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骨质疏松症的发育起源:母体营养的作用。

Developmental origins of osteoporosis: the role of maternal nutrition.

作者信息

Cooper Cyrus, Harvey Nicholas, Cole Zoe, Hanson Mark, Dennison Elaine

机构信息

MRC Epidemiology Resource Centre and Centre for Developmental Origins of Health and Adult Disease, University of Southampton, Southampton General Hospital, Southampton, UK.

出版信息

Adv Exp Med Biol. 2009;646:31-9. doi: 10.1007/978-1-4020-9173-5_3.

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, 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 hypothalamic-pituitary-adrenal (HPA) and growth hormone/insulin-like growth factor-1 (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.

摘要

骨质疏松症是导致发病和死亡的主要原因,因其与年龄相关的骨折有关。尽管预防骨折的大部分努力都集中在减缓与年龄相关的骨质流失速度,以及降低老年人创伤的频率和严重程度上,但越来越多的证据表明,峰值骨量是晚年骨强度的重要贡献因素。骨骼生长的正常模式在横断面和纵向研究中已得到充分描述。已经证实,男孩的骨矿物质含量高于女孩,但体积骨密度并非如此。此外,男女身高增长和骨矿物质积累的峰值速度之间存在脱节。青春期是轴向和附属部位的体积密度似乎都会增加的时期。许多因素影响儿童期和青春期骨矿物质的积累,包括遗传、性别、饮食、身体活动、内分泌状态以及吸烟等偶发风险因素。除了儿童期这些可改变的因素外,也有证据表明骨折风险可能在子宫内生活期间就已编程。流行病学研究表明出生体重、婴儿期体重与成人骨量之间存在关联。这似乎是通过调节垂体依赖的内分泌系统(如下丘脑 - 垂体 - 肾上腺(HPA)轴和生长激素/胰岛素样生长因子 -1(GH/IGF -1)轴)基础活动的设定点来介导的。母亲吸烟、饮食(特别是维生素D缺乏)和身体活动似乎也会调节子宫内生活期间的骨矿物质获取;此外,低出生体重和儿童期生长不良都与后期髋部骨折风险直接相关。尽管是为了后代,但优化母亲营养和子宫内生长也应纳入骨质疏松性骨折的预防策略中。

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