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PubMed1986

A computerized histomorphometric study of the effects of intoxication with vitamin D3 or 1,25 (OH)2D3 on growth and dentin production of impeded and unimpeded rat incisors.

The effects of Vitamin D3 and 1,25(OH)2D3 intoxication on growth and dentinogenesis were studied in impeded and unimpeded rat incisors. Animals were intoxicated either with Vitamin D3 (2 mg/kg/day) or 1,25(OH)2D3 (400 ng/kg/day) for 19 days. Undecalcified transverse sections were obtained from all lower incisors. The outlines of all dental tissues were traced and fed into a computer which depicted the changes in all variables measured (circumference and cross-sectional area of tooth, pulp and dentin, width of dentin, CEJ [cemento-enamel junction] diameter and maximal labio-lingual diameter). Eruption rates, which had been recorded previously every 48 h, were used to compute the physiological age of each tooth site, so that only areas of similar age be compared. Growth. External dimensions of all intoxicated teeth decreased as the experiment progressed in contrast with control incisors which continued to increase in size. This effect was more pronounced in unimpeded incisors and may be due to the inhibitory influence of 1,25(OH)2D3 on cellular proliferation at the apical progenitor end. Dentinogenesis. 1,25(OH)2D3 intoxication had no significant effect on the rate of eruption and dentin formation in both impeded and unimpeded incisors. The same was true for impeded incisors intoxicated with Vitamin D3 but, both eruption and dentin production rates were impaired in Vitamin D3 unimpeded incisors.

Animals↗
PubMed1985

The biosynthesis of dentin phosphophoryns by rat incisor odontoblasts in organ culture.

An in vitro system consisting of rat incisor fragments was used to study the process of dentinogenesis. In order to establish the usefulness of the organ culture, the biosynthesis and deposition of the major noncollagenous components of dentin, the phosphophoryns, were followed for specific lengths of time in culture. Three criteria were satisfied: (1) the synthesis of proteins which appeared to be chemically identical to the native proteins of dentin, (2) the accumulation of the phosphophoryns within the matrix or time, and (3) the association of the secreted proteins with the mineral phase of dentin. The synthesis of phosphophoryns was determined by using both (3H)-serine and (32P)-inorganic phosphate as precursors for synthesis of protein and post-translational modification of serine to phosphoserine. In vitro synthesized phosphophoryns were characterized by 1) their accumulation and EDTA extractability from within dentin, 2) calcium chloride precipitability, 3) elution on anion-exchange columns (DEAE cellulose and AGMP50), and 4) Mr's on SDS-PAGE and Sepharose CL-6B columns. This novel system of studying dentinogenesis provides a model with which to study the regulation of extracellular matrix protein synthesis and may be useful for revealing the effect of other agents which influence tooth development and mineralized tissue metabolism in general.

Animals↗
PubMed1997

Voltage-gated calcium channels and nonvoltage-gated calcium uptake pathways in the rat incisor odontoblast plasma membrane.

Odontoblasts participate actively in the transport and accumulation of Ca2+ ions to the mineralization front during dentinogenesis. These cells are known to carry membrane-bound ATP-driven pumps and Na+/Ca2+ antiports for Ca2+ extrusion, but little is known about Ca2+ influx mechanisms into these cells. It has been shown that the administration of Ca2+ channel blockers in vivo strongly impairs Ca2+ uptake in the mineral phase during dentinogenesis in the rat; the present in vitro study is aimed at further elucidating odontoblast Ca2+ uptake mechanisms. Dissected rat incisor odontoblasts exhibited a pronounced fluorescence when incubated with a fluorescently-labeled (STBodipy) dihydropyridine, which is specific for voltage-gated Ca2+ channels of the L-type, and this binding was competitively abolished by nifedipine. As assayed by fluorescence spectrometry, odontoblast Ca2+ uptake was enhanced by the agonistic dihydropyridine BAYK-8644 (5 micro;M) as well as by plasma membrane depolarization in a high K+ (120 mM) medium. The Ca2+ uptake after depolarization was impaired by nifedipine (5 micro;M). When treated with the Ca2+-ATPase inhibitor cyclopiazonic acid (CPA; 10 micro;M), a nonvoltage-gated uptake of 45Ca2+ was identified. This uptake was not influenced by nifedipine (20 micro;M) but was impaired by lanthanum ions (200 micro;M). A nonvoltage-gated uptake of Mn2+ into CPA-treated cells could be traced using the fura-2 quenching technique. This CPA-induced Ca2+ flux was not caused by an alteration of the plasma membrane potential, as assayed with di-8-ANEPPS. The results demonstrate that Ca2+ flux into dentinogenically active odontoblasts occurs through voltage-gated Ca2+ channels of the L-type and by nonvoltage-gated, agonist-sensitive Ca2+ uptake pathways.

