This paper reviews evidence for the role of subchondral bone and calcified cartilage in the initiation and progression of osteoarthrosis (OA). There is consensus that OA is characterized by subchondral sclerosis, but disagreement about whether bone changes are concurrent with, primary to, or secondary to cartilage deterioration. Clinical observation suggests that bone density and cartilage fibrillation are inversely related. Evidence from the rabbit impulsive loading model is consistent with early bone changes, but evidence from other models of subchondral stiffening, such as the sheep metallic implant model, do not strongly support this idea. However, evidence from tibial angulation models and from the Pond-Nuki (anterior cruciate ligament resection) model show evidence that bone changes precede cartilage fibrillation temporally, and are associated spatially within a single joint. Evidence is also presented for the importance of calcified cartilage changes in pre-disposing the joint towards progression to OA. Microdamage accumulation and repair by vascular invasion may be a component of the pathogenesis of OA in some cases, but more work is needed to demonstrate this conclusively. We conclude that changes in the subchondral mineralized tissues are not required for initiation of cartilage fibrillation, but may be necessary for progression, and that only changes in bone and calcified cartilage close to the joint are significant to the disease process.