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PubMedDate not supplied

Histopathological study on the PTHrP-induced incisor lesions in rats.

Parathyroid hormone related peptide (PTHrP) was discovered as a causative factor of humoral hypercalcemia of malignancy (HHM). The present study elucidates the histopathological characters of incisor lesions in the HHM rat model. Nude rats were implanted with PTHrP-expressing tumor (LC-6) cells, maintained for 12 weeks, after which the mandibular incisors were collected. Incisor fractures were observed grossly. Microscopically, hypercalcified dentin, dentin niche with osteodentin, and thinning of dentin were observed. Hypercalcified dentin was observed as a basophilic line of calcified dentin without associated odontoblastic changes, whereas dentin niche and thinning of dentin occurred with osteodentin and loss of cell height, respectively. In contrast with hypercalcified dentin, which was distributed throughout the dentin, dentin niche and thinning of dentin were localized to the labial area of the apical and middle region, and to the labial and lingual areas of the middle and incisal region, respectively. These results suggest that hypercalcemia affected the entire calcification process resulting in hypercalcified dentin, and that high PTHrP concentrations affected selective populations of odontoblasts resulting in formation of dentin niche and thinning of dentin. The localization of dentin niche and thinning of dentin also suggest that PTHrP may also be involved odontoblastic development in the rat.

Animals↗
PubMed2005

Histopathological study of time course changes in PTHrP-induced incisor lesions of rats.

Parathyroid hormone related peptide (PTHrP) was discovered as a causative factor of humoral hypercalcemia of malignancy (HHM). In the present study using HHM model rats, the time course of odontoblastic response to PTHrP and its relation to incisal fracture were elicited. Nude rats were implanted with PTHrP-expressing tumor (LC-6) cells, mandibular incisors were collected at several time points. Microscopically 3 distinctive types of odontoblastic/dentin lesions were observed. Hypercalcfied dentin, which was reported as hypercalcemia-induced lesion in previous reports, observed in all areas of the dentin from week 5-10 samplings. Dentin niche, observed solely in week-10 sampling point, exhibited a nature identical to that of reparative odontoblast reported in the literatures of various cytotoxic agents. Since cytotoxicites were neither observed prior to the lesions nor reported as a role of PTHrP, the reparative response may have derived from highly sustained levels of PTHrP. Loss of columnar odontoblasts height was initially observed at week-5 time point in the middle section of the incisor. This primary loss of cell height prior to incisor fracture was considered to be the earliest response to the increased PTHrP levels of this model.

Animals↗
PubMed2002

Col1a1-GFP transgene expression in developing incisors.

Previous studies have shown that terminal differentiation of odontoblasts is accompanied by dramatic increases in type I collagen synthesis. Recently transgenic mice in which green fluorescent protein (GFP) expression is under the control of the rat 3.6 (pOBCol3.6GFPtpz) and 2.3 (pOBCol2.3GFPemd) Col1a1 promoter fragments were generated. Our analysis of these GFP-expressing transgenic mice shows that the 2.3-kb promoter fragment directs strong expression of GFP only to bones and teeth, whereas the 3.6-kb fragment of promoter directs strong expression of GFP in bone and tooth, as well as in other type I collagen producing tissues. Our observations of incisors in these transgenic mice show high levels of GFP expression in functional odontoblasts and in differentiated osteoblasts. These observations show that expression of GFP reporter genes closely follow the patterns of expression of alpha 1(I) collagen in various tissues including odontoblasts.

Aging↗
PubMed1987

Comparison of growth and cell proliferation kinetics during mouse molar odontogenesis in vivo and in vitro.

The growth of embryonic first lower mouse molars in vitro was slow and reduced in comparison with in vivo development: the volume of teeth removed on day 15 and 16 of gestation and cultured for 6 days did not exceed the volume reached at day 18 in vivo. The volume of teeth removed on day 17 and 18 and cultured for 6 days either remained constant or decreased. The appearance of post-mitotic odontoblasts and ameloblasts was delayed in vitro. This behaviour might be correlated with a lengthening of the cell cycle (Tc). In vitro, the average durations of Tc (established by the percentage labelled mitoses technique) were 17.4-20.2 hr and 19.1-19.4 hr for pre-odontoblasts and pre-ameloblasts respectively. In vivo, the corresponding Tc values were 13.9 hr and 13.5 hr. The coordination of mitotic activities of pre-odontoblasts and pre-ameloblasts existing in vivo was maintained in vitro, and therefore seemed to require intra-dental control mechanisms. Non-specific extra-dental serum factors may affect the duration of Tc.

