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Origin, cell kinetics, and phenotypic aspects of odontoblast cell lineage are described. Epithelial-mesenchymal interactions regulate odontoblast differentiation. These interactions appear to be mediated by the extracellular matrix. Possible molecular mechanisms of cell-matrix interactions are discussed. Questions still unanswered are recommended for investigation.
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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.
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.
Developing first premolars were used as a model system to obtain information on the nucleolar structure of human odontoblasts at several stages of their life cycle. Four stages were defined by their location within the tooth: a) preodontoblasts were located at the growing tip of the root; b) secretory odontoblasts in the apical region; c) transitional odontoblasts in the middle region; and d) aged odontoblasts in the coronal region. Preodontoblasts have a small nucleolus (0.55 micron 2) with few strands of dense fibrillar material radiating from the fibrillar center. Secretory odontoblasts are characterized by a large (1.24 micron 2), irregular, and reticulated nucleolus. The fibrillogranular material, the largest component in all nucleoli, reaches maximal size at this stage (0.88 micron 2). Fibrillar centers occupy about the same area (0.1 micron 2) throughout the odontoblast's life cycle. As the formation of primary dentin is completed, the nucleolus of transitional odontoblasts is reduced in size (0.54 micron 2). Finally, the aged odontoblasts have a small, compact nucleolus (0.39 micron 2), with segregated components. Morphologic analysis and quantification of size and component areas of nucleoli obtained with an image analyzer indicated that secretory odontoblasts had the most active, and aged odontoblasts the least active, nucleolus.
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.
Although the rat incisor is used widely in the study of dentinogenesis there is little information on the pulp capillaries and the fate of the pulp contents incisally. The capillaries have now been described in relation to the life cycle of the odontoblasts using light microscopy on perfusion fixed teeth and SEM on pulp vascular casts. Odontoblast precursors differentiated to preodontoblasts in the absence of local vessels. Capillaries entered the zone subjacent to preodontoblasts prior to their transformation to odontoblasts. They invaded the odontoblast layer after formation of odontoblast processes and during lengthening of their cell bodies. These capillaries formed a dense plexus which was separated from the predentine by about 10 micron thickness of odontoblast cytoplasm. Electron microscopy near the incisal end showed that the odontoblasts lost their processes and their polarity to form postodontoblasts. This coincided with the deposition of atubular collagenous tissue at the periphery of the pulp. Loss of fenestrations in the capillaries seemed to coincide with the diminution of odontoblast function. Odontoblastic capillaries were lost before the postodontoblasts became separated from one another. There was evidence of degenerating vessels, cells and extracellular debris near the incisal end. Light and transmission electron microscopical evidence from demineralised teeth was correlated with SEM evidence from anorganically prepared specimens and considered in relation to dynamic events at the incisal surface. Thus the pulp closure region was found to include a central zone of mineralised, moribund pulp cells and debris surrounded by atubular tissue.
The relative roles of capillaries and odontoblasts in the process of dentinogenesis and in pulp reactions to trauma and pathology are not clear. Contributing to the problem is the paucity of information on odontoblast--capillary relationships and tight junctions between odontoblasts. Using light microscopy the capillaries have now been examined in semithin transverse sections of perfusion fixed teeth at different positions in the long axis from the apical foramina to the pulp horns. Odontoblastic capillaries were prominent in the coronal and middle regions of canines and present at the same levels of incisors. In the pulp horns and just coronal to the pulp horns capillaries were all subodontoblastic but near the apex there were also a few odontoblastic capillary profiles. Transmission electron microscopy on ultrathin sections revealed that a high proportion of middle and coronal odontoblastic capillary profiles were fenestrated but subodontoblastic profiles coronal to the pulp horns were the most fenestrated. In a search for tight junctions in ultrathin sections some typical strands were observed between odontoblasts. The difficult of obtaining the latter evidence was explained by the cellular arrangement of the odontoblasts which differed markedly from an ideal parallel, apically coplanar arrangement. The results question the possibility that there is a direct exchange of materials between pulp capillaries and dentine in teeth of limited growth and provide a baseline for future experiments to test the permeability of the odontoblast layer.
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.
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.
