Gupta Himadri S, Fratzl Peter, Kerschnitzki Michael, Benecke Gunthard, Wagermaier Wolfgang, Kirchner Helmut O K
Department of Biomaterials, Max Planck Institute of Colloids and Interfaces, MPI-KG Golm, 14424 Potsdam, Germany.
J R Soc Interface. 2007 Apr 22;4(13):277-82. doi: 10.1098/rsif.2006.0172.
The molecular mechanisms for plastic deformation of bone tissue are not well understood. We analysed temperature and strain-rate dependence of the tensile deformation behaviour in fibrolamellar bone, using a technique originally developed for studying plastic deformation in metals. We show that, beyond the elastic regime, bone is highly strain-rate sensitive, with an activation volume of ca 0.6 nm3. We find an activation energy of 1.1 eV associated with the basic step involved in the plastic deformation of bone at the molecular level. This is much higher than the energy of hydrogen bonds, but it is lower than the energy required for breaking covalent bonds inside the collagen fibrils. Based on the magnitude of these quantities, we speculate that disruption of electrostatic bonds between polyelectrolyte molecules in the extrafibrillar matrix of bone, perhaps mediated by polyvalent ions such as calcium, may be the rate-limiting elementary step in bone plasticity.
骨组织塑性变形的分子机制尚未得到充分理解。我们使用一种最初用于研究金属塑性变形的技术,分析了纤维层状骨拉伸变形行为的温度和应变率依赖性。我们发现,在弹性范围之外,骨对应变率高度敏感,激活体积约为0.6立方纳米。我们发现与骨在分子水平塑性变形所涉及的基本步骤相关的激活能为1.1电子伏特。这比氢键的能量高得多,但低于破坏胶原纤维内部共价键所需的能量。基于这些量的大小,我们推测骨纤维外基质中聚电解质分子之间静电键的破坏,可能由钙等多价离子介导,可能是骨塑性的限速基本步骤。