Animals↗
PubMed2004

Platelet-derived growth factor exerts disparate effects on odontoblast differentiation depending on the dimers in rat dental pulp cells.

Platelet-derived growth factor (PDGF) has recently been demonstrated to control the expression of alkaline phosphatase and proteoglycan synthesis of odontoblastic cells in dental pulp tissues. Although PDGF appears to be closely related to dentinogenesis, much about the mode of action of PDGF on odontoblast differentiation remains unclear. In this study, we examined the effects of three PDGF dimers (PDGF AA, AB, and BB) on odontoblastic differentiation of dental pulp cells in long-term mineralized cultures. Dental pulp cells isolated from rat lower incisors were continuously treated with each of PDGF AA, AB, and BB in separate cultures for 20 days. The three PDGF dimers suppressed alkaline phosphatase activity, osteocalcin and calcium content, and the formation of dentin-like nodules. The expression of mRNA for dentin sialoprotein (DSP) in the cells was inhibited by PDGF AA treatment, whereas PDGF AB and BB treatment stimulated the expression of DSP, even though the dentin-like nodule formation was inhibited. Although the effects of PDGF on odontoblastic differentiation varied among the dimers, the cells expressed both PDGF alpha and beta receptors, whose quantities were similar. These results suggest that PDGF exerts diverse effects on odontoblastic differentiation depending on its dimeric form. These in vitro findings explain, at least in part, the in vivo action of PDGF in dentinogenesis during the repair process of damaged dental pulp.

Alkaline Phosphatase↗
PubMed2000

Osteogenesis imperfecta in childhood: prognosis for walking.

OBJECTIVES: We studied the predicted value of disease-related characteristics for the ability of children with osteogenesis imperfecta (OI) to walk. STUDY DESIGN: The severity of OI was classified according to Sillence. The parents were asked to report the age at which the child achieved motor milestones, the fracture incidence, and the age and localization of the first surgical intervention. The present main means of mobility was classified according to Bleck. RESULTS: There were 76 replies to the 98 questionnaires, of which 70 were included (type I, 41; type III, 11; type IV, 18). The type of OI was strongly associated with current walking ability, as was the presence of dentinogenesis imperfecta. Patients with type III and IV had a lower chance of ultimately walking compared with those with type I. Children with more than 2 intramedullary rods in the lower extremities had a reduced chance of walking than patients without rods. Rolling over before 8 months, unsupported sitting before 9 months, the ability to get in sitting position without support before 12 months, and the ability to get in a standing position without support before 12 months showed positive odds ratios. In Bleck > or = 4, multivariate analysis revealed that only the presence of rodding (yes/no) in the lower extremities had additional predictive value to the type of OI. The presence of dentinogenesis imperfecta and rodding (yes/no) had additional value in Bleck > or = 5. CONCLUSION: The type of OI is the single most important clinical indicator of the ultimate ability to walk. Information about motor development adds little. The early achievement of motor milestones contributes to the ability of independent walking when the type of OI is uncertain. Intramedullary rodding of the lower extremities is primarily related to the severity of the disease and in this way provides consequences for the ability to walk.

Adolescent↗
PubMed2002

TGF beta-1 downregulates DMP-1 and DSPP in odontoblasts.

Transforming growth factor beta-1 (TGF beta-1) is a multifunctional growth factor that is expressed in numerous cell types. It has been shown to induce secretion of dentin extracellular matrix components associated with primary dentinogenesis and to play a role in tertiary or reparative dentinogenesis. In this study, we investigated the potential transcriptional regulation by TGF beta-1 of two dentin matrix proteins: dentin matrix protein 1 (DMP-1), and dentin sialophosphoprotein (DSPP). In vitro promoter studies were performed using plasmid constructs containing mouse DMP-1 and DSPP promoter sequences fused to the luciferase reporter gene. Constructs were transiently transfected in the mouse odontoblast cell line M06-G3 and cultured in the presence or absence of TGF beta-1. The integrity of the TGF beta-1 signaling pathway was investigated in the M06-G3 cells by identifying known key effectors of TGF beta-1 signal transduction. Transient transfection studies demonstrate for the first time that TGF beta-1 downregulates both DMP-1 and DSPP genes. Our findings indicate that the TGF beta-1 type I receptor ALK5 is expressed by odontoblasts as well as the signal transduction proteins Smad2, Smad3, and Smad4. These results suggest that TGF beta-1 regulates two key dentin proteins involved in matrix mineralization most likely mediated through the type I ALK5 receptor and transduced by Smads 2, 3, and 4.

