Department of Mechanical Engineering, Johns Hopkins University, Baltimore, MD 21218, USA; Hopkins Extreme Materials Institute, Johns Hopkins University, Baltimore, MD 21218, USA.
Biomaterials & Tissue Engineering Division, Department of Endodontics, Prosthodontics and Operative Dentistry, University of Maryland Dental School, Baltimore, MD 21201, USA.
Mater Sci Eng C Mater Biol Appl. 2017 Apr 1;73:716-725. doi: 10.1016/j.msec.2016.12.065. Epub 2016 Dec 21.
The oral cavity frequently undergoes localized changes in chemistry and level of acidity, which threatens the integrity of the restorative material and supporting hard tissue. The focus of this study was to evaluate the changes in fatigue crack growth resistance of dentin and toughening mechanisms caused by lactic acid exposure. Compact tension specimens of human dentin were prepared from unrestored molars and subjected to Mode I opening mode cyclic loads. Fatigue crack growth was achieved in samples from mid- and outer-coronal dentin immersed in either a lactic acid solution or neutral conditions. An additional evaluation of the influence of sealing the lumens by dental adhesive was also conducted. A hybrid analysis combining experimental results and finite element modeling quantified the contribution of the toughening mechanisms for both environments. The fatigue crack growth responses showed that exposure to lactic acid caused a significant reduction (p≤0.05) of the stress intensity threshold for cyclic crack extension, and a significant increase (p≤0.05) in the incremental fatigue crack growth rate for both regions of coronal dentin. Sealing the lumens had negligible influence on the fatigue resistance. The hybrid analysis showed that the acidic solution was most detrimental to the extrinsic toughening mechanisms, and the magnitude of crack closure stresses operating in the crack wake. Exposing dentin to acidic environments contributes to the development of caries, but it also increases the chance of tooth fractures via fatigue-related failure and at lower mastication forces.
口腔经常发生局部化学变化和酸度变化，这会威胁到修复材料和支持硬组织的完整性。本研究的重点是评估暴露于乳酸后牙本质的疲劳裂纹扩展阻力的变化和增韧机制。从未修复的磨牙中制备人牙本质的紧凑拉伸样品，并对其进行模式 I 开口循环负载。在浸泡在乳酸溶液或中性条件下的中间和外冠牙本质的样品中实现了疲劳裂纹扩展。还评估了通过牙科胶粘剂密封管腔的影响。将实验结果和有限元建模相结合的混合分析量化了两种环境下增韧机制的贡献。疲劳裂纹扩展响应表明，暴露于乳酸会显著降低（p≤0.05）循环裂纹扩展的应力强度阈值，并显著增加（p≤0.05）牙本质外冠两个区域的增量疲劳裂纹扩展率。密封管腔对耐疲劳性几乎没有影响。混合分析表明，酸性溶液对外部增韧机制最不利，并且在裂纹尾迹中起作用的裂纹闭合应力的大小。将牙本质暴露于酸性环境会导致龋齿的发展，但也会通过与疲劳相关的失效和较低的咀嚼力增加牙齿断裂的机会。
