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The research and therapeutic options are limited for skeletal abnormalities found in neurofibromatosis type 1 (NF1)—a haploinsufficient and multisystemic disease caused by inherited or sporadic mutations in the NF1 gene. However, denosumab may be an effective treatment option for osteoporosis in patients with NF1, according to a recent case report.

The largest genomewide association studies ever completed for osteoporosis identified 899 loci, or regions, in the human genome associated with low bone mineral density, 613 of which have not yet been discovered. The Stanford University School of Medicine researcher who made the finding said that widespread genetic screenings could predict a person's future risk of osteoporosis and bone fracture.

The United States Preventive Services Task Force (USPSTF) updated its 2011 recommendation about osteoporosis screening, recommending that women over the age of 65 years continue to get screened and issuing new information about how clinicians should use screening tools to evaluate women younger than 65 years at high risk for developing the bone disease.

A study comparing denosumab (Prolia) with risedronate (Actone) found that denosumab could be a useful treatment option for patients newly initiating or continuing glucocorticoids who are at risk of fractures. It is the first study to show that denosumab can increase bone mineral density at both the spine and the hip in patients with glucocorticoid-induced osteoporosis.

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