Joint health is affected by local and systemic hormones. It is well accepted that systemic factors regulate the metabolism of joint tissues, and that substantial cross-talk between tissues actively contributes to homeostasis. In the current review, we try to define a subtype of osteoarthritis (OA), metabolic OA, which is dependent on an unhealthy phenotype.
Peer-reviewed research articles and reviews were reviewed and summarized. Only literature readily available online, either by download or by purchase order, was included.
OA is the most common joint disease and is more common in women after menopause. OA is a disease that affects the whole joint, including cartilage, subchondral bone, synovium, tendons, and muscles. The clinical endpoints of OA are pain and joint space narrowing, which is characterized by cartilage erosion and subchondral sclerosis, suggesting that cartilage is a central tissue of joint health. Thus, the joint, more specifically the cartilage, may be considered a target of endocrine function in addition to the well-described traditional risk factors of disease initiation and progression such as long-term loading of the joint due to obesity. Metabolic syndrome affects a range of tissues and may in part be molecularly described as a dysregulation of cytokines, adipokines, and hormones (eg, estrogen and thyroid hormone). Consequently, metabolic imbalance may both directly and indirectly influence joint health and cartilage turnover, altering the progression of diseases such as OA.
There is substantial evidence for a connection between metabolic health and development of OA. We propose that more focus be directed to understanding this connection to improve the management of menopausal health and associated comorbidities.
From the 1Department of Rheumatology, Nordic Bioscience, Herlev, Denmark; 2Department of Molecular Epidemiology, Leiden University Medical Center, Leiden, the Netherlands; 3The Netherlands Genomics Initiative–sponsored Netherlands Consortium for Healthy Aging, Leiden, the Netherlands; and 4Center for Clinical and Basic Research–Synarc, Vejle, Denmark.
Received June 11, 2012; revised and accepted September 13, 2012.
Funding/support: Some of the research leading to these results received funding from the European Union’s Seventh Framework Program (FP7/2007-2011) under grant agreement 259679. The Danish Research Fund (Den Danske Forskningsfund) supported this study.
Financial disclosure/conflicts of interest: C.C. is chairman of the board at Nordic Bioscience A/S and Center for Clinical and Basic Research–Synarc. Other authors report no conflict of interest.
Address correspondence to: Anne C. Bay-Jensen, MSc, PhD, Nordic Bioscience, Herlev Hovedgade 207, Herlev DK-2730, Denmark. E-mail: email@example.com