ULTRASTRUCTURAL HISTOPATHOLOGY OF HUMAN DENTAL ENAMEL

长期的假说是釉质晶体的成核、生长， 方向和排列（进入棱镜）取决于一个独特的 晶体与有机基质和成釉细胞的关系。 总体目标是阐明超微结构排列， 正常和病理性牙釉质组织成分排列紊乱 states. 该研究方法承认， 牙釉质组织及其畸形最好在传输中解决 电子显微镜（TEM）。 当TEM结果与 其它技术可以获得关于结构的新的理解， 釉质功能、超微结构和组织病理学的研究。 晶体蚀变 - 目的一是研究晶体的破坏和病理变化 形态学，重点是脱矿/再矿化（demin/remin）。 假设是，提醒可能涉及不同的机制， 釉棱柱相比，棱镜周边。 人牙釉质脱矿/再矿化 和合成磷灰石将通过恒定成分法进行监测 与TEM相关，目的是提醒晶体核心缺陷。 将结果与人类白色斑牙釉质进行比较， 不受术后变化的影响 有机基质分布-第二个目标 确定发育期和成熟期有机基质的分布 搪瓷。 假设是蛋白质被限制在成熟的釉质中， 大多数晶体几乎没有或没有蛋白质外壳。 老鼠，人类，和合成人 将对未经处理和用有机溶剂处理的磷灰石进行检查， 确定在脱有机釉质中是否出现染色伪影。 蛋白 将在人牙釉质中的分布与评级牙釉质进行比较， 将检查釉质发育速率中的成釉细胞残余物。 最后， 为了确定成熟成釉细胞在基质去除中的作用， 将成釉细胞剥离，并在TEM中检查成熟的釉质 来检测体外可能发生的变化。 历史学-第三个目标是 为了确定前两项研究的结果如何被氟化物（F）改变， 二膦酸盐和遗传病 Demin/Remin的局部F效应 并通过透射电镜研究了系统F对基体去除的影响。 将继续通过TEM研究二膦酸盐，特别是其 对大鼠切牙釉质成核、生长和恢复的影响。 最后， 基因缺陷的人类牙釉质将与对照组进行比较， 晶体和基质改变。 结果将与发展有关 无氟牙釉质防龋的最佳环境。

Long-term hypothesis is that enamel crystal's nucleation, growth, orientation, and arrangement (into prisms) is dependent on a unique relationship of the crystal to the organic matrix and the ameloblast. Overall objective is to clarify the ultrastructural arrangement and disarrangement of enamel tissue components in normal and pathological states. The research approach acknowledges that the ultrastructure of enamel tissue and its malformation is best resolved in the transmission electron microscope (TEM). When TEM results are directly correlated wit other techniques new understanding can be gained regarding the structure, function,a and ultrastucural histopathology of enamel. Crystal alterations - first aim is to study posteruptive and pathological changes in crystal morphology with a focus on demineralization/remineralization (demin/remin). Hypothesis is that remin may involve a different mechanism within the enamel prisms compared to the prism periphery. Demin/remin of human enamel and synthetic apatite will be monitored by constant composition methods correlated with TEM with the objective of remin of crystal core defects. Results will be compared with human white spot enamel and distinguished from any posteruptive changes. Organic matrix distribution - second aim is to determine the distribution of organic matrix in developing and mature enamel. Hypothesis is that protein is restricted in mature enamel so that most crystals have little or no protein coat. Rat, human, and synthetic apatite will be examined untreated and treated wit organic solvents to determine if stain artefacts occur in deorganified enamel. Protein distribution in human enamel will be compared to rate enamel, and developing rate enamel will be examined for ameloblast remnants. Finally, to determine the role maturation ameloblasts play in matrix removal, ameloblasts will be stripped away and the maturing enamel examined in TEM to detect changes that may occur in vitro. Histopathology - third aim is to determine how results of first two studies are modified by fluoride (F), diphosphonates, and genetic disturbances. Topical F effects of demin/remin and systemic F effects on matrix removal will be studied via TEM. Diphosphonates will continue to be studied via TEM, particularly for their effects on rat incisor enamel nucleation, growth, and recovery. Finally, genetically defective human enamel will be compared with controls for crystal and matrix alterations. Results will have relevance in developing the optimal environment for enamel caries resistance without fluorosis.