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PubMed1978

Scanning electron microscopic observations of tooth germ in tissue culture with special reference to the migration of epithelial cells.

Tooth germ derived from the mandible of newborn mice was used in this study. The enamel organs were dissected and attached directly to coverslips without using the plasma clot. By this method it was possible, for the first time as far as is known, to attain preparations in which the major part of the outgrowth from the explant consisted purely of epithelial-like cells which probably were aneloblasts. Abundant desmosomes and tonofilaments were confirmed by transmission electron microscopy. Under the scanning electron microscope this outgrowth of epithelial cells revealed characteristic intercellular connections which were divided into four types. 1)In the part nearest to the explant, cell boundaries were indicated with a large number of short microvilli. 2)In the zone beyond the first type, the intercellular connection was represented by bridge-like processes firmly combined with each other. 3)In a still further zone, the tips of bridge-like processes were free from the cell connection and extended to the adjacent cells with the advance of cell migration. 4)In the most peripheral part of the explant, the cytoplasmic processes were capable of further expansion. These cells were soon separated from the adjacent cells to migrate as free cells.

Animals↗
PubMed2002

Relationship between congenitally missing lower third molars and late formation of tooth germs.

In this investigation, we used longitudinal panoramic radiographs from 96 subjects (47 boys, 49 girls) who did not have any congenital disease. The subjects were selected based on their age at the initial radiograph and the number and frequency of radiographs. Lower left premolars and second molars were used as parameters to identify factors that influence the age of formation of the third molar. We classified teeth into eight formation stages according to the method of Demirjian. The age at the beginning of formation of the lower third molar was determined with a regression equation of longitudinal data. The highest correlation existed between the age at the beginning of formation of the third molar and the formation stage of the second molar. We conclude that late formation of tooth germs is one of the factors that leads to the congenital absence of lower third molars. Furthermore, we assume that when the tooth germ of the lower third molar has not appeared at stage 7 of formation of the second molar, the probability of the third molar being missing is 100%.

Anodontia↗
PubMed1995

Fine structure of tooth germs during the formation of enameloid matrix in Tilapia nilotica, a teleost fish.

Tooth germs were examined by light and transmission electron microscopy. Collagen fibrils were relatively dispersed and thin at the early and middle stages of formation of the enameloid matrix, when the enameloid layer was thin. At the late stage, the fibrils became thicker, reaching nearly 30 nm dia, and formed the interwoven thick bundles that are characteristic of teleost cap enameloid. Abundant flocculent and/or fine, network-like material, probably representing glycosaminoglycans or proteoglycans, was located between the collagen fibrils. Tall, columnar, inner dental epithelial cells contained abundant rough endoplasmic reticulum and many mitochondria, and a well-developed Golgi apparatus was seen around the nuclei at the late stage. Elongated vesicles enclosing fine, filamentous material that resembled procollagen granules, and large granules containing fibril-like structures that were 150 nm in thickness and had periodic cross-banding at 32-nm intervals, were usually observed near the Golgi apparatus. The contents of the large granules were well stained with phosphotungstic acid, which suggests that inner dental epithelial cells synthesize collagen fibrils. At this time, odontoblasts also contained abundant rough endoplasmic reticulum and mitochondria, a well-developed Golgi, several kinds of granule including those that probably contained procollagen, and many microtubules. It is proposed that odontoblasts are involved in the formation of a considerable portion of the enameloid matrix, including collagen fibrils.

Amelogenesis↗
PubMed1999

Vimentin localisation in tooth germ cells of two marsupial species, the northern brown bandicoot, Isoodon macrourus, and the brushtail possum, Trichosurus vulpecula.

