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PubMed1981

Collagen type I trimer synthesis by cultured embryonic mouse molars.

Embryonic mouse tooth germs were cultured in vitro and the collagens type I, type III and type I trimer were purified and biochemically characterized. Collagen type I trimer has been identified by means of CM-cellulose chromatography, CNBr peptide analysis, pepsin resistance and molecular sieve chromatography. Already before the odontoblasts were functional, this molecule was found to be a constituent of the dental extracellular matrix. However, the synthesis of collagen type I trimer was considerably increased when odontoblasts polarized and became functional. the incorporation of 5-bromodeoxyuridine into the dental cells inhibited the polarization of odontoblasts as well as the amplification of collagen type I and type I trimer synthesis.

Animals↗
PubMed1980

Epithelio-mesenchymal morphology in ameloblastic fibro-odontoma: a light and electron microscopic study.

Five cases of ameloblastic fibro-odontoma were examined by light and electron microscopy. The ultrastructure of the epithelio-mesenchymal interface was compared with the morphology of the normally developing tooth germ. It was noted that the ultrastructure of the tumors was identical with the normally developing odontogenic tissues up to but not including the differentiation of mesenchymal cells into tall columnar odontoblasts. The absence of odontoblasts in the ameloblastic fibro-odontomas results in an absence of tubular dentin in place of which a homogeneous collagen-containing material is synthesized. The failure of mesenchymal cells to acquire the morphology of tall columnar odontoblasts probably is due to the absence of the normally occurring induction of the mesenchyme by the odontogenic epithelium.

Ameloblasts↗
PubMed1996

Nuclear DNA fragmentation during postnatal tooth development of mouse and hamster and during dentin repair in the rat.

The TUNEL (transferase-mediated, dUTP-biotin nick end labeling) method for in situ labeling of DNA strands was utilized to localize DNA fragmentation in cells involved in tooth formation in the neonatal mouse and hamster. Positive reactions for the presence of DNA fragments were obtained in some epithelial cells of the cervical loop region of incisors, late secretory, transitional and early maturation stage ameloblasts, stratum intermedium cells and in shortened ameloblasts just before eruption. Also, cells of the periodontal ligament of the continuously erupting incisors stained positive shortly before eruption. Odontoblasts were negative but became strongly positive during the formation of physiological osteodentin at the tip of developing incisors. Osteodentin matrix and the surfaces of unerupted enamel and cementum just prior to eruption stained for DNA fragments as well. DNA fragmentation could be elicited in odontoblasts and underlying pulpal tissues of mature erupted molars after mechanical injury to the odontoblast processes during cavity preparation. We conclude that, in rodents, DNA fragmentation and cell death are biological processes which take place in a variety of cells involved in formation of teeth. The TUNEL staining technique is a simple but powerful tool to examine the fate of cells and tissues undergoing either programmed cell death (apoptosis) or fragmentation of nuclear DNA induced by external factors leading to pathological changes.

Amelogenesis↗
PubMed1998

Dentin matrix proteins.

Dentinogenesis consists of highly controlled events occurring a short distance from the periphery of odontoblasts: it involves formation of extracellular collagen fibrils that act as an undergirding for deposition of plate-like carbonate apatite crystals. Odontoblasts also form a set of matrix proteins that are probably secreted at the mineralization front. Although most of these proteins are similar to those of bone, and differ from soft tissue proteins, dentin contains two unique proteins. Dentin phosphoprotein (DPP) is rich in aspartic acid (D) and phosphoserine (S*) and binds large amounts of calcium. DPP contains repeating sequences of DS*S* and S*D in discrete areas of the protein. DS*S* repeats form ridges of phosphates and carboxyllates while the S*D sequences give rise to ridges with phosphates and carboxyllates on opposing sides of the peptide chain. These structures undoubtedly have functional significance since DPP is involved in promotion of mineral initiation and in control of mineral size and shape. Dentin sialoprotein (DSP), found only in dentin, is a 53 kDa glycoprotein rich in aspartic acid, serine, glutamic acid and glycine. DSP is made by odontoblasts and also by pre-ameloblasts, but not by osteoblasts or other cell types. The gene for DSP is now known to be continuous with that of DPP. Thus, DSP and DPP must be secreted as a single protein which is then proteolytically processed to form the individual components found in the dentin matrix. Significantly, the DSP/DPP gene has been localized to human chromosome 4q21 at a site implicated in dentinogenesis imperfecta type II.

