Department of Clinical Medicine, University of Tromsø, Norway.
Bone. 2011 Dec;49(6):1125-30. doi: 10.1016/j.bone.2011.08.009. Epub 2011 Aug 18.
All postmenopausal women become estrogen deficient but not all remodel their skeleton rapidly or lose bone rapidly. As remodeling requires a surface to be initiated upon, we hypothesized that a volume of mineralized bone assembled with a larger internal surface area is more accessible to being remodeled, and so decayed, after menopause. We measured intracortical, endocortical and trabecular bone surface area and microarchitecture of the distal tibia and distal radius in 185 healthy female twin pairs aged 40 to 61 years using high-resolution peripheral quantitative computed tomography (HR-pQCT). We used generalized estimation equations to analyze (i) the trait differences across menopause, (ii) the relationship between remodeling markers and bone surface areas, and (iii) robust regression to estimate associations between within-pair differences. Relative to premenopausal women, postmenopausal women had higher remodeling markers, larger intracortical and endocortical bone surface area, higher intracortical porosity, smaller trabecular bone surface area and fewer trabeculae at both sites (all p<0.01). Postmenopausal women had greater deficits in cortical than trabecular bone mass at the distal tibia (-0.98 vs. -0.12 SD, p<0.001), but similar deficits at the distal radius (-0.45 vs. -0.39 SD, p=0.79). A 1 SD higher tibia intracortical bone surface area was associated with 0.22-0.29 SD higher remodeling markers, about half the 0.53-0.67 SD increment in remodeling markers across menopause (all p<0.001). A 1 SD higher porosity was associated with 0.20-0.30 SD higher remodeling markers. A 1 SD lower trabecular bone surface area was associated with 0.15-0.18 SD higher remodeling markers (all p<0.01). Within-pair differences in intracortical and endocortical bone surface areas at both sites and porosity at the distal tibia were associated with within-pair differences in some remodeling markers (p=0.05 to 0.09). We infer intracortical remodeling may be self perpetuating by creating intracortical porosity and so more bone surface for remodeling to occur upon, while remodeling upon the trabecular bone surface is self limiting because it removes trabeculae with their surface.
所有绝经后妇女都会出现雌激素缺乏,但并非所有人都会迅速重塑骨骼或快速流失骨质。由于重塑需要在表面起始,我们假设,体积较大、内表面积更大的矿化骨更易在绝经后被重塑和侵蚀。我们采用高分辨率外周定量 CT(HR-pQCT)测量了 185 对年龄在 40 至 61 岁之间的健康女性双胞胎的远端胫骨和桡骨的皮质内、骨皮质内和小梁骨表面积及微结构。我们使用广义估计方程分析了(i)绝经过程中的特征差异,(ii)重塑标志物与骨表面积之间的关系,以及(iii)稳健回归估计对每对内差异的关联。与绝经前女性相比,绝经后女性的重塑标志物更高,皮质内和骨皮质内骨表面积更大,皮质内孔隙率更高,小梁骨表面积更小,且两处的小梁数更少(均 P<0.01)。与远端胫骨的皮质骨相比,绝经后女性的皮质骨质量损失更大(-0.98 与 -0.12 标准差,P<0.001),但在桡骨处的损失相似(-0.45 与 -0.39 标准差,P=0.79)。胫骨皮质内骨表面积每增加 1 个标准差,与重塑标志物增加 0.22-0.29 个标准差相关,约为绝经过程中重塑标志物增加 0.53-0.67 个标准差的一半(均 P<0.001)。孔隙率每增加 1 个标准差,与重塑标志物增加 0.20-0.30 个标准差相关。小梁骨表面积每减少 1 个标准差,与重塑标志物增加 0.15-0.18 个标准差相关(均 P<0.01)。两处的皮质内和骨皮质内骨表面积以及胫骨远端的孔隙率的每对内差异与一些重塑标志物的每对内差异相关(P=0.05 至 0.09)。我们推断,皮质内重塑可能通过产生皮质内孔隙率和更多的骨表面积来自我维持,而在小梁骨表面进行的重塑则是自我限制的,因为它会去除带有表面积的小梁骨。