In marsupial teeth, long cellular processes from ameloblasts and odontoblasts are found in the developing enamel and dentinal tubules, respectively. It has been suggested that the odontoblast cytoskeleton plays a role in the dentinal tubule formation of rat. To understand the role of the cytoskeleton in the blast cells, the location of vimentin and cytokeratin in the tooth germ of the bandicoot and the possum was examined using immunohistochemical techniques. Vimentin was detected in differentiating and secretory ameloblasts and may be involved with the secretion of fibronectin. Vimentin labelling was much weaker and irregular in cells of the outer enamel epithelium, the stellate reticulum and the stratum intermedium. Dentinal tubules, odontoblasts and dental papilla fibroblasts also stained positively for vimentin. Positive staining for cytokeratin was observed in all cells in the enamel organ but not in the enamel and dentinal tubules or the cells of the dental papillae. The presence of vimentin in the dentinal tubules indicated that the odontoblast processes in these tubules were still active and they extended to near the enamel-dentin junction. In conclusion, the presence of vimentin in tooth germ cells suggests that it may be involved in the formation of enamel tubules in marsupials.

Animals↗
PubMed1981

Ultrastructure of the epithelial-mesenchymal interface in the mouse tooth germ.

The structure of the epithelial-mesenchymal interface of a developing mouse embryonic tooth germ was examined at the time of cell differentiation by using transmission and scanning electron microscopy. During odontoblast differentiation, the basal lamina was continuous beneath the inner enamel epithelium, and the fibrils at the mesenchymal aspect increased in density and length. Numerous cell processes of the preodontoblasts were seen in close contact with the basal lamina. This supports the idea that the basement membrane is involved in the differentiation of mesenchymal cells into odontoblasts, probably by providing special attachment sites for the aligning mesenchymal cells. The rearrangement of intracellular organelles in the cells of enamel epithelium and a change of epithelial morphology were already seen at the time of the initial predentin secretion by odontoblasts. At this time, the basal lamina was still present. The penetration of epithelial microvilli into the epithelial-mesenchymal interface through breaks in the basal lamina related to the onset of predentin mineralization. This suggests that the determination of epithelial cells into ameloblasts already occurs before the disappearance of the basal lamina.

Ameloblasts↗
PubMed1997

Expressions of c-jun and jun-B proto-oncogenes in odontoblasts during development of bovine tooth germs.

c-jun and jun-B genes are among the nuclear proto-oncogenes induced by growth factors such as the TGF-beta superfamily and play important roles in cell differentiation. These gene products enhance expressions of proteins including osteocalcin, alkaline phosphatase, and collagens. On the other hand, it is well-known that the TGF-beta superfamily affects odontoblast differentiation, and that differentiated odontoblasts express extracellular and membrane proteins as described above. However, there are few reports of factors that participate in the transcriptional regulation of odontoblasts. Especially, little is known about the expression of c-jun and jun-B genes. In this study, we focused on the examination of expressions of c-jun and jun-B genes in dental papillae of bovine tooth germs. Using in situ hybridization, we found that these genes were expressed only in the odontoblastic lineage, but not in other dental papilla cells. Levels of c-jun and jun-B mRNAs increased along the gradient of differentiation of odontoblasts. These levels of c-jun mRNAs were maintained in both young and mature odontoblasts. However, unlike the c-jun gene, expression of the jun-B gene became sparse in mature odontoblasts compared with young odontoblasts. For further analysis, Northern hybridization of total RNA extracted from differentiated odontoblasts was performed for the examination of levels of jun-B mRNAs, indicating that levels of jun-B mRNAs of mature odontoblasts were clearly less than those of young odontoblasts. These results suggest that c-jun and jun-B genes may participate in the transcriptional regulation of odontoblasts of bovine tooth germs, and may control the odontoblast phenotype. Furthermore, our results suggest that these genes can be markers of odontoblasts during dentinogenesis; especially, high expression of jun-B gene can be a marker of young odontoblasts that start to form the new dentin matrix.

Animals↗
PubMedDate not supplied

[3-D reconstruction of a tooth germ with hereditary opalescent dentine].

A computer-aided three-dimensional reconstruction of a tooth-germ with hereditary opalescent dentine for the first time permitted to delineate the characteristic large dentinal canals as being of canal-like shape and to show their spatial relationship to the dentinal contour. The tubules often displayed links to pulpal tissue and extended from pulpo-dentinal junction up to the outer layer of dentine. The results of this study support the hypothesis of a vasal origin of these tubules.

