Two canine acute transarticular loading models have been developed to study the role of acute traumatic cartilage damage in the development of osteoarthritis. One model involves damage to a closed joint and has the advantage of maintaining normal joint biology. The second model involves impaction of an open joint with direct visualization of the cartilage and has the advantages of being able to change the placement, intensity, and geometry of the impaction. Comparison of preliminary histochemical data at 2 weeks and 3 months for the open joint model with previously published data on the closed joint model is consistent with the two models having similar initial features that include surface cracks and step fractures of the zone of calcified cartilage. The early changes include loss of proteoglycan, expression of the pro-inflammatory markers such as TNF-α and IL-1β, and the metalloprotease stromelysin. By 3 months, cloning is present. The models will be useful in evaluating two hypotheses:one, that there is a threshold of damage that must be exceeded before the lesions become progressive and two, the cracks in the zone of calcified cartilage contribute to progression of osteoarthritis by acting as sites of endochondral ossification and thereby decreasing cartilage thickness.