The canine patellofemoral joint was subjected to a standardized transarticular load of 2170 newtons for two milliseconds, and the gross and histological changes were examined at two, twelve, and twenty-four weeks after injury. Initially, the load creates fractures in the zone of calcified cartilage, with minimum damage to the articular cartilage surface. Surface fissures were visible in all patellae only after staining with India ink. Histologically, these surface clefts extended into the transitional or superficial radial zone, and they did not communicate with the subchondral bone except in two patellae. However, there were reproducible clefts in the region of the subchondral bone and the zone of calcified cartilage in all patellae. Six months after loading, there was a loss of safranin-O staining above the deep clefts, and there was new-bone formation in the subchondral region and fibrillation of the cartilaginous surface. Thus, the initial changes had progressed to osteoarthrotic-like conditions at six months. In this animal model, the joint is not invaded and the changes that result from loading are reproducible. The injury to the joint creates superficial disruption of the cartilage and subchondral changes that lead to arthritic-like degeneration of the cartilage within six months.

In this animal model, the joint is not invaded and the changes that result from loading are reproducible. The injury to the joint creates superficial disruption of the cartilage and subchondral changes that lead to arthritic-like degeneration of the cartilage within six months.

CLINICAL RELEVANCE:​ Fractures in the zone of calcified cartilage-bone interface, with no visible abnormalities of the articular cartilage, may represent a previously unrecognized pathological process after traumatic insult to the joint. Recently, there have been reports of magnetic resonance images demonstrating changes in the subchondral bone after traumatic insult to the joint when a fracture was not identifiable on conventional radiographs or when the magnetic resonance images did not reveal disruptions of the articular surface. The load across the surfaces of the joint that is necessary to produce a severe ligamentous disruption has also been correlated with similar findings in bone on magnetic resonance imaging and with intact articular cartilage as seen on arthroscopy. It is possible that the degenerative changes that occur in some patients who are not seen to have a fracture on conventional radiographic examination but who have sustained severe hgamentous injury and other forms of traumatic insult to the joint may represent a phenomenon similar to that described in this animal model.