Activin Receptors, Type I↗
PubMed2002

Mutation of the signal peptide region of the bicistronic gene DSPP affects translocation to the endoplasmic reticulum and results in defective dentine biomineralization.

Dentine dysplasia type II is an autosomal dominant disorder in which mineralization of the dentine of the primary teeth is abnormal. On the basis of the phenotypic overlap between, and shared chromosomal location with, dentinogenesis imperfecta type II, a second disorder of dentine mineralization, it has been proposed that the two conditions are allelic. As recent studies have shown that dentinogenesis imperfecta type II results from mutation of the bicistronic dentine sialophosphoprotein gene (DSPP ), we have tested this hypothesis by sequencing DSPP in a family with a history of dentine dysplasia type II. Our results have shown that a missense change, which causes the substitution of a tyrosine for an aspartic acid in the hydrophobic signal peptide domain of the protein, underlies the phenotype in this family. Biochemical analysis has further demonstrated that this mutation causes a failure of translocation of the encoded proteins into the endoplasmic reticulum, and is therefore likely to lead to a loss of function of both dentine sialoprotein and dentine phosphoprotein.

Dentin↗
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↗
PubMed1983

Heterogeneity of osteogenesis imperfecta type I.

We have studied 166 patients from 71 families with Sillence type I osteogenesis imperfecta (dominant inheritance and blue sclerae). We confirm earlier findings that there are two subgroups, those with and those without dentinogenesis imperfecta; each family can be allocated to one or other group. Our confidence that the two groups represent distinct disorders is increased by finding that the patients with dentinogenesis imperfecta differ not only in their dental characteristics but also in other clinical features. They have a more severe disease with a greater fracture rate and a greater likelihood of growth impairment.

Age Factors↗
PubMed1985

The extracellular matrix of the dental pulp and dentin.

The dental pulp is a loose connective tissue, characterized by its specific anatomical location. Its extracellular components are obvious subjects for study, since such components are largely responsible for the physiological properties of the tissue. Several clinically important processes occur extracellularly, e.g., defense mechanisms such as inflammatory reactions and formation of calcified tissue. The dental mesenchyme has a crucial role during early tooth morphogenesis. The dental pulp, or rather the dental papilla, seems to have only an indirect role during dentinogenesis. This review discusses proteoglycans and glycosaminoglycans, fibronectin and other non-collagenous proteins, and the different types of collagen that have been studied in pulp connective tissue. With regard to its biochemical constituents, the pulp is similar to other loose connective tissues. Collagen type I is the major fibrous component, but collagen type III also constitutes a large portion. Fibronectin is present, as is a high content of proteoglycan. In the proteoglycans, all normally occurring connective tissue glycosaminoglycans can be demonstrated. The composition of the pulpal extracellular matrix during tooth development is quite different from that of the mature tooth. Thus, it is important not to draw any too-far-reaching conclusions about the situation in human pulp from results obtained by studying pulp from animal teeth with ongoing dentinogenesis. In spite of their common ancestry, pulp and dentin differ considerably in extracellular matrix composition. Proteoglycans and collagen type I are present in dentin. No type III collagen or fibronectin can be found in the dentin, although it is present in the dental pulp.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Developmental expression of a 53 KD dentin sialoprotein in rat tooth organs.

Rat dentin contains a major sialic acid-rich glycoprotein, DSP, with an overall composition similar to that of bone sialoproteins but whose biological role in dentinogenesis is unknown. Using polyclonal affinity-purified antibodies to rat DSP and four immunohistochemical methods of detection, we studied the cell and tissue localization of DSP and the time course of its appearance during odontoblast differentiation. DSP first appeared within young odontoblasts concomitant with early secretion of pre-dentin matrix and before the onset of mineralization but was absent in pre-odontoblasts. DSP immunostaining also localized within secretory odontoblasts and was intense in odontoblastic processes. Early pre-dentin stained positive for DSP, in contrast to more mature pre-dentin, where immunoreactivity was less intense and more restricted to odontoblastic processes. In the zone of mineralized dentin matrix, a moderate and uniform staining pattern was evident. Intense immunostaining was also seen within the cells and matrix of dental pulp during dentinogenesis. Other cells and tissues within the tooth organ and those surrounding it were non-reactive. These findings suggest that DSP is developmentally expressed in cells of the odontoblastic lineage and may be a biochemical marker of odontoblastic activity.

