Abstract
Copyright: © 2013 Jayasuriya CT, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Osteoarthritis (OA) was never classically considered to be an inflammatory arthropathy. However, recently this concept has been questioned due to ever increasing evidence suggesting that inflammation plays a key role in the progression of this debilitating degenerative joint disease. Over 55 million Americans suffer from OA for which there is no effective treatment outside of complete joint replacement surgery. Although routine, the invasiveness of this surgical procedure renders it a last resort for alleviating pain associated with the severe late stages of this disease. Today, our current understanding of OA pathogenesis and its intrinsic link to joint inflammation can open up new and innovative avenues of thinking about potential treatment options outside of surgical intervention. The traditional definition of OA differs quite significantly from rheumatoid arthritis (RA), which is primarily classified as a systemic autoimmune disease where inflammation is pivotal to its manifestation. However, recently many have acknowledged that there is also an underlying chronic inflammation present, not only in cartilage tissue but also within the synovium, which perpetuates tissue destruction of the OA joint. While not as pronounced as the inflammatory imbalances characteristic of RA, chronic low levels of inflammation of the OA joint nonetheless persists as a major factor regulating tissue catabolism.
Highlights
Reduces nitric oxide production by OA associated inflammatory cytokines Elevated during OA and acts to inhibit IL-1 and TNF-α expression Inhibits IL-1 and TNF-α expression while elevating IL-1Ra expression Inhibits various catabolic effects of IL-1 Elevated during early and late stage OA and promotes MMP production and inhibits cartilage anabolism Elevated during OA onset and increases nitric oxide and catabolic protease production by chondrocytes Negative regulator of chondrocyte proliferation Regulator of chondrocyte hypertrophy pathology of OA and rheumatoid arthritis (RA) the similarities between these diseases are beginning to unravel
It is reasonable to expect emerging OA therapies/treatments to make more of an effort at readily addressing the chronic inflammation underlying this arthropathy
Summary
Reduces nitric oxide production by OA associated inflammatory cytokines Elevated during OA and acts to inhibit IL-1 and TNF-α expression Inhibits IL-1 and TNF-α expression while elevating IL-1Ra expression Inhibits various catabolic effects of IL-1 Elevated during early and late stage OA and promotes MMP production and inhibits cartilage anabolism Elevated during OA onset and increases nitric oxide and catabolic protease production by chondrocytes Negative regulator of chondrocyte proliferation Regulator of chondrocyte hypertrophy pathology of OA and RA the similarities between these diseases are beginning to unravel.
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