Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Tooth Germ”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources
PubMed1980

Transcriptional activity in lysates of cultured mesenchymal cells from embryonic tooth germs.

Mesenchymal cells isolated from the papilla of embryonic tooth germs of the mouse were cultured in a complex medium for five to six days. Liquid nitrogen lysates, prepared from these cells, incorporated nucleoside monophosphates into a cold acid-insoluble product. The product was sensitive to RNase and no product was formed if the lysate was pretreated with DNase. The reaction was sensitive to EDTA and, in its presence, optimum activity was obtained with 2 mM MgCl2. On sucrose gradients, the reaction product was distributed between two broad peaks; one centered about 18S and the other above 28S. The RNA polymerase inhibitor alpha-amanitin inhibited approximately 50% of the activity at a concentration of 10 microgram/ml.

Amanitins↗
PubMed1994

Immunohistochemical demonstration of bcl-2 protein in human tooth germs.

This study sought to detect patterns of bcl-2 protein expression that could provide more insight into the cellular dynamics of tooth development. As bcl-2 serves to prevent cell death, its occurrence in odontogenic tissues might be helpful in identifying cell populations from which odontogenic tumours may arise. The bcl-2 protein was found only in the epithelial part of the tooth germ and was present in all parts of the enamel organ except the ameloblast. This suggests that bcl-2 protein plays a part in maintaining the viability of the enamel organ. The presence of bcl-2 in the fully matured tooth germ and adjacent dental lamina might indicate that epithelial odontogenic tumours may originate from various parts of the enamel organ.

Enamel Organ↗
PubMed1999

Daunorubicin-induced pathology in the developing hamster molar tooth germ in vitro.

The aim of this study was to evaluate, under organ culture conditions, the cytotoxic effects of daunorubicin on tooth development. Three-day-old maxillary hamster second molars were exposed for 24 h in vitro to 108-10-4 M daunorubicin and then evaluated biochemically and histologically. At 10-6 M daunorubicin dose-dependently decreased tooth germ dry weight, cell proliferation ([3H]thymidine uptake), and insoluble [32P] phosphate uptake (phosphorylation of macromolecules). [45Ca]calcium uptake, a marker for mineralization, was significantly affected only at the highest concentration (10-4 M) tested. Histologically, 10-6 M daunorubicin induced necrosis of the proliferating but not the differentiated protein-secreting cells. At 10-4 M, however, all cells were dead. These results indicate that daunorubicin is particularly toxic to the proliferating cells of the tooth germ. Thus, it can be postulated that children treated with daunorubicin may develop defects in the erupted teeth mainly associated with those regions that were in the proliferating stage at the onset of anticancer chemotherapy.

Amelogenesis↗
PubMed2004

Immunolocalization of heat shock protein 27 in developing jaw bones and tooth germs of human fetuses.

27 kDa Heat shock protein (Hsp27), which is also identified as p29 estrogen-receptor associated protein, plays a crucial role in specific growth stages. It also seems to be involved in the balance between differentiation and apoptosis. To determine whether Hsp27 is involved during craniofacial development and odontogenesis, its expression was studied through immunohistochemistry of developing jaw bone as well as the odontogenesis of heads from human fetuses. Formalin-fixed paraffin-embedded specimens of 7 human fetuses (3 female, 4 male), obtained from miscarriages occurring between the 9th and 16th weeks of pregnancy, were examined by using a monoclonal antibody against Hsp27. Staining intensity (weak, +; moderate, ++; strong, +++) was evaluated semiquantitatively. The sample slice was cut through a coronal plane, which included eyes, nasal cavities, tongue, and primitive dental lamina with tooth germs. A transient and spatially restricted expression of Hsp27 in developing human jaw bones and teeth was observed. Osteoblasts around the uncalcified bone matrix showed Hsp27 immunoreaction products (+++), whereas osteocytes were not immunolabeled. In mandibular condyle, immunolabeling was restricted to hypertrophic chondrocytes (++). In developing tooth germs, Hsp27 immunostaining was detected throughout the bud (+++). At the early cap stage, a strong immunolabeling for Hsp27 was seen in the dental lamina (+++), and a moderate staining was seen in the outer dental epithelium (++). At the late cap stage, Hsp27 expression was detected in the outer dental epithelium (++) as well as in the cells of the future stellate reticulum (++). The spatiotemporal-restricted expression of Hsp27 in craniofacial bones during development suggests that this protein could be involved in the balance between differentiation and apoptosis, by modulating the viability of osteoblasts and chondrocytes. The specific regional and temporal expression patterns of Hsp27 during tooth development sustains that this small Hsp might be related to the morphogenesis and cytodifferentiation processes of tooth germs.

