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 37 records · Page 2Linked to original sources
PubMed1992

Dentinogenesis imperfecta: a case report.

Dentinogenesis imperfecta is a localized form of mesodermal dysplasia of the dentin affecting both the primary and permanent dentitions. Most previous reports on dentinogenesis imperfecta describe treatment with overdentures, which have several disadvantages. The present report describes a case of dentinogenesis imperfecta in an 11-year-old girl. A combination of restorative, prosthetic, and surgical treatment was used to resolve the condition.

Cephalometry↗
PubMed2006

SEM-morphology in dentinogenesis imperfecta type II: microscopic anatomy and efficacy of a dentine bonding system.

AIM: Dentinogenesis Imperfecta is a hereditary defect consisting of opalescent teeth composed of irregularly formed and undermineralised dentin that obliterates the coronal and root pulpal chambers. The aim of this study was to examine the morphology of permanent human enamel, dentine and the dentine-enamel junction, in individuals affected by Dentinogenesis Imperfecta type II in undercalcified sections using scanning electron microscope (SEM) to compare the findings to the normal morphology, and to study the efficacy of modern bonding system to dentine and enamel DI type II affected. MATERIALS AND METHODS: Four third molars extracted from two 19 year-old subjects (one patient affected by Dentinogenesis Imperfecta type II) were included in resin, two divided in slices with a air-cooled diamond disc, and two used to study the characterisation of the resin-dentin interface. The sections of the teeth were examined by means of SEM. The slices were finished up with abrasive paper (400, 600, 1000, and 2000), the half surfaces obtained were etched with 37% phosphoric acid and then joined up to the stubs for SEM analysis. SEM Stereoscan 440 Leica with magnifications of 20X, 100X, 250X, 1000X, 2000X, 3000X was used. As control group were used four third molars with normal anatomy. RESULTS: This study shows that the permanent enamel from patients with DI exhibits few structural changes. No relationships were found between enamel morphology and the DI type II. Enamel appeared to be regularly mineralised. The major findings were anomalies in the dentine-enamel junction, locally a lower degree of mineralisation and an undulating morphology. The dentine showed absence of tubules. CONCLUSION: This study confirms that the problem with teeth affected by DI type II is the defect in dentine and weakness in the way the enamel is attached to the dentine. The adhesive system tested is not able to create a real hybrid layer in dentine DI type II affected and seems to be less effective than on normal substrates.

Adolescent↗
PubMed1997

Development of tight junctions between odontoblasts in early dentinogenesis as revealed by freeze-fracture.

BACKGROUND: Mature odontoblasts possess junctional structures constituted by adherens, gap, and tight junctions. Although adherens and gap junctions appear early between odontoblasts, there is no information on the appearance and development of tight junctions between odontoblasts. In this study, we have examined freeze-fracture replicas of early dentinogenesis to study the development of tight junctions between odontoblasts and to determine whether these junctions are of zonular or macular type. METHODS: Upper first molar tooth germs of Wistar rats between 1 and 3 days old were fixed in buffered 4% glutaraldehyde/4% formaldehyde and subsequently cryoprotected with cacodylate-buffered glycerol. Freeze-fracture replicas were obtained in a Balzers 301 apparatus, and early stages of dentinogenesis were examined in a Jeol 100 CX II electron microscope. RESULTS: In the stage of early dentine matrix prior to mineralization, odontoblasts exhibit only gap junctions. With the progression of development, the distal plasma membranes of odontoblasts show numerous short tight junctions formed by fused particles and grooves. In the stage of advanced mineralization, branched and continuous rows of fused particles or grooves constitute tight junctions of the focal or macular type. CONCLUSIONS: The present study shows that tight junctions of focal or macular type appear on distal plasma membrane of early odontoblasts during differentiation. Formation of tight junctions indicates the establishment of a distal membrane domain and maturation of odontoblasts. These events occur as mantle dentine formation ceases and circumpulpar dentine formation begins.

Age Factors↗
PubMed2000

Highly regulated expression of subtilisin-like proprotein convertase PACE4 (SPC4) during dentinogenesis.

