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温度、应力和微观结构对致密牛骨蠕变的影响。

The effect of temperature, stress and microstructure on the creep of compact bovine bone.

作者信息

Rimnac C M, Petko A A, Santner T J, Wright T M

机构信息

Department of Biomechanics, Hospital for Special Surgery, New York, NY 10021.

出版信息

J Biomech. 1993 Mar;26(3):219-28. doi: 10.1016/0021-9290(93)90360-q.

DOI:10.1016/0021-9290(93)90360-q
PMID:8468335
Abstract

Creep tests of 117 compact bovine bone specimens were conducted at three temperatures (25, 37, and 43 degrees C), with applied stresses between 71 and 115 MPa. Following testing, the amount of secondary haversian bone in the gage region of the specimens was estimated. The resulting steady-state creep rates (epsilon) were fit to an Arrhenius (e-Qc/RT) model (where Qc is the activation energy for the mechanism(s) controlling creep, R is the gas constant, and T is the absolute temperature) of the type used to describe the classic steady-state creep behavior of metals, ceramics, and metamorphic rocks. The empirical model developed was epsilon = 5.6 x 10(-9) e4.6F sigma 5.2 e-5330/T, where epsilon is the estimated mean steady-state creep rate, F is the volume fraction of secondary haversian bone, sigma is the applied stress, and T is the absolute temperature. There was a positive, significant association between the estimated mean steady-state creep rate and F, sigma, and T. Qc was determined to be 44.3 kJ mol-1, a reasonable value when compared to activation energies for creep in ceramics. It is hypothesized that permanent deformation during creep of compact bovine bone is primarily due to damage mechanisms associated with dislocations in the hydroxyapatite mineral lattice structure.

摘要

对117个致密牛骨样本在三个温度(25、37和43摄氏度)下进行了蠕变试验,施加应力在71至115兆帕之间。测试后,估计了样本标距区域内次生哈弗斯骨的数量。将所得的稳态蠕变率(ε)拟合到用于描述金属、陶瓷和变质岩经典稳态蠕变行为的阿累尼乌斯(e -Qc/RT)模型(其中Qc是控制蠕变机制的活化能,R是气体常数,T是绝对温度)。所建立的经验模型为ε = 5.6×10⁻⁹ e⁴.⁶F σ⁵.² e⁻⁵³³⁰/T,其中ε是估计的平均稳态蠕变率,F是次生哈弗斯骨的体积分数,σ是施加的应力,T是绝对温度。估计的平均稳态蠕变率与F、σ和T之间存在正的、显著的关联。确定Qc为44.3千焦/摩尔,与陶瓷蠕变的活化能相比,这是一个合理的值。据推测,致密牛骨蠕变过程中的永久变形主要是由于与羟基磷灰石矿物晶格结构中的位错相关的损伤机制。

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