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PubMed1982

Facts and hypotheses concerning the control of odontoblast differentiation.

Numerous studies using amphibians have demonstrated that preodontoblasts emerging from the dental papilla are derived from cranial neural crest cells [4, 12, 46, 64]. However this has not been established for mammals. The history of odonotogenesis begins during the early stages of cranial-facial development when the maxillary and mandibular processes processes develop. Continuous epithelio-mesenchymal interactions condition the histogenesis and morphogenesis of the teeth [24-26, 43, 44, 49, 51, 58] as well as the terminal differentiation of odontoblasts and ameloblasts [23, 47, 52, 54, 59, 61, 67]. During recent years a considerable amount of experimental data relating to differentiation of odontoblasts has been published. We summarize these data and attempt to integrate them in deductive hypothesis concerning the control of odontoblast differentiation.

Adenylyl Cyclases↗
PubMed1986

Localization of actin during differentiation of the ameloblast, its related epithelial cells and odontoblasts in the rat incisor using NBD-phallacidin.

Using NBD-phallacidin, which specifically binds to F-actin, we investigated changes in the localization of actin during the differentiation of ameloblasts, related epithelial cells and odontoblasts in rat incisors. In cryosections treated with NBD-phallacidin, intense fluorescence was observed in undifferentiated epithelial cells in the apical loop and at the proximal extremity of undifferentiated inner enamel epithelial cells. During differentiation, the distal extremity began to exhibit strong fluorescence. In cross-sections of secretory ameloblasts, the fluorescence took the form of polygons of uniform intensity at the proximal end, and of rectangles of non-uniform intensity at the distal end. At the distal end, the fluorescence was more intense at right angles to the long axis of the incisor. At the distal end, this pattern was established just before the appearance of the enamel layer. These patterns were maintained during the secretory stage of ameloblasts. The location, pattern and time of appearance of these sites were identical to those of the terminal webs in ameloblasts. NBD-phallacidin weakly labelled the peripheral cytoplasm of the cell body of ameloblasts, and also labelled Tomes' process. The cells forming the stratum intermedium were mainly labelled at their periphery (i.e. forming larger polygons), while the overlying epithelial cells exhibited labelling throughout their cytoplasm. Except for the terminal webs, the cell bodies of odontoblasts were weakly labelled throughout the period of differentiation. Young odontoblasts secreting predentin were first labelled on the terminal web, with the fluorescence becoming gradually more intense as the thickness of the dentin increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Actins↗
PubMed1990

High resolution scanning electron microscopy of the subplasmalemmal cytoskeleton in human odontoblasts.

The subplasmalemmal cytoskeleton in human odontoblasts was studied by high resolution scanning electron microscopy. The odontoblast layer was isolated and exposed to formaldehyde, glutaraldehyde, and OsO4 for some specimens, while the membraneous structures and soluble proteins in the dental tissue were removed by Zenker's solution and 1% OsO4 for other specimens, without further fixation of the remaining components. The cytoskeletal elements comprised a dense network of interlacing filaments of different diameters in the cell body. Most cytoskeletal elements were parallel to the axis of the cell processes situated inside the dentinal tubules. The appearance and orientation of the investigated subplasmalemmal cytoskeletal elements was unaffected by the choice of method. Both methods confirm the presence of a subplasmalemmal cytoskeleton in human odontoblasts.

Actin Cytoskeleton↗
PubMed2001

Primary and secondary induction of apoptosis in odontoblasts after cavity preparation of rat molars.

The death regulation of damaged pulp cells after cavity preparation is not well-known. In this study, we examined whether apoptosis is associated with the death regulation of damaged pulp cells. In normal rat molars, terminal deoxynucleotidyl transferase-mediated labeling (TUNEL)-positive cells were not observed. Just after surgery, odontoblasts under cavities were TUNEL-positive, and these signals disappeared in six hours. One day after surgery, we found the reappearance of TUNEL-positive cells in the subodontoblastic region under cavities, and positive signals disappeared in four days. Ultrastructure of TUNEL-positive cells showed characteristics typical of apoptotic cells. Phagocytosis of apoptotic cells by scavenger cells was also observed. By immunohistochemistry, we also found Bcl-2-positive odontoblasts one day after surgery. These results suggest that two waves of apoptosis are induced in odontoblasts after cavity preparation, and that apoptotic cells must be eliminated before the initiation of reparative dentinogenesis.

