Microarchitecture influences microdamage accumulation in human vertebral trabecular bone.

Microarchitecture influences microdamage accumulation in human vertebral trabecular bone.
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DOI:
10.1359/jbmr.080517
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发表时间:
2008-10
期刊:
Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
影响因子:
--
通讯作者:
Delmas PD
Delmas PD
中科院分区:
其他
文献类型:
--
作者:
Arlot ME;Burt-Pichat B;Roux JP;Vashishth D;Bouxsein ML;Delmas PD

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已经表明,随着年龄的增长,微损伤的积累有助于骨骼的脆弱性。然而,与年龄相关的微损伤增加以及人类椎体松质骨微损伤和小梁微结构之间的关联的数据有限。我们对来自23名54 - 93岁(8男15女)供体的人腰椎(L2)椎体松质骨的微损伤进行了定量。使用螯合剂连续标记的组织学技术测量损伤,并通过高分辨率μ CT评估与3D微结构相关。有没有性别之间的显着差异,虽然妇女往往有一个较高的微裂纹密度(Cr. Dn)比男性。Cr、Dn随年龄增长呈指数增加(r = 0.65,P <0.001),并与骨体积分数相关(BV/TV; r =-0.55; p <0.01),小梁数量(Tb. N; r =-0.56 p = 0.008)、结构模型指数(SMI; r = 0.59; p = 0.005)和小梁分离(Tb. Sp; r = 0.59; p <0.009)。所有结构参数彼此之间以及与BV/TV之间都有很强的相关性。逐步回归分析表明,SMI是最好的预测微损伤,解释35%的方差在Cr,Dn和20%的方差在扩散损伤积累。此外,微裂纹长度显着更大的SMI的最高与最低的三分位数。总之,在人椎体松质骨中,微损伤随着年龄的增长而增加,并与低BV/TV和杆状小梁结构相关。
It has been suggested that accumulation of microdamage with age contributes to skeletal fragility. However, data on the age-related increase in microdamage and the association between microdamage and trabecular microarchitecture in human vertebral cancellous bone are limited. We quantified microdamage in cancellous bone from human lumbar (L2) vertebral bodies obtained from 23 donors 54–93 yr of age (8 men and 15 women). Damage was measured using histologic techniques of sequential labeling with chelating agents and was related to 3D microarchitecture, as assessed by high-resolution μCT. There were no significant differences between sexes, although women tended to have a higher microcrack density (Cr.Dn) than men. Cr.Dn increased exponentially with age (r = 0.65, p < 0.001) and was correlated with bone volume fraction (BV/TV; r = −0.55; p < 0.01), trabecular number (Tb.N; r = −0.56 p = 0.008), structure model index (SMI; r = 0.59; p = 0.005), and trabecular separation (Tb.Sp; r = 0.59; p < 0.009). All architecture parameters were strongly correlated with each other and with BV/TV. Stepwise regression showed that SMI was the best predictor of microdamage, explaining 35% of the variance in Cr.Dn and 20% of the variance in diffuse damage accumulation. In addition, microcrack length was significantly greater in the highest versus lowest tertiles of SMI. In conclusion, in human vertebral cancellous bone, microdamage increases with age and is associated with low BV/TV and a rod-like trabecular architecture.
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