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Results for “Dentinogenesis”

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At least 55 records · Page 3Linked to original sources
PubMed1994

The relationship between odontoblasts and immunocompetent cells during dentinogenesis in rat incisors: an immunohistochemical study using OX6-monoclonal antibody.

The relationship between odontoblasts and class II major histocompatibility complex (MHC) antigen-expressing cells in the process of dentinogenesis was studied in rat lower incisors, employing immunohistochemistry using OX6-monoclonal antibody. The dental pulp contained numerous OX6-immunopositive cells that varied in morphology from dendritic to spindle under physiological conditions. Under the electron microscope, these immunopositive cells shared common cytoplasmic features, i.e., multivesicular bodies and characteristic fine tubulovesicular structures in their cytoplasm. At the early stage of dentinogenesis, OX6-immunopositive cells, presumably of the immature type, were located in the subodontoblastic layer. During active dentin formation, the OX6-immunopositive cells increased in number and appeared in the odontoblast layer, associating intimately with fenestrated capillaries situated close to the predentin. These cells showed a dendritic appearance and possessed various sizes of multivesicular bodies and characteristic fine tubulovesicular structures, but never contained typical phagosomes. On the other hand, immunopositive macrophages characterized by typical phagosomes tended to occupy the central portion of the pulp. The results suggest that most, if not all, OX6-immunopositive cells situated deep in the odontoblast layer are dendritic cells playing a role in the defense system of the dental pulp against antigenic molecules arriving from the circulation via the fenestrated capillaries. The increasing number of OX6-immunopositive or immunonegative macrophages appearing near the incisal end of the tooth is thought to be involved in the elimination of degenerated odontoblasts.

Animals↗
PubMed2002

Dental management of severe dentinogenesis imperfecta in a mild form of osteogenesis imperfecta.

Dentinogenesis Imperfecta (DI), in which the teeth are discolored, translucent and brittle, can occur in isolation as a familial trait and as a component of the skeletal dysplasia Osteogenesis Imperfecta (OI). In a Cape Town family, 20 persons in 3 generations had mild OI, with the additional manifestation of severe DI. The family was assessed at the Dental Genetic Unit of the University of the Western Cape and appropriate dental treatment was provided. In this setting, a detailed treatment plan was devised for a severely affected woman. This plan proved to be efficient and cost effective, and the final outcome was pleasing to the patient. Dentinogenesis Imperfecta is not uncommon and may well be encountered in conventional dental practice. The necessary clinical expertise is within the scope of the skills of the general dentist.

Adolescent↗
PubMed1995

Effects of thyro-parathyroidectomy and parathyroidectomy upon dentinogenesis: Part I: Light microscopy.

In order to determine the differential effects of the thyroid hormones and the parathyroid hormone upon dentinogenesis in the rat incisor one control group (C) and four groups of surgically treated rats were studied: parathyroid autotransplanted (PTT), thyroidectomized (TX), parathyroidectomized (PTX), and thyro-parathyroidectomized group. One month after surgery the incisors were dissected and the tissues were prepared for light microscopy and morphometric measurements. This study revealed modifications in the TPTX rats as well as in the PTX rats: an enlargement of the predentin, alterations in the predentin appearance and the presence of mineralization defects. These results confirm that the effects observed are probably due to a PTH deficiency and/or hypocalcemia and suggest that their occurrence is associated with a determined stage of dentinogenesis in the rat.

Animals↗
PubMed1995

Influence of substrate nature and immobilization of implanted dentin matrix components during induction of reparative dentinogenesis.

The biological effects of isolated soluble dentin extracellular matrix components on the induction of reparative dentinogenesis in exposed cavities in ferret canine teeth have been shown to be blocked by immobilizing the extracellular matrix components on nitrocellulose or Millipore membranes during implantation. This contrasts with the picture of induction of odontoblast-like cell differentiation and reparative dentin deposition on existing insoluble dentin matrix of the exposure walls when the extracellular matrix components are implanted in lyophilized form. These data indicate the importance of an existing insoluble dentin matrix in providing a substrate to potentiate the growth factor-like activity of soluble isolated dentin extracellular matrix components in the induction of reparative dentinogenesis.

Animals↗
PubMed1995

Induction of reparative dentinogenesis in vivo: a synthesis of experimental observations.

