Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Odontoblasts”

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 19 recordsLinked to original sources
PubMed1992

The relationship between odontoblasts and pulp capillaries in the process of enamel- and cementum-related dentin formation in rat incisors.

The relationship between odontoblasts and pulp capillaries in the process of dentinogenesis was studied in rat lower incisors, both on the labial and lingual sides, using light and transmission electron microscopy. The odontoblasts showed remarkable differences from the apical to the incisal end. Near the apical end of the tooth, "immature odontoblasts", which were thought to be involved in the formation of the mantle dentin, were arranged in a single layer, and continuous capillaries were located just beneath the odontoblasts. In the middle of the tooth, "mature odontoblasts" with highly developed cell organelles and notable processes formed a pseudostratified layer; fenestrated capillaries were found between these cells close to the predentin. The height of the odontoblast layer and the rate of dentin deposition on the labial (enamel-related) side was significantly greater than that on the lingual (cementum-related) side. Near the incisal end, cementum-related odontoblasts gradually decreased in height and number to become "post-odontoblasts" that produced atubular dentin; continuous capillaries were located subjacent to the post-odontoblasts. On the labial (enamel-related) side, however, odontoblasts retained their pseudostratification; fenestrated capillaries were still observed in the odontoblast layer. No atubular dentin was formed on the labial side.

Animals↗
PubMed1990

Ultrastructural changes in odontoblasts and pulp capillaries following cavity preparation in rat molars.

Responses of odontoblasts and pulp capillaries to cavity preparation were investigated in the upper first molar teeth of rats, using light and transmission electron microscopy. At 100 days of age, the blood vessels of the pulp formed a subodontoblastic network consisting of continuous capillaries at a short distance from the odontoblast layer. Cavity preparation caused the displacement of some odontoblasts into the dentinal tubules, while others were separated from the predentin by rapid inflammatory exudation after drilling. The subodontoblastic capillary network under the injured dentin was shifted inwards together with the separated odontoblasts. The endothelium of the shifted capillaries showed a remarkable increase of pinocytotic vesicles, an event thought to be closely related to the formation of the exudative lesion. By one day after cavity preparation, most of the damaged odontoblasts had degenerated. Many cells with high nucleus/cytoplasm (N/C) ratios and prominent nucleoli accumulated around the subodontoblastic capillaries, some of which had many endothelial fenestrae facing these cells. These cells were suggestive of newly differentiating odontoblasts receiving nutritional supply from the capillaries. Three days after cavity preparation, newly differentiating odontoblasts took the place of the degenerated odontoblasts. They began to produce reparative dentin by five days after cavity preparation. Capillaries were located beneath the newly differentiating odontoblasts, but endothelial fenestrae gradually decreased in number. During the active reparative dentin formation, capillaries remained closely beneath the new odontoblast layer. Although the rate of reparative dentin deposition was not significantly lower than that in the primary dentin formation, one could not recognize an invasion of capillaries into the odontoblast layer nor a remarkable increase of endothelial fenestrae, both of which are common in active primary dentin formation. The results suggest that the function of capillaries differs between primary and reparative dentin formation.

Animals↗
PubMed1989

[Electron microscopic study of canine dentin and odontoblast following the insertion of various composite resin monomers].

