Kotha S P, Guzelsu N
Biomechanics and Biomaterials Laboratory, University of Missouri-Kansas City, 650 E. 25th Street, Kansas City, MO 64108, USA.
J Biomech. 2003 Nov;36(11):1683-9. doi: 10.1016/s0021-9290(03)00169-6.
Plexiform bovine bone samples are repeatedly loaded in tension along their longitudinal axis. In order to induce damage in the bone tissue, bone samples are loaded past their yield point. Half of the bone samples from the damaged group were stored in saline to allow for viscoelastic recovery while the others were decalcified. Tensile tests were conducted on these samples to characterize the effects of damage on the mechanical behavior of the organic matrix (decalcified samples) as well as on bone tissue (stored in saline). The ultimate strain of the damaged decalcified bone is 29% higher compared to that of non-damaged decalcified (control) bone. The ultimate stresses as well as the elastic moduli are similar in both decalcified groups. This phenomenon is also observed in other collagenous tissue (tendon and ligament). This may suggest that damage in bone is caused by shear failure of the organic matrix; transverse separation of the collagen molecules or microfibrils from each other. In contrast, there is a trend towards lowered ultimate strains in damaged bone, which is soaked in saline, with respect to control bone samples (not damaged). The damaged bone tissue exhibits a bi-linear behavior in contrast to the mechanical behavior of non-damaged bone. The initial elastic modulus (below 55 MPa) and ultimate strength of damaged bone are similar to that in non-damaged bone.
丛状牛骨样本沿其纵轴反复承受拉伸载荷。为了在骨组织中诱导损伤,骨样本的加载超过其屈服点。受损组的一半骨样本储存在盐水中以实现粘弹性恢复,而其他样本则进行脱钙处理。对这些样本进行拉伸试验,以表征损伤对有机基质(脱钙样本)以及骨组织(储存在盐水中)力学行为的影响。与未受损的脱钙(对照)骨相比,受损脱钙骨的极限应变高29%。两个脱钙组的极限应力和弹性模量相似。在其他胶原组织(肌腱和韧带)中也观察到这种现象。这可能表明骨损伤是由有机基质的剪切破坏引起的;胶原分子或微原纤维相互横向分离。相比之下,与对照骨样本(未受损)相比,浸泡在盐水中的受损骨的极限应变有降低的趋势。与未受损骨的力学行为相比,受损骨组织表现出双线性行为。受损骨的初始弹性模量(低于55兆帕)和极限强度与未受损骨相似。