Aging↗
PubMed1994

In situ localization and chromosomal mapping of the AG1 (Dmp1) gene.

Dentinogenesis is being used as a model for understanding the biomineralization process. The odontoblasts synthesize a structural matrix comprised of Type I collagen fibrils which define the basic architecture of the tissue. The odontoblasts also synthesize and deliver a number of dentin-specific acidic macromolecules into the extracellular compartment. These acidic macromolecules may be involved in regulating the ordered deposition of hydroxyapatite crystals within the matrix. AG1 is the first tooth-specific acidic macromolecule to have been cloned and sequenced. To identify which cells of the rat incisor pulp/odontoblast complex were responsible for synthesis of AG1, in situ hybridization was used. Digoxigenin labeled sense and anti-sense AG1 riboprobes were prepared. The AG1 mRNA was found to be expressed in the mature secretory odontoblasts. Neither pulp cells nor pre-odontoblasts showed any staining with the anti-sense probes. Chromosomal localization studies placed the AG1 gene on mouse chromosome 5q21, in tight linkage with Fgf5. AG1 has been renamed Dmp1 (dentin matrix protein 1) in accordance with present chromosomal nomenclature. Mouse 5q21 corresponds to the 4q21 locus in humans. This is the locus for the human tooth mineralization disorder dentinogenesis imperfecta Type II (DI-II). These data suggest that the Dmp1 gene is involved in mineralization and is a candidate gene for DI-II.

Animals↗
PubMed1998

Spinal complications in osteogenesis imperfecta: 47 patients 1-16 years of age.

We examined in a cross-sectional study, 47 children (mean age 7.7 (1-16) years) with osteogenesis imperfecta (OI) to find the prevalence of spinal deformities and to correlate these observations with anthropometry. The associations between dentinogenesis imperfecta, joint hypermobility and spinal deformities were also studied. Disproportion in stature in OI type I and type IV was mainly caused by spinal involvement, as evidenced by a greater decrease in body height than in leg length. In OI type I, the decrease in sitting height was mainly caused by platyspondyly, whereas in OI types III and IV, it was also caused by progressive scoliosis and kyphosis. Scoliosis was present in 22 children, and pathological kyphosis in 18, mainly in the severe OI types. Basilar impression was observed in 10 children, mainly in type III. Children with dentinogenesis imperfecta seemed to be prone to develop scoliosis, pathological kyphosis and basilar impression. Children with generalized joint hypermobility were less prone to develop scoliosis and basilar impression. Our observations may contribute to a better understanding of the risk factors for progressive spinal deformities in OI.

Adolescent↗
PubMed1999

Two sibs with an unusual pattern of skeletal malformations resembling osteogenesis imperfecta: a new type of skeletal dysplasia?

We report a 6 year old boy with multiple fractures owing to bilateral, peculiar, wave-like defects of the tibial corticalis with alternative hyperostosis and thinning. Furthermore, he had Wormian bones of the skull, dentinogenesis imperfecta, and a distinct facial phenotype with hypertelorism and periorbital fullness. Collagen studies showed normal results. His sister, aged 2 years, showed the same facial phenotype and dental abnormalities as well as Wormian bones, but no radiographical abnormalities of the tubular bones so far. The mother also had dentine abnormalities but no skeletal abnormalities on x ray. This entity is probably the same as that described in a sporadic case by Suarez and Stickler in 1974. In spite of the considerable overlap with osteogenesis imperfecta (bone fragility, Wormian bones, and dentinogenesis imperfecta), we believe this disorder to be a different entity, in particular because of the unique cortical defects, missing osteopenia, and normal results of collagen studies.

Bone Diseases↗
PubMedDate not supplied

[The use of a bactericidal substance as medication in the indirect capping of healthy dentin].

