Odontoblast dysfunction in osteogenesis imperfecta:: An LM, SEM, and ultrastructural study
Odontoblast dysfunction in osteogenesis imperfecta:: An LM, SEM, and ultrastructural study
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DOI：
10.1080/03008200290001005
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发表时间：
2002-04-01
影响因子：
2.9
通讯作者：
Hemmerlé, J
中科院分区：
文献类型：
--
作者：
Hall, RK;Manière, MC;Hemmerlé, J
遗传性牙本质缺陷牙本质发生障碍（DI），虽然在临床上明显的成骨障碍（OI）类型IB和IC，II，III和IVB，现在被认为是存在于所有儿童与OI，在一个连续的从最小到严重的牙本质病理。这项合作研究进一步阐明了临床上明显DI的OI儿童牙齿的结构和超微结构牙本质变化，并试图从成牙本质细胞功能障碍方面解释这些变化。在澳大利亚的墨尔本和法国的斯特拉斯堡进行了合作研究，使用光学和偏振光显微镜、扫描和透射电子显微镜（SEM、TEM）、选区衍射（SAD）和X射线光谱（EDX）。这些显示结构正常的釉质（但含有长而宽的薄片）和正常的扇形牙本质-釉质连接（DEJ），但牙本质中有严重的病理变化。一个最初的窄带正常出现的牙本质小管（包括外套层）突然停止，取而代之的是一个波浪状的层流区平行于DEJ封闭的小管。直径为5-10 μ m的多个平行通道与DEJ成直角，使该区域凹陷，一些通道终止于"后弯曲“过程。“含有这些通道的异常牙本质几乎完全堵塞了牙髓腔。所见的结构和超微结构变化可以解释的基础上，胶原蛋白缺陷的OI导致成牙本质细胞功能障碍，产生一个独特的表型和一个是不同的骨。
The inherited dentin defect dentinogenesis imperfecta (DI), while clinically obvious in osteogenesis imperfecta (OI) Types IB and IC, II, III, and IVB, is now thought to be present in all children with OI, in a continuum from minimal to severe dentin pathology. This collaborative study further clarifies the structural and ultrastructural dentin changes in the teeth of OI children with clinically obvious DI, and attempts to explain these in terms of odontoblast dysfunction. Collaborative studies were carried out in Melbourne, Australia, and Strasbourg, France, using light and polarized-light microscopy, scanning and transmission electron microscopy (SEM, TEM), selected-area diffraction (SAD), and x-ray spectroscopy (EDX). These showed structurally normal enamel (but containing long and broad lamellae) and a normally scalloped dentino-enamel junction (DEJ), but severe pathologic changes in the dentin. An initial narrow band of normal-appearing dentin tubules (including the mantle layer) ceased abruptly and was replaced by a wavelike laminar zone parallel to the DEJ with occluded tubules. Multiple parallel channels of 5-10 mum diameter were present at right angles to the DEJ indenting this zone, some terminating in retro-curved "processes." The abnormal dentin containing these channels almost completely occluded the pulp chamber. The structural and ultrastructural changes seen can be explained on the basis of the collagen defect in OI resulting in odontoblast dysfunction, which produces a distinct phenotype and one that is different from that in bone.