Abstract
BackgroundTraumatic 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.MethodsThe 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.ResultsACL 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.ConclusionThis 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.Electronic supplementary materialThe online version of this article (doi:10.1186/1471-2474-15-297) contains supplementary material, which is available to authorized users.
Highlights
Traumatic impaction is known to cause acute cell death and macroscopic damage to cartilage and menisci in vitro
Anterior cruciate ligament (ACL) injury is one of the most common injuries to the knee [1]. Concomitant injuries, such as meniscal tears and bone bruising, often occur with traumatic ACL rupture [1]. These injuries are known to play a role in soft tissue damage and the progression of post-traumatic osteoarthritis (PTOA) of the knee
High levels of nitric oxide (NO) can lead to increased apoptosis in chondrocytes [7] and synoviocytes [8], and increased NO levels have been associated with the progression of osteoarthritis
Summary
Traumatic impaction is known to cause acute cell death and macroscopic damage to cartilage and menisci in vitro. Acute morphological and biological perturbations, such as cartilage fissuring, subchondral bone bruising, and chondrocyte death have been associated with rapid joint degeneration [2] Such injuries, along with posterolateral meniscal tearing, have been observed after traumatic impaction that leads to ACL rupture [3,4]. Previous studies have looked at NO release in a lapine model following transection of the anterior cruciate ligament [11] and following partial meniscectomy [12] These studies demonstrated an increase in NO production from meniscal tissue following prolonged ligament and meniscal injury, these studies did not replicate PTOA via traumatic compressive loading, nor were the acute changes to the menisci documented.
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