Expressions of mRNAs for four subtilisin-like proprotein convertases (SPCs: furin, PACE4, PC6, and PC8) and bone morphogenetic protein 4 (BMP4) in the rat molar tooth during development were analyzed by Northern blotting, reverse transcriptase-polymerase chain reaction (RT-PCR), and in situ hybridization to explore the possible involvement of SPCs in the processing of proBMPs. We found a temporospacial expression of PACE4, but not one of the other SPCs, in this tissue; i.e., RT-PCR analysis revealed that the level of PACE4 mRNA, but not that of the other SPC mRNAs became high around the second postnatal day. This increase was in good accordance with the increase in BMP4 mRNA, indicating an apparent association of these molecules with the differentiation and establishment of functional ameloblasts and odontoblasts. During dentinogenesis, PACE4 mRNA was localized in the ameloblasts and odontoblasts. These observations suggest that PACE4 plays a crucial role in dentinogenesis, especially via the activation of BMPs.

Animals↗
PubMed1997

Elucidation of the sequence and the genomic organization of the human dentin matrix acidic phosphoprotein 1 (DMP1) gene: exclusion of the locus from a causative role in the pathogenesis of dentinogenesis imperfecta type II.

The dentin matrix acidic phosphoprotein 1 (DMP1) gene has been mapped to human chromosome 4q21 and shown to exhibit no recombination with the autosomal dominant disorder of dentin formation, dentinogenesis imperfecta type II. In the current study, sequencing of DMP1 cDNA and genomic clones has indicated that the human gene contains an open reading frame of 1539 bp, which predicts a highly acidic, serine-rich protein of 513 amino acids. Comparison of the human DMP1-coding sequence with that of the rat, mouse, and cow indicated that the predicted protein contains a conserved hydrophobic signal peptide sequence and an Arg-Gly-Asp cell attachment sequence. The gene is encoded by six exons, the splicing phase of which is type 0, the first exon containing solely 5' untranslated sequence. Sequencing of each of the coding exons in individuals affected by dentinogenesis imperfecta type II failed to reveal any disease-specific mutations, suggesting that mutations in DMP1 are not causative of this condition at least in the two families examined in this study.

Amino Acid Sequence↗
PubMed2005

Developmental appearance of dentin matrix protein 1 during the early dentinogenesis in rat molars as identified by high-resolution immunocytochemistry.

Dentin matrix protein 1 (DMP 1) is an acidic phosphoprotein that has been postulated to play an important role in mineralized tissue formation. We have examined rat molar tooth germs by applying a high-resolution immunocytochemical approach with the purpose to identify the temporal and spatial localization of DMP 1 at the onset of dentinogenesis. Upper molar tooth germs of 2- to 3-day-old Wistar rats were fixed in a cacodylate-buffered 0.1% glutaraldehyde + 4% formaldehyde fixative, left unosmicated and embedded in LR White resin. The sections were incubated with a polyclonal DMP 1 antibody for postembedding colloidal gold immunolabeling and examined in a Jeol 1010 transmission electron microscope. The earliest localization of DMP 1 was in the Golgi region as well as in the nucleus of differentiating odontoblasts. When mineralization spread from matrix vesicles to the surrounding matrix, DMP 1 was extracellularly detected around the mineralizing globules. In the regions of fully mineralized mantle dentin, it was present in the mineralized regions, mainly around the peritubular dentin. The appearance of DMP 1 during early dentinogenesis implies a direct role for this protein in both odontoblast differentiation and matrix mineralization.

Animals↗
PubMed1986

Quantitative histological analysis of the human coronal dentine in dentinogenesis imperfecta types I and II.

The coronal dentine of 3 teeth from dentinogenesis imperfecta (DI) type I, 9 teeth from DI type II and 4 controls were examined by a quantitative histological technique. In each case, two representative demineralized sections, one stained in H + E and the other in Schmorl's picrothionin were used. The relative amount of dentinal tubule, atubular dentine and canals/clefts were assessed using the point-counting method. Three basic patterns of distribution of tubules were observed. Pattern 1 formed the largest group and showed a gradual decrease in tubule count from enamel-dentine junction (EDJ) pulpwards, pattern 2 was characterized by a drop in tubule count approximately midway between EDJ and pulpal border, and pattern 3 exhibited a gradual increase in tubule score as the pulp was approached. At the 5 per cent level, both patterns 1 and 2 were found to be statistically significant. Pattern 3 was statistically insignificant for the test specimens and highly significant for the controls. The variation in the distribution of the tubules in coronal dentine in this study indirectly supports the concept of abnormal dentinogenesis in DI attributable to a diminution or lack of normal functional odontoblasts.

