Deterioration of trabecular plate-rod and cortical microarchitecture and reduced bone stiffness at distal radius and tibia in postmenopausal women with vertebral fractures.
Deterioration of trabecular plate-rod and cortical microarchitecture and reduced bone stiffness at distal radius and tibia in postmenopausal women with vertebral fractures.
复制标题
DOI：
10.1016/j.bone.2016.04.003
复制
发表时间：
2016-07
期刊：
影响因子：
4.1
通讯作者：
Guo XE
中科院分区：
文献类型：
--
作者：
Wang J;Stein EM;Zhou B;Nishiyama KK;Yu YE;Shane E;Guo XE
经HR-pQCT检测，绝经后女性椎体骨折患者桡骨远端和胫骨的骨微结构异常，与区域BMD无关。然而，女性椎体骨折患者骨小梁板和杆的微结构是否改变尚不清楚。本研究旨在描述绝经后女性椎体骨折患者骨小梁板和棒微结构、皮质和骨硬度的异常。HR-pQCT图像的桡骨远端和胫骨获得了45名妇女椎体骨折和45名对照组无骨折。通过自动分割算法分离骨小梁和皮质隔室，并分别进行个体骨小梁分割（ITS）分析以测量骨小梁板和棒形态以及皮质骨评价以测量皮质厚度和孔隙率。通过有限元分析估计全骨和松质骨刚度。骨折组和对照组受试者在年龄、种族、体重指数、骨质疏松风险因素或药物使用方面没有差异。与对照组相比，椎体骨折的女性皮质更薄，骨小梁面积更大。通过ITS分析，骨折受试者在桡骨和胫骨处的骨小梁板较少，轴向排列的骨小梁较少，骨小梁连接性较低。在桡骨处观察到较少的小梁杆。与对照组相比，女性桡骨椎骨骨折患者的全骨刚度和骨小梁刚度分别降低18%和22%，胫骨骨折患者的全骨刚度和骨小梁刚度分别降低19%和16%。在骨折受试者中，桡骨和胫骨的估计失效载荷也分别降低了13%和14%。总之，绝经后女性椎体骨折患者外周骨骼的骨小梁和皮质微结构均发生恶化，骨小梁板优先丢失，皮质变薄。这些微结构缺陷导致桡骨和胫骨的全骨和松质骨刚度降低。我们的研究结果表明，骨小梁板和杆的微观结构异常可能是绝经后妇女椎体骨折的重要机制。
Postmenopausal women with vertebral fractures have abnormal bone microarchitecture at the distal radius and tibia by HR-pQCT, independent of areal BMD. However, whether trabecular plate and rod microarchitecture is altered in women with vertebral fractures is unknown. This study aims to characterize the abnormalities of trabecular plate and rod microarchitecture, cortex, and bone stiffness in postmenopausal women with vertebral fractures. HR-pQCT images of distal radius and tibia were acquired from 45 women with vertebral fractures and 45 control subjects without fractures. Trabecular and cortical compartments were separated by an automatic segmentation algorithm and subjected to individual trabecula segmentation (ITS) analysis for measuring trabecular plate and rod morphology and cortical bone evaluation for measuring cortical thickness and porosity, respectively. Whole bone and trabecular bone stiffness were estimated by finite element analysis. Fracture and control subjects did not differ according to age, race, body mass index, osteoporosis risk factors, or medication use. Women with vertebral fractures had thinner cortices, and larger trabecular area compared to the control group. By ITS analysis, fracture subjects had fewer trabecular plates, less axially aligned trabeculae and less trabecular connectivity at both the radius and the tibia. Fewer trabecular rods were observed at the radius. Whole bone stiffness and trabecular bone stiffness were 18% and 22% lower in women with vertebral fractures at the radius, and 19% and 16% lower at the tibia, compared with controls. The estimated failure load of the radius and tibia were also reduced in the fracture subjects by 13% and 14%, respectively. In summary, postmenopausal women with vertebral fractures had both trabecular and cortical microstructural deterioration at the peripheral skeleton, with a preferential loss of trabecular plates and cortical thinning. These microstructural deficits translated into lower whole bone and trabecular bone stiffness at the radius and tibia. Our results suggest that abnormalities in trabecular plate and rod microstructure may be important mechanisms of vertebral fracture in postmenopausal women.