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When lesion formation in dental enamel or dentine is studied in vitro, a well-defined area of the material, a 'window', is exposed to the demineralization medium. In the present experiments, we report the effect of window width on lesion formation in enamel and dentine. Rectangular windows, longest dimension always 5 mm and shortest dimension varying from 0.5 to 5 mm, were exposed to demineralization media. Lesions in dentine were formed by placing the specimens in an acidified unstirred 6% carboxymethyl cellulose (CMC) gel, an unstirred 0.5% CMC gel, a mildly stirred 0.5% CMC gel, or in a mildly stirred demineralization solution. Lesions in enamel were formed only in an unstirred acidified 6% CMC gel. pH in the demineralization media was 5.0 in all experiments. The microradiographic technique was used to assess lesion depth and mineral loss (vol% x microm) of lesions formed. Lesions formed in the unstirred gels were deeper, and there was a larger mineral loss, the narrower the window. There was no effect of window size on lesions formed in stirred systems. These effects can be explained by the strong dependence of concentration gradient in stirred gels just outside the exposed window on the window size. The phenomenon found here in vitro may at least partly explain why secondary caries may lead to localized, but relatively deep, lesions.

Thin sections of natural white spot enamel lesions (WS) and of artificial in vitro lesions (VL) were remineralized simultaneously in vitro. The sections, clamped in a PMMA holder, were microradiographed at baseline and after remineralization in a calcium- and phosphate-containing solution (pH = 7.0; 1 ppm F) after 2 and 4 weeks. All data were analyzed with respect to baseline. The results show that the lesion depth values did not change significantly during 2 and 4 weeks of remineralization. The mineral accumulation (change in DeltaZ), however, was substantial and significant in WS and VL. In WS the change in mineral accumulation was roughly proportional to the amount of mineral at baseline. The WS accumulated more than two times the amount of mineral than VL in the same periods of remineralization. After 4 weeks of remineralization the maximum mineral value Vmax in the surface layer of the WS was nearly up to the sound enamel level thick approximate87 vol%. This study shows that the technique and calculation procedure described make this single section method attractive for longitudinal demineralization-remineralization studies in vitro or in situ. Both WS and VL samples obviously remineralized in vitro similarly with respect to the baseline. Furthermore, this in vitro work indicates that remineralization inhibitors present in saliva, and previously penetrated into the enamel tissue, do not influence remineralization later on.

Objectives: To investigate the influence of different electrolyte concentrations on the electrical resistance of sound human enamel-dentine cylinders in vitro., Methods: Forty cylinders of 3-mm diameter and 2-mm length were drilled from 40 extracted caries-free third molar teeth. For ease of handling the samples were fixed in Perspex discs by means of a cyanoacrylate-adhesive. An a.c. source (frequency 500 Hz, amplitude 1 microA) with a high internal resistance was applied. Only Ohm's resistance was measured. The resistance measurements on the samples were made after storage in distilled water, 0.16 mM NaCl, 1.6 mM NaCl and 16 mM NaCl and 160 mM NaCl for 24 h., Results: The mean resistance values were 2026 +/- 152, 1835 +/- 178, 1605 +/- 364, 483 +/- 265 and 60 +/- 33 k omega, respectively. All values were statistically significantly different (Wilcoxon test; P < 0.0001)., Conclusion: It is concluded that the choice of electrolyte solution influences the resistance values of the enamel-dentine samples. This effect should be taken into account when measuring electrical resistances in vivo and in vitro.

Single-section techniques are attractive in enamel de- and remineralization investigations because they allow longitudinal studies in which mineral changes can be assessed by microradiography (TMR). Nail varnish (NV) is in general applied to coat the cut thin-section sides. The aims of this study were to investigate: (1) NV penetration depth in cut surfaces of demineralized enamel, (2) the influence of NV on cut surfaces of demineralized enamel on TMR, (3) the influence of NV penetration on a following remineralization. Cut surfaces of thin sections of demineralized enamel were NV coated; the NV was peeled off and the penetration depth assessed by confocal laser scanning microscopy. The NV penetration was 18+/-5 micrometer (mean+/-SD) in demineralized enamel. To evaluate the possible influence of NV on TMR, cut surfaces of thin sections of demineralized enamel were coated (twice) and microradiographed before and after nail varnishing. The NV effect (total effect of penetrated and surface NV) on the main parameters of TMR, Ld and DeltaZ, was less than 5% of the mean values. In the remineralization experiment (remineralization with 1.5 mM Ca2+, 0.9 mM phosphate, pH 7, 1 ppm F for 1 and 2 weeks), lesions in bulk samples, lesions in thin sections with NV-coated cut surfaces and lesions in thin sections in a PMMA (polymethylmethacrylate) holder were compared. (1) The remineralization of bulk samples and of NV-coated thin sections is different in one aspect. The amounts of mineral deposited in the lesions expressed as DeltaZ are comparable after 1 week. But because the NV penetrates part of the lesion outside, there was an Ld difference. The lesion depth difference between bulk lesions and NV-coated lesions in thin sections was statistically significant and was about 19% less in NV-coated lesions after 1 week; after 2 weeks of remineralization there was no difference in Ld between bulk- and NV-coated lesions any more. (2) There was no difference in remineralization efficacy between lesions in bulk samples and lesions in thin sections in the PMMA holder.

