Hypertrophic repair of canine articular cartilage in osteoarthritis after anterior cruciate ligament transection.

Transection of the anterior cruciate ligament in the dog is used frequently to produce a model of osteoarthritis (OA). Although it results in metabolic, biochemical, biomechanical and morphological changes in the articular cartilage of the unstable knee which resemble those in human OA, it rarely results in full thickness cartilage loss. The lack of progression of the cartilage lesions in this model has generally been attributed to stabilization of the joint by osteophytes and capsular fibrosis which develop following transection of the ligament. In our study transection of the anterior cruciate ligament of adult foxhounds and mongrels resulted in a progressive increase in the amount of articular cartilage in the unstable knee. In articular cartilage from the medial femoral condyle of the unstable knee the total amount of proteoglycan, as assessed by hexuronic acid analysis, and, often, the proteoglycan concentration were increased. Furthermore, the rate of proteoglycan synthesis was commonly elevated, in comparison with that from the contralateral knee. Thus, in these animals knee instability did not lead to loss of cartilage but to an active synthetic response by the chondrocytes resulting in hypertrophic cartilage repair which was sustained for up to 64 weeks of observation.