Age Related Differences in Chondrocyte Viability and Biosynthetic Response to Mechanical Injury

Mechanical trauma has been shown to cause chondrocyte death. The response of the surviving cells has not been fully characterized especially with regards to aging. This study investigates the response to injury in aging chondrocytes. Human articular chondrocytes from younger and older donor knees were cultured in agarose gel disks for three weeks. Disks were submitted to a brief 30% compressive insult (injured), or cultured in IL-1beta (IL-1), or served as controls. Glycosaminoglycan biosynthesis was measured by radiolabeled sulfate (SO4) uptake 48 hours after injury. Chondrocytes from the older group synthesized less glycosaminoglycan as measured by SO4 uptake. This ranged from a 22% to 61% reduction relative to the younger group. After injury, a further decline in glycosaminoglycan synthesis was noted in both older and younger groups. However, the decline in glycosaminoglycan synthesis was more marked in the older group. While mechanical injury results in chondrocyte death, the surviving cells exhibit the effect of injury by reduced biosynthesis and increased loss of matrix. This suggests that the impact of mechanical injury may progress beyond the traumatic event. With age, fewer cells may survive with a further decrease in biosynthetic response. This has implications in the repair response and may provide insights in the development of chondroprotective measures.