Morphological Analysis of enamel hypoplasias as markers of systemic stress – A contribution to the patho-biography of Humans and animals

Die durchgeführten histologischen Untersuchungen von Zähnen mit Schmelzhypoplasien haben gezeigt, dass es möglich ist, Aussagen über die Intensität und die Dauer von Episoden von systemischem Stress zu treffen, die Auswirkungen auf die Amelogenese hatten. Basierend auf den aktuellen Vorstellungen über den Ablauf der Amelogenese und die Zusammenhänge zwischen Morphologie und Funktion sekretorischer Ameloblasten kann, durch die Analyse von Veränderungen der normalen Schmelzstruktur, das Reaktionsmuster der sekretorischen Ameloblasten rekonstruiert werden. Die erhobenen Befunde lassen sich mit einem Schwellenwertmodell beschreiben, das drei Stufen der Einschränkung der sekretorischen Ameloblastentätigkeit umfasst.Histological analysis of teeth that exhibited enamel hypoplasias and the related aberrations in enamel microstructure revealed that inferences on the intensity and duration of episodes of systemic stress affecting amelogenesis can be made. Based on the current understanding of the cellular processes of amelogenesis, deviations from normal enamel microstructure were used to reconstruct functional and related morphological changes of the secretory ameloblasts being caused by the action of stress factors during amelogenesis. In addition to impact duration and intensity, a further influence of ameloblast susceptibility resulting from the age and the stage of the cell within an individual activity cycle was deduced. The reconstructed reaction pattern of the secretory ameloblasts can be grouped in a sequence of increasingly more severe impairment of cell function involving three thresholds. When the lowest of these thresholds is surpassed, matrix secretion is slightly reduced; however, the Tomes’ process retains its normal morphology. The corresponding morphological observation in the enamel is a reduced width between the incremental markings, while the enamel is still of a normal prismatic structure. When the second threshold is surpassed, the synthetic/secretory activity of the ameloblast is impaired to such an extent that it is no longer able to maintain the distal portion of its Tomes’ process. Aprismatic enamel is then formed. When the highest threshold is surpassed, the cell ceases matrix secretion either temporally or permanently. Presence of coronal cementum is seen as indicative of a premature disintegration of the enamel epithelium prior to the completion of amelogenesis. Thereby mesenchymal cells of the dental follicle come into contact with the surface of the immature enamel and deposit coronal cementum. However, it cannot be decided whether this premature breakdown is attributable to specific factors. The external appearance of enamel hypoplasia is further influenced by the variation of tooth crown geometry, i.e. of the orientation of the incremental structures that occur in a single tooth along the corono-cervical tooth axis, between teeth of a dentition, and between species. The present study demonstrates that by including microscopic analysis of tooth sections in the study of enamel hypoplasia it is possible to obtain a more complete picture of the formation of these developmental defects than is possible by inspection of crown surface features alone, and to draw more substantiated conclusions about the possible nature of developmental defects of enamel