Adolescent↗
PubMed1992

Unusual dentinal changes in dentinogenesis imperfecta associated with osteogenesis imperfecta. A case report.

A case is described of a boy with dentinogenesis imperfecta associated with osteogenesis imperfecta. The dentin of extracted deciduous teeth was found to show an abrupt transition to a normal tubular structure before a reversion to the more typical structure seen in dentinogenesis imperfecta. This change in the dentin appeared to have occurred in a chronologic manner. The possibilities that either a metabolic disturbance or a temporary reduced expression of the mutant gene had caused the abnormality and could account for the unusual histologic findings are discussed.

Child↗
PubMed1992

Calcium ion transport kinetics during dentinogenesis: effects of disrupting odontoblast cellular transport systems.

Due to strongly discrepant results in the literature, controversy exists about the timing of the transport of Ca2+ ions to the mineralization front during dentinogenesis and the role of the odontoblasts in this transport. The present study gives evidence, by means of autoradiography as well as by a radiochemical technique, that the transport time for Ca2+ ions into the dentin mineral phase is about 10-15 min in the rat incisor. The results also show that technical factors, such as mode of tracer injection and the use of perfusion fixation, may influence the results more or less strongly. Finally, by disturbing odontoblast microtubules, involved in intracellular transport processes, and by blocking odontoblast calcium uptake channels by nifedipine and neomycin, the Ca2+ ion transport into dentin mineral was found to be strongly impaired. This may be taken as an indication that transcellular calcium transport mechanisms have a role during dentinogenesis.

Animals↗
PubMed2006

Cell pellets from dental papillae can reexhibit dental morphogenesis and dentinogenesis.

We isolated dental papilla mesenchymal cells (DPMCs) from different rat incisor germs at the late bell stage and incubated them as cell pellets in polypropylene tubes. In vitro pellet culture of DPMCs presented several crucial characteristics of odontoblasts, as indicated by accelerated mineralization, positive immunostaining for dentin sialophosphoprotein and dentin matrix protein 1, and expression of dentin sialophosphoprotein mRNA. The allotransplantation of these pellets into renal capsules was also performed. Despite the absence of dental epithelial components, dissociated DPMCs with a complete loss of positional information rapidly underwent dentinogenesis and morphogenesis, and formed a cusp-like dentin-pulp complex containing distinctive odontoblasts, predentin, dentin, and dentinal tubules. These results imply that DPMCs at the late bell stage can reexhibit the dental morphogenesis and dentinogenesis by themselves, and epithelial-mesenchymal interactions at this stage may not be indispensable. Furthermore, different DPMC populations from the similar stage may keep the same developmental pattern.

Animals↗
PubMed1998

An in vitro approach for the study of dentinogenesis by organ culture of the dentine-pulp complex from rat incisor teeth.

Culture of the developing dental tissues has contributed to understanding of developmental processes during early odontogenesis. However, to understand fully the mechanisms involved during dentinogenesis and tissue repair there is a need to develop culture models for the dentine-pulp complex from more mature dental tissues. This study describes the development of a system for the organ culture of mature rodent teeth. Slices of incisors from 28-day-old rats were embedded in a semisolid, agar-based medium and cultured on floating Millipore filters at the liquid-gas interface for up to 14 days. Preservation of cell and tissue morphology was observed throughout the entire dentine-pulp complex after each culture period and autoradiographic studies showed that the odontoblasts were actively synthesizing and secreting extracellular matrix during culture. Transmission electron microscopy confirmed that the phenotypic morphology of the odontoblasts had been maintained during culture. These results demonstrate that the dentine-pulp complex from mature rodent tissues can be cultured successfully for substantial periods of time and will provide a useful model for the study of dentinogenesis and tissue repair.

