Inadequate serum selenium levels may delay the growth and the physiological changes in bone metabolism. In
humans, reduced serum selenium concentrations are associated with both increased bone turnover and reduced bone mineral
density. Moreover, a reduced nutritional intake of selenium may lead to an increased risk of bone disease. Therefore, selenium is an essential nutrient playing a role in bone health, probably due to specific selenium-proteins. Some selenium-proteins
have an anti-oxidation enzymatic activity and participate in maintaining the redox cellular balance, regulating inflammation
and proliferation/differentiation of bone cells too. At least nine selenium-proteins are known to be expressed by fetal osteoblasts and appear to protect bone cells from oxidative stress at bone microenvironment. Mutations of selenium-proteins and
reduced circulating levels of selenium are known to be associated with skeletal diseases such as the Kashin-Beck osteoarthropathy and postmenopausal osteoporosis. In addition, the intake of selenium appears to be inversely related to the risk of
hip fragility fractures. Recent data suggest that an altered selenium state may affect bone mass even in males and seleniumproteins and selenium concentrations were positively associated with the bone mass at femoral, total and trochanteric site.
However, selenium, but not selenium-proteins, seems to be associated with femoral neck bone mass after adjustment for
many bone fracture risk factors. The present review summarizes the findings of observational and interventional studies,
which have been designed for investigating the relationship between selenium and bone metabolism.
Keywords: Selenium, bone metabolism, bone turnover, osteoclasts, anti-oxidation activity, inflammation
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