Heterogeneity in the growth of the axial and appendicular skeleton in boys: Implications for the pathogenesis of bone fragility in men

Citation
M. Bradney et al., Heterogeneity in the growth of the axial and appendicular skeleton in boys: Implications for the pathogenesis of bone fragility in men, J BONE MIN, 15(10), 2000, pp. 1871-1878
Citations number
31
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
JOURNAL OF BONE AND MINERAL RESEARCH
ISSN journal
08840431 → ACNP
Volume
15
Issue
10
Year of publication
2000
Pages
1871 - 1878
Database
ISI
SICI code
0884-0431(200010)15:10<1871:HITGOT>2.0.ZU;2-Y
Abstract
Men with spine fractures have reduced vertebral body (VB) volume and volume tric bone mineral density (vBMD). Men with hip fractures have reduced femor al neck (FN) volume and vBMD, site-specific deficits that may have their or igins in growth. To describe the tempo of growth in regional bone size, bon e mineral content (BMC), and vBMD, we measured bone length, periosteal acid endocortical diameters, BMC, and vBMD using dual-energy X-ray absorptiomet ry in 184 boys aged between 7 and 17 years. Before puberty, growth was more rapid in the legs than in the trunk. During puberty, leg growth slowed whi le trunk length accelerated. Bone size was more advanced than BMC in all re gions, being similar to 70% and similar to 35% of their predicted peaks at 7 years of age, respectively. At 16 years of age, bone size had reached its adult peak while BMC was still 10% below its predicted peak. The legs acco unted for 48%, whereas the spine accounted for 10%, of the 1878 g BMC accru ed between 7 and 17 years. Peripubertal growth contributed (i) 55% of the i ncrease in leg length but 78% of the mineral accrued and (ii) 69% of the in crease in spine length but 87% of the mineral accrued. Increased metacarpal and midfemoral cortical thickness was caused by respective periosteal expa nsion with minimal change in the endocortical diameter. Total femur and VB vBMD increased by 30-40% while size and BMC increased by 200-300%. Thus, gr owth builds a bigger but only slightly denser skeleton. We speculate that e ffect of disease or a risk factor during growth depends on the regions matu rational stage at the time of exposure. The earlier growth of a regions siz e than mass, and the differing growth patterns from region to region, predi spose to site-specific deficits in bone size, vBMD, or both. Regions furthe r from their peak may be more severely affected by illness than those neare r completion of growth. Bone fragility in old age is likely to have its fou ndations partly established during growth.