Effect of high-energy X-ray irradiation on creep mechanisms in bone and dentin

被引:13
作者
Deymier-Back, Alix C. [1 ]
Singhal, Anjali [1 ]
Yuan, Fang [1 ]
Almer, Jonathan D. [2 ]
Brinson, L. Catherine [3 ,4 ]
Dunand, David C. [1 ]
机构
[1] Northwestern Univ, Dept Mat Sci & Engn, Evanston, IL 60208 USA
[2] Argonne Natl Lab, Adv Photon Source, Xray Sci Div, Argonne, IL 60439 USA
[3] Northwestern Univ, Dept Mech Engn, Evanston, IL 60208 USA
[4] Northwestern Univ, Dept Mat Sci & Engn, Evanston, IL 60208 USA
关键词
Bone; Dentin; Creep; Synchrotron; X-ray diffraction; Irradiation damage; ELASTIC PROPERTIES; CORTICAL BONE; LOAD-TRANSFER; NANOSCALE DEFORMATION; NEUTRON-DIFFRACTION; GAMMA-IRRADIATION; COLLAGEN PHASES; ALLOGRAFT BONE; BOVINE DENTIN; FRACTURE;
D O I
10.1016/j.jmbbm.2013.01.016
中图分类号
R318 [生物医学工程];
学科分类号
0831 ;
摘要
Under long-term loading creep conditions, mineralized biological tissues like bone are expected to behave in a similar manner to synthetic composites where the creeping matrix sheds load to the elastic reinforcement as creep deformation progresses. To study this mechanism in biological composites, creep experiments were performed at 37 degrees C on bovine compact bone and dentin. Static compressive stresses were applied to the samples, while wide- and small-angle scattering patterns from high energy synchrotron X-rays were used to determine, respectively, the elastic strain in the hydroxyapatite (HAP) platelets and the strain in the mineralized collagen fibril, as a function of creep time. In these highly irradiated biological composites, the reinforcing hydroxyapatite platelets progressively transfer some of their stress back to the softer protein matrix during creep. While such behavior can be explained by damage at the interface between the two phases, it is not consistent with measurements of the apparent moduli - the ratio of applied stress to elastic HAP strain measured throughout the creep experiments by elastic unload/load segments - which remained constant throughout the experiment and thus indicated good HAP/protein bonding. A possible explanation is a combination of X-ray and load induced interfacial damage explaining the shedding of load from the HAP during long term creep, coupled with interfacial re-bonding of the load-disrupted reversible bonds upon unloading, explaining the unaffected elastic load partitioning during unload/load segments. This hypothesis is further supported by finite element modeling which shows results mirroring the experimental strain measurements when considering interfacial delamination and a compliant interstitial space at the ends of the HAP platelets. (C) 2013 Published by Elsevier Ltd.
引用
收藏
页码:17 / 31
页数:15
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