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Osteoarthritis (OA), one of the most common diseases among humans, is characterised pathologically by focal areas of damage on articular cartilage centred on load-bearing areas, associated with formation of new bone at the joint margins and changes in subchondral bone. Given the huge economic and personal burden of OA, and the fact that this disease is the major cause for the increasing demand for joint replacements, there is urgent need for disease modifying treatments to stop or at least slow the development and progression of OA. But for this to be possible, we need further knowledge about the pathogenesis of disease initiation and progression in OA. The great success of targeted biologic therapy against rheumatoid arthritis (RA) in recent years has meant that much research has been devoted to investigating the pathophysiology of osteoarthritis (OA), in the hope of defining novel therapeutic targets. In contrast to RA, with its pannus and erosions, OA has long been thought of as a degenerative disease of cartilage, with secondary bony damage and osteophytes. In recent years, the importance of the synovium, and in particular the synovial macrophages, in OA, has been highlighted in both in vitro and in vivo studies. This article will give an overview of some important recent findings concerning the ability of macrophages to drive inflammatory and destructive disease mechanisms in OA, the role of their proinflammatory cytokines in doing so, and the potential for macrophages and macrophage-produced cytokines to be used as therapeutic targets for the development of disease-modifying anti-ostroarthritic drugs (DMOADs). There is also an abundance of potential downstream therapeutic targets in OA, including the matrix metalloproteinases, the aggrecanases, the inducible nitric oxide synthetase, and elements of the Wnt pathway.
Bondeson et al. (Thu,) studied this question.