Obesity and type 2 diabetes (T2D) significantly increase the risk of developing an arthritic condition.

We performed a review of literature on the pathophysiological mechanisms that underpin the relationships between obesity, T2D and osteoarthritis (OA).

The pathophysiology of the link between obesity and OA is related to both the direct effect of excess mechanical loads being placed on the cartilage and to an adipose tissue effect. Adipocytes produce and release adipokines (e.g. leptin). They are also the seat of a local inflammatory reaction when the adipose tissue is ectopic (visceral vs. subcutaneous adipose tissue), and then systemic effects that add even more to a micro-inflammatory mechanism. In diabetics, insulin resistance can add to these mechanisms, which can damage cartilage, bone and synovial tissue. These all act together to reduce mobility in obese subjects and contribute to a vicious cycle centered on OA, especially when the obesity is predominantly abdominal and/or associated with T2D.

Prevention of obesity-related OA must be the focus in high-risk subjects, such as those who are obese with metabolic syndrome>“metabolically healthy” obese, have T2D, and normal weight subjects with abdominal obesity (defined as waist circumference>102cm for men and 88cm for women). The primary component of this prevention effort is weight loss combined with a balanced diet and regular physical activity.