Taylor David, Tilmans Antoine
Trinity Centre for Bioengineering, Department of Mechanical Engineering, Trinity College, Dublin 2, Ireland.
J Theor Biol. 2004 Jul 21;229(2):169-77. doi: 10.1016/j.jtbi.2004.03.014.
Microscopic cracks form and grow in compact bone in vivo due to cyclic loading. Their growth can cause stress fractures and has been implicated in the processes of remodelling and adaptation. These cracks are repaired by the actions of BMUs which are mobile resorption cavities. In this work, we studied the interaction between cracks and BMUs by making finite element models representing different stages in the repair process. The tendency of the crack to grow was measured by its stress intensity factor, K. We found that K changes in a complex manner during the repair process, both decreasing and increasing depending on the size of the crack and the type of loading applied. For loading conditions similar to those that exist in vivo, the presence of the BMU can cause K to rise significantly, in some cases by more than 20%, implying a substantial increase in crack growth rate. This information is important for our general understanding of the complexities of the repair process, and especially for the development of theoretical models to simulate damage and repair in bone.
在体内,由于循环载荷作用,密质骨中会形成并生长微观裂纹。这些裂纹的扩展会导致应力性骨折,并且与重塑和适应过程有关。这些裂纹通过骨多能干细胞(BMUs)的作用进行修复,骨多能干细胞是可移动的吸收腔。在这项研究中,我们通过制作代表修复过程不同阶段的有限元模型,研究了裂纹与骨多能干细胞之间的相互作用。裂纹扩展的趋势通过其应力强度因子K来衡量。我们发现,在修复过程中K以复杂的方式变化,根据裂纹的大小和所施加的载荷类型,它会下降或上升。对于与体内存在的载荷条件相似的情况,骨多能干细胞的存在会导致K显著上升,在某些情况下上升幅度超过20%,这意味着裂纹扩展速率大幅增加。这些信息对于我们全面理解修复过程的复杂性非常重要,尤其是对于开发模拟骨骼损伤和修复的理论模型而言。