Department of Mechanical and Manufacturing Engineering, Schulich School of Engineering, University of Calgary, 2500 University Drive, N.W., Calgary, AB, T2N 1N4, Canada.
Osteoporos Int. 2011 Jan;22(1):357-62. doi: 10.1007/s00198-010-1226-1. Epub 2010 May 11.
We used high-resolution peripheral quantitative computed tomography (HR-pQCT) to monitor changes in bone microarchitecture and strength at the distal radius and tibia associated with 18 months of teriparatide therapy in postmenopausal women with osteoporosis. Despite treatment-associated declines in total and cortical BMD, trabecular thinning and reduced trabecular bone volume, bone strength did not change significantly from baseline.
Teriparatide is an established anabolic therapy for osteoporosis; however, treatment effects at the distal radius are unclear. Therefore, we aimed to monitor changes in bone microarchitecture and estimated strength at the distal radius and tibia in osteoporotic postmenopausal women.
We used high-resolution peripheral quantitative computed tomography (Scanco Medical, Switzerland) to perform a standard three-dimensional morphological analysis of the distal radius and tibia in 11 osteoporotic postmenopausal women (mean age, 68.7 ± 12.7 years) at baseline, 6, 12, and 18 months after initiation of 20 μg/day of teriparatide. Ten of the women received bisphosphonate therapy prior to starting on teriparatide. In addition to the standard analysis, we quantified cortical bone mineral density (BMD), porosity, and thickness using an automated segmentation procedure and estimated bone strength (ultimate stress) using finite element analysis.
After 18 months, we observed a decrease in total BMD (p = 0.03) at the distal radius and a decrease in cortical BMD at the distal radius (p = 0.05) and tibia (p = 0.01). The declines in cortical BMD were associated with trends for increased cortical porosity at both sites. At the distal radius, 18 months of teriparatide treatment was also associated with trabecular thinning (p = 0.009) and reduced trabecular bone volume ratio (p = 0.08). We observed similar trends at the distal tibia. Despite these changes in bone quality, bone strength was maintained over the 18-month follow-up.
The observed changes in cortical bone structure are consistent with the effects of parathyroid hormone on intracortical bone remodeling. Controlled trials involving larger sample sizes are required to confirm the effects of teriparatide therapy on trabecular and cortical microarchitecture in the peripheral skeleton.
我们使用高分辨率外周定量计算机断层扫描(HR-pQCT)监测绝经后骨质疏松症患者接受特立帕肽治疗 18 个月时与桡骨远端和胫骨相关的骨微观结构和强度的变化。尽管与治疗相关的总骨密度和皮质骨密度下降、骨小梁变薄和骨小梁体积减少,但骨强度与基线相比无显著变化。
我们使用高分辨率外周定量计算机断层扫描(Scanco Medical,瑞士)对 11 名绝经后骨质疏松症妇女(平均年龄 68.7±12.7 岁)的桡骨远端和胫骨进行标准三维形态学分析,在开始使用 20μg/天特立帕肽治疗前、6、12 和 18 个月时进行分析。其中 10 名妇女在开始使用特立帕肽前接受了双膦酸盐治疗。除了标准分析外,我们还使用自动分割程序量化皮质骨密度(BMD)、孔隙率和厚度,并使用有限元分析估计骨强度(极限应力)。
18 个月后,我们观察到桡骨远端总骨密度下降(p=0.03),桡骨远端和胫骨皮质骨密度下降(p=0.05 和 p=0.01)。皮质骨密度的下降与两个部位皮质骨孔隙率增加的趋势相关。在桡骨远端,特立帕肽治疗 18 个月还与骨小梁变薄(p=0.009)和骨小梁体积比减少(p=0.08)相关。在胫骨远端也观察到类似的趋势。尽管骨质量发生了这些变化,但在 18 个月的随访中,骨强度保持不变。
皮质骨结构的变化与甲状旁腺激素对皮质内骨重塑的影响一致。需要更大样本量的对照试验来证实特立帕肽治疗对周围骨骼的小梁和皮质微观结构的影响。