Animals↗
PubMed1986

Scanning and transmission electron microscopy of tubular structures presumed to be human odontoblast processes.

Tubular structures interpreted as being odontoblast processes can be observed with the scanning electron microscope (SEM) on fractured dentin surfaces which have been demineralized and treated with collagenase. To confirm the nature of these structures, SEM preparations exhibiting similar tubular structures were subsequently examined with the transmission electron microscope (TEM). Newly-erupted human third molars were fractured buccolingually with heavy-gauge industrial nippers or sectioned mesiodistally with a Leitz saw microtome and fixed in glutaraldehyde. The exposed dentin surfaces were decalcified to a depth of approximately 500 microns and then treated with bacterial collagenase. Half of the specimens were critical-point-dried and coated for SEM. The other half were post-fixed and processed for TEM. After examination by SEM, the specimens were embedded and thin-sectioned for TEM. SEM observations of both the fractured and cut surfaces of dentin showed tubular structures running from the surface of the pulp to the dentino-enamel junction. When the SEM preparations were examined with TEM, the tubular structures were seen to be the inner sheath of the peritubular matrix, not odontoblast processes. In the specimens directly processed for TEM, the structures lying inside the sheath could be visualized clearly. In the outer two-thirds of the dentin, the tubules were essentially empty. Well-defined odontoblast processes were seen lying inside the sheath only in the inner dentin.

Adolescent↗
PubMed1990

The crown odontoblasts of rat molars from primary dentinogenesis to complete eruption.

The involution of crown odontoblasts after primary dentinogenesis in teeth of limited eruption is discussed. The odontoblasts of rat first lower molars were analyzed morphometrically from the tenth day to the 40th day of age, i.e., from the late phase of primary dentinogenesis to complete eruption. All the organelles underwent atrophy, but at different rates. In particular, the membranes of the endoplasmic reticulum decreased progressively in surface area from day 10 to day 40, whereas those of the Golgi apparatus decreased significantly between day 10 and day 14, and then remained practically unchanged in size. The volume of the lysosome compartment never increased beyond that during primary dentinogenesis. The profile length of the endoplasmic reticulum in each observed cell section was taken as an estimate of secretory activity. At day 40, this organelle was smaller in approximately 95% of the cells than it had been in any cell at day 10. These results suggest that cell atrophy may occur without any increase in the degradation processes of the cytoplasmic components and that the organelles along the secretory pathway may have independent regulatory systems. In the odontoblasts, as in several types of secretory epithelial cells, only a small fraction of the cells is engaged in appreciable secretory activity. This occurs, however, when the overall activity of the same cell population is relatively low.

Analysis of Variance↗
PubMed1998

Localization of estrogen-receptor-related antigen in human odontoblasts.

Estrogen receptors have been demonstrated in many osteogenic cell lines. Recently, we showed that estrogen deficiency induced by ovariectomy caused enhanced dentin formation in adult rats, suggesting that estrogen receptors may be present in dental tissues. Nothing is known about estrogen receptors in human teeth. We used immunohistochemical staining and immuno-blotting to demonstrate the presence of estrogen receptors in human pulp and/or the pulpo-dentinal border. Unerupted human wisdom teeth were surgically removed, frozen in liquid nitrogen, and prepared for immunological studies. Western blot analysis with monoclonal antibodies specific for human estrogen-receptor-related antigens demonstrated an approximately 29-kDa clear double band in the material scraped from the predentin-odontoblast border and in the fluid that emerged into the pulpal chamber, evidently from the odontoblasts. A weaker double band was also present in pulpal tissue samples. By immunohistochemical staining, estrogen-receptor-related antigens were visualized in the predentinal-odontoblast region and in the pulpal blood vessels. Our results suggest the presence of estrogen receptors in human teeth, and thus the previously reported enhancement of the dentin formation in rats after ovariectomy may be mediated via these receptors.

Adult↗
PubMed2002

Odontoblasts enhance the maturation of enamel crystals by secreting EMSP1 at the enamel-dentin junction.