The aim of this investigation was to study the effect of the interproximal use of fluoride (F)-impregnated and non-impregnated birch toothpicks on the degree of de- and remineralization of enamel and dentine in situ. Ten volunteers with complete dentures in the upper jaw participated. Each subject had four specimens: (1) sound enamel, (2) demineralized enamel, (3) sound dentine and (4) demineralized dentine; placed pairwise at two approximal sites (15/16 and 25/26) of the maxillary prosthesis. The study involved three test periods (A, B and C), each lasting 4 weeks. In A, the subjects used F toothpicks (impregnated in 4% NaF) and, in B, nonimpregnated toothpicks 3 times daily. During period C, no toothpicks were used. Dentifrice or other F-containing products were not allowed during the 4-week periods. Transversal microradiography was used to determine lesion depth (ld) and mineral loss (DeltaZ). The results revealed that all the sound samples lost mineral during the three experimental periods; DeltaZ for both enamel and dentine was less for A and B compared with C (p<0.01) and less for A compared with B and C for dentine (p<0.05, p<0.01). The demineralized samples also lost mineral, apart from dentine, during periods A and B, i.e. when F-impregnated and non-impregnated toothpicks were used; ld for enamel and DeltaZ for dentine were less for A compared with C (p<0.05). Four weeks' use of toothpicks, especially F-impregnated toothpicks, thus reduces the demineralization of enamel and dentine at approximal sites in situ.

In cardiology and research involving the interactions between restorative materials and dental hard tissues, it is important for small changes in tooth mineral content to be measurable. Currently, transverse microradiography (TMR) is the most accepted tool for the above purpose. Electron Probe Microanalysis (EPMA) can yield both qualitative identification of elements and quantitative compositional information. The purpose of this study was to compare the mineral distribution in well-defined artificial lesions, in dentin and enamel, by the use of both TMR and EPMA on the same sample. The good correlation between the two sets of data validates EPMA as a technique and helps in the interpretation of its results. The data from TMR analysis are expressed as vol% of mineral, while EPMA gives the levels of Ca and phosphate in wt%. The conversion between the two sets of data is complicated by the fact that local density is, as yet, unknown.

Three aspects of quantitative transverse microradiography are described and discussed: (1) the average mineral loss parameter of enamel or dentin lesions (R) in vol%; (2) mineral distribution visualization of lesions by means of a computer-assisted videodensitometric (CAV) method; and (3) the microradiography of hyper-remineralized lesions. "R", defined as the average amount of mineral lost (or gained) in a lesion per unit lesion length, is a useful parameter in dental caries. The results show that, in vitro, R is about constant over the demineralization period for enamel and dentin. This was found even for quite different dissolution kinetics. R is strongly reduced by the presence of small amounts of fluoride in the demineralizing system. R of dentin lesions is smaller than for enamel lesions. We conclude that the mineral loss value (delta Z) and the lesion depth (ld) are in general dependent parameters during in vitro or in situ studies on enamel or dentin. During lesion formation, mineral loss from the lesion and acid penetration in the tissue are obviously linked. This is possible only if the mineral content in the lesion does not change very much after passage of the lesion front. The CAV method presented is illustrated for enamel lesions formed in vitro and in situ.

The aim of the study was to compare initial caries development in fluoridated and non-fluoridated deciduous and permanent enamel in situ. Enamel slabs were mounted in removable appliances and worn for 4 wks. Significantly larger lesions developed in deciduous than in permanent enamel when no topical fluorides were used. Fluoride mouthrinsing partly prevented lesion development in deciduous and completely in permanent enamel. Initial enamel caries not detected by microradiography can be visualized by CLSM (confocal laser scanning microscopy).