Ameloblasts↗
PubMed1996

Expression of heat shock protein 27 in adult human third molar dental pulp.

This study is the first to define the expression of hsp 27 in the pulp of the adult human third molar. Using a monoclonal antibody against human hsp 27, immunoreactivity was demonstrated in the odontoblasts, odontoblast processes, pulp fibroblasts, and smooth muscle and endothelial cells of vessel walls. Nerves were negative. Pulp fibroblasts were characterized by cytoplasmic staining and variable nuclear staining. Odontoblasts also displayed consistent cytoplasmic staining and variable nuclear staining. Western, Northern, and RT-PCR analysis confirmed the expression of hsp 27 mRNA and protein. Hsp 27 was also shown to be present in both the unphosphorylated and phosphorylated isoforms. In general, nuclear localization and phosphorylation of hsp 27 has been correlated with cells responding to stress or other stimuli. This study demonstrates that pulp from a single human third molar provides sufficient material to support a detailed molecular analysis of gene expression.

Adult↗
PubMed1975

Pulp reactions in human teeth to tooth colored filling materials.

In each of 49 intact premolars from children between 9 and 15 years of age, one buccal and one lingual cavity were prepared. The 98 cavities were filled with either Silicap, Sevriton Simplified or Adddent XV. After 2 weeks 19, and after 6 months 30 of the teeth were extracted. The histologic investigation included remaining dentin, reduction in the number of odontoblasts, inflammatory cells, necrosis, tertiary dentin and bacteria. After 2 weeks a loss of odontoblasts and inflammation was seen beneath two-thirds of the cavities, and small necrotic areas in 11 of the 38 instances. After 6 months the loss of odontoblasts was a little more pronounced, the inflammation a little less, and necrosis could not be observed. Tertiary dentin was registered beneath most of the cavities after 6 months. The reactions to the three filling materials were quite similar in quality and quantity. The amount of remaining dentin influenced the degree of inflammation and amount of tertiary dentin after 6 months beneath cavities filled with Silicap, and inflammation after 2 weeks and 6 months beneath Addent. Bacteria were observed in nearly all cavities 6 months after the treatment.

Adolescent↗
PubMed1982

Autoradiographic visualization of glycoproteins and glycosaminoglycans in the epithelio-mesenchymal interface of developing mouse tooth germ.

The turnover of basement membrane macromolecules during tooth morphogenesis and odontoblast differentiation was examined by light microscopic autoradiography using 3H-fucose, 35S-sulfate and 3H-glucosamine. Marked incorporation into the basement membrane was found throughout the progressive development. Pulse-chase experiments and prelabeling of tissue components indicated that glycoproteins and glycosaminoglycans in the dental basement membrane are mainly derived from the enamel epithelium. During odontoblast differentiation, incorporation was increased at the epitheliomesenchymal interface at the site of differentiating mesenchymal cells. From these sites the label also disappeared rapidly. This suggests that the active remodeling of extracellular matrix is related to odontoblast differentiation.

Animals↗
PubMed1998

Basement membrane-like structures occurring on the surface of dental papilla mesenchymal cells during odontogenesis in the monkey Macaca fuscata.

The aim of this study was to examine the nature of a basement membrane-like structure occurring along the surface of dental papilla cells during odontogenesis. The tooth germs of Japanese macaques (Macaca fuscata) were prepared for both ultrastructural and immunohistochemical studies. Characteristic discrete structures which resembled basement membranes were observed along the surface of the dental papilla cells, preodontoblasts, and also of the odontoblasts. Immunoperoxidase staining showed that these structures contained major basement membrane components including laminin, heparan sulfate proteoglycan, type IV collagen, as well as fibronectin. They tended to be less prominent along dental pulp fibroblasts and fully developed odontoblasts in comparison with those along the papilla cells localized close to the basement membrane of the inner enamel epithelium. Therefore, possible roles of these basement membrane-like structures would be: 1) to support the cells, 2) to momentarily secure the appropriate positions of differentiating mesenchymal cells, and 3) to regulate epithelial-mesenchymal interactions for odontoblast differentiation.

