Duchenne muscular dystrophy (DMD) is an X-linked progressive myopathy due to mutations in the dystrophin gene, affecting one in every 3’600–10’000 live male births [1,2]. Boys with DMD typically present with delayed motor milestones and muscle weakness, they progress to loss of ambulation around their teens, and respiratory and heart failure during the second decade. Corticosteroids remain the standard supportive therapy for DMD even though new treatments recently emerged [3–6]. Along with other risk factors that are present in DMD such as progressive weakness, immobility and delayed puberty, chronic corticosteroid therapy increases the risk of low bone mineral density, exposing these patients to fractures, pain and decreased quality of life.

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