The aim of the present investigation was to combine 2 techniques suitable for lesion characterization: quantitative microradiography (TMR) and confocal laser scanning microscopy (CLSM) on in vivo induced lesions with and without a fluoride varnish (Duraphat) treatment. Orthodontic bands were attached to premolars to be extracted for orthodontic reasons to induce enamel caries on the buccal surfaces. In the caries development part of the study, 1 tooth of each pair received at the start 1 topical application with the fluoride varnish Duraphat, the contralateral tooth serving as untreated control. All teeth were extracted after 4 weeks. In the caries progression part, the premolars were banded for 4 weeks without any treatment to induce caries, 1 premolar in each pair was then extracted and analyzed. The contralateral tooth received one Duraphat application and was extracted after another 2 weeks. In the caries development part of the study, TMR analysis showed that the Duraphat treatment on sound enamel reduced lesion depth by 48% compared to the untreated control. In the caries progression part, no significant difference was found between the untreated teeth extracted after 4 weeks and the fluoride treated lesions extracted after another 2 weeks. CLSM images agreed well with the TMR measurements. In the fluoride treated lesions, the CLSM images showed more light scattering indicating precipitation of material.

Single crystals of synthetic hydroxyapatite have been examined by orientational micro-Raman spectroscopy. The observed Raman bands include the PO4(3-)/OH-internal and external modes over the spectral range from 180 to 3600 cm-1. The Raman-active symmetry tensors (A, E1, and E2) of crystal-class C6 have been assigned to these bands. Intensities of the Raman bands are invariant to the orientation of the a- or b-axis of a single crystal, but depend solely on the c-axis orientation. Changes in the spectral profile thus reflect changes in the c-axis orientation, which, with respect to the known excitation/observation coordinates, can be determined through the angular dependencies of Raman bands due to A and E2 symmetries. The useful bands are those of the PO4(3-)v4 vibrational mode, which contains relatively well-defined bands due to E2 (581 cm-1) and A (593 cm-1) symmetries. A preliminary Raman study on crystallites near the intact outer surface of human enamel has also been carried out. Strong orientational dependencies similar to those of hydroxyapatite single crystals have been observed among the bands in enamel spectra. This suggests that the crystallites in the region investigated are highly oriented. The results were consistent with an averaged orientation of the crystallite c-axis being perpendicular to the outer surface.

Seventeen subjects with more than 3 x 10(5) mutans streptococci per millilitre of saliva completed this randomised, cross-over study. Four different chewing-gums, containing: (1) 70% xylitol, (2) 35% xylitol + 35% sorbitol, (3) 17.5% xylitol + 52.5% sorbitol, and (4) 70% sorbitol, were tested. The participants used 12 pieces of each gum per day for 25 days. During the four experimental periods, they wore a removable palatinal plate containing two demineralised enamel samples, and brushed their teeth with a non-fluoridated toothpaste. The results showed that an increased concentration of xylitol in the gum resulted in a lower number of mutans streptococci in both saliva and dental plaque, although the decreases were only significant in the saliva samples (p < 0.01). The pH drop in plaque, measured in vivo after a 1-min mouthrinse with a 10% sorbitol solution, was least pronounced after the 70% xylitol gum and most pronounced after the 70% sorbitol gum period (p < 0.01). No significant differences were found after a mouthrinse with a 10% sucrose solution. All demineralised enamel samples lost mineral during the experimental periods. However, the lesion depth as well as the mineral loss values, assessed microradiographically, did not differ significantly between the four chewing-gums.

Raman spectra containing the distinct band at 322 cm-1 due to CaF2 or CaF2-like material formed in/on fluoridated bovine enamel were recorded using a micro-Raman spectrograph. Due to increasing levels of background fluorescence with increasing thickness of enamel, the Raman measurements were carried out on thin regions of wedged enamel sections. The distribution of the CaF2 or CaF2-like material was estimated using a simple model. The results indicate that 1/3 of the total CaF2 was concentrated within the narrow depth < 2 microns with high CaF2 concentrations (> 10 wt%), and that the majority of the CaF2 was distributed over the depths up to 26 microns (1 wt% CaF2). SEM observations on fractured fluoridated enamel confirmed that morphological changes were present in the depth range comparable to that of the high CaF2 concentration region expected from the Raman analysis. In deeper regions where lower concentration (< 10%) but a large amount of CaF2 was still expected, the SEM images failed to distinguish between the normal and fluoridated enamel. After KOH treatment, the Raman spectra did not show evidence of the CaF2 peak and the SEM micrographs also confirmed the removal of globules. The peak position of the Raman band of the CaF2 formed by the fluoridation was identical to that of pure CaF2. However, the linewidth was 23 cm-1 (FWHM) and a factor of 2 broader than that of pure CaF2 (12 cm-1). This implies that the lattice dynamics of the CaF2 formed by fluoridation is different from of pure CaF2, and that the material formed is 'CaF2-like' or 'disordered CaF2'.