The temporal expression patterns and activity distributions of enamelysin and EMSP1, which are the major proteinases in immature enamel, were characterized. Extracellular matrix fractions from developing porcine incisors, individually comprised of predentin, dentin, and four secretory-stage enamel samples, including the highly mineralized enamel (HME) at the enamel-dentin junction (EDJ), were isolated, and their resident proteinases were identified by zymography. Soft-tissue fractions, which included cells from the extension site of enamel formation (ESEF), secretory- and maturation-stage ameloblasts, and odontoblasts, were characterized histologically and by RT-PCR for their expression of enamelysin and EMSP1. A significant finding was that EMSP1, expressed by odontoblasts, concentrates in the HME, but is not detected in predentin or dentin. We conclude that odontoblasts deposit EMSP1 via their cell processes into the deepest enamel layer, which facilitates the hardening of this layer and contributes significantly to the functional properties of the EDJ.

Ameloblasts↗
PubMed1979

Immunohistochemical localization of procollagens. II. Electron microscopic distribution of procollagen I antigenicity in the odontoblasts and predentin of rat incisor teeth by a direct method using peroxidase linked antibodies.

In an attempt to locate procollagen I in rats odontoblasts, antibodies raised in rabbits were purified by affinity methods and linked to peroxidase. They were then incubated with chopped slices from the growing end of rat incisor teeth. The antibodies binding to the antigens in the slices were visualized by reacting the peroxidase moiety with diaminobenzidine in the presence of hydrogen peroxide. The slices were then embedded in Epon and sectioned for ultrastructural study. Within odontoblasts, the immunostaining indicative of procollagen I antigenicity is moderate in rough endoplasmic reticulum cisternae, strong in spherical and cylindrical Golgi distensions, intense in secretory granules, and variable in lysosomal structures. In predentin, immunostaining is intense close to the odontoblast layer, but decreases gradually in a distal direction. Hence, procollagen I (and/or substances endowed with similar antigenicity such as pro alpha (I) chains and procollagen fragments) is present: 1) along the intracellular pathway of collagen precursors where its concentration gradually increases to reach a maximum in secretory granules; 2) in predentin, into which it is released from the granules for transformation into nonimmunoreactive collagen I; and 3) in lysosomal structures where some of it is hydrolyzed.

Animals↗
PubMed1990

Transcription of a mutant collagen I gene is a cell type and stage-specific marker for odontoblast and osteoblast differentiation.

The Mov13 allele of the mouse alpha 1(I) collagen gene carries a retroviral insert in its first intron and had been reported to be transcriptionally silent. We have recently shown, however, that this mutant gene is expressed in odontoblasts of transplanted teeth derived from homozygous and heterozygous carrier embryos. The expression of the Mov13 allele has now been followed throughout in vivo development of mandibular teeth and bone in heterozygous animals, by in situ hybridization with a probe that specifically recognizes transcripts of the mutant gene. We show that the onset of its transcription precisely coincides with the final differentiation of odontoblasts and the onset of dentinogenesis, i.e. on day E16 for the incisor and at birth for the first molar. The mutant allele is also transcribed in osteoblasts of mandibular bone, again starting precisely with the onset of osteogenesis (day E13/14). No other cells were seen to transcribe the mutant gene. By these criteria, transcription of the Mov13 allele constitutes a true differentiation marker for odontoblasts and osteoblasts. Expression of the mutant allele in these two specialized cell types, in contrast to its transcriptional block in all other mesodermal cells ('fibroblasts'), suggests tissue-specific differences in the regulation of the alpha 1(I) collagen gene.

Alleles↗
PubMed1999

Extracellular Ca2+ increases cytosolic free Ca2+ in freshly isolated rat odontoblasts.

Recent evidence suggests that extracellular Ca2+ may modulate cell function in mineralized tissue. To determine whether dentinogenic cells, in particular, are sensitive to extracellular Ca2+, fura-2 microfluorometry was used to monitor intracellular calcium levels in odontoblasts freshly isolated from rat incisor. In response to applications of 0.5-4.0 mM extracellular calcium (CaCl2), most odontoblasts (84%; 107/128) showed an increase in intracellular calcium. For the majority of these cells (70%; 75/107), the typical response was biphasic; there was an initial, transient increase in intracellular calcium which reached peak levels within 30-50 s and decayed rapidly, followed by a slower (> 300 s) recovery toward basal levels. In general, the response of these cells to calcium was repeatable and the mean calcium concentration for the half-maximal response was approximately 1.3 mM. This effect could be partially blocked by either 200 microM lanthanum, a nonspecific blocker of Ca2+ channels, or 20 microM dantrolene, a potent inhibitor of Ca2+ release from internal stores. Used in combination, lanthanum, and dantrolene nearly abolished the calcium response completely. In addition, this response was sensitive to the dihydropyridine-sensitive calcium channel blocking agent nicardipine (60 microM), indicating a role for voltage-gated calcium channels during these events. These results show that odontoblasts respond to external calcium through mechanisms involving both influx of external calcium as well as release of calcium from internal stores and suggest a role for extracellular calcium in regulating the function of these cells.

