Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Dentinogenesis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources
PubMedDate not supplied

Inability of calcium hydroxide to induce reparative dentinogenesis at non-peripheral sites of dog dental pulp.

The ability of 2 calcium hydroxide-containing materials to induce initiation of reparative dentinogenesis was tested at sites remote from the dentinogenically-active regions of the pulp periphery. Pieces of the cements, Dycal and Life, were implanted in central parenchymal sites of dog dental pulps for periods of 6, 14 and 42 days, respectively. Similar pieces were placed in peripheral capping sites as controls. The responses were analyzed by light and transmission electron microscopy. Induction of tubular dentin matrix lined with elongated and polarized odontoblast-like cells was only seen at peripheral capping sites. In response to the centrally implanted cements, only atubular hard tissue with lining fibroblast-like cells was deposited.

Animals↗
PubMed1998

Refined mapping of the human dentin sialophosphoprotein (DSPP) gene within the critical dentinogenesis imperfecta type II and dentin dysplasia type II loci.

Dentinogenesis imperfecta type II and dentin dysplasia type II are diseases resulting in abnormal dentin formation, which have been mapped to overlapping regions of human chromosome 4q defined by markers D4S2691 and D4S2692 (6.6 cM) and D4S3291 and SPP1 (14.1 cM), respectively. Recently, two of the major non-collagenous proteins of dentin, dentin sialoprotein (DSP) and dentin phosphoprotein (DPP, phosphophoryn) have been shown to be encoded by a single gene, termed dentin sialophosphoprotein (DSPP), which has been mapped to human chromosome 4. The purpose of this study was to perform refined mapping of DSPP related to these disease loci by gene content mapping, as well as to place the DSPP gene on the physical map of human chromosome 4 by sequence tagged site (STS) content mapping. Human genomic DSPP clones were isolated, and gene content mapping performed with specific primers for dentin matrix protein 1 (DMP1), bone sialoprotein (BSP) and osteopontin (secreted phosphoprotein 1, SPP1). STS content mapping was then performed with flanking STS markers to these dentin/bone gene loci. Our results demonstrate that the DSPP and DMP1 genes are within a maximum distance of 110 kb. Both DSPP and DMP-1 have been placed on the physical map of human chromosome 4 within the interval defined by markers D4S564 and D4S1292. DSPP is thereby strengthened as a candidate gene for both DGI-II and DD-II.

Amino Acid Sequence↗
PubMed2006

Splicing site mutations in dentin sialophosphoprotein causing dentinogenesis imperfecta type II.

Dentinogenesis imperfecta (DGI) type II (OMIM # 125490) is an inherited disorder affecting dentin. Defective dentin formation results in discolored teeth that are prone to attrition and fracture. To date, several mutations have been described in the dentin sialophosphoprotein (DSPP) gene, causing DGI types II and III and dentin dysplasia type II. DSPP encodes two proteins: dentin sialoprotein (DSP) and dentin phosphoprotein (DPP). Here, we describe a mutational analysis of DSPP in seven Finnish families with DGI type II. We report two mutations and five single nucleotide polymorphisms. In one family we found a mutation that has been described earlier in families with different ethnicity, while in six families we found a novel g.1194C>A (IVS2-3) transversion. Bioinformatic analysis of known DSPP mutations suggests that DGI type II is usually caused by aberration of normal splicing.

Child↗
PubMed1981

Familial dentinogenesis imperfecta, blue sclerae, and wormian bones without fractures: another type of osteogenesis imperfecta?

A unique connective tissue disorder characterised by the triad of dentinogenesis imperfecta, blue sclerae, and multiple wormian bones has been identified in 20 members of three generations of a large kindred of mixed ancestry in South Africa. The skeletons of affected subjects were moderately osteoporotic but, apart from minimal bowing of the femora and some vertebral flattening in late adulthood, this abnormality produced no untoward sequelae. Bone fragility was present in one young male, while a mother and her daughter had deafness of uncertain relationship with the primary disorder. Dental discolouration and a liability to caries were the only important complications. The condition is best regarded as yet another variety of osteogenesis imperfecta. It is inherited as an autosomal dominant trait with relatively consistent phenotypic expression.

