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首页> 外文期刊>Journal of the mechanical behavior of biomedical materials >Aging and the reduction in fracture toughness of human dentin.
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Aging and the reduction in fracture toughness of human dentin.

机译:人牙本质的老化和断裂韧性的降低。

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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.
机译:对人类冠状牙本质的抗裂纹生长性能进行了评估,该技术取自18至83岁的患者。在I型准静态模式下,临床相关长度(0 <或= a <或= 1mm)上实现了稳定的裂纹扩展并垂直于标称肾小管方向。结果表明,人类牙本质随着扩展(即R曲线的上升)而显示出对裂纹扩展的抵抗力的增加,并且韧性的起始(K(o))和平稳期(K(p))分量均显着降低。患者年龄。在年轻的牙本质(18 <或=年龄<或= 35)中,从扩展开始(K(o)= 1.34 MPa m(0.5))到最大值或“平稳”,裂纹扩展阻力增加了25%。韧性(K(p)= 1.65 MPa m(0.5))。相比之下,旧牙本质(55岁或55岁以下)的抗裂纹扩展性从K(o)= 1.08 MPa m(0.5)扩展到K(p)= 1.17 MPa m(0.5)并增加了不到10%。 。在年轻的牙本质中,增韧是通过矿化的胶原蛋白基质的无弹性变形和肾小管周围袖带的微裂纹来实现的。这些机制通过组织不间断韧带的发展和后部裂纹桥接促进了进一步的增韧。随着年龄的增长,微观结构的变化降低了近端无弹性变形和肾小管微裂纹的能力,进而抑制了未断裂韧带的形成和外在增韧的程度。

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