Addressing the musculoskeletal components of fracture risk with calcium and vitamin D: a review of the evidence.
Osteoporotic fractures are an extremely common and serious health problem in the elderly. This article presents the rationale for calcium and vitamin D supplementation in the prevention and treatment of osteoporotic fractures and reviews the literature evidence on the efficacy of this strategy. Two musculoskeletal risk factors are implicated in osteoporotic fractures in the elderly: the loss of bone mass due to secondary hyperparathyroidism and the increased propensity to falls. Calcium and vitamin D reverse secondary hyperparathyroidism with resultant beneficial effects on bone mineral density (BMD). Additionally, calcium and vitamin D supplementation significantly improves body sway and lower extremity strength, reducing the risk of falls. The effects of combined calcium and vitamin D on parathyroid function and BMD provide a strong rationale for the use of this therapy in the prevention and treatment of osteoporosis and osteoporotic fractures. There is general agreement that, in patients with documented osteoporosis, calcium and vitamin D supplementation should be an integral component of the management strategy, along with antiresorptive or anabolic treatment. Frail elderly individuals constitute another major target population for calcium and vitamin D because evidence from randomized studies in institutionalized elderly subjects demonstrates that these supplements reduce osteoporotic fracture risk, particularly in the presence of dietary deficiencies. However, the results of trials in community-dwelling subjects have been equivocal. Within the primary-care setting, further research is required to establish appropriate target subgroups for calcium and vitamin D supplementation; overall, the data are consistent with a benefit individuals with insufficient calcium and/or vitamin D, although patients with documented osteoporosis will derive further benefit in terms of fracture prevention from the addition of an antiresorptive agent.
Boonen
S
S
Leuven University Center for Metabolic Bone Diseases and Division of Geriatric Medicine, Katholieke Universiteit Leuven, Leuven, Belgium. steven.boonen@uz.kuleuven.ac.be
Bischoff-Ferrari
H A
HA
Cooper
C
C
Lips
P
P
Ljunggren
O
O
Meunier
P J
PJ
Reginster
J-Y
JY
D000058:Accidental Falls / Q000517:prevention & control; D000368:Aged; D015519:Bone Density / Q000187:drug effects / Q000502:physiology; D001842:Bone and Bones / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D002118:Calcium / Q000172:deficiency / Q000627:therapeutic use*; D005260:Female; D005598:Fractures, Spontaneous / Q000188:drug therapy* / Q000503:physiopathology / Q000517:prevention & control; D006801:Humans; D006961:Hyperparathyroidism / Q000188:drug therapy / Q000503:physiopathology / Q000517:prevention & control; D008297:Male; D010024:Osteoporosis / Q000188:drug therapy* / Q000503:physiopathology / Q000517:prevention & control; D012307:Risk Factors; D014807:Vitamin D / Q000627:therapeutic use*; D014808:Vitamin D Deficiency / Q000188:drug therapy / Q000517:prevention & control
D014807:Vitamin D; D002118:Calcium