EDTA--and/or guanidine HCl--insoluble dentinal matrix, or demineralized dentin which had been treated with plasma fibronectin, or pieces of Millipore filters coated with a recombinant fibronectin-like engineered polymer, incorporating many RGD sequences, were implanted into central parenchymal sites of young dog molars, via mechanical pulp exposures. Furthermore demineralized dentin and Millipore filters coated with plasma fibronectin were placed into the central pulp of old animals. Histological analysis of buffered formalin-fixed tissues showed that: 1. The dentinogenic activity was retained in the EDTA--and/or guanidine-insoluble dentin matrix. 2. Implantation of Millípore filters supplemented with the recombinant polymer did not induce any odontoblast-like cell differentiation, indicating that the interactions of pulp cells with the exogenous fibronectin are not RGD-dependent. 3. Acid-insoluble dentin matrix or plasma fibronectin (both separately inducing dentinogenesis in dental pulp of young animals) did not show any dentinogenic activity when exposed in pulp sites of old animals. Acid-insoluble dentin matrix and plasma fibronectin also failed to induce dentinogenic activity in the young pulpal tissues, when both factors were combined before to their implantation. Synthesizing the present data with previous relevant information it could be suggested that in the mechanism initiating reparative dentinogenesis, growth factors (endogenous or artificially implanted) and fibronectin are involved and this mechanism seems to be more complex than the simple immobilization of pulp cells onto an adhesion substratum.

Aging↗
PubMed1995

Dentin matrix proteins and dentinogenesis.

The precise mechanisms involved in dentinogenesis are not understood; however, the information to date suggests that a number of highly controlled extracellular events are involved. Mature odontoblasts secrete collagen at the cell border into predentin. They synthesize and secrete other non-collagenous proteins (NCPs) at the mineralization front, possibly through odontoblastic processes. A collagen-NCP complex is formed at the predentin-dentin border and apatite crystal initiation and growth takes place. One of the research needs is to uncover the nature of this dentin collagen-NCP complex and to understand how it controls mineralization. At least three dentin specific NCPs are known: phosphophoryn(s), dentin sialoprotein (DSP) and AG1 (Dmp1). Other macromolecules are commonly made by osteoblasts and odontoblasts and participate in bone and dentin formation. Some progress in understanding dentin mineralization has been gained by focusing upon the role of phosphophoryns. These highly phosphorylated proteins are secreted at the mineralization front, where a small portion binds in the gap region of type I collagen fibrils. This portion of phosphoproteins probably initiates formation of plate-like apatite crystals. Additional phosphoryns in higher concentrations bind to the growing apatite crystals and slow their growth, possibly influencing their size and shape. Other areas which need careful investigations are those involving the mechanisms involved in odontoblast differentiation, how the synthesis of the dentin specific NCPs is controlled and the precise roles of these macromolecules in dentinogenesis. Future experimentation will focus on the gene structures for these NCPs and the mechanisms of tissue specific gene regulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Apatites↗
PubMed1975

[Dentinogenesis imperfecta: a structural and ultrastructural study].

Histopathology of dentinogenesis imperfecta shows a haphazard distribution of dentinal tubules as well as changes in their diameters, sometimes narrowed, sometimes widened. These tubules appear as bundles or sheaves. This kind of dentine is often similar to secondary (also called tertiary) dentine, only mantle dentine preserving a normal structure. There is a complete obliteration of the pulp chamber and an almost complete obliteration of the root canal. Through SEM, the tubules appear to be few in number, their diameters are small and their fine ramifications are intricate through all planes. An heterogenous intertubular substance can be seen. Through TEM, collagenous fibers appear to be uncalcified or incompletely calcified, with a haphazard distribution. There are wide differences in the sizes of crystals and numerous spaces appear between crystals and collagen. Differences between the ultrastructure of human dentinogenesis imperfecta and the dentine of some lower vertebrates are clearly pointed out.

Dental Cementum↗
PubMed1992

Protein kinases in dentinogenesis.