Adolescent↗
PubMed1989

Ultrastructural localization of dentine phosphoprotein in rat tooth germs by immunogold staining.

Dentine phosphoprotein (DPP) was localized on thin frozen sections of fixed rat tooth germs by indirect immunogold staining. Antisera were directed against DPP and against glutaraldehyde-treated DPP and were characterized by immuno-electroblotting. In odontoblasts, DPP was found to be localized in the cisternae of the rough endoplasmic reticulum (RER) and the Golgi apparatus and in Golgi-associated vesicles. Odontoblastic processes were moderately positive for DPP and dentine was intensely labeled on frozen sections of unfixed tissue. Predentine showed a slight immunoreactivity. These results indicate the synthesis of DPP in the RER, its accumulation in the Golgi apparatus and its vesicular transport and secretion via the odontoblastic processes into dentine. The close association of the gold particles with the dentinal collagen fibres makes a role of DPP in linking mineral to collagen conceivable. Matrix vesicles were negative for DPP, suggesting that the protein is not present at the sites of matrix vesicle-associated nucleation.

Animals↗
PubMed1987

Ultrastructural distribution of sulfated glycosaminoglycans in epithelial-mesenchymal interface of developing rat tooth germs.

We investigated the ultrastructural distribution of sulfated glycosaminoglycans in the epithelial-mesenchymal interface of tooth germs by use of the high-iron diamine thiocarbohydrazide silver proteinate (HID-TCH-SP) staining and enzymatic digestion method. At an early stage in odontoblast differentiation, HID-TCH-SP stain deposits were sparsely distributed in the basement membrane and in the intercellular spaces. Subsequently, as formation of the initial predentin matrix began, HID-TCH-SP stain deposits were densely distributed in the interfibrillar spaces and the basement membrane. Testicular hyaluronidase digested most of those in the progenitor pre-dentin, whereas those in the region of basal lamina resisted enzymatic digestion. Testicular hyaluronidase-resistant HID-TCH-SP stain deposits were susceptible to heparitinase, indicating that the sulfated glycosaminoglycan in the basal lamina is heparan sulfate. Furthermore, the heparan sulfate tended to be regularly arranged at the sites of internal and external lamina densa. However, as progenitor pre-dentin matrix formation proceeded, the numbers of stain deposits temporarily increased and their distribution pattern became irregular, finally tending to disappear with the disruption of basal lamina.

Animals↗
PubMed2002

Expression, gene regulation, and roles of Fisp12/CTGF in developing tooth germs.

Odontogenesis involves multiple events, including tissue-tissue interactions, cell proliferation, and cell differentiation, but the underlying mechanisms of regulation are far from clear. Because Fisp12/CTGF is a signaling protein involved in similar events in other systems, we asked whether it is expressed in developing tooth germs and what roles it may have. Indeed, Fisp12/CTGF transcripts were first expressed by dental laminas, invaginating epithelium, and condensing mesenchyme at the bud stage, and then became abundant in enamel knot and preameloblasts. Fisp12/CTGF was present not only in inner dental epithelium but also in stratum intermedium and underlying dental mesenchyme. Fisp12/CTGF expression decreased markedly in secreting ameloblasts. Tissue reconstitution experiments showed that Fisp12/CTGF expression in dental epithelium required interaction with mesenchyme but was maintained by treatment of epithelium with transforming growth factor-1, a factor regulating Fisp12/CTGF expression in other systems, or with bone morphogenetic protein-2. Loss-of-function studies using CTGF neutralizing antibodies revealed that interference with endogenous factor action in tooth germ explants led to a severe inhibition of proliferation in both epithelium and mesenchyme and a marked delay in cytodifferentiation of ameloblasts and odontoblasts. Treatment of dental epithelial and mesenchymal cells in culture with recombinant CTGF stimulated cell proliferation, whereas treatment with neutralizing antibodies inhibited it. The data demonstrate for the first time that Fisp12/CTGF is expressed during odontogenesis. Expression is confined to specific sites and times, is regulated by epithelial-mesenchymal interactions and critical soluble factors, and appears to be needed for proliferation and differentiation along both ameloblast and odontoblast cell lineages.

