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At least 19 recordsLinked to original sources
PubMed1977

On the effect of vinblastine on ameloblasts of rat incisors in vivo. 2. Protracted effect on secretory ameloblasts. A light microscopical study.

The effects of vinblastine sulphate at a dosage of 0.2 mg per 100 g body weight on the secretory ameloblasts of rat incisors were studied 3, 6 and 24 hours and 3 and 7 days after administration of the drug. The vinblastine affected the secretion profoundly, caused a reduction in size of the cells and death of many ameloblasts. Most of the surviving ameloblasts restored initially-induced loss of polarity. Many also resumed secretion and deposition of enamel matrix. The Tomes' processess were extremely sensitive to vinblastine and all matrix deposited after administration of the drug appeared abnormal in structure. Ameloblasts not resuming secretory activity were less than half the size (height) of normal cells. In some areas all the ameloblasts were destroyed with the exception of a varying number of surviving ameloblasts parts consisting only of a nucleus and a small amount of cytoplasm. The ameloblasts which had re-established secretory activity, and most of the ameloblasts which had not, retained their ability to transform into transporting ameloblasts. Large amounts of ameloblast debris present 3 and 6 hours after administration of the vinblastine were effectively engulfed and digested by the cells of the striatum intermedium within 24 hours.

Ameloblasts↗
PubMed1977

On the effect of vinblastine on ameloblasts of rat incisors in vivo. 3. Acute and protracted effect on differentiating ameloblasts. A light microscopical study.

The acute effect of vinblastine sulphate at a dosage of 0.2 mg per 100 g body weight on ameloblasts in the progress of differentiation in rat incisors, and the ability of these cells to develop into secretory ameloblasts after exposure to the drug, were studied under the light microscope. In the early stages of differentiation (exclusively dividing cells) no changes were seen. In more advanced stages of differentiation the cell apices were altered and the nuclei normally placed near the cell base were located at all levels in the ameloblast layer. These changes were reversible and the cells developed into secretory ameloblasts of normal appearance and function. Ameloblasts in the most advanced stage of differentiation in which secretion had begun were severely damaged, and the mature secretory ameloblast population derived from these cells was decimated and produced enamel matrix with abnormal structure. It is concluded that differentiating ameloblasts are relatively invulnerable to vinblastine, whereas in secretory ameloblasts the organelles directly engaged in the secretory processes are particularly exposed to damage from the drug.

Ameloblasts↗
PubMed1978

Fine structure of the secretory and non-secretory ameloblasts in the frog. II. Fine structure of the non-secretory ameloblast.

The non-secretory ameloblasts present at the enamel-free surfaces of maxillary teeth in the frog Rana pipiens were examined by electron microscopy at different stages of tooth development. Their main fine structural features seem to reflect a transport function. During early tooth development, the non-secretory ameloblasts adjacent to odontoblasts and predentin exhibit extensive lateral surface specializations and numerous cytoplasmic vesicles. During late tooth development, the non-secretory ameloblasts adjacent to mineralizing dentin show numerous cellular junctions, well-developed intercellular channels with numerous interdigitating processes and labyrinthine configurations at their distal surfaces. An intact basal lamina is present between the non-secretory ameloblasts and the dentin surface until the dentin becomes fully mineralized. At this stage the adjacent cells no longer exhibit surface specializations. It is suggested that the non-secretory ameloblasts may participate in the mineralization of adjacent dentin at the enamel-free surfaces. This surface dentin becomes fully mineralized at a later stage of development than the underlying dentin.

Ameloblasts↗
PubMed1977

Malignant transformation of ameloblastic fibro-odontoma to ameloblastic fibrosarcoma.

Two cases of malignant transformation of ameloblastic fibro-odontomas are presented, along with a review of the literature on ameloblastic fibrosarcomas. The occurrence of this malignant transformation of ameloblastic fibromas, ameloblastic odontomas, and ameloblastic fibro-odontomas appears to be more frequent than previously thought. This potential transformation alone does not justify radical treatment of all these benign lesions. If there is recurrence accompanied by a histologic pattern change toward a more unorganized fibrous stroma with displacement of the epithelial component, however, then more extensive treatment procedures appear to be indicated.

Adolescent↗
PubMed1977

Light microscopical and ultrastructural observations on the effect of vinblastine on ameloblasts of rat incisors in vivo. I. Short-term effect on secretory ameloblasts.

