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Further unravelling of the mechanisms underpinning the inflammatory pathophysiology of OA is likely to yield new therapeutic approaches that can modify the course of OA. This inflammation comes into play early in the course of OA, as a result of interactions between the immune system and factors including local tissue damage and metabolic dysfunction 5. We no longer view OA as a prototypical degenerative disease resulting from normal bodily wear and tear, but rather as a multifactorial disorder in which low-grade, chronic inflammation has a central role ( BOX 1). The past decade has seen a gradual but fundamental shift in our understanding of the mechanisms underlying OA. Novel therapeutics are needed to inhibit the processes that drive OA pathology. Current therapies for OA focus on pain control, viscosupplementation (via intra-articular injections of hyaluronic acid), and joint replacement, which all simply target the symptoms of advanced disease.
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Women, older individuals, obese individuals, and individuals with prior joint injuries all have an increased risk of developing OA, as do individuals with certain genetic and biomechanical predisposing factors 2– 4. Common clinical features include pain, joint dysfunction, and deformity. OA can affect the knees, hips, spine, and fingers, and is characterized by progressive breakdown of articular cartilage and remodelling of the underlying bone in the synovial joints. Osteoarthritis (OA) is the most prevalent arthritic disease and a leading cause of disability, with radiographically established OA affecting approximately 37% of the US population over 60 years of age 1. Further work is needed to identify effective inhibitors of the low-grade inflammation in OA, and to determine whether therapies that target this inflammation can prevent or slow the development and progression of the disease. Indeed, several anti-inflammatory therapies have shown promise in animal models of OA. However, increasing insight into the inflammatory underpinnings of OA holds promise for the development of new, disease-modifying therapies. Current treatments for OA only control the symptoms, and none has been FDA-approved for the prevention or slowing of disease progression. The inflammation in OA is distinct from that in rheumatoid arthritis and other autoimmune diseases: it is chronic, comparatively low-grade, and mediated primarily by the innate immune system.
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That is, OA is a disorder of the joint as a whole, with inflammation driving many pathologic changes. Furthermore, we now appreciate that OA pathogenesis involves not only breakdown of cartilage, but also remodelling of the underlying bone, formation of ectopic bone, hypertrophy of the joint capsule, and inflammation of the synovial lining. Osteoarthritis (OA) has long been viewed as a degenerative disease of cartilage, but accumulating evidence indicates that inflammation has a critical role in its pathogenesis.
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