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Critical Reviews in Oral Biology and... 1993The formation of dentin, dentinogenesis, comprises a sophisticated interplay between several factors in the tissue, cellular as well as extracellular. Dentin may be... (Review)
Review
The formation of dentin, dentinogenesis, comprises a sophisticated interplay between several factors in the tissue, cellular as well as extracellular. Dentin may be regarded as a calcified connective tissue. In this respect, as well as in its mode of formation, it is closely related to bone. Using dentinogenesis as an experimental model to study biomineralization provides several practical advantages, and the results may be extrapolated to understand similar processes in other tissues, primarily bone. After describing dentin structure and composition, this review discusses items such as the morphology of dentinogenesis; the dentinogenically active odontoblast, transport, and concentrations of mineral ions; the constituents of the dentin organic matrix; and the presumed mechanisms involved in mineral formation.
Topics: Animals; Dentin; Dentinogenesis; Humans; Ion Transport; Minerals; Odontoblasts; Tooth Calcification
PubMed: 8292714
DOI: 10.1177/10454411930040050301 -
The International Journal of... Feb 1995Reactionary dentinogenesis is the secretion of a tertiary dentine matrix by surviving odontoblast cells in response to an appropriate stimulus. Whilst this stimulus may... (Review)
Review
Reactionary dentinogenesis is the secretion of a tertiary dentine matrix by surviving odontoblast cells in response to an appropriate stimulus. Whilst this stimulus may be exogenous in nature, it may also be from endogenous tissue components released from the matrix during pathological processes. Implantation of isolated dentine extracellular matrix components in unexposed cavities of ferret teeth led to stimulation of underlying odontoblasts and a response of reactionary dentinogenesis. Affinity chromatography of the active components prior to implantation and assay for growth factors indicated that this material contained significant amounts of TGF-beta 1, a growth factor previously shown to influence odontoblast differentiation and secretory behavior. Reactionary dentinogenesis during dental caries probably results from solubilization of growth factors, TGF-beta in particular, from the dentine matrix which then are responsible for initiating the stimulatory effect on the odontoblasts. Compositional differences in tertiary dentine matrices beneath carious lesions in human teeth have also been shown indicating modulation of odontoblast secretion during reactionary and reparative dentinogenesis.
Topics: Animals; Dentinogenesis; Extracellular Matrix; Humans; Odontoblasts; Phenotype
PubMed: 7626417
DOI: No ID Found -
Current Stem Cell Research & Therapy 2018Dentinogenesis is a long and complex process not only in tooth development, but also throughout the lifespan. Reporter mice provided us a preferred model to study the... (Review)
Review
BACKGROUND
Dentinogenesis is a long and complex process not only in tooth development, but also throughout the lifespan. Reporter mice provided us a preferred model to study the dentin formation with characteristics of high sensitivity, visualization, and reliability, which makes the long-term and intricate period of dentinogenesis much clear. With the advent of different gene reporters, genetic engineering methods, and tissue specific promoters, various reporter mice can be created to solve different problems.
OBJECTIVE
To understand the fundamental concepts and characteristics to use the reporter mice for dentinogenesis study.
RESULTS
This review introduced the frequently used gene-based reporters, genetic engineering technologies, dentinogenesis-related promoters and the reporter mice commonly used in the dentin study, with the purpose of obtaining a better application of reporter mice and gaining more details about dentinogenesis.
CONCLUSION
Reporter mice is a convenient and reliable model for studying dentinogenesis.
Topics: Animals; Dentinogenesis; Gene Expression Regulation, Developmental; Gene Knockout Techniques; Humans; Mice, Transgenic; Odontoblasts; Tooth
PubMed: 28071582
DOI: 10.2174/1574888X11666161201115754 -
Critical Reviews in Oral Biology and... 2001The predominant proteoglycans present in predentin and dentin are the chondroitin-sulphate-rich decorin and biglycan and the keratan-sulphate-rich lumican and... (Review)
Review
The predominant proteoglycans present in predentin and dentin are the chondroitin-sulphate-rich decorin and biglycan and the keratan-sulphate-rich lumican and fibromodulin. These are small, interstitial, leucine-rich proteoglycans which have recently been shown to exist in gradients across the predentin. Antibodies recognizing chondroitin sulphate show a decreasing gradient from the pulpal aspect toward the mineralizing front, the converse being true for keratan sulphate. Antidecorin shows an increase toward the mineralization front. Evidence from biochemical, autoradiographic, and immunohistochemical studies implies that such changes may be brought about by gradients of metalloproteinases. This offers the possibility that the proteoglycans organize the collagen network for receipt of phosphoproteins and phospholipids, the former being evident only at the onset of dentin formation. The suggestion is raised that glycosaminoglycan-depleted leucine-rich protein cores act as sequester points for receipt of phosphoproteins in particular. The rigid, spatially oriented glycosaminoglycan chains on decorin and biglycan are known to bind calcium and may feature directly in mineral initiation.
