Growth and bone development.
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 characterized in cross-sectional and longitudinal studies. It has been confirmed that boys have higher bone mineral content, 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 birthweight, weight in infancy, and adult bone mass. This appears to be mediated through modulation of the set-point for basal activity of pituitary-dependent endocrine systems such as the hypothalamicpituitary-adrenal and growth hormone/insulin-like growth factor-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 optimization of maternal nutrition and intrauterine growth should also be included within preventive strategies against osteoporotic fracture, albeit for future generations.
Cooper
Cyrus
C
MRC Epidemiology Resource Centre and Centre for Developmental Origins of Health and Adult Disease, University of Southampton, Southampton General Hospital, Southampton, UK. cc@mrc.soton.ac.uk
Harvey
Nicholas
N
Javaid
Kassim
K
Hanson
Mark
M
Dennison
Elaine
E
D000328:Adult; D001724:Birth Weight / Q000502:physiology; D015519:Bone Density; D050071:Bone Density Conservation Agents / Q000008:administration & dosage; D001846:Bone Development / Q000502:physiology*; D001842:Bone and Bones / Q000196:embryology / Q000502:physiology*; D002136:Calcium, Dietary / Q000008:administration & dosage; D004032:Diet; D015444:Exercise / Q000502:physiology*; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D007231:Infant, Newborn; D008297:Male; D039382:Maternal Nutritional Physiological Phenomena / Q000502:physiology; D010024:Osteoporosis / Q000453:epidemiology / Q000209:etiology / Q000235:genetics / Q000517:prevention & control*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D039401:Prenatal Nutritional Physiological Phenomena / Q000502:physiology*; D012307:Risk Factors; D012737:Sex Factors; D014807:Vitamin D / Q000008:administration & dosage
D050071:Bone Density Conservation Agents; D002136:Calcium, Dietary; D014807:Vitamin D