McKay Orthopaedic Research Laboratory, Department of Orthopaedic Surgery, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States.
McKay Orthopaedic Research Laboratory, Department of Orthopaedic Surgery, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States; Department of Radiology, Cumming School of Medicine, McCaig Institute for Bone and Joint Health, University of Calgary, Calgary, Canada.
Bone. 2021 Apr;145:115862. doi: 10.1016/j.bone.2021.115862. Epub 2021 Jan 22.
Postmenopausal osteoporosis affects a large number of women worldwide. Reduced estrogen levels during menopause lead to accelerated bone remodeling, resulting in low bone mass and increased fracture risk. Both peak bone mass and the rate of bone loss are important predictors of postmenopausal osteoporosis risk. However, whether peak bone mass and/or bone microstructure directly influence the rate of bone loss following menopause remains unclear. Our study aimed to establish the relationship between peak bone mass/microstructure and the rate of bone loss in response to estrogen deficiency following ovariectomy (OVX) surgery in rats of homogeneous background by tracking the skeletal changes using in vivo micro-computed tomography (μCT) and three-dimensional (3D) image registrations. Linear regression analyses demonstrated that the peak bone microstructure, but not peak bone mass, was highly predictive of the rate of OVX-induced bone loss. In particular, the baseline trabecular thickness was found to have the highest correlation with the degree of OVX-induced bone loss and trabecular stiffness reduction. Given the same bone mass, the rats with thicker baseline trabeculae had a lower rate of trabecular microstructure and stiffness deterioration after OVX. Moreover, further evaluation to track the changes within each individual trabecula via our novel individual trabecular dynamics (ITD) analysis suggested that a trabecular network with thicker trabeculae is less likely to disconnect or perforate in response to estrogen deficiency, resulting a lower degree of bone loss. Taken together, these findings indicate that the rate of estrogen-deficiency-induced bone loss could be predicted by peak bone microstructure, most notably the trabecular thickness. Given the same bone mass, a trabecular bone phenotype with thin trabeculae may be a risk factor toward accelerated postmenopausal bone loss.
绝经后骨质疏松症影响全球大量女性。绝经后雌激素水平降低导致骨重塑加速,导致骨量减少和骨折风险增加。峰值骨量和骨丢失率都是绝经后骨质疏松症风险的重要预测指标。然而,峰值骨量和/或骨微观结构是否直接影响绝经后雌激素缺乏引起的骨丢失率仍不清楚。我们的研究旨在通过体内 micro-CT(μCT)和三维(3D)图像配准来跟踪骨骼变化,在同质背景的大鼠中建立峰值骨量/微观结构与去卵巢(OVX)手术后雌激素缺乏引起的骨丢失率之间的关系。线性回归分析表明,峰值骨微观结构而非峰值骨量与 OVX 诱导的骨丢失率高度相关。特别是,基线骨小梁厚度与 OVX 诱导的骨丢失程度和骨小梁刚度降低高度相关。在相同骨量的情况下,基线骨小梁较厚的大鼠在 OVX 后骨小梁微观结构和刚度恶化的速度较低。此外,通过我们新的个体骨小梁动力学(ITD)分析进一步评估来跟踪每个个体骨小梁内的变化表明,骨小梁网络较厚的骨小梁不太可能因雌激素缺乏而断开或穿孔,从而导致骨丢失程度较低。总之,这些发现表明,骨丢失率可以通过峰值骨微观结构,尤其是骨小梁厚度来预测。在相同的骨量下,具有薄骨小梁的小梁骨表型可能是加速绝经后骨丢失的危险因素。