Synovial joints are composed of several different kinds of tissue that interact to protect normal joint function. Three subchondral mineralized tissues can be identified-calcified cartilage, subchondral cortical bone, and subchondral trabecular bone-which are distinguished morphologically, physiologically, and mechanically. Each responds to mechanical and pharmaceutical stimuli in different ways through processes of growth, modeling, and remodeling, and changes in each may have a distinct effect on the health of the joint. It is important to distinguish between the structural properties of these tissues and their material properties as these change differently in osteoarthrosis (OA). It is likely that changes in the mineral content and thickness of the calcified cartilage play a greater role in the pathogenesis of OA than has been realized, whereas changes in trabecular bone are probably not causative. Changes in the subchondral cortical bone may accelerate progression of pre-existing disease, but the combined effects of increased subchondral bone turnover and greater subchondral bone volume are not at all clear. Ultimately, the efficacy of bone anti-resorptive therapies for OA will depend upon whether the increased structural stiffness of the subchondral mineralized tissues predisposes the cartilage to deteriorate, whether the increased bone turnover that occurs in OA is itself a causative factor, or whether the lower tissue elastic modulus offsets the increased structural stiffness of the subchondral plate in an attempt to protect the cartilage from damage.