Aging and Fatigue Crack Growth in Dentin
Aging and Fatigue Crack Growth in Dentin
批准号:
7473290
负责人:
Dwayne Dale Arola
金额:
$20.42万
依托单位国家:
美国
项目类别:
财政年份:
2007
资助国家:
美国
项目状态:
已结题
起止时间:
2007-08-01 至 2011-07-31
关键词:
AchievementAddressAgeAgingAreaBehaviorCharacteristicsChemicalsChemistryClinicalConditionCoupledDental Cavity PreparationDental EnamelDental Health SurveysDental InlaysDental MaterialsDental crownsDentinDentistryDentistsDevelopmentEnsureEnvironmentEvaluationFailureFatigueFosteringFoundationsFractureFutureGenderGoalsGrowthHealth Care CostsHealthcareHumanIncidenceInvestigationKnowledgeMechanicsMethodsMicroscopicObject AttachmentOpticsOralOral healthPatientsPopulationProcessPropertyQuality of lifeRangeRateResearchResistanceRiskRoleSavingsServicesSpecimenStressStructureTechniquesTestingTissuesTooth FracturesTooth TissueTooth structureTranslatingage relatedbasedesigndigital imagingimprovednovelnovel strategiespreventrepairedrestorationrestorative dentistryrestorative materialrestorative treatment
中文摘要
描述(申请人提供):牙齿折断导致的修复失败是影响终身口腔健康的主要障碍之一。我们研究的总体假设是,修复牙的断裂是由于牙本质的疲劳裂纹扩展阻力随着年龄的增加而减少所致。我们的初步研究表明,疲劳裂纹经常出现在修复牙的牙本质中,牙本质的疲劳特性是小管方向和患者年龄的函数。尽管牙本质的结构随着年龄的增长而发生明显的变化,而且老年人更容易发生牙齿折裂,但衰老对牙本质疲劳特性的影响仍不清楚。随着部分和全齿老年人的增加,衰老在修复牙失败中的作用变得越来越重要。我们建议将牙本质疲劳裂纹扩展特性量化为患者年龄、性别和牙本质小管方向的函数,区分最有害的变化发生在什么年龄,并确定导致裂纹扩展阻力降低的基本机制。疲劳裂纹的萌生和扩展将在从拔除的原始磨牙的冠状牙本质制备的人牙本质标本中进行评估。裂纹萌生和循环裂纹扩展的机制将使用一种新的数字图像相关应用来表征,并根据患者的年龄和性别进行评估。牙本质的结构和化学变化也将使用分析显微技术进行评估。研究结果将使我们对牙本质的疲劳裂纹扩展特性有一个基本的了解,从而能够发展出详细的结构-特性关系。基于定量结果和对致病机制的理解,我们期望确定现有牙齿折断修复治疗的关键方面,以及在治疗齿状齿人口老龄化方面潜在的新方法的需求。这一结果有望支持临床技术的发展,以阻止牙齿结构中涉及机械和化学修复方法的裂缝。希望我们的发现将有助于确定增强牙齿组织抗疲劳性的方法,无论年龄如何。这些成就应该会减少与牙齿断裂相关的修复失败的发生率,从而节省数十亿美元的医疗费用,并减少人类的痛苦。
英文摘要
DESCRIPTION (provided by applicant): Restoration failures resulting from tooth fracture are one of the primary obstacles to lifelong oral health. The overall hypothesis of our study is that the fracture of restored teeth is fostered by a reduction in the fatigue crack growth resistance of dentin with age. Our preliminary studies have shown that fatigue cracks are often present in the dentin of restored teeth and that the fatigue properties of dentin are a function of both the tubule orientation and patient age. Despite distinct changes in the structure of dentin with age, and identification that tooth fractures occur more frequently in seniors, the influence of aging on the fatigue properties of dentin has remained unknown. With the increase in partially and full dentate seniors, the role of aging on restored tooth failures has become increasingly important. We propose to quantify the fatigue crack growth properties of dentin as a function of patient age, gender and dentin tubule orientation, distinguish at what age the most detrimental changes take place, and identify, the fundamental mechanisms responsible for reduction in crack growth resistance. Fatigue crack initiation axnd growth will be evaluated in human dentin specimens prepared from the coronal dentin of extracted virgin molars. The mechanisms of crack initiation and cyclic crack extension will be characterized using a novel application of digital image correlation and evaluated in terms of the patient's age and gender. Changes in the structure and chemistry of dentin will also be evaluated using analytical microscopic techniques. Results of the investigation will provide a fundamental understanding of the fatigue crack growth properties of dentin that enable development of detailed structure-property relationships. Based on both quantitative results and an understanding of contributing mechanisms, we expect to identify the critical aspects of existing restorative treatments on tooth fracture and the potential need for new approaches in treatment of the aging dentate population. The results are expected to support development of clinical techniques for arresting cracks in tooth structure that involve both mechanical and chemical approaches to repair. Hopefully our findings will help identify approaches for strengthening the fatigue resistance of tooth tissues, regardless of age. These achievements should reduce the incidence of restorative failures associated with tooth fracture, resulting in billions of dollars in savings of health care costs, as well as a reduction in human suffering.
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Aging and Fatigue Crack Growth in Dentin
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批准号:7932521
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项目类别:
-
资助金额:$16.9万
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财政年份:2009
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负责人:Dwayne Dale Arola
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依托单位:
Aging and Fatigue Crack Growth in Dentin
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批准号:7320356
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项目类别:
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资助金额:$22.33万
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财政年份:2007
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负责人:Dwayne Dale Arola
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依托单位:
Aging and Fatigue Crack Growth in Dentin
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批准号:8116239
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项目类别:
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资助金额:$5.86万
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财政年份:2007
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负责人:Dwayne Dale Arola
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依托单位:
Aging and Fatigue Crack Growth in Dentin
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批准号:7652507
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项目类别:
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资助金额:$18.07万
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财政年份:2007
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负责人:Dwayne Dale Arola
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依托单位:
Aging and Fatigue Crack Growth in Dentin
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批准号:7904332
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项目类别:
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资助金额:$18.12万
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财政年份:2007
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负责人:Dwayne Dale Arola
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依托单位:
Fatigue and the Endurance Strength of Dentin
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批准号:6485784
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项目类别:
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资助金额:$6.35万
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财政年份:2002
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负责人:Dwayne Dale Arola
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依托单位:
Fatigue and the Endurance Strength of Dentin
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批准号:6649338
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项目类别:
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资助金额:$7.09万
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财政年份:2002
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负责人:Dwayne Dale Arola
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依托单位:
海外基金