Articular cartilage response to an impact load: In vitro and in vivo models for traumatic joint injury.
Limited information exists on the biological response and possible irreparable damage to cartilage from a blunt impact that does not produce subchondral bone failure, either at the time of injury or post injury. Recent clinical findings based on Magnetic Resonance Imaging (MRI) reported frequent cases of thinning and loss of articular cartilage beneath the location of osseous lesions. The mechanism of how these kinds of injuries occur is not well defined. To better understand how articular cartilage responds to joint insults below subfracture level, we developed in vitro explant impact test system and in vivo impact rabbit model to better predict which mechanical conditions (stress magnitude, stress rate) would predispose the joint to post-traumatic arthritis and which will not.;The in vitro test system was used to determine the threshold stress and stress rate that caused cell death and matrix damage in viable bovine cartilage explants at the time of impaction. The percentage of water loss and depth of cell death increased linearly with increasing magnitude of stress (10--60 MPa), while it decreased exponentially with increasing stress rate (25--1000 MPa/sec). The dynamic impact modulus of the cartilage explants increased exponentially, while their deformation decreased with increasing stress rate.;The in vivo impact test system was used to investigate the post-impact response of the articular cartilage in rabbit knees. In vitro tests were performed to determine damage to the cartilage at the time of injury. The maximum depth of chondrocyte death increased linearly with increasing stress magnitude (1--50 MPa) at a stress rate of 420 MPa. This information was used to study the in vivo response by impacting rabbits with a 35 MPa peak stress at 420 MPa/sec stress rate (sufficient to cause immediate damage) and evaluating the cartilage at 0, 1 and 3 weeks post injury. At the time of impact, the same maximum depth of cell death was reproduced. At one and three weeks post impaction, the articular cartilage showed significant arthritic changes, including matrix damage, abnormal cells, and proteoglycan loss. Visible surface damage was noted at 0 and 1 week, but not at 3 weeks. This finding poses a significant clinical problem when evaluating cartilage damage by visual inspection.