The highly polarized secretory ameloblasts in the incisors of rats fixed by perfusion with glutaraldehyde two or three hours after intravenous administration of vinblastine sulfate at a dosage of 5 mg per 100 g body weight were studied in the light microscope and the electron microscope. The following effects were observed: 1. All cytoplasmic microtubules in the ameloblasts had vanished. This was not accompanied by the appearance of paracrystals of microtubular protein or macrotubules. 2. The ameloblasts preserved their external features of polarized cells but lost their ability to maintain normal orderly segregation of the cell constituents; i.e. their normal internal compartmentalization and polarity had vanished. 3. The ameloblasts lost their capability of directional translocation of the secretory granules towards the cell apex. 4. Secretory granules already translocated to the cell apex regurgitated in the cell and a probably delayed discharge of secretory material had started in abnormal site at the surface. 5. The normal arrangement of ribosomes into polyribosomes on the membranes of the rough endoplasmic reticulum was no longer present; the ribosomes were apparently distributed at random. 6. New secretion was inhibited or brought to a standstill but secretory material already present in the Golgi complex appeared to be transported normally. 7. The centriole had started to develop into a cilium in many of the cells. 8. The number of autophagic vacuoles had increased.

Ameloblasts↗
PubMed1977

Fine structure of the secretory and nonsecretory ameloblasts in the frog. I. Fine structure of the secretory ameloblasts.

Amelogenesis in the tooth germs of the frog Rana pipiens was examined by electron microscopy at different stages of tooth development. Cellular changes in secretory ameloblasts during this process showed many basic similarities to those in mammalian amelogenesis. Amelogenesis can be divided into three stages based on histological criteria such as thickness of enamel and the relative position of the tooth germ within the continuous succession of teeth. These stages are early, transitional and late. The fine structure of the enamel-secreting cells reflects the functional role of these ameloblasts as primarily secretory in the early stage, possibly transporting in the late stage and reorganizing between the two functions in the transitional stage. In early amelogenesis the cell exhibits well-developed granular endoplasmic reticulum, Golgi complex, microtubules, dense granules, smooth and coated vesicles, lysosome-like bodies in supranuclear and distal portions of the cell and mitochondria initially concentrated in the basal part of the cell. Numerous autophagic vacuoles are observed concomitant with the loss of some cell organelles at the transitional stage. During late amelogenesis the ameloblasts exhibit numerous vesicles, granules, convoluted cell membranes, junctional complexes and widely distributed mitochondria. Toward the end of amelogenesis, cells become oriented parallel to the enamel surface and the number of organelles is reduced. Amelogenesis in the frog is an extracellular process and mineralization seems to occur simultaneously with matrix formation.

Ameloblasts↗
PubMed1976

Fine structure of differentiating ameloblasts in the kitten.

The fine structure of differentiating ameloblasts was studied in the lower second molar of 1-week-old kittens after perfusion fixation with and without subsequent decalcification. The differentiation zone was divided into three phases. In Differentiation 1, ameloblasts are about 27 mum long and face an uninterrupted basal lamina. The predentin adjacent to the basal lamina contains a few collagen fibrils oriented mainly at right angles to the ameloblast surface. The specialized predentin forms a well-defined layer, up to 1.5 mum thick, referred to as the junctional layer. In Differentiation 2, ameloblast processes extend through the basal lamina and the thickness of the junctional layer. The processes consist of cytoplasmic sheets forming a honeycomb-like network. Dentin starts to calcify after process-formation is underway. Two distinct types of odontoblast processes, having different shapes and contents, come in contact with the ameloblasts and push into the ameloblastic layer. In Differentiation 3, stippled material appears in the extracellular spaces between ameloblasts. Later, stippled material-like substances appear in the predentin close to the ameloblast apex and close to odontoblast processes within the dentin. Ameloblasts now are up to 40 mum high. Enamel secretion starts in small circumscribed areas which gradually enlarge, leading to the disappearance of the ameloblast processes. These findings are compared with results obtained in other species, including man, and their possible functional significance is discussed.

Ameloblasts↗
PubMed1976

The secretory ameloblast of the mini-pig foetus: Morphology, and effect on morphology of various aldehydes and of delayed fixation.

Electron microscopic investigations of secretory ameloblasts from deciduous tooth germs of mini-pig foetuses and investigations of the ability of various fixatives to preserve these cells in tooth germs immersion-fixed in to 5 min, 10 min, 15 min, 20 min and 40 min after death of the mother gave the following results: 1. The ameloblasts exhibit ultrastructural characteristics typical of exocrine secretory cells of merocrine type. 2. The localization of organelles is as in rodent secretory ameloblasts, but differs from the location in the human analogues. 3. Fixation with 4% formaldehyde invariably gives unacceptable ameloblast preservation. 4. Fixation with 2.5% glutaraldehyde gives fair preservation of the ameloblasts when the germs are fixed within 10 min of the death of the mother. 5. Fixation with a fixative mixture 2% formaldehyde-1.25% glutaraldehyde gives good preservation when the ameloblasts are fixed within 15 min of the death of the mother. 6. Fixation with a fixative mixture 2% formaldehyde-1% glutaraldehyde-1% acrolein gives good ameloblast preservation when the germs are fixed within 15 min of the death of the mother.

