Possible Function of Matrix Proteins in Fluoride Incorporation into Enamel Mineral during Porcine Amelogenesis

Aoba, Takaaki; Collins, Jimmy H.; Moreno, E.C.

doi:10.1177/00220345890680070501

Cited by 23 publications

(12 citation statements)

References 28 publications

(21 reference statements)

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“…Under in vivo situations during the secretory stage of amelogenesis, it is likely that abundant matrix proteins coat enamel crystal surfaces, thereby retarding fluoride incorporation into the forming enamel mineral. In vitro studies (Aoba et al, 1989) In independent studies with the rat incisor model , it was also found that administration of 25 through 100 ppm fluoride in drinking water brings about an increase in the stable fluoride content of secretory enamel tissue but without an appreciable increase in the labile fluoride. The fluoride in the "labile" form is considered as a pool available for incorporation into the enamel crystallites by surface exchange and crystal growth processes.…”

Section: Fluoride Incorporation Into Forming Mammalian Enamelmentioning

confidence: 98%

The Effect of Fluoride On Apatite Structure and Growth

Aoba

1997

Critical Reviews in Oral Biology & Medicine

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Fluoride participates in many aspects of calcium phosphate formation in vivo and has enormous effects on the process and on the nature and properties of formed mineral. The most well-documented effect of fluoride is that this ion substitutes for a column hydroxyl in the apatite structure, giving rise to a reduction of crystal volume and a concomitant increase in structural stability. In the process of enamel mineralization during amelogenesis (a unique model for the cell-mediated formation of well-crystallized carbonatoapatite), free fluoride ions in the fluid phase are supposed to accelerate the hydrolysis of acidic precursor(s) and increase the driving force for the growth of apatitic mineral. Once fluoride is incorporated into the enamel mineral, the ion likely affects the subsequent mineralization process by reducing the solubility of the mineral and thereby modulating the ionic composition in the fluid surrounding the mineral, and enhancing the matrix protein-mineral interaction. But excess fluoride leads to anomalous enamel formation by retarding tissue maturation. It is worth noting that enameloid/enamel minerals found in vertebrate teeth have a wide range of CO3 and fluoride substitutions. In the evolutionary process from elasmobranch through teleost enameloid to mammalian enamel, the biosystems appear to develop regulatory functions for limiting the fluoridation of the formed mineral, but this development is accompanied by an increase of carbonate substitution or defects in the mineral. In research on the cariostatic effect of fluoride, considerable emphasis is placed on the roles of free fluoride ions (i.e., preventing the dissolution and accelerating the kinetics of remineralization) in the oral fluid bathing tooth mineral. Fluoride also has been used for the treatment of osteoporosis, but much still remains to be learned about maximizing the benefit and minimizing the risk of fluoride when used as a public health measure.

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Section: Fluoride Incorporation Into Forming Mammalian Enamelmentioning

confidence: 98%

The Effect of Fluoride On Apatite Structure and Growth

Aoba

1997

Critical Reviews in Oral Biology & Medicine

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186

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“…Most of the fluoride transported in ionic forms can be readily incorporated into growing enamel crystals, if the precipitation reaction is not down-regulated by inhibitors, such as abundant protein moieties existing during the enamel secretion. However, analytical data of the forming enamel in pigs and rats (Aoba et al ., 1989a(Aoba et al ., , 1990b showed that a substantial fraction of the fluoride ions remain in a labile form, which are free in the fluid or associated with organic matter. This labile pool of fluoride corresponds to 25-30% of the total fluoride in the secretory enamel, while the corresponding pool becomes marginal (less than a few % of the total fluoride) in the mature enamel, where most of the matrix proteins have been removed, so that the mineral surface most likely becomes available for reactions with fluoride ions.…”

Section: (4) Fluoride Uptake Into Developing Enamel: Fluoride Pools Imentioning

confidence: 99%

Dental Fluorosis: Chemistry and Biology

Aoba

Fejerskov²

2002

Critical Reviews in Oral Biology & Medicine

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ABSTRACT:This review aims at discussing the pathogenesis of enamel fluorosis in relation to a putative linkage among ameloblastic activities, secreted enamel matrix proteins and multiple proteases, growing enamel crystals, and fluid composition, including calcium and fluoride ions. Fluoride is the most important caries-preventive agent in dentistry. In the last two decades, increasing fluoride exposure in various forms and vehicles is most likely the explanation for an increase in the prevalence of mild-to-moderate forms of dental fluorosis in many communities, not the least in those in which controlled water fluoridation has been established. The effects of fluoride on enamel formation causing dental fluorosis in man are cumulative, rather than requiring a specific threshold dose, depending on the total fluoride intake from all sources and the duration of fluoride exposure. Enamel mineralization is highly sensitive to free fluoride ions, which uniquely promote the hydrolysis of acidic precursors such as octacalcium phosphate and precipitation of fluoridated apatite crystals. Once fluoride is incorporated into enamel crystals, the ion likely affects the subsequent mineralization process by reducing the solubility of the mineral and thereby modulating the ionic composition in the fluid surrounding the mineral. In the light of evidence obtained in human and animal studies, it is now most likely that enamel hypomineralization in fluorotic teeth is due predominantly to the aberrant effects of excess fluoride on the rates at which matrix proteins break down and/or the rates at which the by-products from this degradation are withdrawn from the maturing enamel. Any interference with enamel matrix removal could yield retarding effects on the accompanying crystal growth through the maturation stages, resulting in different magnitudes of enamel porosity at the time of tooth eruption. Currently, there is no direct proof that fluoride at micromolar levels affects proliferation and differentiation of enamel organ cells. Fluoride does not seem to affect the production and secretion of enamel matrix proteins and proteases within the dose range causing dental fluorosis in man. Most likely, the fluoride uptake interferes, indirectly, with the protease activities by decreasing free Ca 2+ concentration in the mineralizing milieu. The Ca 2+ -mediated regulation of protease activities is consistent with the in situobservations that (a) enzymatic cleavages of the amelogenins take place only at slow rates through the secretory phase with the limited calcium transport and that, (b) under normal amelogenesis, the amelogenin degradation appears to be accelerated during the transitional and early maturation stages with the increased calcium transport. Since the predominant cariostatic effect of fluoride is not due to its uptake by the enamel during tooth development, it is possible to obtain extensive caries reduction without a concomitant risk of dental fluorosis. Further efforts and research are needed to settle the currently uncertain ...

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“…Reprinted with permission from Elsevier Science. (Aoba et al, 1989). Due to technical difficulties, the actual concentration of free F -in enamel fluid has not been widely measured.…”

Section: Al-f Complexes and Fluorosismentioning

confidence: 99%