Subchondral Bone in Osteoarthritis

Abstract

Osteoarthritis (OA) is characterised by progressive degenerative damage to articular cartilage, but ultimately the disease affects the whole joint, with important implications for the affected limb and the entire body (Martel-Pelletier and Pelletier, 2010; Edmonds, 2009). There has been an ongoing debate regarding the origins of OA, and specifically whether it initiates in the bone or the cartilage. The debate is somewhat artificial because it assumes that the answer must be one or the other of these possibilities. More likely, OA has multiple etiologies, which converge to produce the recognized manifestations of joint pain and stiffness and degeneration of articular cartilage. Genetic and environmental risk factors for OA, such as increased weight, female sex, joint dysplasias and malalignment, and injury, clearly contribute to the establishment and progression of this condition (Felson, 1988). However, it is most important to consider all possibilities for the underlying cause(s) for OA because our current level of understanding has failed to produce treatments for this condition that offer much more than palliation, with many sufferers proceeding to joint replacement in end stage disease. There are well described changes that are observed in both articular cartilage and subchondral bone in OA (Martel-Pelletier and Pelletier, 2010; Edmonds, 2009; Goldring and Goldring, 2010; Kwan et al., 2010). Changes in the bone include sclerotic changes, typified by increased subchondral plate thickness and osteophyte formation, and the development of bone marrow lesions that can be visualized by MR imaging, and which seem to precede, temporally and spatially, bone cysts in the subchondral compartment (Tanamas et al., 2010). The subchondral bone does much more than provide a substrate on which the articular cartilage sits. While it does give support to the cartilage, it also offers complementarity of shape to the opposite side of the articulation, with important consequences for the joint when this congruency is lost. In addition, the predominantly trabecular structure of the subchondral bone gives compliance and shock absorption to the joint (Madry et al., 2010). It was thought that the sclerotic changes in the subchondral bone in OA made it stiffer and less compliant, resulting in increased loading of the cartilage (Radin et al., 1982) but later work showed that the bone in OA may actually be less mineralised and therefore less stiff (Day et al., 2001). The price paid for the shock absorption role of subchondral bone is the production of damage within the bone matrix by repeated loading. This bone matrix damage is repaired by bone turnover and remodeling, which are highly developed functionalities of bone cells: osteocytes to detect the damage, osteoclasts to remove the damage and osteoblasts to replace sites of damage with healthy new bone (Eriksen, 2010). A