Acrolein↗
PubMed1979

A correlated scanning and transmission electron microscopic study of maturation ameloblasts in developing molar teeth of rats.

Maturation ameloblasts of developing molar teeth of the rate were studied by both scanning and transmission electron microscopy. After fixation, teeth were frozen and split. One face of the fractured tooth was used for SEM, the other for TEM. It was found that in some regions proximal junctional complexes separate the interameloblast space from the intercellular space of the papillary layer. Thereby an intercellular ameloblastic compartment is delineated which in some specimens contains a substance interpreted to be colloidal. Elsewhere the proximal junctions of ameloblasts are not present and free communication between the extracellular spaces is evident. The apical pole of ameloblasts varies in structure. Over some areas there is a distinct distal border zone with membranous infoldings which in some regions resembles a striated or ruffled border, but in other regions the membranes show whorl configurations. The distal border zone also contains granules with flocculent material. Elsewhere the ameloblasts display no distal border zone and the cells show a smooth membrane (except for pinocytotic vesicles and hemidesmosomes) facing the enamel surface. The lateral surface of ameloblasts exhibits a variety of surface configurations similar to but not as pronounced as those reported previously in rat incisor maturation ameloblasts.

Aging↗
PubMed1979

Cytochemical studies of ameloblasts and the surface layer of enamel of the rat incisor at the maturation stage.

In order to elucidate the cytochemical properties of the membranous structure between enamel and ameloblasts of the rat incisor at the maturation stage, chromic phosphotungstic acid (Cr-PTA) and periodic acid-silver methenamine (PA-silver) techniques for electron microscopy were employed in combination with a digestion test with hyaluronidase, neuraminidase, collagenase or trypsin. Also, acid phosphatase activity of ameloblasts at the maturation stage was examined with a modified GOMORI's metal salt method. An intensely Cr-PTA reactive band approximately 0.1 micron thick appeared along the surface layer of enamel at the transitional stage, and at the very beginning of the maturation stage another intensely Cr-PTA reactive band which was seen by uran-lead stain to be a delicate electron-dense membranous structure appeared as well between enamel and ameloblasts. A lot of cytoplasmic small vesicles or tubular structures, both intensely reactive to Cr-PTA, were observed near the apical membranes of the overlying ameloblasts indicating that those organelles must have been responsible for the secretion of the latter band. Acid phosphatase activity was clearly demonstrated at Cr-PTA reactive large vesicles in the cytoplasm of those cells. The PA-silver staining technique manifested a band heavily deposited with silver grains along the surface layer of enamel, i.e., where the former band existed, but showed no particular reaction at the latter, the band-like layer between enamel and ameloblasts. Hyaluronidase or neuraminidase treatment remarkably decreased the Cr-PTA reaction of the latter band. Trypsin or collagenase treatment, on the other hand, not only eliminated the Cr-PTA reaction but digested the band itself. These results suggest that the membranous structure between enamel and ameloblasts of a rat incisor is not so-called enamel cuticle but a basal lamina produced by overlying ameloblasts and that the basal lamina contains collagenous components even though it lies on enamel.

Ameloblasts↗
PubMed1976

Ameloblastic dentinosarcoma- a case report.

A rare case of ameloblastic dentinosarcoma is reported. The literature regarding ameloblastic fibro- and odontosarcomas is reviewed. There have been 16 reported cases of ameloblastic fibrosarcoma and another six cases (one uncertain) of ameloblastic fibrosarcoma which showed induction of dentin or enamel and which therefore according to the WHO Classification should be separately classified as ameloblastic odontosarcomas. Our case showed no enamel and therefore is better called ameloblastic dentinosarcoma. Ameloblastic sarcomas of the jaws are of low grade malignancy, do not often metastasize, and if treated by radical resection have a good prognosis.

Adult↗
PubMed1977

Quantitative analysis of cell turnover in the enamel organ of the rat incisor. Evidence for ameloblast death immediately after enamel matrix secretion.