Animals↗
PubMed2004

New insight into progenitor/stem cells in dental pulp using Col1a1-GFP transgenes.

In recent years there has been increasing progress in identifying stem cells from adult tissues and their potential application in tissue engineering. These advances provide a promising future for tooth replacement/regeneration. Essential for this approach is the identification of donor stem cells for various components of the teeth. Our studies show that pOBCol3.6GFPtpz and pOBCol2.3GFPemd transgenic animals provide a unique model to gain insight into stem cells in the dental pulp. Our in vivo studies of the developing teeth of these transgenic lines show both Col1a1-GFP transgenes are expressed in functional and fully differentiated odontoblasts. The patterns of expression of Col1a1-GFP transgenes during odontoblast differentiation correlates with the expression of DSPP. In the developing craniofacial bones both Col1a1-GFP transgenes are also expressed in osteoblasts and osteocytes of alveolar and calvarial bones. In the alveolar bones, the expression of Col1a1-GFP in osteocytes correlates with the expression of DMP1. Col1a1-3.6-GFP is expressed in the entire layer of the periosteum and in suture mesenchyme containing osteoprogenitor cells. On the other hand, Col1a1-2.3- GFP expression was limited to the osteoblastic layer of the periosteum and was not detected in the fibroblastic layer of the periosteum or in the suture mesenchyme. These observations indicate that Col1a1-3.6-GFP and Col1a1-2.3-GFP transgenes identify different subpopulations of cells during intramembranous ossification. By using the coronal portion of dental pulps isolated from postnatal transgenic mice our observations also provide direct evidence that the dental pulp contains progenitor/stem cells capable of giving rise to a new generation of odontoblast-like cells, as well as osteoblast-like cells.

Ameloblasts↗
PubMedDate not supplied

Delineation of somatic nerve endings in rat teeth by radioautography of axon-transported protein.

We have shown that there is extensive innervation of cusp pulp and dentin in rat molars. The dental nerves either end freely below the odontoblast layer or form gap junction endings on the odontobast cell body or along its dential process. The nerves are largely absent from response dentin, are found in contact with virtually all other odontoblasts at the tip of the cusps, are less frequent in intercuspal regions, and are absent from root dentin and odontoblast layers. The incisors were completely different from the molars, perhaps because they are continuously erupting teeth. The distribution of nerve endings in rat molars may be representative of that in teeth of other species, but the nerve endings should be mapped radioautographically for each type of tooth before generalizations can be made.

Animals↗
PubMed1985

Differentiation of pulpal cells and inductive influences of various matrices with reference to pulpal wound healing.

Based on recent literature, the dynamics of mesenchymal cells in transplantation of various tissues and matrices, as well as the origin of new odontoblasts which participate in the formation of the dentin bridge, are described. Experiments involving implantation of pulp, periosteum, perichondrium, treated dentin, and bone matrices were performed to emphasize the capability of these cells to produce hard tissue. Light and electron microscopic and autoradiographic studies were carried out to clarify the origin of replacement odontoblasts. It appears that the pulp cells, endothelial cells, and pericytes become undifferentiated mesenchymal cells following pulp exposure. These mesenchymal cells differentiate into odontoblasts, which subsequently produce a dentin matrix. Pulp tissues autografted to non-pulpal sites, elaborated bone (or osteodentin) matrix, but they did not graft to tubular dentin. An experiment on dentin bridge formation, using germ-free rats, demonstrated that the pulp tissue has intrinsic healing potential. Therefore, it was concluded that the ability of pulp tissue to elaborate hard tissues depends on its environment.

Animals↗
PubMed1994

Induction of dentin formation on canine amputated pulp by recombinant human bone morphogenetic proteins (BMP)-2 and -4.

Dental pulp cells have the potential to differentiate into odontoblasts. The molecular mechanisms underlying differentiation are not clear. Demineralized dentin matrix is osteoinductive and contains bone morphogenetic protein (BMP) activity. BMPs have been implicated in embryonic odontogenic differentiation and hence may play a role in the differentiation of adult pulp cells into odontoblasts during pulpal healing. This study examined the hypothesis that BMPs induce dentin formation on amputated canine pulp. Recombinant human BMP-2 and BMP-4 were capped with inactivated dentin matrix on amputated pulp. At two months, the amputated pulp was filled with tubular dentin in the lower part and osteodentin in the upper part. The amount of dentin formed was markedly diminished when dentin matrix alone was implanted. These findings imply that recombinant human BMP-2 and BMP-4 induce differentiation of adult pulp cells into odontoblasts. Thus, BMPs may have a role in dentistry as a bioactive pulp-capping agent to induce dentin formation.