The purpose of this study was to evaluate the effect of composite resin monomer on dentinal tubules, odontoblasts and pulp with scanning electron microscopy (SEM) and transmission electron microscopy (TEM). Resin monomers of ethyleneglycol dimethacrylate (EDMA), triethyleneglycol dimethacrylate (Tri-EDMA), urethane dimethacrylate (UDMA), and 2, 2-bis [4- (3-methacryloxy-2-hydroxypropoxy) phenyl] propane (Bis-GMA) were used, and placed on a class V cavity in eighty teeth of adult dogs. Then, these treated animals were sacrificed after 30 to 120 days. The findings obtained were as follows: In the odontoblast body; 1. After 30 days, there were uneven unclear envelopes in all odontoblasts. 2. After 60 and 90 days, there were more invaginations of unclear envelope in Bis-GMA group than those in EDMA, Tri-EDMA and UDMA, and lysosomes and autophagic vacuoles increased in number. 3. In Bis-GMA group after 120 days, there were many degenerative changes of chromatin aggregation and hydropic, and many necrosis cells were seen. Uneven nucleous and lysosomes increased in EDMA, Tri-EDMA and UDMA groups. In the odontoblast process; 4. The odontoblast process disappeared in the dentinal tubule one third of cavity floor side of residual dentin with SEM and TEM after 30 days. However, after 120 days, there were few granular substances and calcified closure was not seen in dentinal tubules. In the region of central one third; 5. Microfilaments and microtubules in the odontoblast process decreased in number, and disarrangement and reticular degeneration of these fibers in all experimental groups after 30 days were seen. After 60 days, shrinkage and reticular degeneration of the odontoblast process were seen. Especially in Bis-GMA group, the odontoblast processes disappeared and the one in other three groups showed reticular degeneration after 90 and 120 days. 6. At the portion of pulp side one third on residual dentin, all odontoblast processes were almost seen normal ultrastructure after 60 days. In the group of Bis-GMA after 90 days, reticular degeneration was seen. Shrinkage of microfilaments and microtubules in EDMA, Tri-EDMA and UDMA groups were slightly seen. In the dentinal tubules after 120 days, reticular degeneration and empty in Bis-GMA group, and disarrangement of microfilaments and microtubules was seen in EDMA, Tri-EDMA and UDMA groups. The above findings indicated that composite resin monomers used in this experiment have effects on the odontoblast respectively. In the clinic, when we restore the cavity with these composite resins, we should intercept the stimulation of residual monomers with perfect dentin lining.

Actin Cytoskeleton↗
PubMed1992

The role of growth factors in determination and differentiation of the odontoblastic cell lineage.

In developing teeth the differentiation of odontoblasts is triggered by the enamel epithelium and is tightly coupled with morphogenesis. There is substantial evidence that even in mature teeth the cells of the dental pulp retain the capability to differentiate into odontoblasts under suitable conditions. However, cells from other than the dental mesenchymal cell lineage apparently do not possess this potential. Thus, it is conceivable that the dental mesenchymal cells acquire cell type-specific potential to differentiate into odontoblasts during their developmental history. Therefore, the understanding of the mechanisms which regulate the terminal differentiation of odontoblasts requires that the molecular changes and mechanisms that are associated with their progressive determination be clarified. It can be speculated that there are key transition points in the developmental sequence during which the mesenchymal cells acquire new levels of differentiation. These include, (1) the condensation of the neural crest-derived mesenchymal cells around the epithelial bud, (2) their entrance into the dental papilla lineage during cap stage, and (3) the differentiation of the cells underlying the enamel epithelium into odontoblasts during bell stage. The transition points are conceivably characterized by amplification or onset of expression of new sets of genes encoding transcription factors, growth factors as well as structural proteins. We have applied in situ hybridization for localization of the expression of two growth factors during mouse molar morphogenesis: transforming growth factor beta 1 (TGF beta 1) and int-2 (a proto-oncogene coding for a fibroblast growth factor-related protein). During bud stage, expression of TGF beta 1 was first detected in the epithelium and shortly thereafter in the condensed dental mesenchyme. The expression was weak during early bell stage but a high number of transcripts appeared in secretory odontoblasts as well as in presecretory ameloblasts. int-2 mRNA appeared in the dental papilla mesenchyme at the onset of cap stage, persisted in the cuspal mesenchyme during bell stage and was lost upon completion of morphogenesis. Our findings suggest that cell type-specific expression of TGF beta 1 and int-2 is associated with phenotypic properties of the odontoblastic cell lineage. For instance, TGF beta 1 may regulate matrix deposition by increasing tenascin and syndecan expression in the condensed dental mesenchyme and by controlling dentin matrix deposition by odontoblasts. TGF beta 1 and int-2 may also be involved in signalling between the epithelial and mesenchymal tissues and in regulation of gene expression at the transition points of the developmental sequence that leads to the differentiation of odontoblasts.

Animals↗
PubMed1989

[Lectin histochemical study on human dental pulp. Special reference to odontoblasts and pulp cells].

