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At least 973 records · Page 54Linked to original sources
PubMed1999

Immunohistochemical and histochemical characterization of the mucosubstances of odontogenic myxoma: histogenesis and differential diagnosis.

To discuss the dental origin of odontogenic myxoma and to provide further information for the differential diagnosis between this tumor and myxoid malignant fibrous histiocytoma (MFH) which occasionally occurs in jaw bones, the contents of glycosaminoglycans (GAGs) and proteoglycans (PGs) in the mucosubstances of 15 odontogenic myxomas, 5 myxoid MFH and 3 human fetal tooth germs in the bell stage of development were characterized using histochemical and immunohistochemical methods. Histochemical staining of hyaluronic acid (HA) was undertaken using biotinylated HA binding protein (B-HABP), and immunohistochemical detection was done using a panel of antibodies against chondroitin 6-sulfate (CS-6), chondroitin 4-sulfate (CS-4), dermatan sulfate (DS), keratan sulfate (KS), heparan sulfate (HS), aggrecan, PG-M/versican, decorin and biglycan. In odontogenic myxoma, CS-6, HA and PG-M/versican were observed in the myxomatous matrix of all cases, while KS and HS were seen in none. As for CS-4, DS, aggrecan, decorin and biglycan, only irregular and mild stainings were shown. Consistent and strong positive straining for CS-6, HA and PG-M/versican were seen in dental papilla and provided evidence supporting the origin of this tumor from dental papilla. Except for the constant staining for HA, the myxoid matrix was rarely stained for most GAGs and PGs in myxoid MFH. Immunodetection of CS-6 and PG-M/version with the use of monoclonal antibodies 3-B-3 and 2-B-1 is therefore recommended as a useful tool in differentiating odontogenic myoma from myxoid MFH.

Diagnosis, Differential↗
PubMed1985

Epidermal growth factor inhibits morphogenesis and cell differentiation in cultured mouse embryonic teeth.

Although local epithelial-mesenchymal tissue interactions which are presumably mediated by extracellular matrix molecules are important regulators of tooth morphogenesis and differentiation, our studies have indicated that these developmental processes also depend on circulating molecules. The iron-carrying serum protein transferrin is necessary for the early morphogenesis of mouse tooth in organ culture (A-M. Partanen, I. Thesleff, and P. Ekblom, 1984, Differentiation 27, 59-66). In the present study we have examined the effects of other growth factors on mouse tooth germs grown in a chemically defined medium containing transferrin. Fibroblast growth factor and platelet derived growth factor had no detectable effects but epidermal growth factor (EGF) inhibited dramatically the morphogenesis of teeth, and prevented odontoblast and ameloblast cell differentiation. EGF stimulated cell proliferation in the explants measured as [3H]thymidine incorporation in DNA. However, when the distribution of dividing cells was visualized in autoradiographs, it was observed that cell proliferation was stimulated in the dental epithelium but was inhibited in the dental mesenchyme. The inhibition of cell proliferation in the dental mesenchyme apparently caused the inhibition of morphogenesis. We do not know whether the dental epithelium or mesenchyme was the primary target for the action of EGF in the inhibition of morphogenesis. It is, however, apparent that the response of the dental mesenchymal cells to EGF (inhibition of proliferation) is regulated by their local environment, since EGF enhanced proliferation when these cells were disaggregated and cultured as monolayers. This indicates that the organ culture system where the various embryonic cell lineages are maintained in their original environment corresponds better to the in vivo situation when the roles of exogenous growth factors during development are examined.

Animals↗
PubMed2006

Effect of calcium, given before or after a fluoride insult, on hamster secretory amelogenesis in vitro.

We tested the hypothesis that high-calcium medium given prior to or immediately after exposure to fluoride (F) reduces the negative effects of F on secretory amelogenesis. Hamster molar tooth germs were grown in organ culture in media with different calcium levels. Deposition of enamel matrix and matrix mineralization were monitored by incorporation of [3H]proline and uptake of 45Ca and acid-soluble 32PO4. Ameloblast structure and the occurrence of a fluorotic enamel matrix were examined by light and electron microscopy. A preculture of explants in high-calcium medium partially prevented the formation of fluorotic (non-mineralizing) enamel matrix, increased matrix secretion but could not prevent F-induced hypermineralization of the pre-exposure enamel. High-calcium medium, applied after F insult, accelerated the recovery of fluorotic matrix, improved ameloblast structure, enhanced amelogenin secretion, and increased enamel thickness. The data indicate that it might be the balance between the amount of mineral deposition and that of matrix secretion which is critical for the mineralization of newly secreted enamel. Exposure to F disturbs this balance by enhancing mineralization of the pre-exposure enamel, probably generating an excess of protons. High calcium may protect against F exposure by enhancing amelogenin secretion into the enamel space, thereby increasing the local buffering capacity at the mineralization front.

