Faculty of Medicine-Endocrinology, Memorial University of Newfoundland, St. John's, Newfoundland, Canada.
J Bone Miner Res. 2017 Apr;32(4):676-680. doi: 10.1002/jbmr.3090. Epub 2017 Feb 28.
During lactation, mammals resorb mineral from the maternal skeleton to provide calcium to milk. Rodents lose 25% to 35% of skeletal ash weight, ash calcium content, and bone mineral content as measured by dual-energy X-ray absorptiometry (DXA), and have compromised material properties of bone as assessed by crushing vertebrae and 3-point bend tests of femora or tibias. The strength, stiffness, and toughness of vertebrae, femora, and tibias are reduced by as much as 60%. The effects of lactation are not uniform throughout the skeleton, but instead resorption is much more marked in the trabecular-rich spine than in the appendicular skeleton or whole body. Women who breastfeed exclusively lose an average of 210 mg calcium in milk each day, whereas nursing of twins or triplets can double and triple the output of calcium. Clinical data are also consistent with skeletal calcium being released during lactation to provide much of the calcium needed for milk production. Lumbar spine bone mineral density (BMD), as assessed by DXA, declines by a mean of 5% to 10% among numerous studies during 3 to 6 months of exclusive lactation, whereas largely cortical sites (hip, forearm, whole body) show half that loss or no significant changes. Micro-CT of rodents and high-resolution peripheral quantitative computed tomography (HR-pQCT) imaging of women confirm that lactation causes microarchitectural deterioration of bone. These skeletal losses occur through two pathways: upregulated osteoclast-mediated bone resorption and osteocytic osteolysis, in which osteocytes remove mineral from their lacunae and pericanalicular spaces. After weaning, the skeleton is fully restored to its prior mineral content and strength in both animal models and humans, despite persistent microarchitectural changes observed in high-resolution imaging. Osteoblasts upregulate to lay down new osteoid, while osteocytes remineralize their surroundings. The factors that stimulate this post-weaning skeletal recovery remain unclear. In most studies, a history of lactation does not increase the risk, but may protect against, low BMD and fragility fractures. © 2017 American Society for Bone and Mineral Research.
哺乳期哺乳动物会从母体骨骼中吸收矿物质，以为乳汁提供钙。通过双能 X 射线吸收法（DXA）测量，啮齿动物的骨骼灰重、灰钙含量和骨矿物质含量会减少 25%至 35%，且其椎骨压碎试验和股骨或胫骨三点弯曲试验的材料特性也受到影响。椎骨、股骨和胫骨的强度、刚度和韧性降低了多达 60%。哺乳期的影响并非在整个骨骼中均匀分布，而是在富含小梁的脊柱中，吸收比在附肢骨骼或整个身体中更为明显。纯母乳喂养的女性每天从乳汁中平均损失 210 毫克钙，而哺乳双胞胎或三胞胎的女性则可能使钙的分泌量增加一倍或三倍。临床数据也表明，在哺乳期，骨骼中的钙会被释放出来，以为乳汁生产提供大部分所需的钙。通过 DXA 评估，在纯母乳喂养 3 至 6 个月期间，许多研究均显示腰椎骨矿物质密度（BMD）平均下降 5%至 10%，而主要是皮质部位（髋部、前臂、全身）的损失为一半或没有明显变化。啮齿动物的微计算机断层扫描（micro-CT）和女性的高分辨率外周定量计算机断层扫描（HR-pQCT）成像证实，哺乳期会导致骨微观结构恶化。这些骨骼损失是通过两种途径发生的：破骨细胞介导的骨吸收和骨细胞性骨溶解增加，其中骨细胞从它们的陷窝和小管周空间中去除矿物质。断奶后，动物模型和人类的骨骼均完全恢复到先前的矿物质含量和强度，尽管在高分辨率成像中仍观察到持续的微观结构变化。成骨细胞上调以形成新的类骨质，同时骨细胞使其周围环境再矿化。刺激这种断奶后骨骼恢复的因素仍不清楚。在大多数研究中，哺乳史并不会增加低 BMD 和脆性骨折的风险，但可能会起到保护作用。 © 2017 美国骨矿研究协会。