Female↗
PubMed2005

Structural features of forming and developing blood capillaries of the enamel organ of rat molar tooth germs observed by light and electron microscopy.

The process of vascularization of the enamel organ, a unique epithelial structure, occurs when the tooth germ is fully developed, i.e., at the onset of dentinogenesis. Although the three-dimensional organization of the capillaries has been previously investigated, the structural features underlying the formation of the new capillaries remains poorly understood. Thus, in the hope of better understanding the mechanism of formation of the stellate reticulum capillaries, upper first molar tooth germs of newborn and 3-day-old rats were fixed in glutaraldehyde-formaldehyde and processed for light and electron microscopy. Our results showed that blood capillaries are initially in close proximity to the outer enamel epithelium. Between and intercalated with the capillaries are round/ovoid clusters of cells, some of which are vacuolated, closely apposed to the outer enamel epithelium. The outer enamel epithelium is not a continuous layer, but exhibits gaps between the cells. This suggests that the capillaries penetrate the enamel organ through these gaps, since no invagination of the epithelium was observed. The presence of a cluster of cells containing vacuoles suggests that vasculogenesis is taking place. Images showing loss of the basal lamina, proliferation of endothelial cells, presence of filopodia and lateral sprouting suggests that angiogenesis is also occurring. Thus, neoformation of capillaries of the molar enamel organ of rat seems to occur simultaneously by mechanisms of vasculogenesis and angiogenesis.

Animals↗
PubMed1987

Developmental appearance of Gla proteins (osteocalcin) and alkaline phosphatase in tooth germs and bones of the rat.

The tissue distribution and developmental appearance of alkaline phosphatase and Gla proteins, relative to mineralization were examined. Undecalcified sections of tooth germs, calvaria and alveolar bone of the rat were immunostained for Gla proteins, (indirect immunofluorescence and avidin-biotin-peroxidase-complex) and then stained for alkaline phosphatase activity. In the growth regions of tooth germs, Gla protein was observed in young odontoblasts and in early predentin, at a stage prior to formation of the first mineralized dentin. Similar results were obtained for bone: young osteoblasts as well as osteoid were immunopositive for Gla protein prior to formation of the first mineralized bone. Histochemical staining revealed that differentiating odontoblasts and osteoblasts exhibited alkaline phosphatase activity at stages prior to appearance of Gla proteins and that cells adjacent to odontoblasts and osteoblasts (not directly involved in the formation of predentin/dentin and osteoid/bone) stained for alkaline phosphatase, but not for Gla proteins. We conclude, that in these bone- and dentin-forming cells, alkaline phosphatase activity is expressed before the appearance of Gla proteins, but that both appear before the onset of mineralization. We also conclude that Gla protein is a more specific marker for bone and dentin formation than histochemical alkaline phosphatase activity, since only the cells directly involved in these processes were immunostained for Gla protein.

Alkaline Phosphatase↗
PubMed1977

[The problem of damage to the tooth germ by ionizing radiation].

Experiments on animals (four-week-old dogs) were conducted in an investigation made to study the possibility of dose-dependent tooth-germ damage produced by ionizing radiation. The individual doses were 50 r and 200 r, respectively, and they were administered once to three times at weekly intervals. Hyperemia and edemata could be observed on tooth-germ pulps from 150 r onward. Both of these conditions became more acute as the radiation dose increased (from 150 r to 600 r). Possible damage to both the dentin and enamel is pointed out.

Animals↗
PubMed1979

Inhibition of tooth germ differentiation in vitro by diazo-oxo-norleucine (DON).

Molar tooth germs from mouse embryos were studied in a Trowell-type organ culture. After 5 days of culture the odontoblasts had secreted predentine and the ameloblasts had differentiated. When cultured in the presence of 10-50 micro M diazo-oxo-norleucine (DON), which is a glutamine analogue, the differentiation of odontoblasts was inhibited, but the teeth looked otherwise healthy. When DON was added after 2 days of culture in control medium (at this time the odontoblasts in the cuspal area were already differentiated), it did not inhibit predentine secretion, ameloblast differentiation, nor enamel secretion. However, this was seen only in the cuspal area and the boundary to the undifferentiated, more cervical cells was distinct. The results support the concept that the mechanism of the differentiation of odontoblasts is different from that of the ameloblasts. We have shown earlier that a close association between the basement membrane and the mesenchymal cells is required for odontoblast differentiation. Because DON interferes with glycosaminoglycan and glycoprotein synthesis we suggest that DON inhibits odontoblast differentiation by affecting the mesenchymal cell surface and/or the basement membrane.

Ameloblasts↗
PubMed2003

Extremely high expression of beta-actin mRNA in osteoclasts resorbing alveolar bone located at the distal area of the developing molar tooth germ in newborn rats.

