Traumatic impaction is known to cause acute cell death and macroscopic damage to cartilage and menisci in vitro. The purpose of this study was to investigate cell viability and macroscopic damage of the medial and lateral menisci using an in situ model of traumatic loading. Furthermore, the release of nitric oxide from meniscus, synovium, cartilage, and subchondral bone was also documented.
The left limbs of five rabbits were subjected to tibiofemoral impaction resulting in anterior cruciate ligament (ACL) rupture and meniscal damage. Meniscal tear morphology was assessed immediately after trauma and cell viability of the lateral and medial menisci was assessed 24 hrs post-injury. Nitric oxide (NO) released from joint tissues to the media was assayed at 12 and 24 hrs post injury.
ACL and meniscal tearing resulted from the traumatic closed joint impact. A significant decrease in cell viability was observed in the lateral menisci following traumatic impaction compared to the medial menisci and control limbs. While NO release was greater in the impacted joints, this difference was not statistically significant.
This is the first study to investigate acute meniscal viability following an in situ traumatic loading event that results in rupture of the ACL. The change in cell viability of the lateral menisci may play a role in the advancement of joint degeneration following traumatic knee joint injury.