Obesity and Osteoarthritis: More Than Just Mechanics

*Richard Conway,1,2 Geraldine M. McCarthy1

1. Department of Rheumatology, Mater Misericordiae University Hospital, Dublin, Ireland
2. University College Dublin, Dublin, Ireland
*Correspondence to drrichardconway@gmail.com

Disclosure: The authors have declared no conflicts of interest.
Received: 20.01.15 Accepted: 18.03.15
Citation: EMJ Rheumatol. 2015;2[1]:75-83.


Osteoarthritis (OA) is the most common form of arthritis worldwide. It results in chronic pain, functional limitations, and significant social and economic burdens. Obesity rates in the developed world are rapidly increasing, leading to warnings of an obesity epidemic. Obesity is associated with increased rates of OA. Traditionally, this increased prevalence was attributed to biomechanical factors including increased joint loading and altered joint dynamics due to the physical burden of obesity. However, a number of factors, including the increased prevalence of OA in non-weight-bearing joints in obese individuals and the increasing awareness of adipose tissue as a functional endocrine organ rather than an inert storage substance, have led to a reappraisal of this viewpoint. Adipose tissue secretes a number of adipokines and cytokines with both local and systemic effects. In addition, adipose tissue has the potential to stimulate a systemic inflammatory state. Differential expression of microRNAs in obese and non-obese osteoarthritic patients has been demonstrated. The potential impact of adipokines on the adipose inflammatory pathway in obese individuals is being actively explored. The traditional view of OA as a mechanical wear-and-tear disease is being revolutionised by the discovery of the key roles of inflammation and cytokines in this most common of joint diseases.

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