Animals↗
PubMed1999

Temporal and spatial expression of c-jun and jun-B proto-oncogenes in pulp cells involved with reparative dentinogenesis after cavity preparation of rat molars.

c-jun and jun-B are nuclear proto-oncogenes induced by growth factors such as bone morphogenetic proteins (BMPs). These gene products enhance the expression of many genes, including osteocalcin and collagen types, indicating that c-jun and jun-B play important roles in the cell differentiation process. It is also known that BMPs affect the differentiation of pulp cells to odontoblast-like cells during reparative dentinogenesis, but little is known about the transcriptional regulation of genes in cells associated with reparative dentinogenesis. In this study, we examined the expression of c-jun and jun-B in pulp cells during reparative dentinogenesis after cavity preparation of rat molars by in situ hybridization. In rat tooth germs, c-jun and jun-B were co-expressed in the odontoblastic lineage. In rat adult molars, c-jun was expressed in the odontoblast layer, but the jun-B expression was absent in all pulp cells. After cavity preparation, we found that c-jun and jun-B were coexpressed in pulp cells underneath cavities. During the early phase of reparative dentinogenesis, levels of c-jun and jun-B greatly increased in pulp cells within and around the reparative dentin matrix formed adjacent to the cavity floor. Fourteen days after cavity preparation, c-jun and jun-B were expressed only in pulp cells lining the irregular surface of the thick reparative dentin. These results suggest that c-jun and jun-B may play important roles both in physiological and in reparative dentinogenesis; in particular, the limited distribution of the jun-B expression suggests a specific role of jun-B only in cells involved with the active formation of the dentin matrix during primary and reparative dentinogenesis.

Animals↗
PubMed2004

Immunolocalization of BMP-2/-4, FGF-4, and WNT10b in the developing mouse first lower molar.

Intercellular signaling controls all steps of odontogenesis. The purpose of this work was to immunolocalize in the developing mouse molar four molecules that play major roles during odontogenesis: BMP-2, -4, FGF-4, and WNT10b. BMP-2 and BMP-4 were detected in the epithelium and mesenchyme at the bud stage. Staining for BMP-2 markedly increased at the cap stage. The relative amount of BMP-4 strongly increased from E14 to E15. At E15, BMP-4 was detected in the internal part of the enamel knot where apoptosis was intense. In contrast to TGFbeta1, BMP-2 and -4 did not show accumulation at the epithelial-mesenchymal junction where the odontoblast started differentiation. When odontoblasts became functional, BMP-2 and BMP-4 were detected at the apical and basal poles of preameloblasts. BMP-2, which induces ameloblast differentiation in vitro, may also be involved physiologically. The decrease in FGF-4 from E14 to E15 supports a possible role for the growth factor in the control of mesenchymal cell proliferation. The relative amount of FGF-4 was maximal at E17. The subsequent decrease at E19 showed correlation with the withdrawal of odontoblasts and ameloblasts from the cell cycle. WNT10b might also stimulate cell proliferation. At E14-15, WNT10b was present in the mesenchyme and epithelium except for the enamel knot, where the mitotic activity was very low. At E19 there was a decreasing gradient of staining from the cervical loop where cells divide to the tip of the cusp in the inner dental epithelium where cells become postmitotic. The target cells for FGF-4 and WNT10b appeared different.

Ameloblasts↗
PubMed2001

The effect of TGF-beta 2 on dentin apposition and hardness in transgenic mice.

Transforming growth factor beta, TGF-beta, is expressed during tooth formation and can induce pre-odontoblast differentiation and formation of functional odontoblast-like cells in vitro. In addition, exogenous TGF-beta can increase reparative dentin formation, presumably by acting on odontoblasts. In this study, we examined the tooth phenotype of transgenic mice, in which TGF-beta 2 expression is directed by the osteocalcin promoter. Previous studies have shown that these mice have a bone phenotype that resembles that of human osteoporosis, including the existence of spontaneous fractures. Microhardness testing of the enamel and dentin showed no differences in the molars of these transgenic mice as compared with those of their wild-type littermates. Consistent with the increase in bone mineral apposition rate previously reported in these mice, the dentin apposition rate appeared to be increased in the TGF-beta 2-overexpressing mice. Thus, in teeth, as in bone, TGF-beta 2 appears to stimulate the synthesis and deposition of matrix. Further studies are needed to understand the effect of TGF-beta 2 on distinct mineralized tissues (bone, dentin, and cementum) and to determine whether exogenous TGF-beta 2 may be useful for tooth repair.