Topics: Animals; Collagen; Dentin; Dentinogenesis; Glycosaminoglycans; Humans; Matrix Metalloproteinases; Phospholipids; Phosphoproteins; Proteoglycans; Tooth Calcification
PubMed: 11603505
DOI: 10.1177/10454411010120040401 -
Organogenesis Dec 2022The development and repair of dentin are strictly regulated by hundreds of genes. Abnormal dentin development is directly caused by gene mutations and dysregulation....
The development and repair of dentin are strictly regulated by hundreds of genes. Abnormal dentin development is directly caused by gene mutations and dysregulation. Understanding and mastering this signal network is of great significance to the study of tooth development, tissue regeneration, aging, and repair and the treatment of dental diseases. It is necessary to understand the formation and repair mechanism of dentin in order to better treat the dentin lesions caused by various abnormal properties, whether it is to explore the reasons for the formation of dentin defects or to develop clinical drugs to strengthen the method of repairing dentin. Molecular biology of genes related to dentin development and repair are the most important basis for future research.
Topics: Dentin; Dentinogenesis; Odontoblasts; Odontogenesis
PubMed: 35023442
DOI: 10.1080/15476278.2021.2022373 -
Journal of Dental Research Jan 2022Small-molecule drugs targeting glycogen synthase kinase 3 (GSK3) as inhibitors of the protein kinase activity are able to stimulate reparative dentine formation. To...
Small-molecule drugs targeting glycogen synthase kinase 3 (GSK3) as inhibitors of the protein kinase activity are able to stimulate reparative dentine formation. To develop this approach into a viable clinical treatment for exposed pulp lesions, we synthesized a novel, small-molecule noncompetitive adenosine triphosphate (ATP) drug that can be incorporated into a biodegradable hydrogel for placement by syringe into the tooth. This new drug, named NP928, belongs to the thiadiazolidinone (TDZD) family and has equivalent activity to similar drugs of this family such as tideglusib. However, NP928 is more water soluble than other TDZD drugs, making it more suitable for direct delivery into pulp lesions. We have previously reported that biodegradable marine collagen sponges can successfully deliver TDZD drugs to pulp lesions, but this involves in-theater preparation of the material, which is not ideal in a clinical context. To improve surgical handling and delivery, here we incorporated NP928 into a specifically tailored hydrogel that can be placed by syringe into a damaged tooth. This hydrogel is based on biodegradable hyaluronic acid and can be gelled in situ upon dental blue light exposure, similarly to other common dental materials. NP928 released from hyaluronic acid-based hydrogels upregulated Wnt/β-catenin activity in pulp stem cells and fostered reparative dentine formation compared to marine collagen sponges delivering equivalent concentrations of NP928. This drug-hydrogel combination has the potential to be rapidly developed into a therapeutic procedure that is amenable to general dental practice.
Topics: Dental Pulp; Dentin, Secondary; Dentinogenesis; Glycogen Synthase Kinase 3; Humans; Hydrogels; Thiadiazoles
PubMed: 34152872
DOI: 10.1177/00220345211020652 -
Journal of Oral Biosciences Mar 2020The Bone Morphogenetic Proteins (BMPs) direct tooth development and still express in the adult tooth. We hypothesized that inhibition of BMP function would therefore...
OBJECTIVES
The Bone Morphogenetic Proteins (BMPs) direct tooth development and still express in the adult tooth. We hypothesized that inhibition of BMP function would therefore disrupt dentinogenesis by differentiated odontoblasts.
METHODS
We generated mice overexpressing the BMP-inhibitory protein Noggin in differentiated odontoblasts and osteocytes under control of a Dmp1 promoter-driven cre transgene. We compared the dentin phenotype in these mice with that in WT littermates and in mice with a Smad4 odontoblast/osteocyte knockout mediated by the same cre and therefore lacking all BMP and Tgfβ signaling in the same tissues.