Animals↗
PubMed2003

Ca2+ signaling mediated by IP3-dependent Ca2+ releasing and store-operated Ca2+ channels in rat odontoblasts.

In the phospholipase-C (PLC) signaling system, Ca2+ is mobilized from intracellular Ca2+ stores by an action of inositol 1,4,5-trisphosphate (IP3). The depletion of IP3-sensitive Ca2+ stores activates a store-operated Ca2+ entry (SOCE). However, no direct evidence has been obtained about these signaling pathways in odontoblasts. In this study, we investigate the characteristics of the SOCE and IP3-mediated Ca2+ mobilizations in rat odontoblasts using fura-2 microfluorometry and a nystatin-perforated patch-clamp technique. In the absence of extracellular Ca2+ ([Ca2+]o), thapsigargin (TG) evoked a transient rise in intracellular Ca2+ concentration ([Ca2+]i). After TG treatment to deplete the store, the subsequent application of Ca2+ resulted in a rapid rise in [Ca2+]i caused by SOCE. In the absence of TG treatment, no SOCE was evoked. The Ca2+ influx was dependent on [Ca2+]o (KD = 1.29 mM) and was blocked by an IP3 receptor inhibitor, 2-aminoethoxydiphenyl borate (2-APB), as well as La3+ in a concentration-dependent manner (IC50 = 26 microM). In TG-treated cells, an elevation of [Ca2+]o from 0 to 2.5 mM elicited an inwardly rectifying current at hyperpolarizing potentials with a positive reversal potential. The currents were selective for Ca2+ over the other divalent cations (Ca2+ > Ba2+ > Sr2+ >> Mn2+). In the absence of [Ca2+]o, carbachol, bradykinin, and 2-methylthioadenosine 5'triphosphate activated Ca2+ release from the store; these were inhibited by 2-APB. These results indicate that odontoblasts possessed Ca2+ signaling pathways through the activation of store-operated Ca2+ channels by the depletion of intracellular Ca2+ stores and through the IP3-induced Ca2+ release activated by PLC-coupled receptors.

Animals↗
PubMed1983

Distribution and organization of odontoblast processes in human dentin.

The distribution and organization of odontoblast processes in young human dentin was examined with a scanning electron microscope. By applying the HCl-collagenase method, the extracellular matrix of dentin was almost completely removed, thereby exposing the odontoblast processes and their branches to direct observation. The odontoblast processes are located close to the dentinoenamel junction. In the middle and outer zones of dentin the processes bear numerous branches. Some of these appeared to bridge the space between the processes and connect them.

Child↗
PubMed1995

An immunocytochemical study of the routes of secretion of collagen and phosphophoryn from odontoblasts into dentin.

Polyclonal antibodies to rat incisor phosphophoryns and to the amino-telopeptide of the alpha1 (I)-chain of type I collagen were used to follow the pathways of movement of collagen I (COL1) and phosphophoryns (PP) from synthesis in the odontoblast to secretion into the mineralized dentin. The antibodies were detected at the transmission electron microscopic level by their reaction with Protein A-colloidal gold conjugates. Special care was given in specimen preparation to retention of maximal antigenicity during fixation while maintaining cellular and extracellular ultrastructure at the mineralization front (MF) in nondemineralized sections. Intracellularly, COL1 and PP were detected within the endoplasmic reticulum (ER), the Golgi (G) and secretory granules (SG). However, as determined by double-immunolabeling with different size gold particles the COL1 and PP were not found together within the same ER, G or SG compartments. PP was localized within the tubular ER, round-shaped transitional vesicles, the Golgi and in narrow asymmetric SG. These asymmetric SG were found in abundance in the odontoblastic process. PP secretion from these vesicles was near the MF at the predentin-dentin boundary. COL1 was localized within rosette form ER compartments, the Golgi and in large, distinctive SG. COL1 was deposited at the cell-predentin boundary. No COL1 SG were seen within the odontoblastic process near the MF. In the region of the MF, prior to mineralization, the PP was localized along the surfaces of the COL1 fibrils of the predentin. The mineral phase etched surfaces revealed both COL1- and abundant mineral-associated PP. These data support the hypotheses that, in dentin, the interaction between COL1 and PP may initiate crystal nucleation and that additional interactions between PP and the growing crystals may modulate the crystal growth pattern and crystal size.