Protein modifications such as phosphorylation and dephosphorylation are known to control several cell functions including regulation of the cell cycle, signal transduction and enzyme activation/inactivation. Bone and dentin contain highly phosphorylated anionic proteins that appear to be involved in the regulation of mineralization. This study was designed to identify and characterize the enzyme(s) responsible for phosphorylation (kinases) of dentin phosphoprotein (DPP) during dentinogenesis. DPP-protein kinase activity was demonstrated in a crude homogenate of dental pulp and odontoblast cells. In parallel studies, oligonucleotides to conserved amino acid sequences present in the active site of kinases were constructed and used to screen a lambda-gt11 tooth organ cDNA library. Several cDNA clones were isolated, the size of the insert determined by PCR (polymerase chain reaction) amplification, and in situ hybridization was used to determine cellular localization during tooth organ development. Preliminary evidence provides additional molecular determinants involved with candidate kinases responsible for DPP phosphorylation and dentinogenesis.

Animals↗
PubMed1992

Repair dentinogenesis following transplantation into normal and germ-free animals.

UNLABELLED: The purpose of this study was to investigate the dentinogenesis of dental pulp tissue following transplantation and during regeneration in normal and germ free animals, as well as in vitro experiments. EXPERIMENTS: (1) Partial and complete exposure of dental pulp in germ free rats by removing the enamel and dentin of molars. (2) The central portion of rat incisor which consisted of pulp and pulp chamber were autografted into various tissues. (3) Explants of rat pulp tissue were cultured on dentin matrix. (4) Resin bonding agent, 4-META/MMA-TBB-O (Superbond), was placed directly on surgically-exposed dental pulp. RESULTS: (1) Dentin bridge formation was recognized at 5 days after operation in germ free rat. (2) The cut surface of the transplant exhibited dentin bridge at 7 days after implantation, and the thickness of the newly formed dentin increased gradually thereafter up to 30 days. (3) Cultured pulp cells had high alkaline phosphatase activity and bone- or dentin-like hard tissue was synthesized on the dentin matrix in vitro. (4) Dentin bridge formation was evident on the surgically-exposed dental pulp even after application of Superbond. From these results, it is suggested that pulp tissue has a high activity of dentinogenesis both in vivo and in vitro and 3 days is enough for pulp cells to express the odontoblast phenotype when inflammatory factors are not present.

Animals↗
PubMed1992

Molecular control of dentinogenesis: a reaction.

This paper represents an invited reaction to three papers presented at the International Conference on Pathobiology of the Dentin/Pulp Complex, June, 1991. Repair dentinogenesis following transplantation into normal and germs free animals are correlated with results elucidating the expression of dentin phosphoproteins, collagen, and osteocalcin. The importance of transcription and translation controls of dentin matrix components are discussed and reviewed. In addition, possible implications of a molecular chaperone protein, Hsp47, in controlling dentinogenesis is introduced. Future research directions are developed and include: (a) identification of odontoblast precursors; (b) delineation of markers for odontoblasts at varying degrees of differentiation; (c) characterization of environmental conditions leading to odontoblast differentiation; (d) determination of the nature of repair and regenerated tissues; (e) elucidation of transcription and translation control factors, and (f) mapping the human genome for dentin matrix constituents.

Collagen↗
PubMedDate not supplied

[Oral rehabilitation in dentinogenesis imperfecta. Report of a case].

We present a case of Amelogenesis imperfecta associated with Dentinogenesis imperfecta, affecting the primary dentition which is rehabilitated under general anesthesia. Dentinogenesis imperfecta is a tooth abnormality which presents clinical, radiological and histological characteristics, they should be recognized by the dentist who will determine the treatment depending on age and grade of affection. In the primary dentition we recommend the use of stainless steel crowns do to it's resistance and easy adaptation which will remain in the mouth until it's normal exfoliation.

Child, Preschool↗
PubMed1989

Immunohistochemistry of extracellular matrix proteins during various stages of dentinogenesis.

During dentinogenesis the expression of extracellular matrix (ECM) proteins by (pre)odontoblasts changes concomitantly with the stage of differentiation. Of these ECM proteins some are present throughout all stages of dentinogenesis, while others can only be demonstrated at particular stages of differentiation. Utilizing immunohistochemical techniques, positive detection of ECM proteins within the (pre)odontoblast or in their extracellular matrices has been demonstrated for (pro)collagen type I, III, IV, V and VI, fibronectin, tenascin, laminin, basement membrane heparan sulfate, nidogen, dentinophosphophoryns (DPP), osteocalcin (OC), osteonectin, osteopontin and 95 kDal glycoprotein. Early predentin before onset of dentin mineralization also reacts with antibodies to enamel matrix proteins. Of these ECM proteins, only DPP are exclusively synthesized by odontoblasts; DPP thus can be regarded as specific biochemical markers for odontoblast activity. A second marker for odontoblasts (but also synthesized by osteoblasts and osteocytes) is OC. In some species however OC levels in dentin seem very low. The initiation of dentin mineralization may be a matrix-mediated process in which preameloblasts also seem to be involved. Current data suggest that the DPP-collagen complex is associated with the mineralization process in dentin.