The present study investigated some lectin affinities of human dental pulps, especially of odontoblasts and pulp cells. The materials were obtained from clinically intact teeth that were caries-free, attrition and/or abrasion-free. Mucopolysaccharide staining was carried out with applied PAS and alcian blue (AB) (pH 1.0 and 2.5). Lectins used were Con A, WGA, RCA-1, UEA-1, DBA, SBA, MPA, LFA, HPA, PNA, and GS-1, and the avidin-biotin peroxidase complex method was employed. Some specimens were tested for PNA binding after treatment with sialidase. The following results were obtained: 1) On PAS and AB staining, the pulp tissue was very weakly or borderline positive. 2) Lectin binding in odontoblasts was intensely positive with Con A, WGA, RCA-1, MPA, and LFA, but negative or very weakly positive with the other lectins examined. 3) Lectin localization in odontoblasts was localized diffusely throughout the cytoplasm. 4) On PNA staining, odontoblasts were negative, but changed to positive after treatment with sialidase. 5) Odontoblast processes showed negative or borderline staining with all lectins used in this study. 6) The pulp cells were clearly positive with Con A, MPA, LFA, RCA-1, and SBA and especially LFA showed an intense reaction with the pulp cells. 7) WGA affinity for odontoblasts was very strong but that for pulp cells was very weak. 8) Lectin binding in pulp cells was observed mainly in the processes of the cells. From the above results, it is clear that the lectin binding pattern of odontoblasts differs from that of pulp cells. The data suggest that D-mannose, N-acetyl-D-glucosamine, D-galactose, and N-acetyl-D-galactosamine residues are localized in the odontoblasts and sialic acid is localized in the pulp cells.

Dental Pulp↗
PubMed1992

The carboxy-terminal extension of the collagen binding domain of fibronectin mediates interaction with a 165 kDa membrane protein involved in odontoblast differentiation.

Terminal differentiation of the odontoblast is characterized by an elongation and a polarization of the cell. The change in the cell shape and the reorganization of the cytoplasm involve the microfilament system. An immunological approach has previously implicated a transmembrane interaction between fibronectin and vinculin in the control of odontoblast differentiation. A 165 kDa protein localized on the cell-surface of odontoblasts mediated this interaction. In order to define the nature of the interaction of the 165 kDa protein with fibronectin, peptides were prepared by proteolytic cleavage of fibronectin with alpha-chymotrypsin. The results indicate that the 165 kDa protein interacted with a 62 kDa peptide located towards the amino-terminal extremity of fibronectin, but not with a 47 kDa related fragment. Both these 62 kDa and 47 kDa peptides included the collagen-binding domain and were retarded on a heparin-Ultrogel column. Microsequences demonstrated that the 62 kDa and 47 kDa fragments had the same amino-terminal extremity and that the larger fragment was extended in the carboxy-terminal direction. This carboxy-terminal extension of the collagen binding domain of fibronectin is implicated in the interaction of this molecule with the 165 kDa protein. On the other hand, odontoblasts differentiated normally when tooth germs were cultured in the presence of GRGDS synthetic peptide, suggesting that RGD-dependent integrins were not involved in odontoblast differentiation. Staining of dental mesenchymal cells in primary culture and of differentiated odontoblasts in situ with antibodies directed against the beta 1-subunit of integrins confirmed previous observations and showed that although beta 1 integrins are involved in the attachment of cultured dental cells, they are not implicated in the process of odontoblast differentiation.

Actin Cytoskeleton↗
PubMed1991

[Micromorphologic studies of the odontoblasts of sheep in different development and maturation stages].

The fine tissue structure of ovine odontoblasts was studied in various developmental and maturational stages. Odontoblasts differentiate from the peripherally-located mesenchymal cells of the dental papilla. On the basis of cytological parameters, it was possible to divide the odontoblasts into the following groups: pre-odontoblasts, juvenile (light) odontoblasts and mature (dark) odontoblasts. The three maturational stages of odontoblasts exhibit substantial differences with respect to their form and to the number and arrangement of their cytoplasmatic organelles. Structural differences in the three cell types appear to be closely correlated to the level of cellular activity.

Animals↗
PubMed1992

Changes in expression of alpha 1 type 1 collagen and osteocalcin mRNA in osteoblasts and odontoblasts at different stages of maturity as shown by in situ hybridization.

