Dental Fluorosis Developed in Post-secretory Enamel

1986 ◽  
Vol 65 (12) ◽  
pp. 1406-1409 ◽  
Author(s):  
A. Richards ◽  
J. Kragstrup ◽  
K. Josephsen ◽  
O. Fejerskov

The aim of this study was to test whether dental fluorosis can be produced by administration of chronic doses of fluoride during only the post-secretory stage of enamel mineralization. Eight control and eight experimental pigs matched by weight and litter were fed a low-fluoride diet (<0.05 mg F-/kg b.w. daily) from weaning to slaughter at 14 months. The test group received an oral dose of 2 mg F -/kg b.w. per day from 8 months of age. Lower fourth pre-molars were at the post-secretory stage at the start of fluoride administration (confirmed by tetracycline marker) and were just erupting at slaughter. All of the fourth pre-molar teeth from the test group developed diffuse enamel hypomineralization indistinguishable from human fluorosis. No such lesions were seen in any of the teeth from the control animals. It was concluded that enamel fluorosis may be caused by fluoride exposure in the maturation phase only. The pathogenic mechanism may be an effect either on the selective loss of protein or on the influx of mineral, both of which occur during the post-secretory or maturation stage of enamel formation.

2019 ◽  
Vol 98 (9) ◽  
pp. 994-1001 ◽  
Author(s):  
S. Houari ◽  
E. Picard ◽  
T. Wurtz ◽  
E. Vennat ◽  
N. Roubier ◽  
...  

Enamel formation and quality are dependent on environmental conditions, including exposure to fluoride, which is a widespread natural element. Fluoride is routinely used to prevent caries. However, when absorbed in excess, fluoride may also lead to altered enamel structural properties associated with enamel gene expression modulations. As iron plays a determinant role in enamel quality, the aim of our study was to evaluate the iron metabolism in dental epithelial cells and forming enamel of mice exposed to fluoride, as well as its putative relation with enamel mechanical properties. Iron storage was investigated in dental epithelial cells with Perl’s blue staining and secondary ion mass spectrometry imaging. Iron was mainly stored by maturation-stage ameloblasts involved in terminal enamel mineralization. Iron storage was drastically reduced by fluoride. Among the proteins involved in iron metabolism, ferritin heavy chain (Fth), in charge of iron storage, appeared as the preferential target of fluoride according to quantitative real-time polymerase chain reaction, Western blotting, and immunohistochemistry analyses. Fluorotic enamel presented a decreased quantity of iron oxides attested by electron spin resonance technique, altered mechanical properties measured by nanoindentation, and ultrastructural defects analyzed by scanning electron microscopy and energy dispersive x-ray spectroscopy. The in vivo functional role of Fth was illustrated with Fth+/-mice, which incorporated less iron into their dental epithelium and exhibited poor enamel quality. These data demonstrate that exposure to excessive fluoride decreases ameloblast iron storage, which contributes to the defective structural and mechanical properties in rodent fluorotic enamel. They raise the question of fluoride’s effects on iron storage in other cells and organs that may contribute to its effects on population health.


2008 ◽  
Vol 389 (6) ◽  
Author(s):  
Yuhe Lu ◽  
Petros Papagerakis ◽  
Yasuo Yamakoshi ◽  
Jan C.-C. Hu ◽  
John D. Bartlett ◽  
...  

Abstract Two proteases are secreted into the enamel matrix of developing teeth. The early protease is enamelysin (MMP-20). The late protease is kallikrein 4 (KLK4). Mutations in MMP20 and KLK4 both cause autosomal recessive amelogenesis imperfecta, a condition featuring soft, porous enamel containing residual protein. MMP-20 is secreted along with enamel proteins by secretory-stage ameloblasts. Enamel protein-cleavage products accumulate in the space between the crystal ribbons, helping to support them. MMP-20 steadily cleaves accumulated enamel proteins, so their concentration decreases with depth. KLK4 is secreted by transition- and maturation-stage ameloblasts. KLK4 aggressively degrades the retained organic matrix following the termination of enamel protein secretion. The principle functions of MMP-20 and KLK4 in dental enamel formation are to facilitate the orderly replacement of organic matrix with mineral, generating an enamel layer that is harder, less porous, and unstained by retained enamel proteins.


2020 ◽  
Vol 117 (32) ◽  
pp. 19201-19208 ◽  
Author(s):  
Yushi Bai ◽  
Zanlin Yu ◽  
Larry Ackerman ◽  
Yan Zhang ◽  
Johan Bonde ◽  
...  

As the hardest tissue formed by vertebrates, enamel represents nature’s engineering masterpiece with complex organizations of fibrous apatite crystals at the nanometer scale. Supramolecular assemblies of enamel matrix proteins (EMPs) play a key role as the structural scaffolds for regulating mineral morphology during enamel development. However, to achieve maximum tissue hardness, most organic content in enamel is digested and removed at the maturation stage, and thus knowledge of a structural protein template that could guide enamel mineralization is limited at this date. Herein, by examining a gene-modified mouse that lacked enzymatic degradation of EMPs, we demonstrate the presence of protein nanoribbons as the structural scaffolds in developing enamel matrix. Using in vitro mineralization assays we showed that both recombinant and enamel-tissue–based amelogenin nanoribbons are capable of guiding fibrous apatite nanocrystal formation. In accordance with our understanding of the natural process of enamel formation, templated crystal growth was achieved by interaction of amelogenin scaffolds with acidic macromolecules that facilitate the formation of an amorphous calcium phosphate precursor which gradually transforms into oriented apatite fibers along the protein nanoribbons. Furthermore, this study elucidated that matrix metalloproteinase-20 is a critical regulator of the enamel mineralization as only a recombinant analog of a MMP20-cleavage product of amelogenin was capable of guiding apatite mineralization. This study highlights that supramolecular assembly of the scaffold protein, its enzymatic processing, and its ability to interact with acidic carrier proteins are critical steps for proper enamel development.