Animals↗
PubMed1986

An autosomal-dominant form of juvenile periodontitis: its localization to chromosome 4 and linkage to dentinogenesis imperfecta and Gc.

Study of a large five-generation kindred from southern Maryland revealed that type III dentinogenesis imperfecta (DGI-III) and a localized form of juvenile periodontitis (JP) were both segregating as autosomal-dominant traits. Linkage analyses demonstrated that these were two distinct clinical entities, making this family the first documented instance of an autosomal-dominant form of JP. Since the locus for the more common form of dentinogenesis imperfecta (DGI-II) is on chromosome 4q [Ball et al, 1982], a linkage analysis of genetic and chromosomal markers on chromosome 4 was undertaken. The results suggested that the locus for the DGI-III subtype is located a similar distance from the Gc locus (theta = 0.12) as the distance previously observed between Gc and DGI-II loci (theta = 0.11) [Ball et al, 1982; Conneally et al, 1984]. Most likely the two DGI subtypes are determined by genes at closely linked loci, by allelic genes, or by the same gene with the variable expression in different families. In addition, close linkage between the Gc locus and that determining the autosomal-dominant form of JP was observed in this family (theta = 0.05). The known map of chromosome 4q and our analysis of the markers tested suggested the gene order to be 4cen----JP----Gc----DGI----MNS----qter with a large distance (at least 15 cM) between 4cen and JP.

Aggressive Periodontitis↗
PubMed1983

Relation of mineralization defects in collagen matrices to noncollagenous protein components. Identification of a molecular defect in dentinogenesis imperfecta.

Hydroxyapatite crystal deposition and stabilization within the collagen matrix of bone and dentin have been linked to the presence of noncollagenous proteins (NCP). Dentinogenesis imperfecta (DI), a genetic disorder of dentin mineralization, is being studied as a model for the analysis of mineralization mechanisms. A comparative study of the NCP in normal human dentin and dentinogenesis imperfecta Type II (hereditary opalescent dentin) dentin has been performed. The proteins of each tissue were extracted and separated using a variety of techniques. The calcium-binding, highly phosphorylated protein phosphophoryn was one of the principal NCP in normal human teeth dentin, whereas there was no evidence for the presence of such a component in the DI teeth. These data imply that dentin phosphophoryn may be related in function to the mineralization process. A similar calcium-binding protein defect should be sought in the various types of osteogenesis imperfecta.

Adult↗
PubMed1981

Thirteen-year-old boy with dentinogenesis imperfecta - pedodontic and orthodontic treatment.

Dentinogenesis imperfecta is a hereditary condition characterized by disturbance in tooth formation. The colour of the teeth vary from opalescent greyish-blue to an amber-like colour on the teeth with splitting of the enamel. On the roentgenogram the marked obliteration of the pulp chambers is a characteristic feature. This case report describe a 13-year-old boy with dentinogenesis imperfecta. High caries activity resulted in extensive caries on the first permanent molars. The boy had to be treated orthodontically to create acceptable occlusion. The treatment was carried out with fixed appliance and started after extraction of the four first permanent molars. No observable injury was recorded during the treatment.

Adolescent↗
PubMed1995

Basic mechanisms of cytodifferentiation and dentinogenesis during dental pulp repair.

Based on recent literature, the specific potential of mature pulp cells to differentiate into polarized cells able to elaborate reparative dentin is described. These odontoblast-like cells are distinguished, by morphological criteria, from the other matrix-formative cells involved in non-specific defensive mechanisms of dental pulp. The suitable tissue conditions and the normal cascade of reparative events, allowing initiation of dentinogenesis in sites of amputated pulp, are presented. This is followed by a review of current observations on specific dentinogenic events, induced in various culture systems or in intrapulpal sites of mature teeth by artificial bio-molecules or bio-matrices. Data from these experiments are focused on the role of extracellular matrix molecules and growth factors in acquisition of the odontoblast-like cell phenotype and initiation of reparative dentinogenesis.

Animals↗