Ameloblasts↗
PubMed1990

Features of the aperiodic microfibrils associated with mouse dental basement membrane demonstrated by ultrastructural histochemistry.

Histochemical features of aperiodic microfibrils (AMF) in mouse tooth germs were examined at the electron microscopic level. Intact and EDTA-isolated materials obtained from one day old first molars were used for ruthenium red (RR) staining, ferritin permeability, periodic acid-silver methenamine (PAM) impregnation, fibronectin localisation, negative staining on cryo-sections and tannic acid fixation. Electron microscopy and negative staining demonstrated that AMF traverse the basal lamina and penetrate below the inner enamel epithelium. In addition to RR staining, PAM impregnation and tannic acid fixation showed deposition on the AMF which was associated with basal laminae. RR staining and tannic acid fixation also indicated the presence of glycoprotein-rich materials in the lamina lucida. The AMF were derived from the lamina lucida which was closely associated with tannic acid-positive granular materials. The precipitation of silver particles by PAM impregnation was seen on banded collagen fibrils, basal lamina and AMF, but the staining features of AMF differed distinctly from those of collagen fibrils. The distribution of ferritin particles revealed that the basal lamina covering EDTA-isolated papilla tissue is a continuous structure. Immuno-reactions for fibronectin were detected on the basal lamina and AMF. Our results suggest that AMF are derived from the glycoprotein-rich lamina lucida and that their histochemical characteristics resemble those of basal lamina.

Animals↗
PubMed1993

Immunocytochemical investigation of the rat cementoblast phenotype.

Recent studies have suggested that cementoblasts may be derived from osteoblast progenitor cells, although the cementoblast phenotype has not been extensively characterized. This immunocytochemical study was carried out to investigate the expression by rat cementoblasts of a number of proteins which are characteristic of the osteoblast phenotype. Paraffin sections from developing rat tooth germs and from fully formed adult rat teeth with surrounding tissues, were incubated with antibodies to type I & III collagen, osteocalcin, transforming growth factor beta (TGE beta), and insulin-like growth factor 1 (IGF1). Frozen sections and unfixed resin-embedded sections were stained for alkaline phosphatase activity. Cementum and bone matrix were strongly positive for type I collagen, although there was only weak staining for type III collagen. Cementum was also positive for osteocalcin, which was particularly strong in the matrix of acellular cementum. Most osteoblasts and cementoblasts of the cellular cementum showed intense staining for TGF beta and IGF1, although some cementocytes and osteocytes were negatively stained. The osteoblast- specific anti-E11 mAb reacted strongly with cementoblasts and newly formed cementocytes in the cellular cementum. Cells associated with acellular cementum did not express TGF beta, IGF1 or stain positively with anti-E11 antibody at any time during root development. Cementoblasts were weakly or negatively stained for alkaline phosphatase in contrast to the osteoblasts examined, which may reflect the low level of synthetic activity in cementoblasts. These results demonstrate that osteoblasts and cementoblasts of cellular cementum share many phenotypic characteristics, and also suggest that there may be phenotypic differences between cementoblasts associated with cellular and acellular cementum.

Animals↗
PubMed2004

Involvement of matrix metalloproteinases in the onset of dentin mineralization.

In order to study the involvement of matrix metalloproteinases (MMPs) on dentin formation and mineralization, day 18 embryonic mouse tooth germs were cultured for 10 d in the presence or absence of Marimastat, a general MMP inhibitor, or CT(1166), a more selective inhibitor of gelatinases (MMP-2 and MMP-9) and stromelysin-1 (MMP-3). With Marimastat a dose-dependent increase in thickness of the predentin layer and a decreased mineralization of dentin were observed. At the highest concentration of the inhibitor used, enamel formation had ceased. With CT(1166), these effects were already apparent at the lowest concentration used. Western blot analyses demonstrated that the two inhibitors inhibited the expression of enamelysin (MMP-20). These observations indicate that MMPs (possibly MMP-2, -3, -9 and/or -20) play a role in the onset of dentin mineralization. The lack of enamel formation was possibly due to diffusion of amelogenin from its normal site of apposition. The protein clearly was not retained at the surface of the non-mineralized dentin layer, and immunopositive amelogenin accumulated in the odontoblast compartment. The diffusion of enamel proteins and the accumulation revealed by immunolabeling of two small leucine-rich proteoglycans, decorin and biglycan, in the predentin may have contributed to impaired dentin mineralization.

Amelogenin↗
PubMed1975

Electron microscopic study of early formation of the tooth enameloid of a fish (Hoplognathus fasciatus). I. Odontoblasts and matrix fibers.

