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PubMed1976

Studies on fluoride distribution in infants and small children.

The fluoride (F) concentrations in hard tissues and blood plasma were determined in biopsy and autopsy specimens from fetuses, infants, and children on varying F intake. In newborn autopsy cases specimens consisting of rib, jawbone with teeth, and blood plasma the F concentrations of bone and dentin were of the same order, those of the enamel lower. Correlations between individual F values in different tissues were all positive, highest for enamel/dentin. Low birth weight entailed only slightly reduced F contents, high water F significantly increased F contents. In the biopsy material (rib and blood plasma) the maximal rib/ash concentration was about 400 parts/10(6) F. A negative correlation between rib F and plasma F is specially commented on. The possible influence of F on bone development as expressed by blood plasma F and phosphatase activity was investigated in three groups of infants aged 2-6 months, either breast-fed or fed dry-milk formulas diluted with drinking waters of different F content. The children of these groups were calculated to ingest F in the ratio of about 1:10:50. The highest F group had higher plasma F values than the two other groups, whereas its alkaline phosphatase was significantly higher than that of the lowest F group only. The influence of disturbances in the skeletal development on F retention studied in physically handicapped children aged 4-15 years living in a city with about 1 part/10(6) F in the drinking water. The severely handicapped showed a higher urinary F excretion than the controls.

Adolescent↗
PubMed1977

A longitudinal radiographic study of the mineralization of 2nd premolars.

Odontogenesis of the 2nd premolar begins in the majority of cases at the age of 3-3 1/2 years, although this period can vary more widely than that for other permanent teeth. For this reason, aplasia of this group of teeth cannot be diagnosed as early and with the same degree of certainty. A group of 104 children aged 3-7 years in whom one or more tooth germs mesial to the 1st permanent molar were not visible in the various age groups was reexamined radiographically in the region where they apparently lacked the development of tooth germs. The second examination took place 16-24 months after the first, and a comparison was made of the two examinations. The study confirms that the 2nd premolar can be very late in developing and that the chance of this being so is greater in the maxilla than in the mandible.

Bicuspid↗
PubMed1983

In vitro study by fluorescence microscopy and microradiography of tetracycline-tooth interaction.

The administration of tetracycline to the growing child may cause discoloration and hypoplasia in developing teeth. Whether tetracycline may also cause changes in fully mineralized enamel and dentin, is still a matter of discussion. The present investigation examines the in vitro reaction between tetracycline chloride and enamel and dentin of extracted human teeth. Specimens were immersed in 0.5 mg/ml to 20 mg/ml aqueous tetracycline solutions. After 24 hr the specimens were sectioned and studied by fluorescence microscopy and microradiography. The tetracycline solutions, which were all very acidic, were found to cause 1) demineralization of enamel and dentin, 2) incorporation of fluorescent material in enamel and, notably, dentin; and 3) formation of yellow, rhombohedral crystals on dental surfaces, especially in the more concentrated solutions. No fluorescence was seen in totally demineralized dentin. The findings indicate that the incorporation of tetracycline into enamel and dentin is caused by physiochemical processes that may take place regardless of the developmental stage of the mineralized tissues.

Dental Enamel↗
PubMed1985

Visualization of human predentin and hypomineralized areas of dentin by silver methenamine staining.

The light microscopic structure of human teeth was studied following silver methenamine staining, with and without previous oxidation in periodic acid. Predentin, hypomineralized dentin and carious dentin stained intensely, whereas highly mineralized dentin and calcospherites at the predentin-dentin junction did not show any reactivity when observed in the light microscope, even following demineralization in strong acid or in EDTA. The reactive sites of the pulp were confined to nuclei, nucleoli and a few thin fibers. This distribution of reactive sites is different from the distribution which is seen following von Kossa's silver stain, and from the distribution seen following silver stain methods for reticular fibers.

Dental Caries↗
PubMed1990

Mineralization of and cementoblast attachment to original and reparative cementum.

Cementoblast attachment to original and reparative cementum as well as the mineralization pattern of the two tissues were studied ultrastructurally. Although differences were found in the mineralization pattern between the two types of cementum, cementoblasts attached to both with focal contacts, indicating a non-motile synthesizing state of the cells. It was concluded that the differences in morphology between the two types of cementum are only reflections of the rate with which they are formed.

Animals↗
PubMed1992

Effects of phosphonoformic acid and 1-hydroxyethylidene-1,1-bisphosphonate (HEBP) on distribution of tetracycline in the developing rat molar.