Animals↗
PubMed2001

Dentin regeneration in vital pulp therapy: design principles.

The nature and specificity of the mechanisms by which the amputated dentin-pulp interface is therapeutically healed determine the properties of the barrier at this site and play a critical role in the outcome of vital pulp therapy. Healing of the dentin-pulp complex proceeds either by natural repair-which results in defensive hard-tissue formation, or therapeutically regulated dentin regeneration, which aims to reconstitute the normal tissue architecture at the pulp periphery. Progress in biomedical research opens new directions for the design of biologically effective pulp therapies. Application of biocompatible and biodegradable carrier vehicles for local delivery of signaling molecules in pulp-capping situations showed induction of fibrodentin/reparative dentin formation, but often at the expense of underlying pulp tissue. An alternative pre-clinical model aiming to reconstitute normal tissue architecture directly at the dentin-pulp interface should be designed on the basis of the direct induction of odontoblast-like cell differentiation and reparative dentin formation at the pulp-capping material interface. Experimental data clearly showed that pulpal cells can differentiate directly into odontoblast-like cells in association with specific extracellular matrices (dentinal or fibrodentinal matrix) or TGF beta 1-containing artificial substrates. Dentin-induced dentinogenesis can be used as a master plan for the achievement of new therapeutic opportunities. In the present study, several short-term experimental studies on dog teeth for potential direct induction of odontoblast-like cell differentiation at the surface of rhTGF beta 1-containing artificial substrates (Millipore filters, hydroxyapatite granules, calcium hydroxide, pure titanium) failed to induce any specific reparative dentinogenic effects.

Animals↗
PubMed2003

Patterns of fluoro-gold entry into rat molar enamel, dentin, and pulp.

Permeabilities of enamel and dentin are not fully understood despite their importance for caries, restorative materials, and pulp-dentin-enamel interactions. We have found that Fluoro-Gold is useful for examining tooth permeability, and we designed studies to test the effects of aging, injury, neural function, and dentinal repair on its influx into vital rat teeth. We used fluorescence microscopy and immunocytochemistry to show that Fluoro-Gold rapidly penetrates enamel, the dentin-enamel junction, and outer dentinal acellular tubules, and then concentrates in odontoblasts, where it remains for weeks. As predicted, influx was greatest in immature teeth, and formation of reparative dentin impeded it. We expected that denervation would disrupt influx, because of neural regulation of dentinal fluid movement, but it did not. Damage to odontoblasts under injured dentin caused increased influx and efflux of Fluoro-Gold. Analysis of our data suggests that permeabilities of enamel and dentin to Fluoro-Gold are age-related, inter-dependent, and regulated by odontoblasts.

Aging↗
PubMed2004

Dentin regeneration by dental pulp stem cell therapy with recombinant human bone morphogenetic protein 2.

Regenerative medicine is based on stem cells, signals, and scaffolds. Dental pulp tissue has the potential to regenerate dentin in response to noxious stimuli, such as caries. The progenitor/stem cells are responsible for this regeneration. Thus, stem cell therapy has considerable promise in dentin regeneration. Culture of porcine pulp cells, as a three-dimensional pellet, promoted odontoblast differentiation compared with monolayers. The expression of dentin sialophosphoprotein (Dspp) and enamelysin/matrix metalloproteinase 20 (MMP20) mRNA confirmed the differentiation of pulp cells into odontoblasts and was stimulated by the morphogenetic signal, bone morphogenetic protein 2 (BMP2). Based on the in vitro experiments, an in vivo evaluation of pulp progenitor/stem cells in the dog was performed. The autogenous transplantation of the BMP2-treated pellet culture onto the amputated pulp stimulated reparative dentin formation. In conclusion, BMP2 can direct pulp progenitor/stem cell differentiation into odontoblasts and result in dentin formation.

Animals↗