Expression of beta-actin is widely utilized as an internal control of mRNA expression in various cells. Here we show evidence that the expression level of beta-actin mRNA in osteoclasts significantly differs in its intensity according to the position in bone tissues. By use of in situ hybridization, we obtained clear data showing that osteoclasts facing the distal part of a developing molar tooth germ expressed extremely high levels of beta-actin mRNA in comparison with other osteoclasts observed in the mandibular bone surface. No signal was detected when beta-nerve growth factor transcripts were observed. Electron microscopic analysis revealed that osteoclasts localized in these areas were functionally active, estimated from the expression of high levels of the osteoclast membrane antigen, Kat1 antigen, which associated with active osteoclasts. These data suggest that osteoclasts expressing extremely high levels of beta-actin are highly related to active osteoclasts induced by the mechanical stress caused by physiological movement of molar tooth germ towards distal directions in the developing mandible.

Actins↗
PubMed2001

Inositol hexasulphate, a casein kinase inhibitor, alters the distribution of dentin matrix protein 1 in cultured embryonic mouse tooth germs.

Immunohistochemical studies using a polyclonal antibody, raised against the recombinant form of dentin matrix protein 1 (DMP1), show that DMP1 was detected mainly in odontoblasts in cultured mouse embryonic tooth germs. However, in restricted areas, DMP1 staining was also observed in secretory ameloblasts, in the stratum intermedium and stellate reticulum, but only when the odontoblasts located in front of them were unstained. When the embryonic tooth germs were cultured in the presence of inositol hexasulfate, a casein kinase I and II inhibitor, staining of odontoblasts was weak or nil, whereas, in contrast, ameloblasts and enamel organ were strongly immunolabelled, suggesting an enhanced translocation of DMP1 after secretion to the secretory ameloblasts and/or stratum intermedium and stellate reticulum. Moreover, DMP1--was shown to be a good substrate for gelatinase A (MMP-2), but not to gelatinase B (MMP- 9). We hypothesized that DMP1--or the sub-fractions cleaved by the MMP--could behave as diffusible signaling molecule (s) rather than as a true dentin extracellular matrix component.

Ameloblasts↗
PubMed2004

The eternal tooth germ is formed at the apical end of continuously growing teeth.

Rodent incisors are known to be continuously growing teeth that are maintained by both the cell-proliferation at the apical end and the attrition of the incisal edge. This type of tooth had a special epithelial structure for the maintenance of stem cells, showing the bulbous epithelial protrusion at the apical end. The morphological transition of the epithelial-mesenchymal compartment by serial transverse sections of the apical end toward the incisal direction is likely to reflect the development of the tooth germ in the prenatal stage. Based on the present histological and previous molecular biological studies, the special structure at the apical end is obviously different from the cervical loop giving rise to Hertwig's epithelial root sheath (HERS), in human, mouse and rat molar tooth germs. Hence, we propose a new concept that the eternal tooth bud producing various dental progeny is formed at the apical end of continuously growing teeth, and a new term "apical bud" for indicating this specialized epithelial structure. Furthermore, BrdU labelling analysis suggested that the guinea-pig molars, which were continuously growing teeth, also possessed plural specific proliferative regions and "apical bud" at the apical end.

Animals↗
PubMed2003

Developmentally regulated expression of Netrin-1 and -3 in the embryonic mouse molar tooth germ.

The Netrins form a small, conserved family of laminin-related signaling proteins regulating axon guidance in the developing nervous system. Here, we analyzed the roles of Netrin-1 and -3 in trigeminal axon guidance to the first lower molar of the embryonic mouse. Netrin-1 showed a restricted epithelial expression domain buccal to the tooth germ, toward which the pioneer tooth axons initially appear to navigate. Later, before birth, transcripts were colocalized with nerve fibers around the bell stage tooth germ. Analysis of Netrin-1-deficient mice, however, did not reveal any obvious disturbances in the axon growth or pattern of tooth innervation. In contrast, Netrin-3 showed a prominent, distinct expression in the axon pathway and target field mesenchyme around the tooth. Hence, it is possible that Netrin-3 may regulate pioneer axon growth toward and within the embryonic tooth target field.

Animals↗
PubMed2001

Sonic hedgehog regulates epithelial proliferation and cell survival in the developing tooth germ.