We investigated whether the expressed phenotype of osteoblasts and odontoblasts is changing with increasing maturity of the cells. Thus we determined, using in situ hybridization techniques, whether the expression of mRNA's for osteocalcin and the alpha 1 type 1 collagen chain was different in newly developed and more mature cuboidal osteoblasts of the primary and secondary spongiosa of radii of 8 day old rats, in mature cuboidal and older flat osteoblasts in the metatarsals of pig embryos, and in apical and coronal odontoblasts of the developing unerupted molars of pig embryos. The results indicate that newly differentiated osteoblasts in the primary spongiosa of the 8 day rat radius contained approximately the same amount of type 1 collagen message as more mature osteoblasts in the secondary spongiosa. Osteocalcin mRNA, on the other hand, was undetectable in the newly differentiated osteoblasts but clearly detectable in the mature osteoblasts of the secondary spongiosa. When we compared expression of osteocalcin and collagen type 1 mRNA in mature cuboidal and older flat osteoblasts, we found that the amount of osteocalcin mRNA relative to collagen type 1 mRNA was higher in flat osteoblasts than in cuboidal osteoblasts. In odontoblasts, however, the steady state level of collagen type 1 mRNA was higher in the older coronal odontoblasts, and the level of osteocalcin message lower, when compared to the younger apical odontoblasts. The results indicate that relative levels of osteocalcin and collagen mRNA in osteoblasts and odontoblasts vary depending on the stage in their secretory lifetime. This heterogeneity of the osteoblast and odontoblast population suggests that the composition of the matrix produced by these cells also differs.

Animals↗
PubMed1989

[Intranuclear rodlet in the odontoblast].

Lower incisors of 6 rabbits (about 3.5 kg, Japanese white, male) were observed by the electron microscopy. The life cycle of rabbit incisor odontoblast is classified into 4 stages by the dentine structure; 1st is outer, 2nd is middle, 3rd is inner and the 4th layer, that is the secondary dentine filling in the center of pulp. Fibrous intranuclear rodlets were observed in the odontoblast of late 2nd and 3rd stages, which forms thick inner half dentine. The odontoblasts of 2nd stage were tall and matrix formation cells, containing well developed golgi apparatus, many RER and secretory granules. The 3rd stage odontoblasts were short and formed the vaso-dentine in the lingual side. Intranuclear rodlets, about 5 nm thick, consisted of 5-20 fibrous or tubular structures. The arrangement of rodlets had no relation to the cell axis. These intranuclear rodlets might be observed only in the last stage odontoblast in the rat incisor. The morphological observations show 1) the term of life cycle of rabbit odontoblast may be more longer than the rat, 2) the intranuclear rodlets may be caused by the stress on the odontoblastic function such as the heat-shock treated fibroblasts.

Animals↗
PubMed1989

Ultrastructure of a new generation of odontoblasts in grafted coronal tissues of mouse molar tooth germs.

Third molar tooth germs were removed from 14-day-old mice and freed from the enamel organ and follicle. After section of the apical tissues, including Hertwig's sheath, they were transplanted in 1-day-old newborn mice of the same lineage. Electron microscopy of grafts removed 7, 14 and 21 days later showed that, following the disappearance of the initial layer of odontoblasts and a period of adaptation, 14 days after transplantation newly differentiated odontoblasts deposited tubular dentine. The dentine matrix production was increased over that of controls, demonstrating that synthesis was accelerated, possibly because of lack of nerves in the grafts. Numerous characteristic structures that might be involved in the transit of proteoglycans from the Golgi apparatus were seen, as far as the extremity of the odontoblast processes. The particular experimental conditions allowed the observation in the neck region of the odontoblast of a concentration of coated vesicles which might be involved in cellular lengthening. Thus, in the presence of a fine and regular vascular network, a new generation of odontoblasts may differentiate, even in the absence of epithelial and nervous elements, and so predentine may contain inductive factors that allow the odontoblastic differentiation of pulp cells in contact with it.

Animals↗
PubMed1990

Autoradiographic analysis of odontoblast replacement following pulp exposure in primate teeth.

Cell migration and replication associated with odontoblast replacement occurring soon after pulp exposure in primate teeth were studied. Class 5 cavity preparations resulting in pulp exposures were restored with a calcium hydroxide-containing capping agent and amalgam. Eighty-four and 96 h after this the animals were injected with 0.5 microCi/g body wt tritiated thymidine (sp. act. 6.7 Ci/mM). Teeth were extracted 6, 8, 10 and 12 days after treatment. The number of labelled cells as well as the number of grains per labelled cell were counted for odontoblast-like, fibroblast-like and perivascular cells in three 60 x 260 microns zones. These zones represented the odontoblast and cell-free (zone 1), cell-rich (zone 2) and deep pulp (zone 3) areas of normal pulp tissue. Ten sections centred around the mid-point of the exposure were counted for each tooth. Matrix formation and labelled odontoblast-like cells were observed at the interface between the capping agent and the pulp as early as day 8. Other significant findings were: (1) an increase in labelled odontoblast-like cells in zone 1 over time, suggesting a continual influx of differentiating cells; (2) an increase in labelled cells in zone 1 over time with a concurrent decrease in zone 3, suggesting that the influx of cells in zone 1 was from the deeper pulp; and (3) differences in grain counts between zones, treatment times and cell types, indicating that at least two DNA replications had occurred between initial treatment and final odontoblast-like cell differentiation.

