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Review: developmental origins of osteoporotic fracture

Review: developmental origins of osteoporotic fracture
Review: developmental origins of osteoporotic fracture
Osteoporosis is a major cause of morbidity and mortality through its association with age-related fractures. Although most effort in fracture prevention has been directed at retarding the rate of age-related bone loss and reducing the frequency and severity of trauma among elderly people, evidence is growing that peak bone mass is an important contributor to bone strength during later life. The normal patterns of skeletal growth have been well characterised in cross-sectional and longitudinal studies. It has been confirmed that boys have higher bone mineral content (BMC), but not volumetric bone density, than girls. Furthermore, there is a dissociation between the peak velocities for height gain and bone mineral accrual in both genders. Puberty is the period during which volumetric density appears to increase in both axial and appendicular sites. Many factors influence the accumulation of bone mineral during childhood and adolescence, including heredity, gender, diet, physical activity, endocrine status, and sporadic risk factors such as cigarette smoking. In addition to these modifiable factors during childhood, evidence has also accrued that fracture risk might be programmed during intrauterine life. Epidemiological studies have demonstrated a relationship between birth weight, weight in infancy, and adult bone mass. This appears to be mediated through modulation of the setpoint for basal activity of pituitary-dependent endocrine systems such as the HPA and GH/IGF-1 axes. Maternal smoking, diet (particularly vitamin D deficiency), and physical activity also appear to modulate bone mineral acquisition during intrauterine life; furthermore, both low birth size and poor childhood growth are directly linked to the later risk of hip fracture. The optimisation of maternal nutrition and intrauterine growth should also be included within preventive strategies against osteoporotic fracture, albeit for future generations.
development, epidemiology, growth, osteoporosis, programming
0937-941X
337-347
Cooper, Cyrus
e05f5612-b493-4273-9b71-9e0ce32bdad6
Westlake, Sarah
91d63b6c-1af8-45d1-a7e1-302407b78e3d
Harvey, Nicholas
ce487fb4-d360-4aac-9d17-9466d6cba145
Javaid, Kassim
69bf78c2-9bb1-48b8-8c26-157a823b3421
Dennison, Elaine
ee647287-edb4-4392-8361-e59fd505b1d1
Hanson, Mark
1952fad1-abc7-4284-a0bc-a7eb31f70a3f
Cooper, Cyrus
e05f5612-b493-4273-9b71-9e0ce32bdad6
Westlake, Sarah
91d63b6c-1af8-45d1-a7e1-302407b78e3d
Harvey, Nicholas
ce487fb4-d360-4aac-9d17-9466d6cba145
Javaid, Kassim
69bf78c2-9bb1-48b8-8c26-157a823b3421
Dennison, Elaine
ee647287-edb4-4392-8361-e59fd505b1d1
Hanson, Mark
1952fad1-abc7-4284-a0bc-a7eb31f70a3f

Cooper, Cyrus, Westlake, Sarah, Harvey, Nicholas, Javaid, Kassim, Dennison, Elaine and Hanson, Mark (2006) Review: developmental origins of osteoporotic fracture. Osteoporosis International, 17 (3), 337-347. (doi:10.1007/s00198-005-2039-5).

Record type: Article

Abstract

Osteoporosis is a major cause of morbidity and mortality through its association with age-related fractures. Although most effort in fracture prevention has been directed at retarding the rate of age-related bone loss and reducing the frequency and severity of trauma among elderly people, evidence is growing that peak bone mass is an important contributor to bone strength during later life. The normal patterns of skeletal growth have been well characterised in cross-sectional and longitudinal studies. It has been confirmed that boys have higher bone mineral content (BMC), but not volumetric bone density, than girls. Furthermore, there is a dissociation between the peak velocities for height gain and bone mineral accrual in both genders. Puberty is the period during which volumetric density appears to increase in both axial and appendicular sites. Many factors influence the accumulation of bone mineral during childhood and adolescence, including heredity, gender, diet, physical activity, endocrine status, and sporadic risk factors such as cigarette smoking. In addition to these modifiable factors during childhood, evidence has also accrued that fracture risk might be programmed during intrauterine life. Epidemiological studies have demonstrated a relationship between birth weight, weight in infancy, and adult bone mass. This appears to be mediated through modulation of the setpoint for basal activity of pituitary-dependent endocrine systems such as the HPA and GH/IGF-1 axes. Maternal smoking, diet (particularly vitamin D deficiency), and physical activity also appear to modulate bone mineral acquisition during intrauterine life; furthermore, both low birth size and poor childhood growth are directly linked to the later risk of hip fracture. The optimisation of maternal nutrition and intrauterine growth should also be included within preventive strategies against osteoporotic fracture, albeit for future generations.

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Published date: 2006
Keywords: development, epidemiology, growth, osteoporosis, programming

Identifiers

Local EPrints ID: 25597
URI: http://eprints.soton.ac.uk/id/eprint/25597
ISSN: 0937-941X
PURE UUID: d3b0fb92-60a9-47f1-bb3a-c03f8842982b
ORCID for Cyrus Cooper: ORCID iD orcid.org/0000-0003-3510-0709
ORCID for Nicholas Harvey: ORCID iD orcid.org/0000-0002-8194-2512
ORCID for Elaine Dennison: ORCID iD orcid.org/0000-0002-3048-4961
ORCID for Mark Hanson: ORCID iD orcid.org/0000-0002-6907-613X

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Date deposited: 09 May 2007
Last modified: 18 Mar 2024 02:58

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Contributors

Author: Cyrus Cooper ORCID iD
Author: Sarah Westlake
Author: Nicholas Harvey ORCID iD
Author: Kassim Javaid
Author: Elaine Dennison ORCID iD
Author: Mark Hanson ORCID iD

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