Shh expression is highly restricted to the future sites of tooth development during the initiation of odontogenesis. This suggests a role for Shh as a proliferative factor, as localized epithelial thickenings invaginate to form a tooth bud. We have investigated this role by blocking Shh signaling between E10.5 and E12.5 in murine mandibular processes using a 5E1 blocking antibody and the PKA activator Forskolin. This results in down-regulation of Ptc, a principle target of Shh signaling. The effects of inhibition varied with developmental time. At E10.5, tooth development was arrested as epithelial thickenings and the numbers of teeth developing were considerably reduced. Inhibition at E12.5 produced localized apoptosis in the epithelium at the tip of the tooth buds, although some teeth were able to develop. Thus, Shh has dual roles in early odontogenesis, first in bud formation by stimulating epithelial proliferation, and second in the development of cap-stage tooth germs by increasing epithelial cell survival.

Animals↗
PubMed2004

Immunocytochemistry of keratan sulfate proteoglycan and dermatan sulfate proteoglycan in porcine tooth-germ dentin.

Keratan sulfate proteoglycan and dermatan sulfate proteoglycan have been reported to inhibit collagen fibrillogenesis. We investigated their distribution in order to evaluate the role of proteoglycan in dentinogenesis. Specimens of porcine tooth-germ dentin and erupted teeth were the materials on which antibodies to keratin sulfate and dermatan sulfate proteoglycan were used. Predentin was found to be positive for both antibodies and the reaction ceased in the calcification front. Uniformly thick collagen fibrils (30-70 nm in diameter) were distributed in the predentin matrix, which would become intertubular dentin in the future. Both antibodies reacted positively along these fibrils. In contrast, along the surface layer of dentin in the tooth germ and that in erupted teeth, collagen fibrils of 10-300 nm in diameter were noted occasionally in dentinal tubules whose odontoblastic processes had disappeared and these heterogeneous fibrils were negative for both antibodies. Our findings suggest that keratan sulfate proteoglycan and dermatan sulfate proteoglycan distributed in the predentin inhibit calcification of collagen fibrils in the uncalcified matrix and disappear in the calcification front. It is further suggested that keratan sulfate proteoglycan and dermatan sulfate proteoglycan distributed along collagen fibrils in the predentin matrix maintain uniform thickness, whereas collagen fibrils in dentinal tubules varied in thickness because of the absence of involvement of both proteoglycans. Therefore, keratan sulfate proteoglycan and dermatan sulfate proteoglycan were thought to be involved in both calcification and matrix formation.

Animals↗
PubMed1983

Studies of alkaline phosphatase inhibition by p-bromotetramisole in non-mineralizing and mineralizing neonatal hamster tooth germs in vitro.

The effects of l and d-, p-bromotetramisole (pBTM) on alkaline phosphatase were studied in relation to 45Ca2+, 32phosphate and 3H-thymidine uptakes in non-mineralizing second (M2) and mineralizing first (M1) maxillary hamster molar tooth germs under the conditions of organ culture. At the concentration used in culture (10(-3)M), l-pBTM completely inhibited alkaline phosphatase activity in tooth germ homogenates. About 30% of the enzyme activity was inhibited by d-pBTM at the same concentration. In culture, there were no significant differences between the effects of l and d-pBTM isomers on all the parameters measured. In the non-mineralized M2 molars, l and d-pBTM significantly reduced both TCA-soluble and TCA-insoluble 32phosphate uptakes but not 45Ca2+. However, 3H-thymidine uptake was also significantly decreased. In M1 molars, the pBTM isomers significantly reduced the uptake of TCA-soluble 32phosphate and 45Ca2+ but not TCA-insoluble 32phosphate. Ouabain, a specific inhibitor of Na+-K+-ATPase (but not alkaline phosphatase), also significantly reduced 3H-thymidine uptake to the same extent as the pBTM isomers in the non-mineralizing M2 molars, but it did not significantly affect either 32phosphate (TCA-soluble and TCA-insoluble) or 45Ca2+ uptake. Although this inhibitor significantly reduced both 45Ca2+ and TCA-soluble 32phosphate uptake in the mineralizing M1 molars, this effect was much less dramatic than was the case with the pBTM isomers. The reduced 45Ca2+ uptake in the M1 molars is probably a consequence of reduced mineralization since in the non-mineralizing M2 molars calcium uptake was not significantly affected by the pBTM isomers.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗
PubMed1993

Inhibition of in vitro mineralization in osteoblastic cells and in mouse tooth germ by phosphatidylinositol-specific phospholipase C.

We have examined the effect of phosphatidylinositol-specific phospholipase C (PIPLC) on the in vitro mineralization during cultivation of both osteoblast-like MC3T3-E1 cells and the lower molar tooth germ from mouse embryo. PIPLC not only caused the release of alkaline phosphatase (ALP) from cell membranes into the culture medium but also produced a disturbance of in vitro mineralization in MC3T3-E1 cells and in mouse embryonic tooth germ. These findings strongly suggest that ALP, functioning as an ectoenzyme, is involved in the physiological mineralization process of both bone and teeth.

Alkaline Phosphatase↗