IMR Press / FBE / Volume 4 / Issue 1 / DOI: 10.2741/e361

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.


Osteoarthritis: genetic factors, animal models, mechanisms, and therapies

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1 Department of Orthopedics and Traumatology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, No.725 South Wan-ping Road, Shanghai, 200032, China
2 Institute of Spine, Shanghai University of Traditional Chinese Medicine, No.725 South Wan-ping Road, Shanghai, 00032, China
3 Institute of integrated Traditional Chinese Medicine and Western Medicine, Huashan Hospital, Fudan University, No.12 Middle Wu lu mu qi Road, Shanghai, 200040, China
4 Department of Pathology, University of Alabama at Birmingham, SHEL 810, 1825 University Blvd, Birmingham AL 35294-2182

*Author to whom correspondence should be addressed.

Academic Editor: Yi-Ping Li

Front. Biosci. (Elite Ed) 2012, 4(1), 74–100;
Published: 1 January 2012
(This article belongs to the Special Issue Skeletal biology and diseases)

Osteoarthritis (OA) is the most common form of joint disease. OA frequently affects knees, hips, hands, and the spine. It is characterized by the progressive destruction of articular cartilage and subchondral bone accompanied by low-grade inflammation that together result in pain and deformity. Recent studies have shed light on the nature of OA genetic susceptibility and confirmed a number of candidate genes involved in the destruction of the synovium, articular cartilage, and subchondral bone in OA pathogenesis. During the progression of OA, there are several cellular changes in joints, including an increase in the number of activated osteoclasts and macrophages and an infiltration of the synovium by activated T-cells and B-cells. Pro-inflammatory mediators (e.g. interleukin IL-1, IL-1beta, IL-6, IL-17, and IL-18, and Tumor necrosis actor-alpha), proteinases (e.g. matrix metalloproteinase 9 and cathepsin K), and regulators of cartilage and bone formation (e.g. BMPs) have been shown to have important roles in OA progression at the molecular level. Studies have suggested that OA shares several common characteristics with rheumatoid arthritis (RA). To systematically understand OA, this review summarizes OA disease genes, mouse models of human disease experimental mouse models, mechanisms of OA pathogenesis, and current OA therapies.

Animal model
Articular cartilage
Subchondral bone
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