Animals↗
PubMed2003

Dentin sialophosphoprotein knockout mouse teeth display widened predentin zone and develop defective dentin mineralization similar to human dentinogenesis imperfecta type III.

Dentin sialophosphoprotein (Dspp) is mainly expressed in teeth by the odontoblasts and preameloblasts. The Dspp mRNA is translated into a single protein, Dspp, and cleaved into two peptides, dentin sialoprotein and dentin phosphoprotein, that are localized within the dentin matrix. Recently, mutations in this gene were identified in human dentinogenesis imperfecta II (Online Mendelian Inheritance in Man (OMIM) accession number 125490) and in dentin dysplasia II (OMIM accession number 125420) syndromes. Herein, we report the generation of Dspp-null mice that develop tooth defects similar to human dentinogenesis imperfecta III with enlarged pulp chambers, increased width of predentin zone, hypomineralization, and pulp exposure. Electron microscopy revealed an irregular mineralization front and a lack of calcospherites coalescence in the dentin. Interestingly, the levels of biglycan and decorin, small leucine-rich proteoglycans, were increased in the widened predentin zone and in void spaces among the calcospherites in the dentin of null teeth. These enhanced levels correlate well with the defective regions in mineralization and further indicate that these molecules may adversely affect the dentin mineralization process by interfering with coalescence of calcospherites. Overall, our results identify a crucial role for Dspp in orchestrating the events essential during dentin mineralization, including potential regulation of proteoglycan levels.

Animals↗
PubMed2006

Effect of GaAIAs laser on reactional dentinogenesis induction in human teeth.

OBJECTIVE: This study investigated the biomodulatory effect of the gallium- aluminum-arsenate laser (GaAlAs) in pulp cells on reactional dentinogenesis, and on the expression of collagen type III (Col III), tenascin (TN), and fibronectin (FN) in irradiated dental tissues and controls (not irradiated). BACKGROUND DATA: Several studies suggest a biomodulatory influence of low-intensity laser radiation in the inflammatory and reparative processes of biological tissues. METHODS: Sixteen human premolar teeth were selected (after extraction due to orthodontal reasons) and divided into irradiated and control groups. Black class V cavity preparations were accomplished in both groups. For the irradiated group, GaAlAs laser (670 nm, 50 mW) with an energy density of 4 J/cm2 was used. Soon after, the cavities were restored with a glass ionomer and the extractions made after 14 and 42 days. RESULTS: Histological changes were observed by light microscopy; less intense inflammatory reaction in the irradiated group was found when compared to the controls. Only the irradiated group of 42 days exhibited an area associated with reactional dentinogenesis. After immunohistochemical analysis by the streptoavidin-biotin complex (SABC) method, the expression of Col III, TN, and FN was greater in the irradiated groups. CONCLUSION: Our results suggest that a GaAlAs laser with energy density of 4 J/cm2 and wavelength of 670 nm caused biomodulation in pulp cells and expression of collagen, but not collagen of the extracellular matrix, after preparation of a cavity.

Aluminum↗
PubMed1994

Mechanisms controlling secondary initiation of dentinogenesis: a review.

Dentinogenesis can be initiated secondarily as an intrinsic ability of the dental pulp to repair, or after interaction of pulp cells with specific exogenous inductive factors. In the present article the basic developmental aspects, highlighting the mechanism by which dentinogenesis is initiated during tooth development, are discussed. Furthermore, clinical and experimental observations concerning the events taking place during secondary initiation of dentine formation, as part of exposed or non-exposed pulp tissue repair, or as a result of dentine matrix or other chemical-pulp cell interactions, are reviewed. Discussion includes hypotheses relating to the crucial biological steps leading to expression of odontoblastic-like cell phenotype and secondary initiation of dentine histogenesis.

Animals↗
PubMed1980

Dentinogenesis imperfecta: evidence of qualitative alteration in the organic dentin matrix.

