Bala Yohann, Bui Quang Minh, Wang Xiao-Fang, Iuliano Sandra, Wang Qingju, Ghasem-Zadeh Ali, Rozental Tamara D, Bouxsein Mary L, Zebaze Roger M D, Seeman Ego
Endocrine Center, Austin Health, University of Melbourne, Melbourne, Australia.
J Bone Miner Res. 2015 Apr;30(4):621-9. doi: 10.1002/jbmr.2388.
Fragility fractures commonly involve metaphyses. The distal radius is assembled with a thin cortex formed by fusion (corticalization) of trabeculae arising from the periphery of the growth plate. Centrally positioned trabeculae reinforce the thin cortex and transfer loads from the joint to the proximal thicker cortical bone. We hypothesized that growth- and age-related deficits in trabecular bone disrupt this frugally assembled microarchitecture, producing bone fragility. The microarchitecture of the distal radius was measured using high-resolution peripheral quantitative computed tomography in 135 females with distal radial fractures, including 32 girls (aged 7 to 18 years), 35 premenopausal women (aged 18 to 44 years), and 68 postmenopausal women (aged 50 to 76 years). We also studied 240 fracture-free controls of comparable age and 47 healthy fracture-free premenopausal mother-daughter pairs (aged 30 to 55 and 7 to 20 years, respectively). In fracture-free girls and pre- and postmenopausal women, fewer or thinner trabeculae were associated with a smaller and more porous cortical area (r = 0.25 to 0.71 after age, height, and weight adjustment, all p < 0.05). Fewer and thinner trabeculae in daughters were associated with higher cortical porosity in their mothers (r = 0.30 to 0.47, all p < 0.05). Girls and premenopausal and postmenopausal women with forearm fractures had 0.3 to 0.7 standard deviations (SD) fewer or thinner trabeculae and higher cortical porosity than controls in one or more compartment; one SD trait difference conferred odds ratio (95% confidence interval) for fracture ranging from 1.56 (1.01-2.44) to 4.76 (2.86-7.69). Impaired trabecular corticalization during growth, and cortical and trabecular fragmentation during aging, may contribute to the fragility of the distal radius.
脆性骨折通常累及干骺端。桡骨远端由生长板周边小梁融合形成的薄皮质骨(皮质化)构成。位于中央的小梁加强了薄皮质骨,并将负荷从关节传递至近端较厚的皮质骨。我们推测,与生长和年龄相关的小梁骨缺陷会破坏这种节俭组装的微结构,导致骨脆性增加。使用高分辨率外周定量计算机断层扫描对135例桡骨远端骨折女性的桡骨远端微结构进行测量,其中包括32名女孩(7至18岁)、35名绝经前女性(18至44岁)和68名绝经后女性(50至76岁)。我们还研究了240名年龄相仿的无骨折对照者以及47对健康的无骨折绝经前母女对(分别为30至55岁和7至20岁)。在无骨折的女孩、绝经前和绝经后女性中,小梁数量减少或变细与皮质面积更小、孔隙更多相关(在调整年龄、身高和体重后,r = 0.25至0.71,所有p < 0.05)。女儿的小梁数量减少和变细与母亲较高的皮质孔隙率相关(r = 0.30至0.47,所有p < 0.05)。与对照者相比,发生前臂骨折的女孩、绝经前和绝经后女性在一个或多个区域的小梁数量减少或变细0.3至0.7个标准差(SD),且皮质孔隙率更高;一个SD的性状差异使骨折的比值比(95%置信区间)范围为1.56(1.01 - 2.44)至4.76(2.86 - 7.69)。生长过程中小梁皮质化受损以及衰老过程中皮质和小梁碎片化可能导致桡骨远端的脆性增加。