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通过骨骼生长从骨质疏松症中恢复:早期骨量获取对成人骨密度影响不大。

Recovery from osteoporosis through skeletal growth: early bone mass acquisition has little effect on adult bone density.

作者信息

Gafni Rachel I, McCarthy Edward F, Hatcher Tracy, Meyers Jodi L, Inoue Nozomu, Reddy Chitra, Weise Martina, Barnes Kevin M, Abad Veronica, Baron Jeffrey

机构信息

Unit on Growth and Development, Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892-1862, USA.

出版信息

FASEB J. 2002 May;16(7):736-8. doi: 10.1096/fj.01-0640fje. Epub 2002 Mar 26.

DOI:10.1096/fj.01-0640fje
PMID:11923218
Abstract

It is often assumed that bone mineral accretion should be optimized throughout childhood to maximize peak bone mass. In contrast, we hypothesized that bone mineral acquisition early in life would have little or no effect on adult bone mass because many areas of the juvenile skeleton are replaced in toto through skeletal growth. To test this hypothesis, we induced osteoporosis by administering dexamethasone to 5-week-old rabbits for 5 weeks and then allowed them to recover for 16 weeks. Tibial bone mineral density (ash weight/volume) was decreased in the dexamethasone-treated animals at the end of treatment but recovered completely. Bone structure in the femur was assessed by histomorphometry. Trabecular and cortical bone in the distal metaphysis was made osteoporotic by dexamethasone, but was then replaced through endochondral bone formation and recovered. Periosteal bone formation rate in the diaphysis was decreased during dexamethasone treatment but afterwards rebounded above controls and normalized cortical width. Our data suggest that bone mineral acquisition early in life has little effect on adult bone density because the juvenile bone is largely replaced through growth. If this concept generalizes, then interventions to maximize peak bone mass should be directed at adolescents rather than young children.

摘要

人们常常认为,在整个童年时期都应优化骨矿物质的积累,以实现峰值骨量最大化。相比之下,我们提出假说,认为生命早期的骨矿物质获取对成年后的骨量影响很小或没有影响,因为幼年骨骼的许多部位会在骨骼生长过程中完全被替换。为了验证这一假说,我们给5周龄的兔子注射地塞米松5周以诱导骨质疏松,然后让它们恢复16周。在治疗结束时,地塞米松处理组动物的胫骨骨矿物质密度(灰重/体积)降低,但随后完全恢复。通过组织形态计量学评估股骨的骨结构。地塞米松使远端干骺端的小梁骨和皮质骨发生骨质疏松,但随后通过软骨内成骨被替换并恢复。在使用地塞米松治疗期间,骨干的骨膜骨形成速率降低,但之后反弹至高于对照组水平,皮质宽度恢复正常。我们的数据表明,生命早期的骨矿物质获取对成年后的骨密度影响很小,因为幼年骨骼在很大程度上会通过生长被替换。如果这一概念具有普遍性,那么旨在最大化峰值骨量的干预措施应针对青少年而非幼儿。

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