This article reviews evidence that subchondral bone plays a role in the degeneration of cartilage in osteoarthrosis. Whether the bony changes precede the cartilage degeneration remains unproven but may best be considered necessary for progression of the disease. Epidemiologic studies clearly show increasing subchondral sclerosis with disease progression. Recent evidence demonstrates specific architectural changes in the subchondral trabecular bone in osteoarthrosis that are consistent with an acceleration of bone turnover, which appears to be a part of the pathophysiologic process in progression of the disease. The now well-documented acceleration of bone turnover in osteoarthrosis decreases the stiffness of the bone as a material, but because of structural modifications in both trabecular bone (i.e., increased trabecular number and reduced separation) and subchondral bone (i.e., increased plate thickness), the stiffness (rigidity) of the structure as a whole undoubtedly increases. There is no evidence that growth factors, cytokines, or enzymes play any role in the bony changes associated with the disease, other than as the naturally occurring sequelae of normal bone remodeling processes.