An electron microscope study was made on the tooth germs of Hoplognathus fasciatus in early developmental stage. Special attention was given to the odontoblasts, enameloid matrix fibers, calcification of enameloid and the hitherto controversial origin of the enameloid. 1. The ameloblasts and the odontoblasts are demarcated by a single layer of basement membrane which persists until immediately before the calcification of the enameloid matrix. 2. This histogenesis of the enameloid matrix begins with the formation of non-striated fibers 140-180 A thick. They are arranged in a direction vertical to the basement membrane and parallel to the sides of odontoblasts. Fibers with regular cross striations of 640 A periodicity later appear and the entire enameloid matrix is formed by these fibers. 3. Along with the formation of the enameloid, the odontoblasts assume a high columnar form, with a marked increase in cell organelles which show marked polarity suggesting active protein synthesis. Numerous odontoblastic processes are noted in the enameloid matrix. Granules, representing precurosors of enamleoid matrix fibers occur in the odontoblasts. Based on these findings, the enameloid matrix fibers must be of mesodermal origin. 4. Deposition of crystals of small size, needle and tube in shape, occurs in the circumference of the fiber bundles. As calcification progresses, crystals appear in the central portion of the bundles. Later, large crystals of rod and platelet shapes become intermingled. In addition to this, small crystals are fused, forming aggregates.

Ameloblasts↗
PubMed1993

Immunohistochemical detection of an enamel protein-related epitope in rat bone at an early stage of osteogenesis.

Monoclonal antibody MI315 was produced against hamster tooth germ homogenate by in vitro immunization. It was found that MI315 reacted with enamel matrix, ameloblasts, and bone matrix at an early stage of osteogenesis. Decalcified tissues of rat femurs and mandibles were examined with MI315 using indirect immunofluorescence. In endochondral ossification of femurs, immunoreactivity was found in bone extracellular matrix (ECM) deposited on the surface of the cartilage core of primary spongiosa, but not in the cartilage core itself. In intramembranous ossification of 0-day-old rat mandibles, intense immunofluorescence was detected in bone ECM and a few young osteocytes, but not in osteoblasts. Immunoreactivity in bone ECM of 2-day-old rats decreased and almost disappeared from bone ECM of 4-day-old rats. Although in nondecalcified sections of 0-day-old rats, negligible immunofluorescence was detected in bone ECM which showed positive staining in decalcified tissues, the immunostaining appeared after decalcification using ethylenediaminetetraacetic acid (EDTA). These results indicate that a substance(s), which had a common epitope with an enamel-derived protein(s), existed in immature bone ECM of both endochondral and intramembranous ossification, and that it might be masked by bone mineral. Monoclonal antibody MI315 is a useful tool to investigate the time- and position-specific changes in osteogenesis and amelogenesis.

Animals↗
PubMed2000

Immunohistochemical demonstration of an enamel sheath protein, sheathlin, in odontogenic tumors.

Enamel proteins can be useful markers for assessment of the functional differentiation of neoplastic epithelium and the nature of extracellular matrices in odontogenic tumors. In the present study, we examined immunohistochemical localization of sheathlin, a recently cloned enamel sheath protein, in various odontogenic tumors to evaluate functional differentiation of tumor cells and the nature of hyalinous or calcified matrices in odontogenic neoplasms. Distinct immunolocalization of sheathlin was observed in the immature enamel of the tooth germ at the late bell stage. Secretory ameloblasts facing the enamel matrix also showed positive staining in their cytoplasm. Definite localization of sheathlin was demonstrated in the enamel matrix in odontogenic tumors with inductive dental hard tissue formation such as ameloblastic fibroodontomas and odontomas. Immunoexpression of sheathlin was, furthermore, demonstrated in eosinophilic droplets in solid nests of adenomatoid odontogenic tumor (AOT) and ghost cells in the epithelial lining of calcifying odontogenic cyst (COC). In AOT, cells facing the eosinophilic droplets also expressed the protein in their cytoplasm. There was neither intracellular staining for sheathlin in the tumor cells nor extracellular staining in the matrix of ameloblastomas and calcifying epithelial odontogenic tumors. Dentin, dysplastic dentin-like hyaline material and cementum in the tumors examined were negative for sheathlin. These results show that immunodetection of sheathlin is a useful marker for functional differentiation of secretory ameloblasts and enamel matrix, which is often hard to differentiate from other hard tissues in odontogenic tumors. Our findings from the view point of sheathlin expression support that the tumor cells of ameloblastomas do not attain full differentiation into functional ameloblasts. It is very interesting that epithelial cells in odontogenic tumors can differentiate into functional ameloblasts without induction by odontogenic mesenchyme, as shown by immunoexpression of sheathlin in eosinophilic droplets within solid epithelial sheets in AOT and ghost cells in the epithelial lining of COC where inductive participation of mesenchymal cells was most unlikely.

