Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) stimulate bone formation in vitro and in rodents. Recent data from separate studies suggest that statins used in the treatment of hypercholesterolemia decrease fracture risk and increase bone mineral density (BMD). Current statin use and BMD were evaluated in 573 women (aged 50-95 years) with incident fracture and in a random sample of 802 women (aged 50-94 years) without incident fracture, drawn from the same community. There were 16 statin users in the fracture group and 53 in the nonfracture group. Unadjusted odds ratio (OR) for fracture associated with statin use was 0.40 (95% confidence interval [CI], 0.23-0.71). Adjusting for BMD at the femoral neck, spine, and whole body increased the OR to 0.45 (95% CI, 0.25-0.80), 0.42 (95% CI, 0.24-0.75), and 0.43 (95% CI, 0.24-0.78), respectively; adjusting for the potential confounders age, weight, dietary calcium intake, alcohol consumption, smoking, activity levels, and exposure to hormone replacement therapy, glucocorticoids, or calcium and/or vitamin D supplements had no effect on the OR. Statin use was associated with a 3% greater age- and weight-adjusted BMD at the femoral neck (P = .08), and BMD tended to be greater but did not achieve statistical significance at the spine and whole body. Results suggest that increases in BMD associated with statin use are small and may be insufficient to account for the observed 60% reduction in fracture risk. Unless confounded by unrecognized factors, statin use is associated with substantial protection against fracture, but the mechanisms of action remain unclear.