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We studied changes in subchondral bone and articular cartilage in an animal model of osteoarthrosis. In this model we applied repetitive impulsive loads to rabbits' knees. Their legs were held in short leg splints so the rabbits were unable to dampen the peak applied load with ankle flexion. After sacrifice, at 1 day to 6 weeks, we studied proximal tibial load-bearing cartilage histologically, biochemically, and with radioactive sulfate uptake. We also studied the subchondral bone under that cartilage histologically, histomorphometrically, with bone scan (99mTc pyrophosphate), and by tetracycline labeling. An increase in 99mTc labeling of the subchondral bone was the first reliable change observed. This was followed by an increase in tetracycline labeling, bone formation, and a decrease in porosity, which has been associated with relative stiffening of bone. Horizontal splitting and deep fibrillation of the overlying articular cartilage followed the early bone changes. All of these changes preceded changes in content and characterization of cartilage proteoglycans or increased chondrocyte activity as manifested by incorporation of radioactive sulfate. In this model the early bone changes preceded changes in the articular cartilage. The deep splitting of articular cartilage occurred prior to metabolic alteration of that tissue.

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The purpose of this work was to determine whether subchondral bone changes are an integral part of the development of osteoarthrosis of the knee following experimentally created tibial angulation. Thirty degree varus or valgus proximal tibial osteotomies were created in female New Zealand white rabbits. Bone and cartilage changes were assessed grossly, radiologically, and histologically. Thirty-four weeks following osteotomy, severe cartilage changes, including osteophytes, fibrillation, derangement of cell columns, and cloning, were evident on the overloaded condyle, accompanied by increased subchondral bone density. The pattern of cartilage deterioration was different from that found in other experimental, mechanically induced arthroses. We conclude that osteoarthrosis is a final common pathway for mechanically induced joint failure, and that progressive cartilage change is associated with increased subchondral bone density.