Investigations on the caries-preventive effect of calcium fluoride have been seriously hampered by the lack of adequate detection techniques. In this paper, the micro-Raman technique is introduced as a suitable method for CaF2 quantification with a spot size typically 5 microns. Advantages of this measuring technique and associated problems are described for CaF2 determination in the presence of large amounts of hydroxyapatite. The data show that a comparative analysis of Raman intensities of calcium fluoride and phosphate ions of hydroxyapatite can be used for quantification of CaF2 concentrations. The intensity behaviour of the CaF2 and hydroxyapatite Raman lines is explained considering the absorption-scattering cross-sections of the two components. The ratio of the Raman intensity (322 cm-1) of CaF2 to the phosphate Raman intensity (432/447 cm-1) of hydroxyapatite was found to be related linearly to the ratio of the concentration of CaF2 to that of hydroxyapatite. At present, the lower limit of CaF2 quantification is approximately 3 wt%. The technique has already been applied on fluoridated bovine enamel, and Raman emissions due to CaF2 or CaF2-like material formed on/in enamel have been detected for the first time.

Fluoridated composites are able to reduce or inhibit secondary caries around fillings. The aims of this study were firstly to investigate the amount of F released in vitro from composites with a F content between 0 and 26 vol% as a function of time over a 1-year period. A second aim was to correlate the in vitro data on F release with enamel demineralisation data in situ after a 1-month period. The results show that all fluoridated composites release sizable amounts of F in solution, the total amounts of F released from three composites were proportional to log t over at least 1 year. In one case proportionality of the total amount of F released with t was observed. Possible mechanisms of F release are considered. The results presented also show a linear relation between the log of in vitro F release data and the effects on enamel demineralisation in situ next to the composite. Extrapolation of the data reveals that a F release of about 200-300 micrograms/cm2 over a 1-month period from a fluoridated composite would completely inhibit secondary caries under plaque conditions.

This paper compares the experimental techniques utilized to assess the de- or remineralization of enamel or dentin in intra-oral studies. In in situ studies, it is important for one to know how much mineral has been lost or gained, and where the loss or gain occurred. The main emphasis in this paper is on techniques suitable for direct or indirect mineral quantification. The measuring techniques considered are microradiography, iodine absorptiometry, various microhardness tests, polarized light, light-scattering, iodide permeability, and wet chemical analysis. The various techniques are compared concerning suitability for the determination of mineral content in vol% (or wt%), mineral changes in vol% micron (or kg.m-2), and mineral distributions. Furthermore, sample preparation, the importance of protein penetration, nominal mineral loss range, the estimated mineral loss threshold, and the applicability to dentin are compared and considered. It is concluded that, although more than ten techniques are available for the measurement of changes after de- or remineralization in situ, transverse microradiography is the most practical technique for the direct and quantitative measurement of mineral content, mineral changes, and mineral distributions. Cross-sectional microhardness testing and light-scattering are also practical indirect techniques for quantitative mineral loss (or gain) determination in intra-oral studies.

This paper describes the effect of a 2 ppm fluoride containing, slightly acidic mouthrinse (pH = 6) on the remineralization of enamel lesions in vitro. The rinse was applied twice daily for 2 min, on about 85 microns in depth artificial lesions. Artificial enamel lesions were formed at pH = 5 in a 6% CMC gel. The lesions were subsequently remineralized in vitro in a neutral remineralizing solution (1.5 mM Ca and 0.9 mM phosphate) with or without the application of the rinse. After 3 weeks the samples were evaluated by means of quantitative microradiography. The results showed that a statistically significant reduction in lesion depth occurred of 48 and 29% with or without rinse application, with respect to the original lesion depth. The effect of the rinse compared with no rinse decreased the lesion depth by 40%. The data indicate that application of a slightly acidic rinse with 2 ppm fluoride applied twice a day, stimulates the remineralization at the lesion front and does not lead to blocking of enamel pores observed after acidic, high level F applications (APF).

