In a previous study, we demonstrated that chronic administration of systemic glucocorticoids decreases cortical bone mineral density (BMD) and induces development of pathologic fractures in asthmatic patients. To investigate cortical bone porosity due to glucocorticoids, we studied cortical bone volume, BMD, bone strength, and fractures in patients with asthma in this report. A total of 82 postmenopausal asthmatic patients were enrolled in the study. Vertebral fractures were diagnosed via plain spinal radiograms. Peripheral quantitative computed tomography (pQCT) was used to measure cortical BMD, relative cortical volume, and Strength Strain Index (SSI). Multiple regression analysis, Student's t test, and other statistical analyses were performed. Patients with systemic glucocorticoids therapy had lower cortical BMD, relative cortical volume, SSI, and more number of vertebral fractures than patients without it. Lifetime cumulative dose of glucocorticoids was related to cortical BMD, relative cortical volume, SSI, and the number of vertebral fractures. The cortical volumedensity relationship appeared to remain constant regardless of systemic glucocorticoid administration. The number of vertebral fractures correlated highly with cortical BMD, relative cortical volume, and SSI at the radius. In conclusion, systemic glucocorticoid administration decreases cortical bone density, cortical bone volume, and bone strength. G lucocorticoid administration appears to be responsible for the process of cortical bone porosity at both endosteal and intracortical sites. Given that both cortical bone density and volume provide bone strength, cortical bone porosity was seen to contribute to glucocorticoid - induced bone strength loss and fractures.