An association of trimethoprim and sulphamethoxazol (Bactrim, Roche) was employed in the indirect capping of healthy teeth in the dog. Tetracycline labelling showed dentinogenesis in these teeth and comparison was made with the controls, A quantitative and qualitative change in dentinogenesis was noted below the control cavities. This alteration was less marked in Bactrim-treated teeth. It is deduced, therefore, that the operations involved in the preparation and filling of cavities in healthy teeth leads to pulp damage that can be partly prevented by using a bactericide.

Animals↗
PubMed1990

Distinct biochemical phenotypes predict clinical severity in nonlethal variants of osteogenesis imperfecta.

We reviewed clinical and biochemical findings from 132 probands with nonlethal forms of osteogenesis imperfecta (OI) whose fibroblasts were sent to the University of Washington for diagnostic studies in the years 1981-87. In cells from 86% of probands with nonlethal OI we identified biochemical alterations compatible with heterozygosity for a mutation that affected expression or structure of alpha chains of type I procollagen. We observed two major biochemical phenotypes. Cells from 40 probands (group A) secreted about half the normal amount of normal type I procollagen and no identifiable abnormal molecules; these patients were generally of normal stature, rarely had bone deformity or dentinogenesis imperfecta, and had blue sclerae. Cells from 74 probands (group B) produced and secreted normal and abnormal type I procollagen molecules; these patients were usually short and had bone deformity and dentinogenesis imperfecta, and many had grey or blue-grey sclerae. In cells from an additional 18 probands (group C) we were unable to identify altered type I procollagen synthesis or structure. Detection of these abnormalities has value in the determination of mode of inheritance and in the prediction of clinical severity.

Cells, Cultured↗
PubMed1982

Histological and biochemical studies of vitamin C requirements of hamster molars during development in vitro.

The dose response relationship between medium concentrations of vitamin C (0-350 micrograms/ml) and the hydroxylation of in vitro incorporated 3H-proline showed that in (small) 2nd molars 50 micrograms/ml vit C at level of a maximum hydroxylation was attained at whereas in (larger) 1st molars higher medium concentrations seemed to be required (150 micrograms/ml or more). No cytotoxic effects were observed in media containing concentrations of vit C up to 350 micrograms/ml. In the absence of vit C odontoblasts in young 2nd molars failed to differentiate normally and an abnormal jelly-like substance was produced. Dentinogenesis in the 2nd molars was normal in the presence of at least 50 micrograms/ml vit C. In the 1st molars, in which production of collagenous dentine matrix had already started at the time of explantation, significantly less 3H-hydroxyproline was measured during vit C deficiency as early as the first day of culture, suggesting that there is a high need for vit C during dentinogenesis in vitro.

Animals↗
PubMed1996

Structure and organization of odontoblasts.

Differentiation of odontoblasts involves cell-to-cell recognition, contact stabilization involving the formation of attachment specializations, cytoplasmic polarization, development of the protein synthetic and secretory apparatus, and the active transport of mineral ions. The secretory odontoblast is characterized by an extensive rough-surfaced endoplasmic reticulum, a highly developed Golgi complex, and the presence of specific secretion granules. Type I collagen, a major constituent of dentin matrix, appears to be secreted by the odontoblast into predentin at the proximal portion of the odontoblast process, the major cytoplasmic process extending from the odontoblast cell body into the dentin. The odontoblast process contains a rich network of microtubules and microfilaments. The proximal portion of the process is also a site of fluid-phase endocytosis. Adjacent odontoblasts are held together by numerous macula adherens junctions and a well-developed distal junctional complex adjacent to be predentin. Junctional strands of the occludens type have been observed to be a component of this junctional complex. Tracer studies employing horseradish peroxidase indicate that this junctional complex does not form a tight barrier to the diffusion of tissue fluid from the interodontoblast spaces into the predentin. Many well-developed gap junctions are formed between adjacent odontoblasts and between odontoblasts and the fibroblasts that make up the subodontoblastic layer. Ca-ATPase activity is demonstrated in the Golgi complex and mitochondrial cristae and along the distal plasma membranes of odontoblasts. ALPase activity is also intense along the entire odontoblast cell surface. The osmium tetroxide-pyroantimonate technique for calcium localization demonstrates prominent reaction precipitates in mitochondria of odontoblasts. Energy-dispersive x-ray microanalysis of anhydrously fixed and processed odontoblasts detected Ca and P peaks throughout the cytoplasm. A sulfur peak is noted in the distal cytoplasm of odontoblasts and in matrix vesicles. Together, these results demonstrate the complexity and variety of cell functions involved in dentinogenesis.

Animals↗