Role of Inflammation in Osteoarthritis

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.

[1]  W. Robinson,et al.  Plasma proteins present in osteoarthritic synovial fluid can stimulate cytokine production via Toll-like receptor 4 , 2012, Arthritis Research & Therapy.

[2]  Qian Chen,et al.  CXCR4/SDF1 mediate hypoxia induced chondrosarcoma cell invasion through ERK signaling and increased MMP1 expression , 2010, Molecular Cancer.

[3]  Johanne Martel-Pelletier,et al.  Cartilage in normal and osteoarthritis conditions. , 2008, Best practice & research. Clinical rheumatology.

[4]  E. Lavallie,et al.  Involvement of protein kinase Cζ in interleukin‐1β induction of ADAMTS‐4 and type 2 nitric oxide synthase via NF‐κB signaling in primary human osteoarthritic chondrocytes , 2007 .

[5]  R. Loeser Molecular mechanisms of cartilage destruction: mechanics, inflammatory mediators, and aging collide. , 2006, Arthritis and rheumatism.

[6]  Qian Chen,et al.  Synovectomy reduces stromal-cell-derived factor-1 (SDF-1) which is involved in the destruction of cartilage in osteoarthritis and rheumatoid arthritis. , 2004, The Journal of bone and joint surgery. British volume.

[7]  J. Dayer The process of identifying and understanding cytokines: from basic studies to treating rheumatic diseases. , 2004, Best practice & research. Clinical rheumatology.

[8]  T. Wyss-Coray,et al.  Identification of a central role for complement in osteoarthritis , 2016 .

[9]  E. Lavallie,et al.  Involvement of protein kinase Czeta in interleukin-1beta induction of ADAMTS-4 and type 2 nitric oxide synthase via NF-kappaB signaling in primary human osteoarthritic chondrocytes. , 2007, Arthritis and rheumatism.

[10]  Qian Chen,et al.  Stimulation of matrix metalloprotease 3 release from human chondrocytes by the interaction of stromal cell-derived factor 1 and CXC chemokine receptor 4. , 2002, Arthritis and rheumatism.