Although the complete pathogenesis of cartilage damage in canine hip dysplasia has not been completely worked out, it appears that joint laxity with resultant excessive stresses upon articular cartilage is the initiating factor. Grossly, this damage is characterized by cartilage thinning with potential exposure of subchondral bone, osteophyte formation, and pannus formation. Microscopically, there is a marked variation in chondrocyte cellularity, with focal regions of hypocellularity and chondrocyte clusters and synovial lining cell hyperplasia and hypertrophy as well as a decrease in proteoglycan content. This latter change has been substantiated biomechanically. Ultrastructural studies indicate that there is extensive alteration of collagen organization within the cartilage.