨化和主要胶原蛋白和蛋白聚糖表达变化的存在。我们的结果表明,急性损伤后修复组织未恢复正常。在第 4 周时,33%的样本中观察到异位软骨生成,而在第 12 周时,50%的样本中观察到被软骨样细胞包围的异位骨化。在修复组织中的肌腱基质中,存在着聚集蛋白聚糖的持续表达和聚集蛋白聚糖和核心蛋白聚糖的减少表达。修复组织中细胞外基质的错误沉积和异位软骨 - 骨化可能相互影响,可能是急性损伤后组织质量差的原因。在修复组织中的异位软骨 - 骨化部位观察到更高表达的聚集蛋白聚糖和聚集蛋白聚糖,表明它们可能在异位软骨 - 成骨发生中发挥作用。