Endocrine Abstracts

Until recently obesity was believed to be protective against fractures as a result of higher bone mass and the cushioning effect of subcutaneous tissue during falls. However, recent studies indicate that fractures in obese postmenopausal women and older men make a substantial contribution to the overall fracture burden in this population. The effect of obesity on fracture risk is site-dependent, with some protection against hip and wrist fractures but increased risk of ankle and lower leg fractures. Risk factors for fractures in the obese are similar in many respects to those in the non-obese population, although increased risk of falling and reduced mobility are likely to play a prominent role.

The pathophysiology of bone fragility in obese individuals has not been clearly established. Visceral adipose tissue produces adipokines and cytokines, many of which have adverse effects on bone, and its presence is inversely related to bone mineral density. Increased intramuscular adipose tissue is likely to contribute to reduced muscle strength, reducing bone mass and increasing the risk of falls. Other potential pathogenetic factors include vitamin D insufficiency, secondary hyperparathyroidism and hypogonadism.

The evidence base for efficacy of anti-osteoporosis medication in the obese is weak, since pivotal clinical trials have included relatively few obese individuals. There is some evidence from post hoc subgroup analyses that anti-resorptive medications may not be effective in reducing non-vertebral fractures in obese postmenopausal women; however, whether this reflects inadequate dosing or other factors is unclear. Weight loss in association with exercise regimens may be beneficial. However, further studies are needed to enable the development of effective strategies to reduce the growing fracture burden in the obese population.