Enamel mineralization in the absence of maturation stage ameloblasts (original) (raw)
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The Anatomical record, 1987
In the continuously erupting rat incisor the ameloblasts progress through distinct stages associated with the secretion and maturation of enamel. We have examined the possibility that the so-called "postsecretory" ameloblasts of the maturation stage of amelogenesis remain biosynthetically active and are engaged in the synthesis, secretion, and degradation of enamel gene products. The ultrastructural distribution of antigenic sites for enamel proteins was studied within enamel organ cells during the early maturation stage of amelogenesis in rat incisors by using the protein A-gold immunocytochemical technique and rabbit polyclonal antibodies developed against mouse amelogenins. All regions of amelogenesis from late secretion through the first complete modulation from ruffle-ended to smooth-ended ameloblasts were examined. Specific immunolabelling was found within the rough endoplasmic reticulum, Golgi saccules, secretory granules, and lysosomes of ameloblasts throughout the...
The Anatomical record, 1977
During renewal of the enamel organ in the rat incisor cohorts of epithelial cells are transported sequentially through presecretory, secretory and maturation zones to the gingival margin where the life cycles of these cells terminate. This process was examined kinetically by determining the absolute flux of cells within each of these zones of amelogenesis. It was found that the efflux of ameloblasts, stratum intermedium and papillary layer cells from the presecretory zone was about equal to the efflux plus expected growth within the secretory zone. However, between the secretory and maturation zones about 50% more ameloblasts entered the maturation zone than were required to account for the egress at the gingival margin and the expected growth. Since there was no similar imbalance between these zones for papillary layer cells, it was concluded that this discrepancy must represent a 50% reduction in the size of the ameloblast population during the maturation stage of amelogenesis. It...
Histology of enamel organ and chemical composition of adjacent enamel in rat incisors
Calcified Tissue International, 1981
By avoiding chemical fixation and using a freeze-drying technique, it proved possible to examine the enamel organ of rat mandibular incisors histologically while retaining the adjacent enamel of the same tooth for chemical analysis. The dramatic alterations which occur in enamel organ histology, such as ameloblast shortening and the development of the papillary layer, could then be compared directly with mineral uptake and mineral content of the adjacent enamel. Both enamel and adjacent enamel organ were sampled as a continuous series of pieces, 0.5 mm in width, from youngest (apical) to oldest (incisal) tissue. Short ameloblasts were associated directly with the beginning of a rapid uptake of phosphate ions during the maturation phase and also coincided with the beginning of a steep rise in mineral content. By implication, some loss of matrix may also occur at this point. Development of the highly vascular papillary layer preceded ameloblast shortening and may be associated with changes in the organic matrix prior to its disappearance from the tissue. Further development of this layer was associated with ameloblast shortening. This may also therefore be associated with mineral uptake during maturation.
Molecular genetics & genomic medicine, 2016
Amelogenin is required for normal enamel formation and is the most abundant protein in developing enamel. Amelx(+/+), Amelx(+/-) , and Amelx(-/-) molars and incisors from C57BL/6 mice were characterized using RT-PCR, Western blotting, dissecting and light microscopy, immunohistochemistry (IHC), transmission electron microscopy (TEM), scanning electron microscopy (SEM), backscattered SEM (bSEM), nanohardness testing, and X-ray diffraction. No amelogenin protein was detected by Western blot analyses of enamel extracts from Amelx(-/-) mice. Amelx(-/-) incisor enamel averaged 20.3 ± 3.3 μm in thickness, or only 1/6th that of the wild type (122.3 ± 7.9 μm). Amelx(-/-) incisor enamel nanohardness was 1.6 Gpa, less than half that of wild-type enamel (3.6 Gpa). Amelx(+/-) incisors and molars showed vertical banding patterns unique to each tooth. IHC detected no amelogenin in Amelx(-/-) enamel and varied levels of amelogenin in Amelx(+/-) incisors, which correlated positively with enamel thi...
The International journal of developmental biology, 1995
In this survey we summarize data on mineralization of enamel mostly obtained in organ culture experiments in our laboratory. Historically, the enzyme alkaline phosphatase has been proposed to stimulate mineralization by supplying phosphate or by splitting away inorganic pyrophosphate PPi, a potent inhibitor of mineralization. Localization of alkaline phosphatase in developing teeth by enzyme histochemistry shows that cells of the stratum intermedium contain extremely high levels of alkaline phosphatase but secretory ameloblasts that are engaged in deposition of the matrix and in transport of mineral ions lack alkaline phosphatase. The function therefore must be an indirect one, since no activity was seen at the site of enamel mineralization. We propose that the main function of alkaline phosphatase in the stratum intermedium is to transport phosphate or nutrients from blood vessels near the stratum intermedium into the enamel organ. Another function of the enzyme in stages of cell d...
American Journal of Physical Anthropology, 2008
We studied the abnormalities in enamel microstructure associated with enamel hypoplasia in human teeth from the early medieval (5th–7th century AD) cemetery of Barbing, Germany, using light and scanning electron microscopy. The main aim of the study was to test the hypothesis that by analyzing the microstructure of fully formed enamel it is possible to reconstruct the reaction pattern of secretory ameloblasts to stress events leading to enamel hypoplasia. From the histological findings, a sequence of increasing impairment of secretory ameloblast function involving three thresholds was deduced. Surpassing of each of these thresholds is assumed to result in characteristic changes in enamel microstructure attributable to specific functional/morphological alterations of secretory ameloblasts. Based on our results we propose a model identifying the principal factors influencing the reaction of secretory ameloblasts to stress. The present study demonstrates that by including microscopic analysis 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. Am J Phys Anthropol, 2008. © 2008 Wiley-Liss, Inc.