Harvey W. Lyon

An electron optic analysis and explanation for the etiology of dentinal dysplasia

Abstract Metallurgically polished and fractured sections of teeth with dentinal dysplasia were prepared and studied under the scanning electron microscope. The morphologic data obtained suggested that the defect was one of the epithelial root sheath. A hypothetical model for the defect is presented and is supported both by scanning electron microscopy and classic histopathology.

The surface of genetically determined hypoplastic enamel in human teeth

Abstract A localized form of hypoplastic amelogenesis imperfecta was compared to a form of febrile hypoplastic enamel to ascertain the potential for alternative surface enamel morphologies predicated on differing influences during development. Surface observations with the scanning electron microscope (SEM) in febrile altered enamel revealed surfaces resembling that of developing enamel. The genetically determined form of the defect suggested that other influences rather than alteration of ameloblasts were included in the phenotype; these were suggested to be vascular in origin.

Electron-optic analyses of hypomineralized amelogenesis imperfecta in man

Abstract A hypomineralized-type of amelogenesis imperfecta was investigated with the scanning electron microscope, analyzed with an electron microprobe and compared with normal enamel. Perikymata, imbrication lines and a prismless zone were absent in the abnormal enamel. Two-hour etching of the samples with EDTA revealed the presence of cross-striations in abnormal enamel but not in normal enamel. Pathological enamel showed the presence of macroporosities and disoriented prisms which extended below the surface of enamel. In addition, hypocalciflcation of prism sheaths and surface prisms were observed. Electron microprobe analyses of formed prisms in amelogenesis imperfecta showed that the values for calcium, phosphorus and the Ca:P ratio were normal, and fibrillar disorientated surface prisms were hypomineralized. Selective aplasia of ameloblasts and hypocalcification of enamel matrices were suggested as causes of the enamel defects.