Low bone density and bone metabolism alterations in Duchenne muscular dystrophy: response to calcium and vitamin D treatment

Osteoporos Int. 2011 Feb;22(2):529-39. doi: 10.1007/s00198-010-1275-5. Epub 2010 May 11.


Boys with Duchenne muscular dystrophy often have reduced bone mass and increased fracture risk. In this prospective study on 33 patients, calcifediol (25-OH vitamin D(3)) plus adjustment of dietary calcium to the recommended dose reduced bone resorption, corrected vitamin D deficiency, and increased bone mass in about two-thirds of cases.

Introduction: Low BMC and BMD and bone metabolism alterations are frequent in boys with Duchenne muscular dystrophy (DMD), especially now that long-term glucocorticosteroid (GC) treatment is the standard of care. This prospective study was designed to evaluate the effects of a first-line treatment (25-OH vitamin D(3) [calcifediol] plus adjustment of dietary calcium to the recommended daily dose) on bone.

Methods: Thirty-three children with DMD on GC treatment were followed for 3 years: one of observation and two of treatment.

Main outcome: spine and total body BMC and BMD increase; secondary outcome: changes in bone turnover markers (C-terminal [CTx] and N-terminal [NTx] telopeptides of procollagen type I; osteocalcin [OC]).

Results: During the observation year, BMC and BMD decreased in all patients. At baseline and after 12 months, serum CTx and urinary NTx were higher than normal; OC and parathyroid hormone at the upper limit of normal; 25-OH vitamin D(3) significantly lower than normal. After 2 years of calcifediol and calcium-rich diet, BMC and BMD significantly increased in over 65% of patients, and bone metabolism parameters and turnover markers normalized in most patients (78.8%). During the observation year, there were four fractures in four patients, while during the 2 years of treatment there were two fractures in two patients.

Conclusions: Calcifediol plus adequate dietary calcium intake seems to be an effective first-line approach that controls bone turnover, corrects vitamin D deficiency, and increases BMC and BMD in most patients with DMD. Lack of response seems related to persistently high bone turnover.

MeSH terms

  • Adolescent
  • Bone Density / drug effects*
  • Bone Density Conservation Agents / administration & dosage
  • Bone Density Conservation Agents / pharmacology*
  • Bone Remodeling / drug effects*
  • Bone Resorption / drug therapy
  • Calcifediol / administration & dosage
  • Calcifediol / pharmacology*
  • Calcium, Dietary / administration & dosage
  • Calcium, Dietary / pharmacology*
  • Child
  • Child, Preschool
  • Collagen Type I / metabolism
  • Glucocorticoids / adverse effects
  • Humans
  • Male
  • Muscular Dystrophy, Duchenne / complications*
  • Muscular Dystrophy, Duchenne / drug therapy
  • Osteocalcin / blood
  • Parathyroid Hormone / blood
  • Peptides / metabolism
  • Prospective Studies
  • Treatment Outcome
  • Vitamin D / analogs & derivatives
  • Vitamin D / blood
  • Vitamin D Deficiency / drug therapy


  • Bone Density Conservation Agents
  • Calcium, Dietary
  • Collagen Type I
  • Glucocorticoids
  • Parathyroid Hormone
  • Peptides
  • collagen type I trimeric cross-linked peptide
  • Osteocalcin
  • Vitamin D
  • 25-hydroxyvitamin D
  • Calcifediol