External bone size identifies different strength-decline trajectories for the male human femora.

External bone size identifies different strength-decline trajectories for the male human femora.
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外部骨骼大小可以识别男性人类股骨的不同强度轨迹轨迹。

DOI:
10.1016/j.jsb.2020.107650
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发表时间:
2020-12-01
影响因子:
3
通讯作者:
Kohn DH
Kohn DH
中科院分区:
生物学3区
文献类型:
--
作者:
Bolger MW;Romanowicz GE;Bigelow EMR;Ward FS;Ciarelli A;Jepsen KJ;Kohn DH

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随着老年人口的增加,了解骨骼老化和预测骨折风险变得越来越重要。我们假设,当按外部骨大小分类时,男性股骨干将显示不同的强度-年龄轨迹,这可以通过形态学,组成和胶原交联的变化来解释。根据中轴总截面积与骨长标准化(Tt.Ar/Le),将尸体男性股骨分为窄(n = 15, 26-89岁)组和宽(n = 15, 29-82岁)组,并进行全骨强度、组织水平强度和组织水平屈服后应变测试。形态学,皮层TMD (Ct。TMD),孔隙度,酶促胶原交联和戊苷的直接测量。单独宽骨组与年龄在组织水平强度(R2 = 0.50, p = 0.002)、组织水平屈服后应变(R2 = 0.75, p < 0.001)和全骨强度(R2 = 0.14, p = 0.108)上呈显著负相关。Ct。TMD与两组的全骨和组织水平强度相关,但戊苷归一化为酶交联仅与宽组的所有力学性能负相关。多变量分析表明,每种力学性能的三个特征解释了整个骨强度的大部分差异(Ct。区域,Ct。TMD, Log(PEN/Mature; R2 = 0.75),组织水平强度(Age, Ct。TMD、日志(DHLNL / HLNL);R2 = 0.56),屈服后应变(Age, Log(Pyrrole), Ct.Area;R2 = 0.51)。总的来说,这突出了骨骼结构、组成和强度的个体间差异是如何随着年龄的增长而变化的,而且对骨骼衰老的一刀切的理解是不够的。
Understanding skeletal aging and predicting fracture risk is increasingly important with a growing elderly population. We hypothesized that when categorized by external bone size, the male femoral diaphysis would show different strength-age trajectories which can be explained by changes in morphology, composition and collagen cross-linking. Cadaveric male femora were sorted into narrow (n = 15, 26–89 years) and wide (n = 15, 29–82 years) groups based upon total cross-sectional area of the mid-shaft normalized to bone length (Tt.Ar/Le) and tested for whole bone strength, tissue-level strength, and tissue-level post-yield strain. Morphology, cortical TMD (Ct.TMD), porosity, direct measurements of enzymatic collagen cross-links, and pentosidine were obtained. The wide group alone showed significant negative correlations with age for tissue-level strength (R2 = 0.50, p = 0.002), tissue-level post-yield strain (R2 = 0.75, p < 0.001) and borderline significance for whole bone strength (R2 = 0.14, p = 0.108). Ct.TMD correlated with whole bone and tissue-level strength for both groups, but pentosidine normalized to enzymatic cross-links correlated negatively with all mechanical properties for the wide group only. The multivariate analysis showed that just three traits for each mechanical property explained the majority of the variance for whole bone strength (Ct.Area, Ct.TMD, Log(PEN/Mature; R2 = 0.75), tissue-level strength (Age, Ct.TMD, Log(DHLNL/HLNL); R2 = 0.56), and post-yield strain (Age, Log(Pyrrole), Ct.Area; R2 = 0.51). Overall, this highlights how inter-individual differences in bone structure, composition, and strength change with aging and that a one-size fits all understanding of skeletal aging is insufficient.
DOI: 10.1002/ar.22962
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