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At least 19 recordsLinked to original sources
PubMed1979

Amelogenesis imperfecta among Israeli Jews and the description of a new type of local hypoplastic autosomal recessive amelogenesis imperfecta.

Amelogenesis imperfecta (AI) was detected in nine of 70,359 school children surveyed, a prevalence approximating 1:8,000. Of these cases, eight were the hypoplastic type and one the snow-capped hypomaturation type. Family studies demonstrated that hypoplastic AI was an autosomal dominant trait in two children and an autosomal recessive in six. Of three additional families referred to our clinic, two had autosomal recessive hypoplastic AI and one the hypocalcified type, inherited as an autosomal dominant trait. In four families, a new type of local hypoplastic autosomal recessive AI was observed, characterized by horizontal pitting and grooving more pronounced in the middle third of the crowns of most teeth in both dentitions.

Adolescent↗
PubMed1977

Ultrastructural study of amelogenesis imperfecta.

An ultrastructural study of teeth with amelogenesis imperfecta revealed various aspects of microcavities in the enamel surface, which ranged from isolated imprints of ameloblasts corresponding to the mildest lesions at the end of amelogenesis, to pits caused by the death of 20 to 30 ameloblasts at the beginning of amelogenesis. Abnormalities in the shape of the prisms can be observed. Further, crystals are distributed randomly within a prism or at the junction of 2 contiguous prisms while intercrystalline spaces are widened, indicating in various places the lack of a preferred orientation of the crystals. In amelogenesis imperfecta, two different crystalline periods are found: 1 of about 250 A, the other of about 500 A and over. The fact that amorphous areas are found among the crystals of enamel may be related to different stages of crystallization. However, it was not possible to find any lattice defect.

Ameloblasts↗
PubMed1979

Amelogenesis imperfecta with taurodontism.

Reports of families having a combination of amelogenesis imperfecta and taurodontism are limited. This study of members of three families shows that the combination is inherited as an autosomal dominant trait. In each of the patients examined, neither condition was seen without the other. The enamel was rough and dysplastic and varied in color from white to yellow. Radiographically, taurodontism was present in the deciduous and permanent dentitions. The pulp chambers of the incisor teeth were larger than is usually seen at all ages. All patients had normal-appearing hair, fingernails, and bones. The distinction between amelogenesis imperfecta with taurodontism and the tricho-dento-osseous syndrome is discussed.

Amelogenesis Imperfecta↗
PubMed1979

An antisera for the fluorescent labeling of mouse amelogenesis.

Embryonic mammalian enamel extracellular matrix is immunogenic. Antisera has been produced in New Zealand white rabbits using 5-day-old (post-natal) C57B1/6J mandibular and maxillary incisor and molar tooth organs as immunogens. The expression of secretory amelogenesis in mouse molar tooth organs was studied from the "cap stage" (circa 17-day fetus) to the fifth day of postnatal odontogenesis using indirect immunofluorescent microscopy. The specificity of the antisera for enamel matrix secretion was unequivocal. Secretory amelogenesis was observed in molar tooth organs as early as day-2 postnatal age. These reagents and methods provide a significant strategy in studies of epithelial-mesenchymal interactions during tooth development.

Amelogenesis↗
PubMed1979

Enamel matrix proteins in normal and abnormal amelogenesis.

Histochemical techniques have been used to study three stages of enamel maturation in normal (fetal calf, newborn human, adult human) and abnormal amelogenesis (odontodysplasia, fluorosis, a compound-complex odontome, and an invaginated odontome). The amount of Type I matrix secreted decreases as amelogenesis progresses. Pockets of Type II matrix may be left at the dentino-enamel junction after maturation of enamel to Type III. Fluorosed enamel contains pockets which may extend the width of the enamel. All stages of enamel maturation may be seen in the compound-complex odontoma.

Amelogenesis↗
PubMed1979

Blood supply of the rat periodontal space during amelogenesis as studied by the injection replica SEM method.

Distribution of blood vessels at the labial periodontal space of the rat lower incisor teeth was studied, using Mercox-resin vascular casts, which were coated with gold-palladium and observed in a scanning electron microscope (SEM). Three different layers were identified in the vascular bed of the periodontium. In the inner layer the enamel organ was supplied by a blood capillary network that changed from a circular mesh to a ladder-like pattern during amelogenesis. The middle layer was supplied by small arteries and arterioles. Small arteries originated from the inferior alveolar artery; arterioles, arising from them, became blood capillaries. In the outer layer, the sinusoid veins continued with the blood capillaries which ran into the proximal and the distal sites of the inner layer. This venous layer is located near the alveolar bones. As capillary networks change in pattern during amelogenesis, the circular mesh is considered convenient to provide the required materials for the proliferation and differentiation of inner enamel epithelial cells as well as for early enamel matrix formation, whereas the ladder pattern seems suitable to supply numerous organic or inorganic materials for the advanced enamel matrix formation and calcification.

Amelogenesis↗
PubMed1979

Amelogenesis in vitro.

