The association between OA and obesity is well known. But is this a simple matter of physical loading, or are more complicated factors at work? Presentations at the recent annual meeting of the American College of Rheumatology added to our knowledge about this important issue and other matters relating to obesity and OA. (Click on the abstract numbers to see abstracts of the presentations.)
• The hormone leptin, which is involved in energy regulation, hunger and satiety, is associated wtih cartilage loss. Australian researchers found that loss of knee cartilage, as measured in 163 patients, was significantly associated with serum leptin levels, after adjusting for BMI and other measures of body fat. Because leptin appeared to mediate known associations between adiposity and cartilage loss, there could be interesting implications for treatment. (Abstract #2537)
• Not just fat mass, but also skeletal muscle mass, contribute to the risk of knee OA. A team in the Netherlands matched data about osteoarthritis (both self-reported and documented by MRI) against measures of BMI, fat mass (FM), and skeletal muscle mass (SMM). They found that the FM/SMM ratio was associated with OA, meaning that having more fat relative to skeletal muscle is unfavorable. But further analysys suggested that skeletal muscle also plays a role in the underlying mechanisms of knee OA development. (Abstract #2538)
• Weight loss directly slows joint narrowing. Among subjects in the Osteoarthritis Initiative, not only did heavier body weight correlate with radiographic measures of joint space narrowing, but subjects who lost weight had slower progression of narrowing than those who gained. (Abstract #2533)
• However, a prospective study of weight loss has sobering results: No direct impact on structural signs of progression, and reasons for concern about bone density. Physicians involved in the Intensive Diet and Exercise for Arthritis Trial (IDEA) trial confirm that while weight loss has "potent" effects on symptoms, it does not appear to ameliorate progression of tibiofemoral osteoarthritis. Also, intential weight loss induced a troubling decline in hip and femoral (but not spine) bone mineral density (BMD), which exercise did not modify. The obvious conclusion: Watch BMD carefully among your patients who succeed in losing weight. (Abstracts #2534 and #2536)