In this paper, data are presented on the in situ demineralization of human enamel as a function of the demineralization period. To quantify the mineral loss parameters versus time, it is important to obtain information on the kinetics, and thus on the mechanism of dental caries. The results show that for in situ enamel demineralization, the lesion depth as well as the mineral loss parameter both vary linearly with the demineralization time. This is in contrast to in vitro lesion formation where the third power, or the square power of the lesion depth is linearly related to the demineralization time. In in situ demineralization, the rate-determining step of the demineralization process is the inhibitor-controlled dissolution process at the enamel crystallite surfaces, while the inhibitor content (F-, proteins etc.) in the lesion originating from the plaque, saliva and enamel is high. Furthermore, the study indicates that in in situ demineralization, interprismatic mineral loss is very important.

The aim of this article was to investigate the effects of methanehydroxydiphosphonate (MHDP) and fluoride (F) separately and combined, on the demineralization process in enamel and in dentine under constant composition conditions. The demineralization was carried out in solutions containing 3 mM calcium, 3 mM phosphate, pH = 5.0, and either 6 microM MHDP, 12 microM F or 6 microM MHDP and 12 microM F. After demineralization periods (t) between 24 and 140 h, the lesion depth l and the mineral loss delta Z were measured by transverse microradiography of the enamel and dentine specimens. The amount of mineral lost during demineralization averaged over the lesion depth, R = delta Z/l, was calculated. R approximately 17 vol% for both enamel and dentine, both delta Z and l being greater for dentine than for enamel by approximately the same factor. The results show that under the same conditions dentine is attacked much more strongly than enamel. The lesion progress with time is quite different for the two tissues: in enamel the lesion depth progresses als l3 = alpha t + beta, in dentine as l2 = alpha't + beta'. The slopes alpha and alpha' decrease in the order MHDP > F > MHDP+F. In enamel the combined inhibitor effect is only slightly larger than the effect of F alone; in dentine the inhibiting effects of F and MHDP are approximately additive. The inhibitor interactions can be described by the Langmuir adsorption theory.(ABSTRACT TRUNCATED AT 250 WORDS)

Shark enamel consists of nearly pure fluorapatite and has been shown to demineralize in an in situ caries model. The present study was conducted to investigate whether additional fluoride supplementation in the form of mouthrinsing would inhibit lesion development in shark enamel. The study slabs of shark enamel were mounted in dental appliances. Six individuals wore the appliances while rinsing daily with a neutral 0.2% NaF solution for 4 wk. The specimens were analyzed by means of quantitative microradiography, and the data compared with a previous study using untreated shark enamel and the same participants. It was found that fluoride rinsing did not measurably inhibit enamel demineralization in 4 wk. Scanning electron microradiographs showed that calcium fluoride-like material was not formed on shark enamel after neutral fluoride treatment, supporting a previous study. The present study indicates, therefore, that formation of a calcium fluoride-like material on the enamel surface may be essential for the cariostatic effect of topical agents.

The depth of caries lesions produced in bovine enamel situated in an unstirred 0.1 mol/L lactic acid buffer at pH 4.5 has been studied as a function of time and of concentration of the inhibitor ethane-1-hydroxy-1, 1-diphosphonate, EHDP. At concentrations of EHDP up to 5 mmol/L, the lesion progress decreased with increasing concentration of inhibitor. At higher concentrations, the opposite effect was observed. At low inhibitor concentration (0.1 mmol/L), the lesion depth to the third power varied linearly with time. At intermediate concentrations (0.25-5 mmol/L), the square of the lesion depth varied linearly with time. At high inhibitor concentrations (25-100 mmol/L), the lesion depth varied linearly with time. It was also shown that the rate of dissolution of calcium hydroxyapatite crystals was retarded by low concentrations of EHDP, but accelerated by high concentrations of EHDP. The results are related to a physico-chemical model describing lesion formation.

A comparison was made between the demineralization of enamel and dentine with and without abraded surfaces. This was done in a pH-cycling experiment for different demineralization/remineralization ratios--in the range from 1:1 to 1:4--and for different fluoride additions (up to 2 ppm) in solution. A new automatic pH-cycling system, in which the de- and remineralization solutions have a constant composition during the de- and remineralization cycles, was used to create mineral loss in human dentine and enamel. Changes in mineral content were monitored by means of longitudinal microradiography. A linear correlation was found between the amount of mineral lost and the total demineralization time for both dentine and enamel. The demineralization rates were comparable for abraded enamel and dentine and for polished enamel and dentine, and this rate was roughly doubled by the removal of the outer surface for both tissues. This showed that the presence of the outer surface is equally important to dentine and enamel. Under the pH-cycling conditions used, a logarithmic relation was found between the addition of fluoride and the decrease in demineralization for both enamel and dentine. The inhibitory effect of fluoride on demineralization was most pronounced on abraded enamel, followed by pumice-polished enamel, abraded dentine and pumice-polished dentine. About 2 ppm fluoride was needed under the conditions used to stop enamel demineralization completely; in the case of dentine, however, this amount of added fluoride did not inhibit demineralization.

