Technical Abstract: Selenium (Se), a chemical component of selenoproteins (such as glutathione peroxidases and thioredoxin reductase), plays a major role in cellular redox status and may have beneficial effects on bone health. The deficiency of Se has been linked to increased oxidative stress with increased levels of reactive oxygen species (ROS). Oxidative stress and ROS have been shown to stimulate bone resorption and osteoclast activity. The objective of the study was to determine whether Se deficiency affects bone microarchitecture and whether Se from pinto beans (SeBean) is bioavailable as compared to that of Se in the form of selenomethionine (SeMet) in supporting normal bone development in a mouse model. Thirty-three male C57BL/6J mice, 18-wk-old, were assigned randomly to three groups. Mice were fed either purified Se-deficient diet (SeDef) containing ~ 0.9 µg Se/kg diet, or diets containing ~ 100 µg Se/kg diet as either SeMet or SeBean for four months. Liver Se concentration, glutathione peroxidase (GPx1) activity, as well as GPx1 mRNA levels were higher in mice fed the SeMet or SeBean diet than those fed the SeDef diet (P < 0.05). Mice fed the SeMet or SeBean diet had higher femoral trabecular bone volume/total volume and trabecular number and lower trabecular separation than mice fed SeDef diet. Selenium deficiency did not affect any femoral mid-shaft cortical bone parameters (P > 0.05). There were no significant differences in bone structural parameters between SeMet group and SeBean group (P > 0.05). Taken together, this study demonstrates that Se deficiency is detrimental to bone microarchitecture and Se from pinto beans is equally bioavailable to support normal bone development in mice as compared to Se in the form of selenomethionine.