Nazari A, Bajaj D, Zhang D, Romberg E, Arola D
Department of Mechanical Engineering, University of Maryland Baltimore County, Baltimore, MD 21250, United States.
J Mech Behav Biomed Mater. 2009 Oct;2(5):550-9. doi: 10.1016/j.jmbbm.2009.01.008. Epub 2009 Feb 5.
An evaluation of the crack growth resistance of human coronal dentin was performed on tissue obtained from patients between ages 18 and 83. Stable crack extension was achieved over clinically relevant lengths (0< or = a < or =1mm) under Mode I quasi-static loading and perpendicular to the nominal tubule direction. Results distinguished that human dentin exhibits an increase in crack growth resistance with extension (i.e. rising R-curve) and that there is a significant reduction in both the initiation (K(o)) and plateau (K(p)) components of toughness with patient age. In the young dentin (18< or =age< or =35) there was a 25% increase in the crack growth resistance from the onset of extension (K(o)=1.34 MPa m(0.5)) to the maximum or "plateau" toughness (K(p)=1.65 MPa m(0.5)). In comparison, the crack growth resistance of the old dentin (55< or =age) increased with extension by less than 10% from K(o)=1.08 MPa m(0.5) to K(p)=1.17 MPa m(0.5). In young dentin toughening was achieved by a combination of inelastic deformation of the mineralized collagen matrix and microcracking of the peritubular cuffs. These mechanisms facilitated further toughening via the development of unbroken ligaments of tissue and posterior crack-bridging. Microstructural changes with aging decreased the capacity for near-tip inelastic deformation and microcracking of the tubules, which in turn suppressed the formation of unbroken ligaments and the degree of extrinsic toughening.
对年龄在18至83岁患者的组织进行了人牙冠部牙本质抗裂纹扩展性能的评估。在I型准静态加载下,沿与牙本质小管名义方向垂直的方向,在临床相关长度(0≤a≤1mm)上实现了稳定的裂纹扩展。结果表明,人牙本质的抗裂纹扩展能力随裂纹扩展而增加(即R曲线上升),并且随着患者年龄的增长,韧性的起始(K(o))和平原(K(p))分量均显著降低。在年轻牙本质(18≤年龄≤35岁)中,从裂纹扩展开始(K(o)=1.34MPa·m(0.5))到最大或“平原”韧性(K(p)=1.65MPa·m(0.5)),抗裂纹扩展能力增加了25%。相比之下,老年牙本质(年龄≥55岁)的抗裂纹扩展能力从K(o)=1.08MPa·m(0.5)增加到K(p)=1.17MPa·m(0.5),扩展量不到10%。在年轻牙本质中,增韧是通过矿化胶原基质的非弹性变形和管周袖套的微裂纹共同作用实现的。这些机制通过组织未断裂韧带的形成和后方裂纹桥接促进了进一步增韧。随着年龄增长的微观结构变化降低了小管尖端附近非弹性变形和微裂纹形成的能力,进而抑制了未断裂韧带的形成和外部增韧程度。