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

Qin Bian, Yong Jun Wang, Shu Fen Liu, Yi Ping Li

Research output: Contribution to journalArticlepeer-review

44 Scopus citations


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 Bcells. 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.

Original languageEnglish (US)
Pages (from-to)74-100
Number of pages27
JournalFrontiers in Bioscience - Elite
Volume4 E
Issue number1
StatePublished - Jan 1 2012
Externally publishedYes


  • Animal model
  • Articular cartilage
  • BMPs
  • Gene
  • Mechanisms
  • Osteoarthritis
  • Review
  • Subchondral bone
  • Synovium
  • Therapies

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology
  • General Immunology and Microbiology


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