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Osteoarthritis (OA) is the most common musculoskeletal disease in developed countries, and although OA presents a considerable global health burden, the most widely prescribed treatments such as analgesics and total joint replacements are at best palliative. Epidemiological studies have shown that OA is a complex, multifactorial disorder with a number of risk factors, including environmental and genetic components. Progress has been made in understanding the pathophysiology of the disease, but the molecular mechanisms underlying disease initiation and progression remain elusive. Genetic investigations into complex diseases like OA have proven successful in not only confirming the role of candidate genes in the disease process but also in identifying novel disease pathways that offer new avenues for therapeutic intervention. In this review, we discuss three of the most compelling OA susceptibility genes to date: secreted frizzled-related protein 3 (FRZB), asporin (ASPN), and growth/differentiation factor 5 (GDF5), and discuss how these genes offer insight into the underlying OA-causing pathway. © 2007 Future Medicine Ltd.

Original publication




Journal article


Future Rheumatology

Publication Date





607 - 620