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      Demineralization of Enamel in Primary Second Molars Related to Properties of the Enamel

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          Abstract

          Enamel structure is of importance in demineralization. Differences in porosity in enamel effect the rate of demineralization, seen between permanent and deciduous teeth. Individual differences have been shown in the mean mineral concentration values in enamel, the role of this in demineralization is not thoroughly investigated. The aim of this study was to study variations of depths of artificial lesions of demineralization and to analyze the depth in relation to variations in the chemical and mineral composition of the enamel. A demineralized lesion was created in second primary molars from 18 individuals. Depths of lesions were then related to individual chemical content of the enamel. Enamel responded to demineralization with different lesion depths and this was correlated to the chemical composition. The carbon content in sound enamel was shown to be higher where lesions developed deeper. The lesion was deeper when the degree of porosity of the enamel was higher.

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          Most cited references31

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          The chemistry of enamel caries.

          The chemical changes which occur during the process of carious destruction of enamel are complex due to a number of factors. First, substituted hydroxyapatite, the main component of dental enamel, can behave in a very complex manner during dissolution. This is due not only to its ability to accept substituent ions but also to the wide range of calcium phosphate species which can form following dissolution. In addition, the composition, i.e., the extent of substitution, changes throughout enamel in the direction of carious attack, i.e., from surface to interior. Both surface and positively birefringent zones of the lesion clearly illustrate that carious destruction is not simple dissolution. Selective dissolution of soluble minerals occurs, and there is the probability of reprecipitation. The role of fluoride here is crucial in that not only does it protect enamel per se but also its presence in solution means that rather insoluble fluoridated species can form very easily, encouraging redeposition. The role of organic material clearly needs further investigation, but there is the real possibility of both inhibition of repair and facilitation of redeposition. For the future, delivering fluoride deep into the lesion would appear to offer the prospect of improved repair. This would entail a delivery vehicle which solved the problem of fluoride uptake by apatite at the tooth surface. Elucidation of the role of organic material may also reveal putative mechanisms for encouraging repair and/or protecting the enamel mineral.
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            Improved resin infiltration of natural caries lesions.

            In artificial lesions, improved penetration and the caries-inhibiting properties of infiltrating resins could be observed with increasing penetration coefficients (PCs). The aim of the present study was to compare the penetration abilities of an experimental 'infiltrant' into natural lesions with those of an adhesive in vitro. Extracted human molars and premolars showing proximal white spots were cut across the lesions perpendicular to the surface. Corresponding lesion halves were etched for 120 sec with 15% hydrochloric acid gel and were subsequently treated with either an adhesive (PC: 31 cm/sec) or an infiltrant (PC: 273 cm/sec). Specimens were observed by confocal microscopy and transverse microradiography. Penetration depths of the adhesive were significantly lower compared with those of the infiltrant (p < 0.001; Wilcoxon). It can be concluded that resins with higher PCs (infiltrants) show superior ability to penetrate natural lesions compared with resins with lower PCs.
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              What constitutes dental caries? Histopathology of carious enamel and dentin related to the action of cariogenic biofilms.

              Substantial pH fluctuations within the biofilm on the tooth surface are a ubiquitous and natural phenomenon, taking place at any time during the day and night. The result may be recordable in the dental tissues at only a chemical and/or ultrastructural level (subclinical level). Alternatively, a net loss of mineral leading to dissolution of dental hard tissues may result in a caries lesion that can be seen clinically. Thus, the appearance of the lesion may vary from an initial loss of mineral, seen only in the very surface layers at the ultrastructural level, to total tooth destruction. Regular removal of the biofilm, preferably with a toothpaste containing fluoride, delays or even arrests lesion progression. This can occur at any stage of lesion progression, because it is the biofilm at the tooth or cavity surface that drives the caries process. Active enamel lesions involve surface erosion and subsurface porosity. Inactive or arrested lesions have an abraded surface, but subsurface mineral loss remains, and a true subsurface remineralization is rarely achievable, because the surface zone acts as a diffusion barrier. The dentin reacts to the stimulus in the biofilm by tubular sclerosis and reactionary dentin.
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                Author and article information

                Journal
                ScientificWorldJournal
                ScientificWorldJournal
                TSWJ
                The Scientific World Journal
                The Scientific World Journal
                1537-744X
                2012
                2 May 2012
                : 2012
                : 587254
                Affiliations
                1Department of Pedodontics, Institute of Odontology at the Sahlgrenska Academy, University of Gothenburg, Box 450, SE-405 30 Göteborg, Sweden
                2Department of Pediatric Dentistry, Public Dental Service, Odontologen, Box 7162, SE-402 33 Göteborg, Sweden
                3Centre of Electron Microscopy, Friedrich-Schiller-University, Bachstr. 18, DE- 07743 Jena, Germany
                Author notes

                Academic Editors: M. Alexandre Coelho Sinhoreti and N. Tanoue

                Article
                10.1100/2012/587254
                3354421
                22629152
                3f74bd6b-ef79-4cb8-9e61-675ffa0022b0
                Copyright © 2012 N. Sabel et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 25 October 2011
                : 18 December 2011
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