Ameloblastoma↗
PubMed2002

Expression of neural cell-adhesion molecule mRNA during mouse molar tooth development.

This study employed in situ hybridisation using a probe recognising all isoforms of the molecule. Expression of the molecule in tooth germs started at embryonic day 13, when they were at the bud stage. Both inner cells of the epithelial bud and peripheral cells of the dental mesenchyme were positive. At the cap stage, positive cells were found in the inner part of the enamel organ but only in a limited area near the outer enamel epithelium. In the mesenchyme at the cap stage, expression was weak in the dental papilla and strong in the follicle. From the bell stage onward, epithelial cells in the enamel organ were negative except for the cells of the stratum intermedium, which were transiently positive at early and late bell stages. In the dental papilla, expression had mostly ceased during and after the bell stage, although transient expression was found in cuspal areas at the early bell stage. The dental follicle strongly expressed neural cell-adhesion molecule (NCAM) to the end of the experimental period, at post-natal day 4. In contrast to the first molar at its earliest stage of appearance, in which both the thickened epithelium and surrounding mesenchyme were negative for the expression of the molecule, the second molar appeared as a combination of extending epithelial thickenings and mesenchymal cells strongly positive for its expression. This study newly identifies the dental papilla and the stratum intermedium as NCAM-expressing sites.

Animals↗
PubMed1989

[Lectin-binding sites in the growing end of rat incisors].

Tooth germs of rat incisors were examined by lectin-histochemistry in the portion from the apical end to enamel forming stage. Tissue sections were prepared from paraformaldehyde-fixed and paraffin-embedded tissues with or without EDTA-decalcification. They were stained with fluorescein-isothiocyanate-labeled (F- for short) lectins and observed by a fluorescent microscope. The boundary between inner enamel epithelia and dental papilla cells was stained with F-Con A, F-MPA and F-PNA. The boundary between the epithelia and dentin was stained with F-Con A and F-MPA. Stratum intermedium cells were stained with F-Con A, F-MPA and F-PNA, and were different in the time when they began to be stained with each lectin during their development. Distal cytoplasm of secretory ameloblasts and odontoblasts were stained with F-MPA and F-Con A, respectively. The staining with these lecting became stronger gradually from the apical to the incisal side. These results suggest that F-MPA and F-Con A are useful as a marker indicating the time when enamel and dentin begins to form, respectively. Distal cytoplasm of secretory ameloblasts was also stained with F-Con A and F-PNA. The odontoblastic layer was stained only with F-Con A, but the dental papilla was stained with F-Con A, F-MPA, and F-PNA. Stellate reticulum and outer enamel epithelia were stained with F-Con A and F-MPA. The comparison of the results from decalcified and non-decalcified tissues showed that the EDTA-decalcification scarcely affected these lectin bindings.

Amelogenesis↗
PubMed1978

Mobility of concanavalin A receptors and distribution of cytoplasmic actin in odontogenic epithelial and mesenchymal cells.

The distribution of concanavalin A (Con A) surface receptors and cytoplasmic actin in the same cell was studied in monolayer cultures of 2 odontogenic epithelial cells of different developmental age and in ecto-mesenchymal cells derived from the same tooth germ. Con A receptors were demonstrated by fluorescein-isothiocyanate-labelled Con A (FITC-Con A) and cytoplasmic actin by a specific anti-actin autoantibody (AAA) traced with a rhodamine-labelled goat anti-human globulin (R-AHG). All 3 cell types, incubated with FITC-Con A at 37 degrees C for increasing time periods, showed progressive changes in staining patterns from clusters, caps to perinuclear globules. Capping was seen in the majority of immature epithelial cells at 120--180 min, in cells of more mature epithelium at 180--240 min and in ecto-mesenchymal cells at 240--360 min. Binding of FITC-Con A to cell surfaces resulted in sequential changes in AAA staining from filamentous to an aggregated or diffuse pattern, co-capping of aggregated or diffusely stained areas with those capped by FITC-Con A, presence of aggregated or diffusely stained areas in sites similar to the perinuclear globules stained by FITC-Con A, to final re-emergence of filamentous staining. Prior treatment of cells with cytochalasin B or colchicine promoted capping in epithelial but not in ecto-mesenchymal cells while presence of either drug throughout the staining procedure inhibited capping. The results show that Con A receptors are more mobile in epithelial compared to ecto-mesenchymal cells and in immature epithelial cells compared to their more mature counterparts, and that binding and mobility of Con A receptors on the cell surface is associated with redistribution of cytoplasmic actin. The cytochalasin B and colchicine experiments suggest that both microfilaments and microtubules may have synergistic roles in the opposing functions of receptor anchorage and mobility, and that the relative receptor immobility of ectomesenchymal compared to epithelial cells may be attributed to firmer receptor anchorage to the cytoskeleton.

Actins↗