Deciduous teeth affected by dentinogenesis imperfecta were obtained from two patients with osteogenesis imperfecta. Electronmicroscopy of the dentin revealed some structural alterations. The striation of the collagen fibrils was not clear, and the crystals were less dense than in normal dentin. The amino acid analysis of dentin collagen was slightly different from normal dentin. There were slight increases in the amounts of hydroxylysine, serine and acidic acids. On the other hand, lysine and arginine were reduced. The elevation of hexosyllysine content and an increase of carbohydrate were also observed. These results indicate that either dentin collagen is altered, or noncollagenous matrices associated with collagen are increased in dentinogenesis imperfecta dentin.

Adolescent↗
PubMed2005

Dentinogenesis imperfecta associated with short stature, hearing loss and mental retardation: a new syndrome with autosomal recessive inheritance?

The follow-up history and oral findings in two brothers from consanguineous parents suggest that the association of dentinogenesis imperfecta (DI), delayed tooth eruption, mild mental retardation, proportionate short stature, sensorineural hearing loss and dysmorphic facies may represent a new syndrome with autosomal recessive inheritance. Histological examination of the dentin matrix of a permanent molar from one of the siblings reveals morphological similarities with defective dentinogenesis as presenting in patients affected with Osteogenesis Imperfecta (OI), a condition caused by deficiency of type I collagen. A number of radiographic and histological characteristics, however, are inconsistent with classical features of DI. These findings suggest that DI may imply greater genetical heterogeneity than currently assumed.

Body Height↗
PubMed1999

Genetic linkage of the dentinogenesis imperfecta type III locus to chromosome 4q.

Dentinogenesis imperfecta type III (DGI-III) is an autosomal-dominant disorder of dentin formation which appears in a tri-racial southern Maryland population known as the "Brandywine isolate". This disease has suggestive evidence of linkage to the long arm of human chromosome 4 (LOD score of 2.0) in a family presenting with both juvenile periodontitis and DGI-III. The purpose of this study was to screen a family presenting with only DGI-III to determine if this locus was indeed on chromosome 4q. Furthermore, we wanted to determine if DGI-III co-localized with dentinogenesis imperfecta type II (DGI-II), which has been localized to 4q21-q23. Therefore, a large kindred from the Brandywine isolate was identified, oral examination performed, and blood samples collected from 21 family members. DNA from this family was genotyped with 6 highly polymorphic markers that span the DGI-II critical region of chromosome 4q. Analysis of the data yielded a maximum two-point LOD score of 4.87 with a marker for the dentin matrix protein 1 (DMP1) locus, a gene contained in the critical region for DGI-II. Our results demonstrated that the DGI-III locus is on human chromosome 4q21 within a 6.6 cM region that overlaps the DGI-II critical region. These results are consistent with the hypothesis that DGI-II is either an allelic variant of DGI-III or the result of mutations in two tightly linked genes.

Aggressive Periodontitis↗
PubMed2001

Presence or absence of tertiary dentinogenesis in relation to caries progression.

Studies have shown that dental caries may or may not be associated with tertiary dentin formation in the pulp. On the basis of histological examinations of 69 clinical well-defined caries lesions, a hypothesis is proposed on the dynamics of the hard-tissue responses of the pulp to caries. In active non-cavitated lesions, the formation of tertiary dentin seems to be initiated by primary odontoblast cells that subsequently result in atubular dentin/fibrodentinogenesis, whereas, in similarly aged but more rapidly progressing cavitated enamel lesions, no tertiary dentin is laid down by primary odontoblast cells. In all old-dentin exposed lesions, a so-called closed lesion environment was defined with subjacent atubular dentin formation. As these lesions progress, a shift from a closed to a more large and open lesion environment may develop in the very old lesions, and a new tubular dentinal matrix is noted on the top of the fibrodentin, also defined as reparative dentinogenesis. In very old slowly progressing lesions, a relatively small open lesion environment is also observed, with tubular tertiary dentin resembling the primary dentin being strictly tubular. It is suggested that the absence of tertiary dentinogenesis can be expected in very rapid caries lesions, whereas a variety of tertiary dentin is observed in older dentin cavitated lesions guided by a changing external lesion environment over time.

Dental Caries↗