1989 ◽  
Vol 3 (2) ◽  
pp. 168-176 ◽  
Author(s):  
I. Gedalia ◽  
L. Shapira

Fluoride passes from the mother to fetal teeth. Much of the fluoride is taken up in secretory enamel, probably by the forming mineral apatite crystals. Some is retained with residual proteins. The low concentration of fluoride in the inner enamel is incorporated mainly during the secretory stage, while the enhanced concentration in the surface enamel is produced during the much longer maturation stage. Mature, hard enamel is generally absent during fetal life. The clinical question is whether prenatal fluoride imparts an additional benefit to the universally accepted effect of postnatal fluoride. In general, surface enamel fluoride levels of deciduous teeth increase with increasing pre- and postnatal fluoride administration. A consistent level of caries protection has been reported with pre- and postnatal administration of fluoride unrelated to the acquisition of fluoride in the surface enamel. Many children develop enamel opacities in their deciduous dentition related by various factors to enamel mineralization disturbances in drinking water areas even low in fluoride. Accumulation of fluoride due to an increased fluoride intake is a feature of fluorosed enamel in the deciduous as well as permanent dentition. The resulting mature fluorosed enamel retains a relatively high proportion of immature matrix proteins onto the crystal surface. The degree of fluorosis of the deciduous dentition is less compared with that of the permanent dentition, due probably to a partial protection afforded by the maternal loss of fluoride, formerly known as the "placental barrier".


2008 ◽  
Vol 106 (1) ◽  
pp. 214-222 ◽  
Author(s):  
Eija Salmela ◽  
Carin Sahlberg ◽  
Satu Alaluusua ◽  
Pirjo-Liisa Lukinmaa

1987 ◽  
Vol 1 (2) ◽  
pp. 267-275 ◽  
Author(s):  
P.R. Garant ◽  
T. Sasaki ◽  
P.E. Colflesh

Ouabain-sensitive, K-dependent p-nitrophenyl phosphatase (p-NPPase) activity was localized ultra-Ocytochemically in the lateral plasma membranes of secretory ameloblasts and the stratum intermedium and principally in the papillary layer cells of aldehyde-fixed rat incisor enamel organs by the one-step lead method. Daily intraperitoneal injection of ouabain (250 μg, 500 μg, and 1 mg/100 g body weight) for two weeks reduced p-NPPase activity in the enamel organ cells. However, the degree to which this activity was reduced appeared to vary among the experimental animals. Addition of ouabain to the cytochemical incubation medium completely inhibited p-NPPase activity in the tissues. Although long-term ouabain injection did not result in any morphological alterations of the enamel organ cells, it caused, in part, an appearance of electron-dense, homogeneous matrix-like substances (MS) in the extracellular spaces of the ameloblast layers at both the secretion and maturation stages. In addition, long-term ouabain injection appeared to have resulted in delayed maturation of enamel as measured by energy-dispersive x-ray analysis of Ca and P in surface enamel. These results suggest that Na-K-ATPase of enamel organ cells may participate in the net flow (removal) of organic matrix components and water from the enamel during the maturation stage of enamel formation. It is suggested that this flow is maintained by local osmotic gradients generated by Na-K-ATPase within the papillary layer.


2009 ◽  
Vol 54 (4) ◽  
pp. 313-321 ◽  
Author(s):  
Isabel Maria Porto ◽  
José Merzel ◽  
Frederico Barbosa de Sousa ◽  
Luciano Bachmann ◽  
Jaime Aparecido Cury ◽  
...  

2013 ◽  
Vol 38 (4) ◽  
pp. 358-362 ◽  
Author(s):  
Y Wang ◽  
Y Sa ◽  
S Liang ◽  
T Jiang

SUMMARY Dental fluorosis is a developmental disturbance of enamel caused by excessive fluoride on ameloblasts during enamel formation. Patients often present to the dentist with a main goal of improving their esthetic appearance. This case report describes a minimally invasive technique for treating a severe case of enamel fluorosis with brown surface aspect and small defects. A selective mega-abrasion and microabrasion were used to recreate macro- and micro- surface morphology, followed by power bleaching, home bleaching, and resin infiltration to improve the esthetic appearance.


1987 ◽  
Vol 66 (8) ◽  
pp. 1360-1363 ◽  
Author(s):  
J.W. Bawden ◽  
T.G. Deaton ◽  
M.A. Crenshaw

This study investigated the diffusion of fluoride through the enamel organ in vitro. The rat molar explants used were entirely in the secretory stage or predominantly in the maturation stage of enamel formation. The removal of the enamel organ or metabolic inhibition with iodoacetate caused significant increases in enamel fluoride uptake at both stages of enamel formation. Inhibition with dinitrophenol caused a significant increase only in the maturation phase. Uptake of fluoride in enamel was related to the fluoride concentration in the medium, except in the maturation stage explants, where increasing the medium fluoride concentration from 0.05 ppm to 0.08 ppm did not significantly increase fluoride uptake at any of the three observation times. The findings indicate that the enamel organ exists as a diffusion-limiting membrane to the movement of fluoride from the extracellular fluid compartment to the developing enamel.


Author(s):  
E. Angeles Martínez-Mier

Fluoride is a naturally occurring element with multiple implications for human health. This review discusses its metabolism and toxicity, along with the current understanding of the mechanism of action of fluoride and its role as a safe and effective agent in the prevention of dental caries. The relationship between excessive fluoride intake during periods of dental enamel formation and the development of dental fluorosis is also reviewed.


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