Department of Biomedical Engineering, Stony Brook University, Stony Brook, NY 11794, USA.
Bone. 2012 Mar;50(3):596-604. doi: 10.1016/j.bone.2011.12.012. Epub 2011 Dec 28.
Bone's microporosities play important biologic and mechanical roles. Here, we quantified 3D changes in cortical osteocyte-lacunae and other small porosities induced by estrogen withdrawal and two different osteoporosis treatments. Unlike 2D measurements, these data collected via synchrotron radiation-based μCT describe the size and 3D spatial distribution of a large number of porous structures. Six-month old female Sprague-Dawley rats were separated into four groups of age-matched controls, untreated OVX, OVX treated with PTH, and OVX treated with Alendronate (ALN). Intracortical microporosity of the medial quadrant of the femoral diaphysis was quantified at endosteal, intracortical, and periosteal regions of the samples, allowing the quantification of osteocyte lacunae that were formed primarily before versus after the start of treatment. Across the overall thickness of the medial cortex, lacunar volume fraction (Lc.V/TV) was significantly lower in ALN treated rats compared to PTH. In the endosteal region, average osteocyte lacunar volume (<Lc.V>) of untreated OVX rats was significantly lower than in age-matched controls, indicating a decrease in osteocyte lacunar size in bone formed on the endosteal surface after estrogen withdrawal. The effect of treatment (OVX, ALN, PTH) on the number of lacunae per tissue volume (Lc.N/TV) was dependent on the specific location within the cortex (endosteal, intracortical, periosteal). In both the endosteal and intracortical regions, Lc.N/TV was significantly lower in ALN than in untreated OVX, suggesting a site-specific effect in osteocyte lacuna density with ALN treatment. There also were a significantly greater number of small pores (5-100 μm(3) in volume) in the endosteal region for PTH compared to ALN. The mechanical impact of this altered microporosity structure is unknown, but might serve to enhance, rather than deteriorate bone strength with PTH treatment, as smaller osteocyte lacunae may be better able to absorb shear forces than larger lacunae. Together, these data demonstrate that current treatments of osteoporosis can alter the number, size, and distribution of microporosities in cortical rat lamellar bone.
骨的微孔起着重要的生物学和机械作用。在这里,我们定量了雌激素缺乏和两种不同骨质疏松症治疗引起的皮质骨细胞陷窝和其他小孔隙的 3D 变化。与 2D 测量不同,这些通过基于同步辐射的 μCT 收集的数据描述了大量多孔结构的大小和 3D 空间分布。将 6 个月大的雌性 Sprague-Dawley 大鼠分为 4 组:年龄匹配的对照组、未治疗的 OVX、接受 PTH 治疗的 OVX 和接受 Alendronate(ALN)治疗的 OVX。在样本的骨内膜、皮质内和骨膜区域定量测量内侧股骨干的皮质内微孔,允许定量分析主要在治疗开始之前和之后形成的骨细胞陷窝。在整个内侧皮质的厚度上,与 PTH 相比,ALN 治疗的大鼠的骨细胞陷窝体积分数(Lc.V/TV)显著降低。在内膜区域,未治疗的 OVX 大鼠的平均骨细胞陷窝体积(<Lc.V>)明显低于年龄匹配的对照组,表明雌激素缺乏后骨内膜表面形成的骨中骨细胞陷窝大小减小。治疗(OVX、ALN、PTH)对单位组织体积的陷窝数(Lc.N/TV)的影响取决于皮质内的特定位置(骨内膜、皮质内、骨膜)。在内膜和皮质内区域,ALN 治疗的 Lc.N/TV 明显低于未治疗的 OVX,表明 ALN 治疗对骨细胞陷窝密度具有特定部位的影响。与 ALN 相比,PTH 在骨内膜区域的小孔(体积为 5-100 μm3)数量明显更多。这种改变的微孔结构的力学影响尚不清楚,但可能会增强而不是恶化 PTH 治疗的骨强度,因为较小的骨细胞陷窝可能比较大的陷窝更能吸收剪切力。总的来说,这些数据表明,目前的骨质疏松症治疗方法可以改变皮质大鼠板层骨中微孔的数量、大小和分布。