Actin filaments, intermediate filaments, and microtubules in the odontoblasts of rat incisors were investigated electron microscopically using heavy meromyosin and taxol. Actin filaments were abundant at the periphery of the odontoblast process in the form of a network or in bundles. In a branch of the odontoblast process, longitudinally oriented actin filament bundles were found. Most actin filaments were associated with the plasma membrane via electron-dense material which stained with tannic acid. The intermediate filaments had a diameter of 11 to 13 nm. They were distributed throughout the cytoplasm of odontoblasts. They ran lengthwise in the core of the odontoblast process, which showed a different distribution compared with that of actin filaments. Microtubules, which were disrupted after Triton X-100 but preserved by addition of taxol, tended to be associated with intermediate filaments. Such a relation was also seen in conventional preparations. Coated vesicles, which were abundant at the periphery of the odontoblast process, were often associated with actin filaments. Therefore, it is suggested that actin filaments, in the odontoblast process at least, play a role associated with the coated vesicles at the periphery of the process, and may be involved in coated vesicle transport.
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.
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.
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.
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.
Three stages during cell differentiation of rat incisor odontoblasts were classified, and change of microtubular arrangement around centrioles in the odontoblasts was examined with three-dimensional analyses using serial ultrathin sections. In the undifferentiated odontoblasts, microtubules were observed to radiate from the pericentriolar area, whereas, in the differentiating odontoblasts, some microtubules became poorly related to the centrioles. In the differentiated odontoblasts, arrangement of most microtubules appeared to have a poor relationship to the centrioles. Throughout the differentiation of the odontoblasts, one of the centriolar pair was ciliated, and Golgi apparatus was invariably observed near the centrioles. The present study suggests that a pericentriolar area, or a centrosome, could function as a microtubule-organizing center (MTOC) in the undifferentiated odontoblasts, but their function might be attenuated during cell differentiation.
A computerized histomorphometric method was devised to estimate the kinetics of odontoblast turnover and dentinogenesis in rat incisors. The method was applied to two groups of rats: one group with lower incisors in impeded eruption and another group with the left lower incisor in the unimpeded state. The teeth were divided into six equal segments, from which consecutive ground sections were obtained. The distance of each ground section from the posterior border of the alveolar bone was calculated. Each section was magnified, traced, and the tracings fed into a computer by a sonic digitizer. The perimeters and areas of dentine and pulp in each ground section were calculated by the computer. The mean odontoblast density along the predentine was evaluated from histological sections taken both from the same tooth segments and from teeth sectioned midsagittally. These served for the estimation of the predentine area occupied by the average odontoblast. In the impeded group, this area was 11% larger than in the unimpeded one. Outer dimensions of teeth, namely the circumference of the dentine, the labiolingual width, and the mesiolateral width remained constant and equal for both groups. Daily rates of dentine apposition were computed and were found to vary according to the age of the odontoblasts. Odontoblasts of impeded teeth started to secrete matrix at a rate of 17 microns/day, which increased slightly to 19 microns/day and later declined to 7 microns/day on the 38th day. Dentine production of unimpeded odontoblasts, on the other hand, started at a rate of 16 microns/day and gradually increased to 34 microns/day on the 17th day.(ABSTRACT TRUNCATED AT 250 WORDS)
Odontoblasts are known to be involved in the process of dentinogenesis but it is not clear whether substances may also be deposited in predentine and dentine by passing between these cells. Although tight junctions have been described, it is not clear if they are macular or "leaky" as opposed to continuous or "tight". In this study use has been made of the permeability of fenestrated capillaries amongst the odontoblasts to deposit the penetrative tracer lanthanum in the interodontoblastic space. This was done by perfusion of anaesthetized rats with physiological solutions containing lanthanum nitrate at 37 degrees C. Immersion fixation of transverse segments of mandibular incisors and examination with an electron microscope showed that lanthanum could permeate 40-50 microns between the odontoblasts to reach the peripheral pulp. Towards the predentine, often less than 10 microns from the capillaries, its progress was abruptly and completely halted by the junctions at the apical ends of the odontoblast cell bodies. Lanthanum was not found in the predentine. The mature secretory odontoblasts in the rat incisor have therefore been shown to be joined by continuous tight junctions. In the process of dentinogenesis this means that all substances deposited in predentine and dentine must arrive by passing through the odontoblasts.