Torzilli P A, Grigiene R, Borrelli J, Helfet D L
Laboratory for Soft Tissue Research, Hospital for Special Surgery, New York, NY 10021-4892, USA.
J Biomech Eng. 1999 Oct;121(5):433-41. doi: 10.1115/1.2835070.
Significant evidence exists that trauma to a joint produced by a single impact load below that which causes subchondral bone fracture can result in permanent damage to the cartilage matrix, including surface fissures, loss of proteoglycan, and cell death. Limited information exists, however, on the effect of a varying impact stress on chondrocyte biophysiology and matrix integrity. Based on our previous work, we hypothesized that a stress-dependent response exists for both the chondrocyte's metabolic activity and viability and the matrix's hydration. This hypothesis was tested by impacting bovine cartilage explants with nominal stresses ranging from 0.5 to 65 MPa and measuring proteoglycan biosynthesis, cell viability, and water content immediately after impaction and 24 hours later. We found that proteoglycan biosynthesis decreased and water content increased with increasing impact stress. However, there appeared to be a critical threshold stress (15-20 MPa) that caused cell death and apparent rupture of the collagen fiber matrix at the time of impaction. We concluded that the cell death and collagen rupture are responsible for the observed alterations in the tissue's metabolism and water content, respectively, although the exact mechanism causing this damage could not be determined.
有大量证据表明，单次冲击负荷对关节造成的创伤，若低于引起软骨下骨骨折的负荷，可能会导致软骨基质的永久性损伤，包括表面裂缝、蛋白聚糖丢失和细胞死亡。然而，关于变化的冲击应力对软骨细胞生物生理学和基质完整性的影响，现有信息有限。基于我们之前的研究工作，我们假设软骨细胞的代谢活性和活力以及基质的水合作用存在应力依赖性反应。通过用名义应力范围为0.5至65MPa的冲击作用于牛软骨外植体，并在冲击后立即以及24小时后测量蛋白聚糖生物合成、细胞活力和含水量，对这一假设进行了检验。我们发现，随着冲击应力的增加，蛋白聚糖生物合成减少，含水量增加。然而，似乎存在一个临界阈值应力（15 - 20MPa），在冲击时会导致细胞死亡和胶原纤维基质的明显破裂。我们得出结论，细胞死亡和胶原破裂分别是观察到的组织代谢和含水量变化的原因，尽管导致这种损伤的确切机制尚无法确定。