Animals↗
PubMed1978

Acute and protracted effects of vinblastine on odontoblasts and dentinogenesis in rat incisors.

The effects of a large dose of vinblastine sulfate (2 mg/kg body weight) on proliferating odontoblast precursors and secretory odontoblasts in the continuously growing rat incisor were studied. The rats were killed 6 h, 24 h, 3 d and 7 d after vinblastine injection. Most cells in the proliferating zone contained arrested mitoses, or had perished after 24 h. After 3 and 7 d, the odontoblasts derived from this zone were reduced in number, and showed altered cell shapes. The odontoblasts had produced irregular dentin. The secretory odontoblasts had displaced nuclei and altered cell shapes after 24 h. Those most affected were opposite early mineralized dentin. In some incisors the cells had perished. In the protracted experiments almost all the odontoblasts were changed and had produced abnormal dentin. In the early mineralized dentin area, accumulations of cells were present after 3 d, and osteodentin-like material after 7 d.

Animals↗
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↗
PubMed1992

A permeability barrier to lanthanum and the presence of collagen between odontoblasts in pig molars.

Previous experiments in rat incisors indicate that the odontoblasts form an impermeable barrier which prevents fluid movement between pulp and dentine. The permeability of the odontoblast layer has now been investigated in pig molars which are more analogous to human teeth. The heads and necks of anesthetised piglets were perfused intra-arterially with lanthanum nitrate in Ringer's solution or with Ringer's solution alone. Molar tooth germs were removed, sliced, fixed by immersion and embedded in resin. Ultrathin sections including pulp and dentine were examined by transmission electron microscopy. Fenestrated capillaries were permeable to the electron dense lanthanum which thus entered the extracellular space between the odontoblast cell bodies. The lanthanum was excluded from predentine indicating that a barrier to permeability is present. In the above specimens and in others from 2 animals which were fixed by perfusion fixation, longitudinally oriented bundles of collagen fibrils were found passing from dentine through predentine into the odontoblast layer. Longitudinal collagen was also present between odontoblast cell bodies and entering the pulp at their basal ends. This suggests that classical von Korff fibres are present during primary circumpulpal dentinogenesis. In some sections longitudinally oriented collagen was absent. The junctions showed features of classical tight junctions but open tight junctions containing longitudinal collagen were also observed, suggesting that the junctions may modulate. Despite a trace of evidence that lanthanum can leak through adjacent to longitudinally penetrating collagen we concluded that the biological permeability barrier is maintained. The presence of the barrier indicates that other than the longitudinal collagen fibrils of which the source is unknown, all molecules incorporated into dentine are deposited there by the odontoblasts. An advantage of the barrier may be that it provides a closed environment for the orderly process of matrix deposition and mineralisation of dentine.

Animals↗
PubMed1992

Calcium transport in dentinogenesis. An experimental study in the rat incisor odontoblast.

Since cellular calcium transport mechanisms during biological calcification are less known, a series of experiments were performed by in vivo as well as in vitro methodologies in the dentinogenically active rat incisor. By means of micro-electrode technique, the pH and pCa (calcium ion activity) in predentin in situ were found to be 7.0 and 2.9, respectively. It was concluded that there exists a Ca2+ion concentrating mechanism over the odontoblast layer in direction towards the mineralization front. The kinetics of this calcium flow was determined in vivo by radiotracer technique. The time for 45Ca2+ uptake into the dentin mineral phase was determined to 10-15 min. Transmembraneous Ca2+ ion pumps and channels in odontoblasts were further analyzed. The resting membrane potential of rat incisor odontoblasts was determined to -24 mV. Using ion-specific mini-electrode technique as well as fluorescence spectrophotometry, calcium channels, Ca(2+)-ATPase and Na+/Ca2+ antiports, responsible for cellular Ca2+ uptake and extrusion, were identified in the odontoblast plasma membrane. Dissected odontoblasts were subjected to subcellular fractionation. An electrophoretic uniporter and a Na2+/Ca2+ exchanger, for Ca2+ release and uptake, respectively, were demonstrated in mitochondria, whereas a Ca(2+)-ATPase was present in the microsomal fraction. Mitochondria, microsomes and whole, digitonin-permeabilized odontoblasts, were able to maintain a steady state Ca2+ activity at pCa = 6.4-6.6 in vitro. In rats treated with colchicine, the incorporation of 45Ca2+ into dentin mineral was severely altered. Similarly, administration to rats of specific calcium channel blockers strongly inhibited 45Ca2+ incorporation. Together, the results indicate that a transcellular pathway is a major route for Ca2+ ion transport during dentinogenesis, and that this may be under a relatively strict cellular control.