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 was calculated that a little over 25% of the loss occurred immediately at the start of maturation within the region of postsecretory transition and the remaining 25% of the loss occurred throughout the subsequent regions of the maturation zone. In addition to the kinetic analysis graphic reconstructions, or surface maps, of ameloblast nuclei were prepared. These maps illustrated the characteristics of ameloblast nuclear packing within the three zones of amelogenesis and they provided quantitative confirmation that as ameloblasts progress through the maturation zone, there is a loss of cells in an amount predicted by the kinetic analysis.

Ameloblasts↗
PubMed1977

Multinucleate ameloblasts in the rat incisor.

Cytological examination of the rat incisor enamel organ with the light and electron microscope revealed a small number of ameloblasts which contained two and sometimes three or more nuclei per cell. A multinucleate ameloblast usually contained two vertically apposed nuclei situated near the base of the cell. A narrow cytoplasmic band was interposed between adjacent nuclear envelopes. The apical nucleus was often the more elongated of the two nuclei and it fitted a convexity or a concavity within the more basally positioned nucleus. In serial sections examined with the electron microscope no connections were observed between the nuclei. In animals injected with 3H-thymidine instances of multinucleate ameloblasts were found within the advancing front of labeling where only one of the nuclei contained label. Finally, quantitative analysis by nuclear counting established that multinucleate ameloblasts were 60 times more frequent within the maturation zone as in the secretory zone of amelogenesis. As well, the numbers of multinucleate ameloblasts increased progressively in the course of the maturation stage. It was concluded that multinucleate ameloblasts increase with cell age and likely arise by the process of cell fusion.

Ameloblasts↗
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

Physiological cell death of secretory ameloblasts in the rat incisor.

The migration of the ameloblasts in the continuously erupting incisors of the rat is accompanied by cell loss. Ameloblasts degenerate near the mesial and lateral cemento-enamel junctions in the secretory zone and in the middle two thirds of the region of postsecretory transition, degeneration being most marked where these areas merge. These findings support the hypothesis that the prism decussation in the enamel results from alternating transverse rows of secretory ameloblasts sliding past each other whilst elaborating their rods. The distribution of the degenerating cells suggests, however, that the sliding cell rows are not exactly transverse but arcuate, with the opening facing incisally. The progress of structural alterations of the nuclei in the degenerating ameloblasts appears to follow the pattern earlier described in vinblastine-damaged ameloblasts.

Ameloblasts↗
PubMed1978

Electron probe analysis of maturation ameloblasts of the rat incisor and calf molar.

Rapidly frozen upper incisor teeth of rats and molar teeth of calves were freeze fractured, freeze dried and dry dissected in preparation for energy dispersive x-ray emission microanalysis in the scanning electron microscope. Successive zones of ameloblasts adjacent to maturing rat incisor enamel were examined, beginning with cells adjacent to the least mature enamel and progressing to cells over increasingly more mature enamel. Pronounced Kalpha1,2 x-ray peaks were obtained for P, S, Cl, K and Fe but not for Ca. Ca levels were also very low compared with P, S, Cl and K in calf molar maturation ameloblasts, whereas they were high in the distal poles of the secretory odontoblasts in the same specimens. The findings indicate that both intra- and extracellular Ca levels are extremely low in maturation ameloblasts. It is concluded that Ca is neither stored nor concentrated in large amounts by the maturation ameloblasts prior to its entry into the enamel. The suggestion is made that the maturation ameloblasts might regulate entry of calcium into enamel by serving as a selective barrier.

Ameloblasts↗
PubMed1978

Electron microscopic localization of 5'-nucleotidase in the stratum intermedium and ameloblasts.

5'-nucleotidase was demonstrated at the fine structural level in the stratum intermedium and ameloblasts of the first mandibular molars of CD-1 mice. The enzyme was localized with the Wachstein & Meisel (1957) method along the plasma membranes of the cells of the stratum intermedium and ameloblasts. While 5'- nucleotidase was present throughout the stratum intermedium, only the proximal region of the plasma membranes of ameloblasts was demonstrably active for this enzyme. 5'-Nucleotidase has been implicated in transport of metabolites across cell membranes, and its localization in the present study supports this implication as well as the transport functions of the stratum intermedium and the stratum intermedium--ameloblastic interface.

Ameloblasts↗
PubMed1979

Ameloblastic fibroma and its sarcomatous transformation.

A case of ameloblastic fibroma, and one of its more aggressive variety, the ameloblastic "fibrosarcoma", are presented. The clinical and morphologic differences are discussed. In our opinion, ameloblastic "fibrosarcoma" is a semimalignant tumor. Therefore we propose "proliferating ameloblastic fibroma" as a more appropriate designation.

Adolescent↗