Abnormalities, Multiple↗
PubMed1999

A light microscopic study of odontoblastic and non-odontoblastic cells involved in tertiary dentinogenesis in well-defined cavitated carious lesions.

This study examines cellular and microradiographic findings in thin, undemineralized sections of 46 cavitated lesions, that were clinically well-defined with respect to lesion activity and estimated lesion age at extraction time. The progressive stages of surface breakdown ranged from enamel cavitation to larger dentine exposures classified as closed and open lesion environments. Measurements of the following parameters were performed using computerized image processing software: (a) the cytoplasm:nucleus ratio of primary odontoblast cells; (b) the cell:dentinal tubule ratio; (c) the adjacent predentine area (mum2), and (d) the cytoplasm: nucleus ratio of non-odontoblastic cells, and secondary odontoblast-like cells, where estimation of these cell types were based on structural criteria. In active enamel cavitated lesions, reduced odontoblast-predentine regions and indistinct subodontoblastic regions were noted. During initial dentine exposures, non-odontoblastic cells along the pulp-dentinal interface were observed as well. The first indication of tertiary dentine was seen in old lesions with exposed dentine. The tertiary dentine appeared more atubular in the closed/active lesions than in the open/slow-progressing lesions. The involved odontoblastic cells in tubular tertiary dentine in small open/slow-progressing lesions were comparable to the primary odontoblast cells, however, new dentinal tubules were also noted presenting a mixture between reactionary and reparative dentinogenesis. In close/active lesions non-primary odontoblastic cells were aligning the atubular tertiary dentine, whereas well-defined signs of secondary odontoblast-like cells were first seen in larger open lesions, producing tubular tertiary dentine. In conclusion, a strong relationship between external lesion environments and corresponding different formations of tertiary dentine was noted in advanced cavitated lesions. It is additionally suggested that the stimulation of tubular tertiary dentine could be a closely related reaction when an active lesion complex changes into a slower progressing lesion environment.

Adult↗
PubMed1984

Crystal growth in calcifying fronts during dentinogenesis.

Additional dentinogenesis in calcifying fronts of permanent tooth germs in kittens was examined using a transmission electron microscope. The irregular island-like structures were observed in calcifying fronts. These islands, increased in size, formed the coalescence. Pairs of fine crystals ran parallel in the marginal zone of these islands. At the inner part of the islands, long and wide crystals were abundant. Furthermore, a three-dimensional visualization of crystals revealed that dentin crystals were of needle-like shape. These findings suggest that pairs of fine, needle-like crystals first appear and additional calcification progresses due to fusions between fine crystals, and maturation in crystallization occurs along the long axis following these fusions.

Animals↗
PubMed1986

Early dentinogenesis in mice: von Korff fibres and their possible significance. A preliminary study by light and electron microscopy.

By light and electron microscopy we have confirmed the collagenous nature of von Korff fibres in early dentinogenesis in mice. Each fibre array begins as an argyrophil 'stem' lying between the outermost cells of the dental papilla, with finer divisions passing into the papilla. With the appearance of odontoblasts, a cone-like 'spray' of nonargyrophil fibres in continuity with the stem spreads peripherally between these cells to the dental epithelial basement membrane. After the sprays become immured in dentine matrix, the stems are removed. Later, new stems appear. Sprays are restricted to enamel-bearing parts of teeth. The possible nature and functions of von Korff fibres are discussed.

Animals↗
PubMed2000

The non-collagenous dentin matrix proteins are involved in dentinogenesis imperfecta type II (DGI-II).