Amino Acid Sequence↗
PubMed1998

Blood vessels and nerve fibers in rat incisor pulp. Immunoelectron microscopic observation with anti-substance P antibody.

The distribution of nerve fibers with special reference to their positional relationship with blood vessels in the pulp of the rat mandibular incisor was investigated by light and electron microscopic immunohistochemistry using polyclonal anti-substance P antibody. In the center of the pulp, numerous immunoreactive nerve fibers with varicosities were found along larger blood vessels. In the periphery of the pulp, there were two layers of capillary plexus; an odontoblastic and a subodontoblastic. Many nerve fibers, showing varicosities, were located in the subodontoblastic region, and some revealed a close association with pericytes of capillaries of the subodontoblastic plexus. A few nerve fibers entered the odontoblast layer, but no nerve fibers were seen to be associated with the odontoblastic capillary plexus. The results suggest that the local regulation of blood flow takes place not only in larger blood vessels but also in the capillaries of the rat incisor pulp.

Animals↗
PubMed2006

Dentin-pulp complex responses to carious lesions.

To understand the molecular events underlying the dentin-pulp complex responses to carious progression, we systematically analyzed tissue morphology and dentin matrix protein distribution in non-carious teeth and in teeth with enamel and dentin caries. Dentin matrix proteins analyzed included collagen type I, phosphophoryn (PP) and dentin sialoprotein (DSP), all of which play decisive roles in the dentin mineralization process. Human non-carious and carious third molar teeth were freshly collected, demineralized, and processed for hematoxylin and eosin staining. The ABC-peroxidase method was used for immunohistochemical staining of collagen type I, PP and DSP proteins using specific antibodies. In situ hybridization was also performed. In contrast to elongated odontoblasts in non-carious teeth, odontoblasts subjacent to dentin caries were cuboidal and fewer in number. The predentin zone was also dramatically reduced in teeth with dentin caries. The staining intensity for collagen type I, PP and DSP in the dentin-pulp complex increased progressively from non-carious teeth, to teeth with enamel and dentin caries. In situ hybridization studies showed DSP-PP mRNA expression in odontoblasts and dental pulp that was consistent with our immunohistochemical results. These results suggest that carious lesions stimulate the dentin-pulp complex to actively synthesize collagen type I, PP and DSP proteins. This response to carious lesions is likely to provide a basis for reparative and/or reactionary dentin formation.

Animals↗
PubMed1999

Aberrant gene expression in epithelial cells of mixed odontogenic tumors.

Comparative investigations of odontogenic cells in normally forming teeth and tumors may provide insights into the mechanisms of the differentiation process. The present study is devoted to late phenotypic markers of ameloblast and odontoblast cells, i.e., proteins involved in biomineralization. The in situ expression of amelogenins, keratins, collagens type III and IV, vimentin, fibronectin, osteonectin, and osteocalcin was performed on normal and tumor odontogenic human cells. The pattern of protein expression showed some similarities between ameloblasts and odontoblasts present in normally developing human teeth and cells present in neoplastic tissues of ameloblastic fibroma, ameloblastic fibro-odontomas, and complex odontomas. Amelogenins (for ameloblasts) and osteocalcin (for odontoblasts) were detected in cells with well-organized enamel and dentin, respectively. In contrast, "mixed" cells located in epithelial zones of mixed odontogenic tumors co-expressed amelogenins and osteocalcin, as shown by immunostaining. The presence of osteocalcin transcripts was also demonstrated by in situ hybridization in these cells. Keratins and vimentin were detected in the same epithelial zones. Tumor epithelial cells were associated with various amounts of polymorphic matrix (amelogenin- and osteocalcin-immunoreactive), depending on the types of mixed tumors. No osteocalcin labeling was found in epithelial tumors. This study confirms that the differentiation of normal and tumor odontogenic cells is accompanied by the expression of some common molecules. Furthermore, the gene products present in normal mesenchymal cells were also shown in odontogenic tumor epithelium. These data may be related to a tumor-specific overexpression of the corresponding genes transcribed at an undetectable level during normal development and/or to an epithelial-mesenchymal transition proposed to occur during normal root formation. A plausible explanation for the results is that the odontogenic tumor epithelial cells are recapitulating genetic programs expressed during normal odontogenesis, but the tumor cells demonstrate abnormal expression patterns for these genes.