The relative cariostatic effects of fluoride as fluorapatite, CaF2, loosely-bound fluoride, or KOH-soluble fluoride are debated. The present study was carried out to investigate this further in an intra-oral caries model. Pairs of premolars extracted for orthodontic reasons were used. Enamel from one tooth of each pair was used as control (untreated). Two slabs were cut from the enamel of the other contralateral premolar. These slabs were treated with 2% NaF for 24 h. One slab was then treated with 1 mol/L KOH twice for 24 h for removal of all loosely-bound fluoride. The slabs treated with 2% NaF and then with 1 mol/L KOH would contain the KOH-insoluble fluoride. Those treated with only 2% NaF would, in addition, contain KOH-soluble fluoride. Each slab, control, KOH-insoluble F, and KOH-soluble and insoluble F was mounted on different upper removable appliances. The slabs were covered with orthodontic banding material, thus allowing space for plaque accumulation. Five individuals wore the appliance in three separate four-week periods. The slabs were analyzed by quantitative microradiography. The average mineral loss (delta Z) was 1680 +/- 1000 vol% x microns in the control teeth, 620 +/- 76 vol% x microns in the KOH-soluble and -insoluble F teeth, and 2167 +/- 1278 vol% x microns in the KOH-insoluble F teeth. The average lesion depths were 90 +/- 41 microns in the control teeth, 35.3 +/- 5.5 microns in the KOH-soluble F teeth, and 88 +/- 35 microns in the KOH-insoluble F teeth. It was concluded that only KOH-soluble fluoride reduced mineral loss and lesion depths significantly, compared with the untreated teeth.

To determine the fluoride uptake in enamel and dentin, a fluoridating composite resin was fixed at a 100-microns distance from bovine enamel and dentin for 2 weeks. The results revealed a substantial increase in the level of fluoride in both enamel and dentin. This model investigation showed that the fluoride released by the composite resin was effectively taken up by the surrounding tissues. The fluoride released from the composite resin and the subsequent uptake by the tissues would be expected to protect against secondary caries.

This paper discusses loosely bound fluoride and its role in dental caries and prevention. Loosely bound fluoride (abbr. by Fa) is fluoride adsorbed onto enamel mineral crystallites. Several recent studies indicate that a high total level of fluoride in enamel does not guarantee protection against caries. This leads to the conclusion that a major part of fluoride present in the solid enamel is not active in prevention. The adsorption of Fa to the mineral under acidic conditions is described. Most likely there is a dynamic equilibrium between fluoride in solution and adsorbed Fa at the crystal surface interface. When the crystallite is completely covered by adsorbed Fa, there is a maximum inhibition of dissolution. The rate of dissolution of mineral depends on pH, the actual concentrations of calcium and phosphate in the liquid in contact with the crystallites, and on the fraction of the surface covered by adsorbed fluoride. The fluoride, Fs, localized in the inner part of the crystallites is relatively unimportant. "CaF2-like" material can be formed on and in enamel depending on conditions. The in vivo-formed globular "CaF2-like" material is not pure CaF2 and releases F- ions when dissolving; these ions will also be partly adsorbed as Fa in and on enamel. Presently, the amount and importance of Fa originating from in vivo-formed "CaF2-like" material are not known. The level of fluoride, Fa, necessary for strong inhibition of enamel demineralization in vitro is estimated to correspond to a fluoride concentration, FL, in the liquid phase of 1 ppm or 50 mumol/L fluoride ions.(ABSTRACT TRUNCATED AT 250 WORDS)

The in situ remineralization of 100-microns-deep enamel lesions positioned in a full prosthesis just under the first molar was determined in 13 participants after 3 months. The outer surface of the samples was always flush with the acrylic surface: there was no measurable plaque accumulation on the samples. The effect of not brushing of the samples (A) is compared with the effect of brushing with a nonfluoridated dentifrice (B) or with a fluoridated paste (C) containing 1,250 ppm F. The results show that lesion depth (and mineral loss) data increase by about 50% (case A), do not change statistically in case B and decrease by about 40% in case C. The increase of lesion depth in case A is most likely due to acidic food and/or beverage intake by the participants. With respect to nonbrushing, the remineralization effect of brushing with an F-free paste is about 50% and with the fluoridated paste about 90% in 3 months. It is suggested that the remineralization efficacy of fluoridated pastes is due to the cleaning effect of the brushing by the dentifrice (presumably on the pellicle) as well as due to the fluoride effect on mineral nucleation and growth.

