Purpose of review: Labeling osteoarthritis as a degenerative arthritis is a misnomer. It is now clear that an active genetic and proteomic profile suggests inflammation. The cytokine milieu is similarly inflammatory and neatly parallels that found in the metabolic syndrome.
Recent findings: Important cellular changes in the osteoarthritis lesion include not only chondrocytes but also macrophages. Important catabolic mediators of osteoarthritis include metalloproteinases, a disintegrin and metalloproteinase with thrombospondin motif, a disintegrin and a metalloprotease, interleukin (IL)-1beta, IL-17, IL-18 and tumor necrosis factor alpha. The striking finding that hand osteoarthritis in older women is linearly correlated to their degree of atherosclerosis suggests that a connection between osteoarthritis and atherosclerosis exists independently of putative overuse factors directly related to obesity. Therefore, it is not surprising that oxidative stress, endothelial dysfunction, and leptin dysregulation all characterize the osteoarthritis lesion. Better understanding of vitamin D metabolic effects and the Wnt, frizzled, secreted frizzled-related protein, Dickkopf, and low-density lipoprotein receptor-related protein gene families are promising regarding osteoarthritis genesis and therapeutics.
Summary: Current information suggests that osteoarthritis shares a similar biochemical and inflammatory profile to the metabolic syndrome. Mounting evidence exists to call attention to the fact that osteoarthritis deserves a seat at the Metabolic Syndrome 'table' of disorders.