Ameloblastoma↗
PubMed2004

CELLS AND EXTRACELLULAR MATRICES OF DENTIN AND PULP: A BIOLOGICAL BASIS FOR REPAIR AND TISSUE ENGINEERING.

Odontoblasts produce most of the extracellular matrix (ECM) components found in dentin and implicated in dentin mineralization. Major differences in the pulp ECM explain why pulp is normally a non-mineralized tissue. In vitro or in vivo, some dentin ECM molecules act as crystal nucleators and contribute to crystal growth, whereas others are mineralization inhibitors. After treatment of caries lesions of moderate progression, odontoblasts and cells from the sub-odontoblastic Höhl's layer are implicated in the formation of reactionary dentin. Healing of deeper lesions in contact with the pulp results in the formation of reparative dentin by pulp cells. The response to direct pulp-capping with materials such as calcium hydroxide is the formation of a dentinal bridge, resulting from the recruitment and proliferation of undifferentiated cells, which may be either stem cells or dedifferentiated and transdifferentiated mature cells. Once differentiated, the cells synthesize a matrix that undergoes mineralization. Animal models have been used to test the capacity of potentially bioactive molecules to promote pulp repair following their implantation into the pulp. ECM molecules induce either the formation of dentinal bridges or large areas of mineralization in the coronal pulp. They may also stimulate the total closure of the pulp in the root canal. In conclusion, some molecules found in dentin extracellular matrix may have potential in dental therapy as bioactive agents for pulp repair or tissue engineering.

Journal Article↗
PubMed1999

Cbfa1 is required for epithelial-mesenchymal interactions regulating tooth development in mice.

Osteoblasts and odontoblasts, cells that are responsible for the formation of bone and dentin matrices respectively, share several molecular characteristics. Recently, Cbfa1 was shown to be a critical transcriptional regulator of osteoblast differentiation. Mutations in this gene cause cleidocranial dysplasia (CCD), an autosomal dominant disorder in humans and mice characterized by defective bone formation. CCD also results in dental defects that include supernumerary teeth and delayed eruption of permanent dentition. The dental abnormalities in CCD suggest an important role for this molecule in the formation of dentition. Here we describe results of studies aimed at understanding the functions of Cbfa1 in tooth formation. RT-PCR and in situ hybridization analyses show that Cbfa1 has a unique expression pattern in dental mesenchyme from the bud to early bell stages during active epithelial morphogenesis. Unlike that observed in osteoblast differentiation, Cbfa1 is downregulated in fully differentiated odontoblasts and is surprisingly expressed in ectodermally derived ameloblasts during the maturation phase of enamel formation. The role of Cbfa1 in tooth morphogenesis is further illustrated by the misshapen and severely hypoplastic tooth organs in Cbfa1-/- mice. These tooth organs lacked overt odontoblast and ameloblast differentiation and normal dentin and enamel matrices. Epithelial-mesenchymal recombinants demonstrate that dental epithelium regulates mesenchymal Cbfa1 expression during the bud and cap stages and that these effects are mimicked by the FGFs but not by the BMPs as shown by our bead implantation assays. We propose that Cbfa1 regulates the expression of molecules in mesenchyme that act reciprocally on dental epithelium to control its growth and differentiation. Taken together, our data indicate a non-redundant role for Cbfa1 in tooth development that may be distinct from that in bone formation. In odontogenesis, Cbfa1 is not involved in the early signaling networks regulating tooth initiation and early morphogenesis but regulates key epithelial-mesenchymal interactions that control advancing morphogenesis and histodifferentiation of the epithelial enamel organ.

Animals↗
PubMed2000

Sonic hedgehog regulates growth and morphogenesis of the tooth.