RESULTS
Three-month-old first molars from both Noggin-expressing and Smad4-deleted mice showed decreased dentin volume with enlarged pulp cavities, and both displayed less organized and mineralized dentinal tubules compared to WT. The Smad4-ablated phenotype was more severe. While dentin sialophosphoprotein (DSPP) and bone sialoprotein (BSP) were decreased in the dentin of both lines, dentin matrix protein 1 (DMP1) was sharply increased in Noggin-expressing teeth.
CONCLUSIONS
The phenotypes we observed in Noggin-overexpressing and Smad4-conditional knockout teeth resemble the phenotype of Dentinogenesis Imperfecta (DGI) type III. Our results show that BMPs regulate post-natal dentinogenesis and that BMP-inhibitory proteins like Noggin play a role in that regulation. The increased severity of the Smad4 phenotype indicates that Tgfβ ligands, in addition to BMPs, play a crucial role in post-developmental dentinogenesis.
Topics: Animals; Carrier Proteins; Dentin; Dentinogenesis; Extracellular Matrix Proteins; Mice; Phosphoproteins; Sialoglycoproteins
PubMed: 31862386
DOI: 10.1016/j.job.2019.11.001 -
Operative Dentistry 1992The formation of dentin involves secretion of matrix proteins by odontoblasts, prior to the deposition of apatite crystals. These matrix proteins probably play a role in... (Review)
Review
The formation of dentin involves secretion of matrix proteins by odontoblasts, prior to the deposition of apatite crystals. These matrix proteins probably play a role in transformation of predentin to dentin. The physical and chemical properties of dentin collagen, similar to those of bone, are especially adapted for binding matrix proteins and as a grid for mineral deposition. Phosphophoryns, polyanionic, and dentin-specific proteins are secreted at the mineralization front and are involved in some way in the mineralization process of circumpulpal dentin. Dentin sialoprotein is specifically made by odontoblasts and pulp cells and may be in the family of bone proteins known to promote cell attachment. Several proteins originally isolated from bone are also found in dentin and are expressed by odontoblasts. Although the mechanisms of dentinogenesis have not been elucidated, detailed studies of dentin matrix proteins should give valuable insights into this process.
Topics: Collagen; Dentin; Dentinogenesis; Extracellular Matrix Proteins; Humans; Odontoblasts; Osteocalcin; Phosphoproteins; Sialoglycoproteins
PubMed: 1470547
DOI: No ID Found -
Molecules (Basel, Switzerland) May 2021Dental pulp vitality is a desideratum for preserving the health and functionality of the tooth. In certain clinical situations that lead to pulp exposure, bioactive... (Review)
Review
Dental pulp vitality is a desideratum for preserving the health and functionality of the tooth. In certain clinical situations that lead to pulp exposure, bioactive agents are used in direct pulp-capping procedures to stimulate the dentin-pulp complex and activate reparative dentinogenesis. Hydraulic calcium-silicate cements, derived from Portland cement, can induce the formation of a new dentin bridge at the interface between the biomaterial and the dental pulp. Odontoblasts are molecularly activated, and, if necessary, undifferentiated stem cells in the dental pulp can differentiate into odontoblasts. An extensive review of literature was conducted on MedLine/PubMed database to evaluate the histological outcomes of direct pulp capping with hydraulic calcium-silicate cements performed on animal models. Overall, irrespective of their physico-chemical properties and the molecular mechanisms involved in pulp healing, the effects of cements on tertiary dentin formation and pulp vitality preservation were positive. Histological examinations showed different degrees of dental pulp inflammatory response and complete/incomplete dentin bridge formation during the pulp healing process at different follow-up periods. Calcium silicate materials have the ability to induce reparative dentinogenesis when applied over exposed pulps, with different behaviors, as related to the animal model used, pulpal inflammatory responses, and quality of dentin bridges.
Topics: Aluminum Compounds; Animals; Biocompatible Materials; Calcium Compounds; Ceramics; Dental Materials; Dental Pulp; Dental Pulp Capping; Dentin; Dentin, Secondary; Dentinogenesis; Dogs; Drug Combinations; Humans; Inflammation; Models, Animal; Oxides; Silicates
PubMed: 34066444
DOI: 10.3390/molecules26092725 -
Oral Surgery, Oral Medicine, and Oral... May 1959
Topics: Dentin; Dentinogenesis; Humans
PubMed: 13644922
DOI: 10.1016/0030-4220(59)90162-8