Animals↗
PubMed1988

Ultrastructural localization of osteocalcin in rat tooth germs by immunogold staining.

Osteocalcin was localized by indirect immunogold staining of thin frozen sections of rat tooth germs which had been fixed by different methods. Acrolein fixation proved to be satisfactory considering the preservation of fine structure and antigenicity. In odontoblasts, osteocalcin was found to be localized in the cisternae of the rough endoplasmic reticulum and Golgi apparatus. Few positive transport vesicles were found. Staining for osteocalcin in odontoblastic processes was only observed after strong fixation and was intense in odontoblasts engaged in early dentine formation. Predentine was slightly positive in the neighbourhood of positive processes. Matrix vesicles were negative and strong osteocalcin labeling of dentine seemed to appear after the onset of mineralization.

Animals↗
PubMed1996

In vitro characterization of enamel epithelium and pulp cells in mouse tooth germs.

Mixed cell populations consisting of enamel epithelium and pulp cells obtained from 18-day embryonic mouse tooth germs were cultured in vitro. Epithelial cells and pulp cells were also cultured individually and examined. Isolated cells were cultured in alpha-MEM supplemented with 10% fetal bovine serum for up to four weeks and examined morphologically using histological procedures including immunostaining, light and electron microscopy, and electron probe microanalysis. The pulp cells proliferated and differentiated in the absence of epithelium, but the number of epithelial cells showed a strong dependence on the pulp cells. Pulp cells showing fibroblastic morphology in the mixed culture gradually became elliptical, and eventually transformed into spherical cells surrounded by a calcified extracellular matrix. Alkaline phosphatase (ALPase) activity was expressed on the pulp cells prior to calcification of the extracellular matrix, as shown by von Kossa's and alizarin-red staining. Calcification deposition, which is closely associated with thick banded type-I collagen fibrils, was shown to be composed of calcium and phosphorous using electron probe microanalysis. Type-I collagen immunoreactivity was detected on the extracellular matrix after two weeks of culturing. The present results show that the proliferation and differentiation of pulp cells, and subsequent calcification of the extracellular matrix occur in the presence or absence of epithelial elements, but that the proliferation of epithelial cells depends on the presence of pulp cells.

Ameloblasts↗
PubMed2000

Transgenically ectopic expression of Bmp4 to the Msx1 mutant dental mesenchyme restores downstream gene expression but represses Shh and Bmp2 in the enamel knot of wild type tooth germ.

Bmp4 is a downstream gene of Msx1 in early mouse tooth development. In this study, we introduced the Msx1-Bmp4 transgenic allele to the Msx1 mutants in which tooth development is arrested at the bud stage in an effort of rescuing Msx1 mutant tooth phenotype in vivo. Ectopic expression of a Bmp4 transgene driven by the mouse Msx1promoter in the dental mesenchyme restored the expression of Lef-1 and Dlx2 but neither Fgf3 nor syndecan-1 in the Msx1 mutant molar tooth germ. The mutant phenotype of molar but not incisor could be partially rescued to progress to the cap stage. The Msx1-Bmp4 transgene was also able to rescue the alveolar processes and the neonatal lethality of the Msx1 mutants. In contrast, overexpression of Bmp4 in the wild type molar mesenchyme down-regulated Shh and Bmp2 expression in the enamel knot, the putative signaling center for tooth patterning, but did not produce a tooth phenotype. These results indicate that Bmp4 can bypass Msx1 function to partially rescue molar tooth development in vivo, and to support alveolar process formation. Expression of Shh and Bmp2 in the enamel knot may not represent critical signals for tooth patterning.

Alleles↗