Tetracycline was used as a marker to study the effect of phosphonoformic acid and 1-hydroxyethylidene-1,1-bisphosphonate (HEBP) on the mineralization of the developing dental hard tissues. Groups of young rats were given a single subcutaneous injection of tetracycline and at the same time were injected with a single dose of either phosphonoformic acid or HEBP (10 mg P/kg b.w.). Alternatively, rats were injected with the tetracycline after different time intervals from the phosphonate injection. Rats were sacrificed at intervals ranging from 1 to 4 days. Frozen-sections were obtained at the level of the maxillary first molar and prepared for light and fluorescence microscopy. The results of the present study indicate that the distribution pattern of tetracycline in the developing dental hard tissues is greatly affected by the pathologic changes induced by phosphonoformic acid and HEBP. Both drugs caused similar changes in the pattern of tetracycline uptake in the developing enamel. There seems to be a direct relation between the presence of developmental defects of enamel and the degree of discoloration induced by tetracycline. Aberrations in the mineralization of dentin were caused only by HEBP. As demonstrated by this study, HEBP is capable of inducing a provisional inhibitory effect on dentin mineralization.

Ameloblasts↗
PubMed1993

Dentin formation in miniature pigs with special reference to indomethacin and orthodontic treatment.

The rate of dentin mineralization and the influence of indomethacin on the dentin mineralization rate during orthodontic treatment was determined in miniature pigs by intravital labeling with tetracycline. The results demonstrated that the dentin mineralization rate in the control animals was 3.8 microns/day, a rate corresponding to that of human teeth. Both indomethacin and orthodontics had an effect on the dentin mineralization rate, indomethacin reducing and orthodontic forces increasing it. In combination, the two factors neutralized each other.

Animals↗
PubMed1994

Effect of hypocalcemic state on enamel formation in rat maxillary incisors.

Several authors have proposed that hypocalcemia can interfere with amelogenesis, resulting in enamel aberrations. Therefore, the purpose of this investigation was to study the effects of a diet-induced hypocalcemic state in young rats on enamel formation of the maxillary incisors. The experimental rats were fed a special diet, free from vitamin D and very low in calcium. The control rats were fed a normal diet. The experimental period was 3 wk. After termination, the blood analysis showed that the experimental rats had developed hypocalcemia with very low values of both total and ionized blood calcium. The experimental rats were smaller than their controls after 3 wk, with smaller skulls and teeth. At the light microscope level, the enamel and the ameloblasts did not seem to be affected, except in one rat, the smallest, which showed enamel hypoplasias in both maxillary incisors and a delayed increase of the mineral content during the maturation stage process. It is concluded that the hypocalcemic state induced did not greatly affect enamel formation. However, occasional enamel aberrations may occur.

Ameloblasts↗
PubMed1996

A comparative study of the transition between predentin and dentin, using various preparative procedures in the rat.

The appearance of the junction between predentin and dentin of rat incisors was investigated after chemical fixation (aldehyde), physical fixation (high pressure freezing and freeze substitution) and by histochemistry. Physical fixation revealed a 1-2 micron wide intermediary zone, in which only the collagen fibers were mineralized. In dentin, which looked denser and more homogeneous, both collagen fibers and intercollagenous spaces were mineralized. The intermediary layer could not been seen after aldehyde fixation. When cationic dyes were used during fixation in order to retain proteoglycans, a 0.5-5 micron border zone located at the junction between predentin and dentin was densely stained on the dentin side, whereas in dentin only the interglobular network displayed electron density. The periodic acid-thiocarbohydrazide-silver proteinate reaction, visualizing glycoproteins, and the phosphotungstic acid/chromic acid mixture, which reveals glycoproteins and phosphorylated proteins, produced extensive staining of the transitional zone located at the dentin edge, whereas staining was weaker in dentin. These morphological and histochemical investigations support the existence of an intermediary zone in which mineralization occurs. This transitional zone between predentin and dentin has specific properties; therefore we propose it be termed metadentin.

Aldehydes↗
PubMedDate not supplied

Developmental dental defects associated with long breast feeding.

Despite its unequivocal advantages, breast feeding may be associated with undesired side-effects. Recently, we have shown an association between exposure via mother's milk to dioxins and developmental defects of the child's teeth. The present study was undertaken to analyze further the association between the duration of breast feeding and the occurrence of dental defects. For this purpose, 2 different populations were selected. The first population comprised 40 children who had mineralization defects in the permanent 1st molars, and their age-living area- and sex-matched controls. The median duration of breast feeding was 9 months in the affected children compared to 6 months in the controls. The defects were more extensive after prolonged breast feeding. The second population consisted of 97 children whose mothers had been encouraged to extensive and prolonged breast feeding. Of these children, 24 had mineralization defects. They all had been breastfed longer than 8 months. In both study populations mineralization defects were associated with the duration of breast feeding. The result suggests that long breast feeding may increase the risk of mineralization defects in healthy children, possibly because of environmental contaminants that interfere with tooth development.