During mammalian tooth development, the oral ectoderm and mesenchyme coordinate their growth and differentiation to give rise to organs with precise shapes, sizes and functions. The initial ingrowth of the dental epithelium and its associated dental mesenchyme gives rise to the tooth bud. Next, the epithelial component folds to give the tooth its shape. Coincident with this process, adjacent epithelial and mesenchymal cells differentiate into enamel-secreting ameloblasts and dentin-secreting odontoblasts, respectively. Growth, morphogenesis and differentiation of the epithelium and mesenchyme are coordinated by secreted signaling proteins. Sonic hedgehog (Shh) encodes a signaling peptide which is present in the oral epithelium prior to invagination and in the tooth epithelium throughout its development. We have addressed the role of Shh in the developing tooth in mouse by using a conditional allele to remove Shh activity shortly after ingrowth of the dental epithelium. Reduction and then loss of Shh function results in a cap stage tooth rudiment in which the morphology is severely disrupted. The overall size of the tooth is reduced and both the lingual epithelial invagination and the dental cord are absent. However, the enamel knot, a putative organizer of crown formation, is present and expresses Fgf4, Wnt10b, Bmp2 and Lef1, as in the wild type. At birth, the size and the shape of the teeth are severely affected and the polarity and organization of the ameloblast and odontoblast layers is disrupted. However, both dentin- and enamel-specific markers are expressed and a large amount of tooth-specific extracellular matrix is produced. This observation was confirmed by grafting studies in which tooth rudiments were cultured for several days under kidney capsules. Under these conditions, both enamel and dentin were deposited even though the enamel and dentin layers remained disorganized. These studies demonstrate that Shh regulates growth and determines the shape of the tooth. However, Shh signaling is not essential for differentiation of ameloblasts or odontoblasts.

Animals↗
PubMed1997

Gene expression patterns of murine dentin matrix protein 1 (Dmp1) and dentin sialophosphoprotein (DSPP) suggest distinct developmental functions in vivo.

Although the precise mechanisms of the conversion of predentin to dentin are not well understood, several lines of evidence implicate the noncollagenous proteins (NCPs) as important regulators of dentin biomineralization. Here we compared the in vivo temporospatial expression patterns of two dentin NCP genes, dentin matrix protein 1 (Dmp1), and dentin sialophosphoprotein (DSPP) in developing molars. Reverse transcription-polymerase chain reaction was performed on embryonic day 13 to 1-day-old first molars using Dmp1- and DSPP-specific primer sets. Dmp1 transcripts appeared at the late bud stage, while DSPP mRNA was seen at the cap stage. Expression of both genes was sustained throughout odontogenesis. In situ hybridization analysis revealed interesting differences in the expression patterns of these genes. While Dmp1 and DSPP showed coexpression in young odontoblasts before the start of mineralization, the expression of these genes was notably distinct at later stages. Dmp1 expression decreased in secretory odontoblasts after the appearance of mineral, while high levels of DSPP were sustained in odontoblasts. In early secretory ameloblasts, DSPP expression was transient and down-regulated with the appearance ofdentin matrix. Interestingly, Dmp1 expression became evident in ameloblasts during the maturative phase of amelogenesis. In contrast to Dspp expression that was tooth-specific, Dmp1 was expressed by osteoblasts throughout ossification in the skeleton. Probes directed to the "DSP" and "DPP" regions of the DSPP gene showed identical patterns of mRNA expression. These data show that the developmental expression patterns of Dmp1 and DSPP are distinct, implying that these molecules serve different biological functions in vivo.

Animals↗
PubMed2005

Fibromodulin-deficient mice display impaired collagen fibrillogenesis in predentin as well as altered dentin mineralization and enamel formation.

To determine the functions of fibromodulin (Fmod), a small leucine-rich keratan sulfate proteoglycan in tooth formation, we investigated the distribution of Fmod in dental tissues by immunohistochemistry and characterized the dental phenotype of 1-day-old Fmod-deficient mice using light and transmission electron microscopy. Immunohistochemistry was also used to compare the relative protein expression of dentin sialoprotein (DSP), dentin matrix protein-1 (DMP 1), bone sialoprotein (BSP), and osteopontin (OPN) between Fmod-deficient mice and wild-type mice. In normal mice and rats, Fmod immunostaining was mostly detected in the distal cell bodies of odontoblasts and in the stratum intermedium and was weaker in odontoblast processes and predentin. The absence of Fmod impaired dentin mineralization, increased the diameter of the collagen fibrils throughout the whole predentin, and delayed enamel formation. Immunohistochemistry provides evidence for compensatory mechanisms in Fmod-deficient mice. Staining for DSP and OPN was decreased in molars, whereas DMP 1 and BSP were enhanced. In the incisors, labeling for DSP, DMP 1, and BSP was strongly increased in the pulp and odontoblasts, whereas OPN staining was decreased. Positive staining was also seen for DMP 1 and BSP in secretory ameloblasts. Together these studies indicate that Fmod restricts collagen fibrillogenesis in predentin while promoting dentin mineralization and the early stages of enamel formation.

