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The presence of peri-articular osteoporosis and focal bone erosions at the joint margins and within the subchondral bone adjacent to inflamed joints has been considered the radiographic hallmark of rheumatoid arthritis (RA).1-4 In addition, in recent years there has been an increased awareness that RA also produces adverse effects on systemic bone remodelling at sites not directly involved with joint inflammation. Numerous reports have documented that people with RA have reduced axial and appendicular bone mass and that this bone loss is associated with an increased risk of fracture.5-11 Thus, it is possible to identify three distinct patterns of bone loss in RA. These include systemic osteoporosis, juxta-articular osteopenia adjacent to inflamed joints and focal marginal and subchondral bone erosions that are associated directly with inflamed synovial tissues. Each of these disorders represents an example of disturbed skeletal tissue remodelling in which there is a net loss of bone, although the precise mechanisms responsible for the bone loss in each of these conditions may involve differential cellular and regulatory processes. This review will focus on the mechanisms involved in the pathogenesis of focal bone erosions that are directly associated with the inflammatory synovial lesion.
Insights into the processes underlying the development of focal bone erosions in RA have been derived principally from histopathological evaluation of joint tissues from patients with RA and from animal models of inflammatory arthritis. Early studies by Bromley and Woolley demonstrated the presence of multinucleated cells with phenotypic features of osteoclasts in resorption lacunae at the pannus-bone interface.12-14 More recently, in our own studies,15 we have used in situ hybridisation to demonstrate that multinucleate and some mononuclear cells in resorption lacunae at the bone-pannus interface exhibit the entire repertoire of phenotypic markers that are associated with the fully differentiated osteoclast. This includes …