ULTRASTRUCTURAL HISTOPATHOLOGY OF HUMAN DENTAL ENAMEL

长期的假设是釉质晶体的成核、生长、 方向和排列(成棱镜)取决于唯一的 晶体与有机基质和成釉细胞的关系。 总体目标是澄清超微结构的排列和 正常和病理性牙釉质组织成分紊乱 各州。研究方法承认，细胞的超微结构 釉质组织及其畸形在传递中得到最好的解决 电子显微镜(TEM)。当瞬变电磁测试结果直接与 可以获得关于该结构的其他技术的新理解， 牙釉质的功能、α和超微结构组织病理学。结晶蚀变 -第一个目标是研究晶体的后遗症和病理变化 形态学，重点是脱矿/再矿化(脱矿/再矿化)。 假设remin可能涉及一种不同的机制 釉面棱镜与棱镜外围相比。人牙釉质的明胶/明胶 合成磷灰石将通过恒定组成方法进行监测 并与透射电子显微镜的观察结果进行了对比，以消除晶核缺陷为目标。 将结果与人类白斑牙釉质进行比较并加以区分 免受任何后遗症的影响。有机基质分配--第二个目标 是确定有机基质在发育和成熟过程中的分布 珐琅。假设蛋白质仅限于成熟的牙釉质中，因此 大多数晶体很少或根本没有蛋白质外壳。大鼠、人类和人造动物 磷灰石将在未经处理的情况下进行检查，并使用有机溶剂进行处理 确定脱机牙釉质中是否存在污渍伪影。蛋白 在人牙釉质中的分布将与等级牙釉质进行比较，以及 发育率釉质将检查成釉细胞残留物。最后， 为了确定成熟的成釉细胞在基质去除中所起的作用， 成釉细胞将被剥离，成熟的釉质将在透射电子显微镜下检查 以检测在体外可能发生的变化。组织病理学-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)修改， 二膦酸盐和遗传障碍。DEMIN/REMIN的局部F效应 并用透射电子显微镜研究了系统F对基质去除的影响。 双膦酸盐将继续通过透射电子显微镜进行研究，特别是它们的 对大鼠切牙釉质成核、生长和修复的影响。最后， 基因缺陷的人牙釉质将与对照组进行比较 晶体和基质的变化。结果将对开发具有相关性 无氟牙釉质防龋性的最佳环境。

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.