Dentinogenesis Imperfecta type II (DGI-II) is a localized form of mesodermal dysplasia of the dentin affecting both the primary and permanent dentitions. This is an autosomal-dominant disease in which there is a disorder in dentin mineralization. Several studies have localized DGI-II to human chromosome 4 in the region 4q 12-21. Many ECM genes-such as OPN, DMP1, DMP2, DMP3 (DSPP), and BSP-have been mapped to the same locus. Biochemical studies indicated that dentin phosphophoryn (DMP2) might be a candidate gene in DGI-II. In this study, we have used histological and RFLP analyses of tissues from a DGI-II-affected patient, as compared with two normal controls, to determine if DMP1, 2, or 3 was linked to DGI-II. The histology of the affected tooth was very different in the DGI-II patient as compared with the normals. In particular, the dentinal tubules in the DGI-II patient were very irregular, which could be the result of perturbations in the process of dentin formation. Patient and control DNA samples were digested with EcoRI or PstI and Southern-hybridized with the DMP1, DMP2, and DMP3 cDNAs. Few differences in the restriction pattern were observed between affected and normal samples for DMP1 and DMP3-3' region (phosphophoryn-like sequences) probes. On the other hand, DMP2 showed a dramatic shift in the restriction pattern in DGI-II. This study suggests that the different restriction enzyme digestion profiles of the DNA from the DGI-II patient, as probed by DMP2, might be related to the defective mineralization of dentin in DGI-II.

Chromosomes, Human, Pair 4↗
PubMed2001

Intrafibrillar mineral may be absent in dentinogenesis imperfecta type II (DI-II).

High-resolution synchrotron radiation computed tomography (SRCT) and small-angle x-ray scattering (SAXS) were performed on normal and dentinogenesis imperfecta type II (DI-II) teeth. The SRCT showed that the mineral concentration was 33% lower on average in the DI-II dentin with respect to normal dentin. The SAXS spectra from normal dentin exhibited low-angle diffraction peaks at harmonics of 67.6 nm, consistent with nucleation and growth of the apatite phase within gaps in the collagen fibrils (intrafibrillar mineralization). In contrast, the low-angle peaks were almost non-existent in the DI-II dentin. Crystallite thickness was independent of location in both DI-II and normal dentin, although the crystallites were significantly thicker in DI-II dentin (6.8 nm [SD = 0.5] vs. 5.1 nm [SD = 0.6]). The shape factor of the crystallites, as determined by SAXS, showed a continuous progression in normal dentin from roughly one-dimensional (needle-like) near the pulp to two-dimensional (plate-like) near the dentin-enamel junction. The crystallites in DI-II dentin, on the other hand, remained needle-like throughout. The above observations are consistent with an absence of intrafibrillar mineral in DI-II dentin.

Adolescent↗
PubMed2001

Growth-hormone-stimulated dentinogenesis in Lewis dwarf rat molars.

In dentinogenesis, certain growth factors, matrix proteoglycans, and proteins are directly or indirectly dependent on growth hormone. The hypothesis that growth hormone up-regulates the expression of enzymes, sialoproteins, and other extracellular matrix proteins implicated in the formation and mineralization of tooth and bone matrices was tested by the treatment of Lewis dwarf rats with growth hormone over 5 days. The molar teeth were processed for immunohistochemical demonstration of bone-alkaline phosphatase, bone morphogenetic proteins-2 and -4, osteocalcin, osteopontin, bone sialoprotein, and E11 protein. Odontoblasts responded to growth hormone by more cells expressing bone morphogenetic protein, alkaline phosphatase, osteocalcin, and osteopontin. No changes were found in bone sialoprotein or E11 protein expression. Thus, growth hormone may stimulate odontoblasts to express several growth factors and matrix proteins associated with dentin matrix biosynthesis in mature rat molars.

Alkaline Phosphatase↗
PubMed1990

Inductive influences of demineralized dentin and bone matrix on pulp cells: an approach of secondary dentinogenesis.

The effects of demineralized dentin and bone matrix on dental ectomesenchymal cells were evaluated after observation periods of two or three weeks. Autogenous dentin and bone matrix, obtained from the crowns of primary molars or maxillary cortical bone, respectively, were demineralized with 3% acetic acid and implanted into pulpal or papilla sites of erupting dog teeth: first molars, fourth premolars, and canines. Dentin histogenesis associated with odontoblastic arrangement was demonstrated in relation to all dentin implants in pulpal sites. Deposition of osteodentin, followed in some areas by tubular predentin formation, was observed in contact with bone implants in pulpal sites. In papilla sites, the dentin implantation exhibited bone-like matrix formation, while bone implants were encapsulated by connective tissue. The interactions of pulp cells with demineralized dentin matrix constitute a model for experimental induction of secondary dentinogenesis and odontoblast-like cell differentiation.