Amelogenin↗
PubMed2006

Potential of dental mesenchymal cells in developing teeth.

The tooth, composed of dentin and enamel, develops through epithelium-mesenchyme interactions. Neural crest (NC) cells contribute to the dental mesenchyme in the developing tooth and differentiate into dentin-secreting odontoblasts. NC cells are known to differentiate into chondrocytes and osteoblasts in the craniofacial region. However, it is not clear whether the dental mesenchymal cells in the developing tooth possess the potential to differentiate into a lineage(s) other than the odontoblast lineage. In this study, we prepared mesenchymal cells from E13.5 tooth germ cells and assessed their potential for differentiation in culture. They differentiated into odontoblasts, chondrocyte-like cells, and osteoblast-like cells. Their derivation was confirmed by tracing NC-derived cells as LacZ(+) cells using P0-Cre/Rosa26R mice. Using the flow cytometry-fluorescent di-beta-D-galactosidase system, which makes it possible to detect LacZ(+) cells as living cells, cell surface molecules of dental mesenchymal cells were characterized. Large number of LacZ(+) NC-derived cells expressed platelet-derived growth factor receptor alpha and integrins. Taken together, these results suggest that NC-derived cells with the potential to differentiate into chondrocyte-like and osteoblast-like cells are present in the developing tooth, and these cells may contribute to tooth organogenesis.

Animals↗
PubMed1993

Expression and regulation of insulin-like growth factor-I in the rat incisor.

Growth factors play an important role in the regulation of cell growth, division and differentiation. In this study the distribution and regulation of insulin-like growth factor-I (IGF-I) in the continuously erupting rat incisor was determined by immunohistochemistry. Results were evaluated both visually and with a computer-based image analysis system. The distribution and intensity of IGF-I immunoreactivity varied with developmental stage of the rat incisor. Strong IGF-I immunoreactivity was observed in differentiating odontoblasts and ameloblasts. The most intense immunoreactivity was observed in secretory ameloblasts, secretory odontoblasts and in maturation ameloblasts. Staining was weak or absent in post-secretory ameloblasts but persisted in post-secretory odontoblasts. Weak to moderate immunoreactivity was also seen in cells of the stratum intermedium and in the reduced enamel epithelium. Surrounding alveolar bone showed strong IGF-I immunoreactivity in osteoblasts and in the stratum basale and stratum spinosum of the adjacent labial gingival epithelium. In order to assess the role of GH in IGF-I expression, GH (65 micrograms/100 g bw) was administered for six days to dwarf GH deficient rats, producing a significant increase in body weight (P < 0.01). Measurements at different stages of odontogenesis showed that the staining intensity of secretory ameloblasts (P < 0.01) and maturation ameloblasts (P < 0.001) was significantly different between untreated and treated animals. These results indicate that IGF-I is present in cell populations of the enamel organ of the rat incisor found previously to exhibit growth hormone receptors, and that expression of IGF is GH dependent.(ABSTRACT TRUNCATED AT 250 WORDS)

Ameloblasts↗
PubMed1994

[Molecular cloning and expression of homeobox-containing genes during hard tissue development].

