Analysis of Acute Mechanical Insult in an Animal Model of Post-traumatic Osteoarthrosis

Abstract

Chronic degeneration of articular cartilage and bone in a rabbit model of post-traumatic osteoarthrosis has been hypothesized to occur due to acute stresses that exceed a threshold for injury. In this study, we impacted the rabbit patellofemoral joint at low and high intensities. High-intensity impacts produced degenerative changes in the joint, such as softening of retropatellar cartilage, as measured by indentation, an increase in histopathology of the cartilage, and an increase in thickness of subchondral bone underlying the cartilage. Low-intensity impacts did not cause these progressive changes. These data suggest that low-intensity impacts produced acute tissue stresses below the injury threshold, while high-intensity impacts produced stresses that exceeded the threshold for disease pathogenesis. This study begins to identify "safe" and "unsafe" ranges of acute tissue stress, using the rabbit patella, which may have future utility in the design of injury prevention devices for the human.

Analysis of the Relationship between Peak Stress and Proteoglycan Loss following Injurious Compression of Human Post-mortem Knee and Ankle Cartilage

“…Injury of knee cartilage resulted in an increase in GAG loss to the medium after injury compared to location-matched controls (P < 0.001 by paired t test), whereas there was no observed difference after injury of ankle cartilage (P = 0.97) add to the evidence that knee and ankle cartilages, whether by design or adaptation, respond differently to mechanical and biological stimuli. The concept of a threshold for cartilage injury is interesting for its implications both in understanding chondrocyte mechanotransduction and in clinical practice (Newberry et al 1998;Torzilli et al 1999;Loening et al 2000). In one of the first in vitro investigations of this phenomenon, Torzilli et al (1999) showed evidence for a threshold level of injury in terms of cell death and collagen damage in their injury model using adult bovine occipital joint cartilage.…”

“…Several researchers have suggested that there may be a threshold level of peak stress that separates injurious from harmless loads to the cartilage (Repo and Finlay 1977;Newberry et al 1998;Torzilli et al 1999;Clements et al 2001). At the same time, others have observed associations of cartilage injury with loading parameters such as the final strain Ewers et al 2001) and the rate of loading (Chen et al 1999;Kurz et al 2001;Quinn et al 2001).…”

Molecular basis of osteoarthritis: biomechanical aspects

“…Radin et al [13 -15] impacted patellofemoral joints of rabbits, causing damage to the bone and cartilage and subsequently leading to OA-like degradation. Even impacts that do not appear to fracture the bone can result in cartilage degradation [16].…”

The limitation of acute necrosis in retro-patellar cartilage after a severe blunt impact to the in vivo rabbit patello-femoral joint

“…In a recent study using this model, a rigid impact mass was dropped with 6 J of energy onto the flexed patello-femoral joint, resulting retro-patellar surface cartilage, and thickening of underlying subchondral bone after 3 years [lo]. In another study, this impact was found to produce patello-femoral contact pressures of approximately 25 MPa [22]. Another laboratory, using the New Zealand white rabbit subjected to a 10 J impact, found advanced OA-like changes in the patello-femoral joint, with fibrillation, ulceration, and erosion of retro-patellar cartilage within 6 months post-contusion [19].…”