Animals↗
PubMed1992

Odontoblast response under carious lesions.

The local regulation of odontoblast response to caries is viewed through initiation and elaboration of sclerotic as well as reparative dentin. Dentin tissue represents a multiple source of potent environment factors when teeth are affected by the demineralization phases of carious process. Some of them have already been identified in sound tissue (matrix glycoproteins, proteoglycans, growth factors, Bone Morphogenetic Protein) and may act on the cell through membrane receptors. Thus, the amplification in collagen synthesis and alkaline phosphatase activity previously observed during sclerotic dentin deposition can be related to the interaction between matrix signals and cell receptors such as the 165 kDa protein shown only by odontoblasts under the affected zone. Similarly, under established lesions generating cell death, the specific matrix made of odontoblasts debris and damage tissues, probably rich in active molecules, may trigger pulp cells to elaborate a cartilage-like layer (identified by type II and XI collagen) followed by odontoblast-like cells to give rise to abnormal tubular dentin. Here, odontoblast response is identical to bone-cells response to injury. What remains to be elucidated concern: The nature of signals found in carious dentin (matrix components, growth factors, bacterial products). The nature and regulation of expression of cell membrane receptors during tooth repair. How the odontoblast produces specific responses to each of these signaling molecules will be the focus of important new investigations.

Cell Differentiation↗
PubMed1978

Odontoblast alkaline phosphatases and Ca2+ transport.

The same isoenzyme of nonspecific alkaline phosphatase (APase), assayed with p-nitrophenylphosphate (p-NPP), was shown be present in different calcifying tissues, bone, calcifying cartilage, odontoblasts and enamel organ. Indications were also found that the enzymatic degradation of inorganic pyrophosphate (PPi) in calcifying tissues is mediated by APase. By using specific APase inhibitors, it was shown that two enzymes capable of degrading ATP exist. These were characterized in dentinogenically active odontoblasts, and it was concluded that one is the classical APase, the other is a Ca2+ and Mg2+ activated ATPase, named Ca2+-ATPase. The two phosphatases were solubilized from odontoblasts and separated. The localization of APase and Ca2+-ATPase in odontoblasts was investigated by subcellular fractionation and EM histochemistry. Routine methods for fixation were found to almost completely inactivate the enzymes. By using a mild fixation technique that preserved 80% of the enzyme activity, the main localization for both APase and Ca2+-ATPase was found to be in the membranes of intercellular vesicles located in the cell body and odontoblasts process. No activity was found in the cell membranes. It is concluded that there are at least two enzymes able to degrade phosphate compounds at alkaline pH in hard tissue forming cells. One is the nonspecific alkaline phosphatase (APase; EC 3. 1. 3. 1), which is active against p-NPP, PPi, glycerophosphates and ATP among other substrates. The other is a more specific Ca2+-ATPase (EC 3. 6. 1. 3). There seems to be an intimate relation between these two enzymes in the tissue. The function of APase in biological calcification is still obscure. In contrast, the finding of an ATP dependent, intravesicularly directed, transmembranous Ca2+-transport in vesicles derived from the microsomal fraction of odontoblasts may explain the role of Ca2+-ATPase.

Alkaline Phosphatase↗
PubMed1977

[Histoautoradiographic studies on protein synthesis by odontoblasts].

The protein-producing function of the odontoblasts was studied in 120 Wistar rats with an initial weight ranging from 30 to 40 g determining the rate of the migration of radio-active isotopes (glycine-2-14C, lysine-1-14C) from the odontoblasts to the predentine. The odontoblasts exert a protein-synthetizing function and play an active part in predentine formation. Under the influence of a cariogenic saccharose-casein diet and the simultaneous induction of experimental caries, the intensity of the migration of the labelled amino acids from the odontoblasts to the predentine increases during the first and second stages of caries, which must be interpreted as an increase of the protein-synthetizing function of the odontoblasts associated with an intensification of dentinogenesis. During the third stage of caries, the protein-producing function of the odontoblasts decreases.

Animals↗