Animals↗
PubMed1995

Characterization of cellular responses involved in reparative dentinogenesis in rat molars.

During primary dentin formation, differentiating primary odontoblasts secrete an organic matrix, consisting principally of type I collagen and non-collagenous proteins, that is capable of mineralizing at its distal front. In contrast to ameloblasts that form enamel and undergo programmed cell death, primary odontoblasts remain metabolically active in a functional tooth. When dentin is exposed to caries or by operative procedures, and when exposed dentinal tubules are treated with therapeutic dental materials, the original population of odontoblasts is often injured and destroyed. The characteristics of the replacement pool of cells that form reparative dentin and the biologic mechanisms that modulate the formation of this matrix are poorly understood. Based on the hypothesis that events governing primary dentinogenesis are reiterated during dentin repair, the present study was designed to test whether cells that form reparative dentin are odontoblast-like. Cervical cavities were prepared in rat first molars to generate reparative dentin, and animals were killed at various time intervals. In situ hybridization with gene-specific riboprobes for collagen types I and III was used to study de novo synthesis by cells at the injured dentin-pulp interface. Polyclonal antibodies raised against dentin sialoprotein (DSP), a dentin-specific protein that marks the odontoblast phenotype, were used in immunohistochemical experiments. Data from our temporal and spatial analyses indicated that cells forming reparative dentin synthesize type I but not type III collagen and are immunopositive for DSP. Our results suggest that cells that form reparative dentin are odontoblast-like.

Animals↗
PubMed1996

Immunoreactivity of tenascin-C in dentin matrix in dentinogenesis imperfecta associated with osteogenesis imperfecta.

Osteogenesis imperfecta (OI) is a heterogeneous group of heritable connective tissue disorders, assigned to different mutations in type I collagen genes. A variety of structural abnormalities of dentin have been described in dentinogenesis imperfecta (DI) associated with OI. To clarify further the constitution of the dentin matrix in OI, we immunostained frozen and paraffin sections of deciduous teeth from four patients, each from a different family, with two monoclonal antibodies (MAbs) to the matrix glycoprotein tenascin-C (TN-C). One of the MAbs recognizes an epitope common to all TN-C isoforms (BC-4), and the other is specific for a splicing variant (BC-2). Normal teeth, oral mucosa, and skin were analyzed for comparison. Staining patterns with the two MAbs did not differ markedly. Normal dentin matrix and odontoblasts were lacking reactivity, but the pulp stained clearly. TN-C reactivity was present in the dentin matrix of all teeth obtained from two patients with different OI phenotypes and DI, and in one out of three teeth from one patient who also had DI. The reactivity was distributed in layers, but the staining patterns varied from one patient to another and from tooth to tooth. Intratubular staining seen in a tooth from the patient with clinically and histologically normal teeth was comparable with that present in normal deciduous teeth. The variation in TN-C expression suggests that, besides genetic heterogeneity, epigenetic factors could influence the composition of the dentin matrix in OI.

Adolescent↗
PubMed1996

Immunolocalization of fibronectin during reparative dentinogenesis in human teeth after pulp capping with calcium hydroxide.

Exposed dental pulp is known to possess the ability to form a hard-tissue barrier (dentin bridge). The exact mechanisms by which pulp cells differentiate into odontoblasts in this process are unknown. Fibronectin has been demonstrated to play a crucial role in odontoblast differentiation during tooth development. This study tested the hypothesis that fibronectin is involved in the initial stages of replacement odontoblast differentiation and reparative dentin formation. We observed its immunohistochemical localization during dentin bridge formation in human teeth, after pulp was capped with calcium hydroxide [Ca(OH)2]. One day after the capping, precipitation of crystalline structures was observed at the TEM level in association with cell debris at the interface between the superficial necrotic zone and underlying pulp tissue. This layer of dystrophic calcification showed positive reaction for fibronectin, and pulp cells appeared to be closely associated with this layer, seven to ten days post-operatively. At 14 days, an alignment of cells, some of which were elongated and odontoblast-like, was observed adjacent to the fibronectin-positive irregular matrix. Between the cells, corkscrew fiber-like fluorescence was visible. At 28 days, the irregular fibrous matrix was followed by the formation of tubular dentin-like matrix lined with odontoblast-like cells. Therefore, it would seem that fibronectin associated with the initially formed calcified layer might play a mediating role in the differentiation of pulp cells into odontoblasts during reparative dentinogenesis, after pulp was capped with Ca(OH)2.