The processess by which diversity is acquired and maintained during embryogenesis have been repeatedly described but are as yet not understood. One fascinating example of diversity following gastrulation is epidermal organogenesis and in particular embryonic tooth morphogenesis. Tooth morphogenesis in situ and in vitro encompasses such interesting developmental problems as epithelial-mesenchymal interactions, cytodifferentiation, dentine and enamel extracellular matrix production, mineralization, issues of form and enamel maturation. In vitro methods provide access to many of these problem areas. This presentation will review selected issues related to amelogenesis in vitro and will emphasize avenues for future research.

Ameloblasts↗
PubMed1979

Amelogenesis imperfecta: local hypoplastic type with pulpal calcification.

A case report of a patient with local hypoplastic type of amelogenesis imperfecta is presented. Developmentally absent canines and unerupted teeth in the anterior maxilla and calcifications in the apical third of the pulp chambers of the molars were noticed and discussed. A family history was analyzed as consistent with an autosomal dominant form of transmission of the disorder.

Adult↗
PubMed2016

Ultrastructure of early amelogenesis in wild-type, Amelx-/-, and Enam-/- mice: enamel ribbon initiation on dentin mineral and ribbon orientation by ameloblasts.

INTRODUCTION: Dental enamel is comprised of highly organized, oriented apatite crystals, but how they form is unclear. METHODS: We used focused ion beam (FIB) scanning electron microscopy (SEM) to investigate early enamel formation in 7-week-old incisors from wild-type, Amelx-/-, and Enam-/- C56BL/6 mice. FIB surface imaging scans thicker samples so that the thin enamel ribbons do not pass as readily out of the plane of section, and generates serial images by a mill and view approach for computerized tomography. RESULTS: We demonstrate that wild-type enamel ribbons initiate on dentin mineral on the sides and tips of mineralized collagen fibers, and extend in clusters from dentin to the ameloblast membrane. The clustering suggested that groups of enamel ribbons were initiated and then extended by finger-like membrane processes as they retracted back into the ameloblast distal membrane. These findings support the conclusions that no organic nucleator is necessary for enamel ribbon initiation (although no ribbons form in the Enam-/- mice), and that enamel ribbons elongate along the ameloblast membrane and orient in the direction of its retrograde movement. Tomographic reconstruction videos revealed a complex of ameloblast membrane processes and invaginations associated with intercellular junctions proximal to the mineralization front and also highlighted interproximal extracellular enamel matrix accumulations proximal to the interrod growth sites, which we propose are important for expanding the interrod matrix and extending interrod enamel ribbons. Amelx-/- mice produce oriented enamel ribbons, but the ribbons fuse into fan-like structures. The matrix does not expand sufficiently to support formation of the Tomes process or establish rod and interrod organization. CONCLUSION: Amelogenin does not directly nucleate, shape, or orient enamel ribbons, but separates and supports the enamel ribbons, and expands the enamel matrix to accommodate continued ribbon elongation, retrograde ameloblast movement, and rod/interrod organization.

Ameloblast↗
PubMed1979

Radioautographic studies on amelogenesis.

Radioautography has been used to visualize various aspects of morphogenesis and differentiation in the continuously erupting rat incisor. Formation of the entire incisor involves continuous production of "tooth segments" at the growing end of the tooth, each of which undergoes a similar history of development as it is carried by eruption towards the oral cavity. The sequence of differentiation which characterizes the life cycle of the ameloblasts was timed using 3H-thymidine, a precursor of DNA. The cells pass through presecretory, secretory and maturative stages whose collective activity results in the layer of mature enamel. 3H-Amino acids, as precursors of proteins were used to evaluate the protein synthetic activity of ameloblasts, before, during and after they produced the layer of enamel. Quantitative analysis (grain counts) of the differential utilization of 3H-proline and 3H-tyrosine by the various types of ameloblasts suggests that the cells produce structural proteins throughout their life cycle, but they produce enamel proteins only in the zone of secretion. The data further suggest that near the end of the presecretory zone structural proteins are used in the formation of Tomes' processes and that during secretion structural proteins contribute to the persistent growth of those processes as the rods are lengthening. Sugars such as 3H-N-acetylmannosamine and 3H-fucose were used to examine glycoprotein formation by ameloblasts. In the secretion zone labeled glycoproteins were not present in the enamel layer, but were confined to the cell bodies and Tomes' processes of ameloblasts at time intervals up to 4 hours after injection. This was contrary to the behaviour of extracellular proteins labeled with 3H-amino acids which left the cell and were present in the enamel at similar time intervals. The distribution of labeled sugars was indicative of turnover of membrane-associated glycoprotein possibly related to growth. This was interpreted as further support for the concept of a lengthening Tomes' process which remains embedded in the enamel until it is obliterated by the forming rod. Preliminary attempts were made to define the role of hormones in tooth development. Specific receptor sites for 125I-insulin were localized to the endothelial lining of capillaries in the papillary layer during maturation. Although the significance is unclear, the potential of this tool in studying dental morphogenesis is considerable.

Ameloblasts↗