The inhibiting effect of a 24 hours application of a fluoridated varnish with various fluoride contents on demineralization of human sound enamel was evaluated in vitro. The varnishes used had the same polyurethane base (Fluor Protector) and contained 0.7; 0.1; 0.05 and 0 wt% fluoride, resp. A constant composition technique was used to demineralize varnished and non-varnished specimens at a pH of 5 for periods upto 2 weeks. Microhardness measurements were carried out after several time intervals to follow mineral loss in time longitudinally. At the end of each experimental run microradiography was carried out to investigate 1) lesion type, 2) lesion depth and 3) mineral loss. It is shown in this study that the fluoride releasing varnishes applied on the enamel for 24 hours can inhibit demineralization completely. No demineralization inhibition with the 0% fluoride varnish application was observed.

The effect of 4% SnF2 on brushite, hydroxyapatite and powdered bovine enamel applied for short, 15 or 30 minute, periods was investigated using infra-red spectroscopy. It was found that brushite was converted into a fluoridated hydroxyapatite, a reaction which was both time and temperature dependent. The reactions of hydroxyapatite and powdered enamel with SnF2 were similar. There was a drop in the OH- peak intesities. X-ray diffraction analysis of these samples showed that F- ions occupied mainly OH positions in the hydroxyapatite lattice structure. In all reactions an increase in temperature from 37 degrees C to 50 degrees C increased the reaction speed by at least a factor 2. The most probable result of in vivi SnF2 application on sound enamel is the formation of a fluoridated hydroxyapatite together wity stannous complexes and amorphous CaF2. In demineralized areas some of the brushite is converted into a fluoridated hydroxyapatite as is some of the remaining hydroxyapatite. In the more protected area of an enamel lesion these reactions may well continue for some time after the topical fluoride application; Sn2F3PO4 may also therefore be formed.

In this investigation, microhardness changes in partially demineralized human enamel were studied after in vivo use of fluoridated toothpaste systems. Flattened enamel specimens were demineralized in vitro and subsequently positioned in approximal positions in the prostheses of 27 participants for three weeks; the samples were plaque-covered in vivo. After brushing for one week with a non-fluoridated paste to achieve an in vivo equilibrium, participants brushed with an assigned product for a two-week period. This test was a six-way cross-over design which used randomization of subjects. Five fluoridated and one non-fluoridated paste were tested. Knoop hardness measurements were carried out on sound and on in vitro demineralized enamel, and after in vivo exposure of the enamel to the dentifrice treatments. The results showed that during the two weeks of in vivo exposure to the fluoride products, net rehardening of the demineralized enamel did not occur, and no correlation was observed between fluoride uptake into the demineralized enamel and changes in microhardness. That we failed to observe rehardening may be due to the fact that the duration of this study was too short for any net remineralization to have occurred, especially because the samples were constantly covered with plaque. Other possibilities, such as the type and/or severity of the lesions used in this study, may account for the lack of rehardening.

In this study, the total fluoride uptake in partially demineralized enamel from in situ brushing with six dentifrice systems was investigated in vivo among 22 panelists. Five dentifrices with different fluoride systems were compared with a placebo control. Two demineralized enamel discs were placed in proximal positions on specially fabricated dentures worn by each participant. Each treatment involved use of the placebo dentifrice for one week, followed by two weeks of twice-daily use of the test dentifrice. The F- contents of the dentifrices were: A = 1000 ppm F as Na2PO3F + 450 ppm F as NaF; B = 1100 ppm F as NaF; C = 1000 ppm F as Na2PO3F; D = 1000 ppm F as SnF2; E = 1500 ppm F as Na2PO3F; and P = 0 ppm F (placebo). The F- uptakes from A, C, D, and E were not significantly different from each other but were all significantly higher than the placebo. Statistical analysis showed a significantly higher F- level from the NaF-based paste B than that from all other systems. No differences existed between mesial-distal specimens; there was no correlation between F- uptake and age. Significant uptake differences were found between panelists with full and partial prostheses.