Adult↗
PubMed2001

Utilization of MO6-G3 immortalized odontoblast cells in studies regarding dentinogenesis.

Tooth formation is the result of reciprocal instructive interactions between oral epithelium and cranial neural-crest-derived ectomesenchymal tissues. These interactions lead to the cytodifferentiation of highly specialized matrix-forming cell types, the ameloblast, odontoblast, and cementoblast, that produce the mineralized tissues enamel, dentin, and cementum, respectively. Our laboratory has been developing immortalized dental cell lines representative of these various cell types to facilitate studies on gene regulation, cell differentiation, matrix formation, and mineralization. Odontoblasts are solely responsible for the synthesis and secretion of the dentin extracellular matrix bilayer that consists of non-mineralized predentin and mineralized dentin. The mouse immortalized MO6-G3 cell line expresses the major matrix proteins associated with the odontoblast phenotype, producing a matrix that is capable of mineralization. This cell line serves as a useful tool in studies designed to explore the various processes of dentinogenesis. In this paper, we present studies using the mouse odontoblast cell line MO6-G3 as examples of the various research applications. Studies highlighted are: in vitro promoter studies investigating the tooth-specific gene regulation of the major non-collagenous dentin matrix protein, dentin sialophosphoprotein; regulation of tertiary dentin formation by cytokines, such as transforming growth factor-Beta 1; and the utilization of dentally relevant cells in dental material biocompatibility testing.

Ameloblasts↗
PubMed2003

Comparison of stem-cell-mediated osteogenesis and dentinogenesis.

The difference between stem-cell-mediated bone and dentin regeneration is not yet well-understood. Here we use an in vivo stem cell transplantation system to investigate differential regulation mechanisms of bone marrow stromal stem cells (BMSSCs) and dental pulp stem cells (DPSCs). Elevated expression of basic fibroblast growth factor (bFGF) and matrix metalloproteinase 9 (MMP-9, gelatinase B) was found to be associated with the formation of hematopoietic marrow in BMSSC transplants, but not in the connective tissue of DPSC transplants. The expression of dentin sialoprotein (DSP) specifically marked dentin synthesis in DPSC transplants. Moreover, DPSCs were found to be able to generate reparative dentin-like tissue on the surface of human dentin in vivo. This study provided direct evidence to suggest that osteogenesis and dentinogenesis mediated by BMSSCs and DPSCs, respectively, may be regulated by distinct mechanisms, leading to the different organization of the mineralized and non-mineralized tissues.

Adult↗
PubMed2006

Phenotypic variation in dentinogenesis imperfecta/dentin dysplasia linked to 4q21.

Dentinogenesis imperfecta (DGI) and dentin dysplasia (DD) are allelic disorders that primarily affect the formation of tooth dentin. Both conditions are autosomal-dominant and can be caused by mutations in the dentin sialophosphoprotein gene (DSPP, 4q21.3). We recruited 23 members of a four-generation kindred, including ten persons with dentin defects, and tested the hypothesis that these defects are linked to DSPP. The primary dentition showed amber discoloration, pulp obliteration, and severe attrition. The secondary dentition showed either pulp obliteration with bulbous crowns and gray discoloration or thistle-tube pulp configurations, normal crowns, and mild gray discoloration. Haplotype analyses showed no recombination between three 4q21-q24 markers and the disease locus. Mutational analyses identified no coding or intron junction sequence variations associated with affection status in DMP1, MEPE, or the DSP portion of DSPP. The defects in the permanent dentition were typically mild and consistent with a diagnosis of DD-II, but some dental features associated with DGI-II were also present. We conclude that DD-II and DGI-II are milder and more severe forms, respectively, of the same disease.

Adult↗