Peripheral arterial disease is associated with higher rates of hip bone loss and increased fracture risk in older men.

BACKGROUND Peripheral arterial disease (PAD) and osteoporosis are chronic illnesses that increase in prevalence with aging and certain metabolic disorders. The association between PAD, rates of bone loss, and fracture risk in older men is uncertain. METHODS AND RESULTS We sought to test the hypothesis that PAD is associated with higher rates of bone loss and increased fracture risk. We analyzed data from a prospective cohort study involving 6 US centers and 5781 men at least 65 years of age. We assessed ankle-brachial index and hip bone mineral density, followed up prospectively for changes in hip bone mineral density and fractures. PAD was defined as a baseline ankle-brachial index <0.9. Hip bone mineral density was measured with dual x-ray absorptiometry at baseline and again an average of 4.6 years later. Incident nonspine fractures were ascertained by self-report and confirmed with radiography reports during an average of 5.4 years of follow-up. At baseline, the prevalence of PAD was 6.2%. After adjustment for age, race, site, and baseline bone mineral density, the mean annualized rate of bone loss at the total hip was -0.66% per year (95% confidence interval -0.78 to -0.54) in men with PAD compared with -0.34% per year (95% confidence interval -0.36 to -0.31) in men without PAD (P<0.001). After further adjustment for multiple potential confounders, the difference was attenuated (-0.49% in men with PAD versus -0.35% in men without PAD) but remained significant (P=0.02). Findings were similar at hip subregions. Twelve percent of men with PAD and 7.9% of those without PAD experienced an incident nonspine fracture (hazard ratio adjusted for age, race, and site=1.47, 95% confidence interval 1.07 to 2.04); this association was not altered substantially by further adjustment for multiple confounders. CONCLUSIONS In community-dwelling older men, PAD was associated with higher rates of hip bone loss and increased risk of nonspine fractures. Further research should examine the biological mechanisms underlying the association between reduced limb blood flow and fractures.