Amelogenesis↗
PubMed2006

Overexpression of transforming growth factor-beta1 in teeth results in detachment of ameloblasts and enamel defects.

Transforming growth factor-beta1 (TGF-beta1) is a key regulator of many cellular processes, including cell adhesion, the immune response and synthesis of extracellular matrix proteins. In the present study, we report the characterization of enamel defects in a transgenic mouse model overexpressing TGF-beta1 in odontoblasts and ameloblasts, its expression being driven by the promoter sequences of the dentin sialophosphoprotein gene. As reported earlier, these mice develop distinct dentin defects similar to those seen in human dentin dysplasia and dentinogenesis imperfecta. A further detailed examination of enamel in these mice revealed that from the early secretory stage, ameloblasts began to detach from dentin to form cyst-like structures. A soft X-ray analysis revealed that this cyst-like structure had a disorganized and partially mineralized matrix with an abnormal mineralization pattern and a globular appearance. In the molars, the enamel was not only pitted and hypoplastic, but enamel rods were completely lost. Thus, altered TGF-beta1 expression in the tooth seems to trigger detachment of ameloblasts and abnormal secretion and deposition of minerals in the cyst-like structures adjoining the dentin. We speculate that the altered expression of TGF-beta1 in teeth impacts the adhesion process of ameloblasts to dentin.

Ameloblasts↗
PubMed2006

How do enamelysin and kallikrein 4 process the 32-kDa enamelin?

The activities of two proteases--enamelysin (MMP-20) and kallikrein 4 (KLK4)--are necessary for dental enamel to achieve its high degree of mineralization. We hypothesize that the selected enamel protein cleavage products which accumulate in the secretory-stage enamel matrix do so because they are resistant to further cleavage by MMP-20. Later, they are degraded by KLK4. The 32-kDa enamelin is the only domain of the parent protein that accumulates in the deeper enamel. Our objective was to identify the cleavage sites of 32-kDa enamelin that are generated by proteolysis with MMP-20 and KLK4. Enamelysin, KLK4, the major amelogenin isoform (P173), and the 32-kDa enamelin were isolated from developing porcine enamel. P173 and the 32-kDa enamelin were incubated with MMP-20 or KLK4 for up to 48 h. Then, the 32-kDa enamelin digestion products were fractionated by reverse-phase high-performance liquid chromatography (RP-HPLC) and characterized by Edman sequencing, amino acid analysis, and mass spectrometry. Enamelysin cleaved the 32-kDa enamelin only after it was deglycosylated. Kallikrein 4 digestion of the 32-kDa enamelin generated nine major cleavage products, six of which were successfully characterized. After 12 h of digestion with KLK4, all of the 32-kDa enamelin had been cleaved, but some cleavage products persisted after 48 h of digestion.

Amelogenesis↗
PubMed2006

A developmental comparison of matrix metalloproteinase-20 and amelogenin null mouse enamel.

Mutations in both the human amelogenin and human matrix metalloproteinase-20 (MMP20, enamelysin) genes cause amelogenesis imperfecta. Both genes have also been individually deleted from the mouse and each deletion results in defective dental enamel. Here, we compare the stage-specific progression of enamel development in continuously erupting mouse incisors from amelogenin null and MMP-20 null mice. Our goal was to closely examine differences in enamel and enamel organ structure between these mice that would allow a better understanding of each protein's function. The predominant feature of the amelogenin null incisors was the late onset of mineral deposition, with little or no protein present within the forming mineral. Conversely, the developing MMP-20 null incisors had a layer of protein between the apical surface of the ameloblasts and the forming enamel. Furthermore, the protein present within the enamel matrix was disorganized. An analysis of crystal structure demonstrated that the thin amelogenin null enamel was plate-like, while the MMP-20 null enamel had a disrupted prism pattern. These results suggest that amelogenin is essential for appositional crystal growth during the early to mid-secretory stage and for the maintenance of the crystal ribbon structure. They also suggest that MMP-20 is responsible for enamel matrix organization and for subsequent efficient reabsorption of enamel matrix proteins. Both genes are essential for the generation of full-thickness enamel containing the characteristic decussating prism pattern.

Absorption↗