Animals↗
PubMedDate not supplied

Extent of the odontoblastic process. Analysis by SEM and confocal microscopy.

BACKGROUND: Towards the middle of the eighteenth century, Tomes described membranous structures of cellular origin inside the dentinal tubules. Subsequent studies of the terminal segment of the odontoblasts have been controversial. According to Fusayama, this cellular process reaches as far as the junction; others, including Brännström, affirm that this process is present only in the inner third of the dentin. AIMS: The aim of the present study was to verify the exact length of the odontoblastic terminal segment with the aid of advanced confocal microscopy (CLSM) and high resolution field-emission scanning electron microscopy (FE-SEM). METHODS: Premolars due for extraction for orthodontic reasons, were used for this study; vestibular class V cavities about 2 mm in diameter and 3 mm in depth prepared and subsequently filled with IRM (Caulk Dentsply). All teeth were extracted after four weeks fixed and prepared for examination under SEM and CLSM. RESULTS: CLSM revealed cylindrical structures inside the tubules even in the absence of odontoblasts. SEM evidenced the presence tubular structures only in the inner third of the dentin (towards the pulp). CONCLUSIONS: Structures previously described as cellular processes can be identified as the lamina limitans of the peritubular dentin.

Bicuspid↗
PubMed1975

[Epithelial-mesenchymal interactions in the differentiation of odontoblasts and adamantoblasts].

In the present study we report experiments which indicate that the adamantal epithelium (inner dental epithelium) plays a specific role in the initiation of differentiation and in the initial maintenance of odontoblasts. The preodontoblasts do not differentiate in the pulps cultures alone or in association of pulps with no specific epithelium. The early stages in the process of odontoblasts differentiation are labile and dependent upon their environment. The odontoblasts and the ameloblasts cannot differentiate in advance in the isochronic and heterochronic associations. A previous maturation of these cells or of their environment is indispensable.

Ameloblasts↗
PubMed1975

[Functional morphology of the odontoblast cell].

The most highly differentiated cells of the dental pulp - odontoblasts, taken from normal and carious teeth of persons of various age groups were investigated by the aid of electron microscope. Aim of the investigation to determine the relationship between the fine structure and function. Ultrastructural investigation shows that odontoblasts beside the 1) production of dentin take part in the 2) transport of substances and 3) tissue fluids. In the beginning and continuous promoting of the 4) crystallization of the enamel layers odontoblasts play a role of a border-surface which provide a necessary concentration 5) On the end part of nerve fibres they may function as supporting cells (replacement of the Schwann-cells). 6) When pathological processes present (caries) the ultrastructure shows cell-activity of defence type.

Amelogenesis↗
PubMed2002

[Transforming growth factor beta(1) and bone morphogenetic protein 2 induce the differentiation of odontoblasts in vitro].

OBJECTIVE: To investigate the effects of transforming growth factor beta(1) (TGF-beta(1)) and bone morphogenetic protein 2 (BMP2) combined with heparin on odontoblast differentiation. METHODS: Trypsin-isolated dental papillae from day 17 mandibular first molar were cultured in semisolid-agar medium for 6d. Recombinant human TGF-beta(1) and BMP2 combined with heparin were added to the medium. RESULTS: TGF-beta(1) and BMP2 combined with heparin induced differentiation of odontoblasts and promoted matrix secretion. Odontoblast differentiation never occurred when TGF-beta(1) or BMP2 were added alone to the medium, whereas an increase in extracellular matrix production was observed. CONCLUSION: These results demonstrate that both TGF-beta(1) and BMP2 stimulate the cytological and functional differentiation of preodontoblasts, and that heparin might play important role as a substrate.

Animals↗