Gilsanz V, Roe T F, Antunes J, Carlson M, Duarte M L, Goodman W G
Department of Radiology, Children's Hospital of Los Angeles, University of Southern California School of Medicine.
Am J Physiol. 1991 Mar;260(3 Pt 1):E471-6. doi: 10.1152/ajpendo.1991.260.3.E471.
Reductions in peak bone mass at skeletal maturity may increase the risk for the subsequent development of osteoporosis. Although changes in calcium intake can modify the rate of decline in bone density in the mature skeleton, longitudinal assessments of the effect of dietary calcium supplementation during skeletal growth on peak bone mass have not been done in humans or experimental animals. Thus quantitative computed tomography (QCT) was used to monitor changes in vertebral bone density at 6-wk intervals during growth from 8 wk of age until skeletal maturity at 35 wk in male New Zealand White rabbits maintained on diets containing 0.15% (low Ca), 0.45% (normal Ca), or 1.35% (high Ca) calcium. Serum parathyroid hormone (PTH) and calcitriol levels increased, and renal calcium excretion decreased in low Ca compared with normal Ca; in contrast, serum calcitriol levels decreased and renal calcium excretion increased from control values in high Ca. Vertebral bone density by QCT did not differ during growth between high Ca and normal Ca, and peak values at epiphyseal closure also did not differ in these two groups. Vertebral bone density was lower, however, throughout the study in low Ca, and peak values at epiphyseal closure remained below those in either normal Ca or high Ca. Quantitative bone histology revealed decreases in cortical thickness in the third lumbar vertebra in low Ca, whereas trabecular bone area did not differ among groups; there was no histological evidence of osteomalacia in low Ca. Thus dietary calcium restriction during growth reduces peak bone mass at skeletal maturity, but raising dietary calcium intake above normal levels does not increase peak bone mass in this experimental model.
骨骼成熟时峰值骨量的降低可能会增加随后发生骨质疏松症的风险。虽然钙摄入量的变化可以改变成熟骨骼中骨密度的下降速度,但在人类或实验动物中,尚未对骨骼生长期间膳食补钙对峰值骨量的影响进行纵向评估。因此,使用定量计算机断层扫描(QCT)来监测雄性新西兰白兔从8周龄生长至35周龄骨骼成熟期间,每隔6周的椎体骨密度变化。这些兔子分别食用含0.15%(低钙)、0.45%(正常钙)或1.35%(高钙)钙的饮食。与正常钙饮食组相比,低钙饮食组血清甲状旁腺激素(PTH)和骨化三醇水平升高,肾钙排泄减少;相反,高钙饮食组血清骨化三醇水平降低,肾钙排泄量高于对照组。高钙饮食组和正常钙饮食组在生长过程中通过QCT测得的椎体骨密度没有差异,两组在骨骺闭合时的峰值也没有差异。然而,在整个研究过程中,低钙饮食组的椎体骨密度较低,骨骺闭合时的峰值仍低于正常钙饮食组或高钙饮食组。定量骨组织学显示,低钙饮食组第三腰椎皮质厚度降低,而小梁骨面积在各组之间没有差异;低钙饮食组没有骨软化的组织学证据。因此,生长期间限制膳食钙会降低骨骼成熟时的峰值骨量,但在这个实验模型中,将膳食钙摄入量提高到正常水平以上并不会增加峰值骨量。