Division of Endocrinology, Department of Medicine, College of Physicians and Surgeons, Columbia University, New York, NY, USA.
J Bone Miner Res. 2012 Apr;27(4):865-75. doi: 10.1002/jbmr.1503.
Despite the dramatic bone loss that occurs during lactation, bone mineral density rapidly recovers after offspring are weaned and milk production stops. The goal of this study is to quantify site-specific changes in bone quantity and quality during and after lactation in a mouse model. We used micro computed tomography (µCT), individual trabecula segmentation (ITS), digital topological analysis (DTA)-based tissue mineral density (TMD) analysis, and micro finite element analysis (µFEA) to quantify the effects of lactation and weaning on bone microarchitecture, mineralization, and stiffness at the spine, tibia, and femur. We found a significant decrease in trabecular plate microarchitecture, tissue mineralization of the trabecular surface, trabecular central skeleton, and intervening envelopes, and whole bone stiffness in lactating versus nulliparous mice at all three sites. In recovered mice, all these different aspects of bone quality were comparable to nulliparous mice at the spine. In contrast, trabecular plate microarchitecture and whole bone stiffness at the tibia and femur in recovered mice were lower than nulliparous mice, as were central trabecular tissue mineralization and cortical structure at the femur. These findings are consistent with clinical observations of partial recovery of femoral bone mineral density BMD after lactation in humans. The observed differences in trabecular surface tissue mineralization in nulliparous, lactating, and recovered mice are consistent with prior observations that maternal bone turnover shifts from resorption to formation at the time of pup weaning. The significant differences in trabecular central tissue mineralization during these three states suggest that osteocytes may contribute to the reversible loss of mineral during and after lactation. Future studies are necessary to determine whether differing functions of various bone cells at individual skeletal sites cause site-specific skeletal changes during and after lactation.
尽管哺乳期会发生明显的骨质流失，但在断奶和停止产奶后，骨密度会迅速恢复。本研究的目的是在小鼠模型中定量研究哺乳期和断奶后骨骼数量和质量的特定部位变化。我们使用微计算机断层扫描（µCT）、单独的小梁分割（ITS）、基于数字拓扑分析（DTA）的组织矿物质密度（TMD）分析和微有限元分析（µFEA）来定量研究哺乳期和断奶对脊柱、胫骨和股骨的小梁微观结构、矿化和刚度的影响。我们发现，与未产小鼠相比，哺乳期小鼠的小梁板微观结构、小梁表面组织矿化、小梁中央骨架和间隔包络以及整个骨骼刚度均显著降低。在恢复的小鼠中，所有这些不同方面的骨质量在脊柱上都与未产小鼠相当。相比之下，恢复小鼠的胫骨和股骨的小梁板微观结构和整个骨骼刚度均低于未产小鼠，而股骨的中央小梁组织矿化和皮质结构也低于未产小鼠。这些发现与人类哺乳期后股骨骨密度（BMD）部分恢复的临床观察结果一致。未产、哺乳期和恢复小鼠小梁表面组织矿化的观察差异与之前的观察结果一致，即母体骨转换在幼崽断奶时从吸收转为形成。在这三种状态下，小梁中央组织矿化的显著差异表明，破骨细胞可能导致哺乳期和断奶后矿物质的可逆丢失。需要进一步的研究来确定在个体骨骼部位，不同骨细胞的不同功能是否会导致哺乳期和断奶期间骨骼的特定部位变化。
