Bone Abstracts

Selenium (Se) is an essential trace element active in the catalytic sites of many redox enzymes, including glutathione peroxidase and the iodothyronine deiodinases that metabolize thyroid hormones. In humans 25 genes encode selenoproteins, in which a specific tRNA incorporates the amino acid selenocysteine during protein translation. Although specific roles for many selenoproteins are unclear, studies suggest an important role for Se in skeletal development and bone maintenance. In animal studies deletion of the Se transport protein selenoprotein P, or key components of the selenocysteine incorporation machinery during protein translation, results in growth retardation and defects of endochondral ossification. Kashin–Beck disease is an osteoarthropathy that is endemic in Se- and iodine-deficient areas of Asia and which may result from oxidative damage to skeletal tissues due to Se deficiency or in response to combined deficiencies of both elements. Dietary supplementation studies in rodents indicate an important role for Se in bone, but they also identify interactions between Se and iodine that could be confounded by the critical role of both Se and iodine in thyroid hormone metabolism.

We investigated Se status in a well-defined cohort of 1144 healthy euthyroid post-menopausal women from the Osteoporosis and Ultrasound Study (OPUS) and determined its relationship to thyroid status, bone turnover markers, bone mineral density (BMD) and vertebral, hip and non-vertebral fractures. Higher Se and selenoprotein P levels were positively associated with higher BMD and negatively associated with lower levels of bone formation and resorption markers. These associations persisted after adjustment for thyroid status, vitamin D levels and PTH. Effects of changes in thyroid status on BMD and fracture risk were similarly independent of Se status.

Overall, these studies demonstrate that variation in Se status is related to BMD and bone turnover in healthy postmenopausal women.