Although much is known about the hormonal regulation of hard tissue development, much less is known about the nuclear regulatory molecules that affect the process. Homeobox-containing genes are thought to encode DNA-binding transcriptional factors which control the expression of other genes. In this study, molecular cloning of Msx homeobox-containing genes from a bovine odontoblast library and a human dental pulp-derived cells library was performed, and also the expression of mRNAs for Hox and Msx homeobox-containing genes during ectopic bone formation induced by BMP was investigated. Screening of a bovine odontoblast cDNA library and a human dental pulp-derived cells library with murine Msx-1 and Msx-2 cDNA probes led to the isolation of several positive clones. All of the clones from a bovine odontoblast library encoded the bovine counterpart for human MSX-1. All of the clones from a human dental pulp-derived cells library encoded the human counterpart for murine Msx-2. Northern blot analysis probed with a human MSX-2 cDNA indicated the expression of 2.2kb and 1.2kb mRNA in human dental pulp-derived cells. Polymerase chain reaction (PCR)-based analysis in the BMP-implanted tissue revealed that nine rat homologues of Hox homeobox-containing genes were expressed in the early cell migration stage and that two Msx genes were expressed in the cartilage and bone differentiation stages. The PCR study provided evidence of dynamic changes in the BMP-induced homeobox gene expression.

Amino Acid Sequence↗
PubMed1997

[Studies on aging enzyme activities of the human dental pulp blood vessels].

Histochemical distribution and age changes of alkaline phosphatase (AKPase E. C. 3. 1. 3. 1) and adenosine triphosphatase (ATPase E. C. 3. 6. 1. 3) in normal human dental pulp blood were investigated qualitatively and quantitatively. 42 dental pulp samples from patients aged 10 to 70 years old were divided into three groups. Results showed that accompanying aging, activities of AKPase and ATPase of dental pulp blood vessels decreased. AKPase staining quantities for group one (10-30 years), group two (31-50 years) and group three (51-70 years) were 40.62 +/- 13.79, 36.75 +/- 9.78 and 19.20 +/- 5.35 and ATPase staining quantities were 33.00 +/- 10.09, 27.53 +/- 16.60 and 23.27 +/- 5.04 respectively. The endothelial cells of capillaries in dental pulp changed greatly. With aging, metabolic ability of dental pulp decreased gradually. In addition, it was observed that the capillaries in sub-odontoblasts decreased and odontoblast layer became thin with aging. The close association of the capillaries of the pulp to the odontoblasts had been demonstrated.

Adenosine Triphosphatases↗
PubMed1998

[Effect of bovine plasma fibronectin on rat papilla cells in vitro].

OBJECTIVE: To observe the effect of exogenous fibronectin (FN) on the rat dental papilla tissues and cells. METHODS: Tooth germs of first mandibular molars obtained from 17-day-old rat (SD) embryos were cultured for 3, 6, 9 days on millipore filters in DMEM supplemented with 10% FCS, 50 mg/L Vitamin c. The dental papilla were isolated by trypsin treatment of homologous tooth germs and cultured on uncoated (control) and FN coated millipore filters for 3, 6 days, bovine plasma FN deposited on millpore filters by treated for 2 hours with 80 mg/L FN. RESULTS: As shown by histological and cytological data, some mesenchymal cells differentiated into odontoblasts and deposited predentine in cultured tooth germs. In cultured dental papillas, polarized functional cells were observed in FN coated group, odontoblast-like cells never differentiated in control cultures. CONCLUSION: FN may be involved in odontoblast polarization.

Animals↗
PubMed2002

Nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry detecting NOS in healthy and chronically inflamed pulp.

The aim of this study was to examine the expression of nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) activity in human dental pulps and determine whether there are changes of the activity in chronically inflamed pulp tissue. Nineteen pulps with clinical diagnosis of chronic pulpitis were collected during endodontic treatment. The healthy controls were obtained from teeth extracted for orthodontic therapy. The clinical diagnosis was confirmed by histological analysis. Healthy pulps showed stratified odontoblasts in peripheral parts, while in central area there was normal connective tissue. Chronically inflamed pulps showed less expressed stratification of odontoblasts and infiltration of lymphocytes, polymorphonuclear leukocytes, plasma cells and mastocytes. NADPH-d granular reactivity was assessed semi quantitatively under the light microscope by a single observer and scored on an intensity scale from negative reaction to very strong reaction. In healthy human pulps, NADPH-d activity was strong to very strong in odontoblastic layer. Endothelial cells and Schwann cells showed strong NADPH-d reactivity, while the other parts of central area were weakly positive. Similar distribution of reactivity was expressed also in chronically inflamed pulp; moderate to strong reaction was observed in stromal area as result of positive reaction in inflammatory cells and endothelial cells of abundant newly formed capillaries.

Case-Control Studies↗