A chemical system based on the dialysis principle was used to study protein loss of dental enamel during demineralization with an acetic-acid buffer solution containing calcium and phosphate, in which the fluoride-ion activity was kept constant. This resulted in a subsurface lesion, with a depth of about 130 microns. After demineralization, protein material was isolated from the demineralization solution. u.v. Spectra of the protein showed strong absorbance between 240 and 300 nm. Amino-acid composition showed high glycine, glutamic acid, proline, serine and aspartic acid contents. After 10 days demineralization, the total protein loss was 3 micrograms cm-2; the mineral loss was 16 mg cm-2. Compared with the total enamel-protein content (0.06-0.09 wt per cent) protein loss (0.018 per cent of total lost material) was not proportional to the mineral loss, when a subsurface lesion was formed.

In this paper the mechanism of dental enamel dissolution is discussed. Special attention is given to the anisotropic solubility behaviour (hollow tube formation) of demineralized enamel crystallites. The combined evidence strongly indicates that this peculiar dissolution behaviour is caused by dislocations. The dislocations--linear lattice defects--are present in the crystallite center and are the cause of two active dissolution sites in each crystallite. Initial as well as later stages in the caries process are discussed. Experimental evidence is presented which indicates that the active sites can be inactivated by agents like EHDP and MFP. After inactivation, acid penetration is either prevented or strongly retarded.

Microhardness measurements with the indenter load perpendicular to the artificial carious enamel surfaces can be employed to investigate lesion depth in de- and remineralization of fluoridation studies in vitro or in vivo. In this study, microhardness and lesion depth studies were made on bovine enamel subjected to demineralizing solutions on a gelatin base at pH = 4.5 and 37 degrees C. The parameters studied were load, demineralization period and dialysis of the gelatin. All experimental data are compared with lesions formed in acidified 6% HEC solutions under identical conditions. The results show that lesion formation and mechanical properties of artificially carious enamel are comparable for nonchared HEC and charged gelatin based systems. Because of the higher sensitivity, lesions formed in HEC are to be preferred for lesion depth determinations by means of microhardness indentations. Both gelatin - and HEC based systems show a lesion depth proprotional to the square root of the demineralization period. If gelatin or HEC is dialyzed first, and subsequently used in the demineralizing buffers, the results show that no subsurface lesions are formed but "acid-softening" of the enamel takes place.

Almost twice as much fatty acid was extracted without demineralization from the mature enamel of erupted teeth treated with 2:1 chloroform-methanol as from the enamel of unerupted teeth (32.64 micrograms/g versus 15.60 micrograms/g). Palmitic C16:0, stearic C18:0, oleic C18:1 omega 9 and linoleic acids C18:2 omega 6 were the chief fatty acids detected by gas-liquid chromatography. The percentage of free fatty acids and diglycerides was larger in unerupted than erupted teeth, whereas that of triglycerides, phosphatidylethanolamine and phosphatidylcholine was larger in erupted teeth. These changes may be due to bacteria and other contaminants (saliva and pellicle). The large amounts of free fatty acids, diglycerides, cholesterol and phospholipids as intrinsic components were probably due to the persistence of membrane remnants entombed during enamel formation, as indicated by the visualization of holes and by the increase in the size and number of focal holes after lipid-solvent interaction with the enamel surface. These defects always occurred in rods and never in inter-rod material. Other minute defects, including empty-widened intercrystal spaces, were also observed inside some rods.

Citric acid dissolves crystallites of enamel by initially etching out approximately hexagonal holes in the core of the crystallites, parallel to their long axis. Such acid-treatment influences the crystallite diameter only slightly since the distribution of the diameters of crystallites with a hollow core is not essentially different from those found in sound enamel. In both cases, the average diameter is 37 nm. Crystallites having a central defect and an outer diameter of about 40 nm are split into two parts of approximatley 15 nm in diameter following acid treatment. The central defect is caused exclusively by the acid and not by damage from the electron beam, nor by a combination of acid treatment and electron beam damage.

The diffusion of 45Ca ions in sound bovine enamel at pH 7.0 was studied as a function of temperature in the range 20 degrees-40 degrees C. The experimental data show that the diffusion is governed by two processes with activation energies of about 0.7 and 1.3 eV respectively. These values are considerably larger than the activation energy of calcium ion diffusion in water (0.2 eV). The diffusion process with the activation energy of 1.3 eV is dependent upon the calcium concentration in solution. A model based on the complex pore structure of enamel and on interactions of diffusing ions with the enamel constituents is discussed.