Javaid M K, Cooper Cyrus
MRC Environmental Epidemiology Unit, Southampton General Hospital, Southampton, SO16 6YD, UK.
Best Pract Res Clin Endocrinol Metab. 2002 Jun;16(2):349-67. doi: 10.1053/beem.2002.0199.
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, in both genders there is a dissociation between the peak velocities for height gain and bone mineral accrual. 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. Measures for maximizing bone mineral acquisition, particularly through encouraging physical activity and adequate dietary calcium intake, are likely to affect the risk of fracture in later generations. In addition to these modifiable factors during childhood, evidence has also accrued that the risk of fracture 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 - pitutiary - adrenal (HPA) and growth hormone/insulin-like growth factor I (GH/IGF-I) axes. Maternal smoking, diet and physical activity levels 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.
骨质疏松症因其与年龄相关的骨折关联,是发病和死亡的主要原因。尽管预防骨折的大部分努力都旨在减缓与年龄相关的骨质流失速度,并降低老年人创伤的频率和严重程度,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,在男女两性中,身高增长峰值速度与骨矿物质积累之间存在脱节。青春期是轴向和附属部位的体积密度似乎都增加的时期。许多因素影响儿童期和青春期的骨矿物质积累,包括遗传、性别、饮食、身体活动、内分泌状况以及吸烟等偶发风险因素。最大化骨矿物质获取的措施,特别是通过鼓励身体活动和充足的膳食钙摄入,可能会影响后代的骨折风险。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) 和生长激素/胰岛素样生长因子 I (GH/IGF-I) 轴)基础活动的设定点来介导的。母亲的吸烟、饮食和身体活动水平似乎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,但预防骨质疏松性骨折的策略也应包括优化母亲营养和子宫内生长。