The effect of fluoride on apatite structure and growth.
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 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.
Aoba
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Nippon Dental University, Department of Pathology, Tokyo, Japan.
D000566:Amelogenesis; D000818:Animals; D001031:Apatites / Q000737:chemistry*; D002130:Calcium Phosphates / Q000737:chemistry; D002254:Carbonates / Q000737:chemistry; D002327:Cariostatic Agents / Q000737:chemistry; D003460:Crystallization; D003743:Dental Enamel / Q000378:metabolism; D003746:Dental Enamel Proteins / Q000737:chemistry; D003747:Dental Enamel Solubility; D005459:Fluorides / Q000737:chemistry*; D009050:Fluorosis, Dental / Q000378:metabolism; D006801:Humans; D006868:Hydrolysis; D006878:Hydroxides / Q000737:chemistry; D015394:Molecular Structure; D014074:Tooth Calcification; D014089:Tooth Remineralization
D001031:Apatites; D002130:Calcium Phosphates; D002254:Carbonates; D002327:Cariostatic Agents; D003746:Dental Enamel Proteins; D006878:Hydroxides; C030782:carboapatite; C031356:hydroxide ion; D005459:Fluorides