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The application of a self-assembling peptide on noncavitated caries lesions is supposed to be a feasible approach to facilitate remineralization and mask their unfavorable appearance. However, demineralizing conditions are common in the oral environment, so the aim of this pH-cycling study was to compare recommended and novel treatment methods regarding their ability to hamper demineralization and as a consequence mask artificial enamel caries lesions. Artificial caries lesions were prepared in bovine enamel and randomly allocated to 11 groups (n = 22). Treatments before pH-cycling were as follows: the application of a self-assembling peptide (Curodont™ Repair [C]), a low-viscosity resin (Icon® [I]), 2 fluoride solutions (10,000 ppm F-: Elmex fluid [E] and 43,350 ppm F-: Tiefenfluorid® [T]), and no intervention (N). During pH-cycling (28 days, 6 × 60 min demineralization/day) half of the specimens in each group were brushed (10 s; 2 ×/day) with either fluoride-free (named e.g., C0) or NaF (1,100 ppm F-; e.g., C1) dentifrice slurry. In another subgroup specimens were pH-cycled but not brushed (NNB). Differences in integrated mineral loss (ΔΔZ), lesion depth (ΔLD), and colorimetric values (ΔΔE) were calculated between values after pre-demineralization, surface treatment, and pH-cycling. Specimens of C0, C1, NNB, N0, N1, T0, and E0 showed significantly increased ΔZ and LD values after pH-cycling (p ≤ 0.003; paired t test). C0, C1, NNB, and N0 showed significantly higher changes in ΔΔZ than E1, I0, I1, and T1 (p < 0.001; ANOVA). Significantly reduced colorimetric values could only be observed for I1, I0, E1, and E0 after treatment and after pH-cycling (p ≤ 0.027; paired t test). In conclusion, under the conditions chosen only the application of a low-viscosity resin could mask caries lesions significantly, whereas self-assembling peptides could neither inhibit lesion progression nor mask the lesions considerably. [ABSTRACT FROM AUTHOR]

High fluoride dentifrice (FD; 5,000 ppm F) has been recommended to arrest root dentine lesions and to control enamel caries in high-risk patients. Also, standard FD (1,100 ppm F) in combination with professional fluoride application has been recommended to control dentine caries, but the effect of this combination on enamel has been considered modest. Considering the lack of evaluation comparing the use of 5,000 ppm FD (5,000-FD) versus acidulated phosphate fluoride (APF) application combined with 1,100 ppm FD (1,100-FD) on the inhibition and repair of caries lesions in both enamel and dentine, we conducted this in situ, double-blind, crossover study of 3 phases of 14 days. In each phase, 18 volunteers wore palatal appliances containing enamel and root dentine specimens, either sound or carious, to evaluate the effect of the treatments on the inhibition or repair of caries lesions, respectively. The treatments were non-FD (negative control), 5,000-FD, or 1 APF gel application on dental specimens combined with 1,100-FD used twice per day (APF + 1,100-FD). The reduction of demineralization and enhancement of remineralization were assessed by surface and cross-sectional hardness. Fluoride concentration was determined on dental specimens and on the formed biofilm. For enamel, APF + 1,100-FD and 5,000-FD did not differ regarding the inhibition of demineralization and repair of caries lesions. However, for dentine the difference between these treatments was inconclusive because while APF + 1,100-FD was more effective than 5,000-FD in caries lesion reduction and repair, 5,000-FD was more effective than APF + 1,100-FD in the reduction of surface demineralization. Therefore, the findings show that the combination of APF + 1,100-FD is as effective as 5,000-FD in enamel inhibition of demineralization and enhancement of remineralization. [ABSTRACT FROM AUTHOR]

Recent advances regarding the caries process indicate that ecological phenomena induced by bacterial acid production tilt the de- and remineralization balance of the dental hard tissues towards demineralization through bacterial acid-induced adaptation and selection within the microbiota - from the dynamic stability stage to the aciduric stage via the acidogenic stage [Takahashi and Nyvad, 2008]. Dentin and root caries can also be partly explained by this hypothesis; however, the fact that these tissues contain a considerable amount of organic material suggests that protein degradation is involved in caries formation. In this review, we compiled relevant histological, biochemical, and microbiological information about dentin/root caries and refined the hypothesis by adding degradation of the organic matrix (the proteolytic stage) to the abovementioned stages. Bacterial acidification not only induces demineralization and exposure of the organic matrix in dentin/root surfaces but also activation of dentin-embedded and salivary matrix metalloproteinases and cathepsins. These phenomena initiate degradation of the demineralized organic matrix in dentin/root surfaces. While a bacterial involvement has never been confirmed in the initial degradation of organic material, the detection of proteolytic/amino acid-degrading bacteria and bacterial metabolites in dentin and root caries suggests a bacterial digestion and metabolism of partly degraded matrix. Moreover, bacterial metabolites might induce pulpitis as an inflammatory/immunomodulatory factor. Root and dentin surfaces are always at risk of becoming demineralized in the oral cavity, and exposed organic materials can be degraded by host-derived proteases contained in saliva and dentin itself. New approaches to the prevention and treatment of root/dentin caries are required. [ABSTRACT FROM AUTHOR]

Objectives: The aim of this double-blinded, randomized, cross-over in situ study was to evaluate the re- and demineralization characteristics of sound enamel as well as lowly and highly demineralized caries-like enamel lesions after the application of different fluoride compounds.Methods: In each of three experimental legs of 4 weeks, 21 participants wore intraoral mandibular appliances containing 4 bovine enamel specimens (2 lowly and 2 highly demineralized). Each specimen included one sound enamel and either one lowly demineralized (7 days, pH 4.95) or one highly demineralized (21 days, pH 4.95) lesion, and was positioned 1 mm below the acrylic under a plastic mesh. The three randomly allocated treatments (application only) included the following dentifrices: (1) 1,100 ppm F as NaF, (2) 1,100 ppm F as SnF2 and (3) 0 ppm F (fluoride-free) as negative control. Differences in integrated mineral loss (x0394;x0394;Z) and lesion depth (x0394;LD) were calculated between values before and after the in situ period using transversal microradiography.Results: Of the 21 participants, 6 did not complete the study and 2 were excluded due to protocol violation. Irrespectively of the treatment, higher baseline mineral loss and lesion depth led to a less pronounced change in mineral loss and lesion depth. Except for x0394;x0394;Z of the dentifrice with 0 ppm F, sound surfaces showed significantly higher x0394;x0394;Z and x0394;LD values compared with lowly and highly demineralized lesions (p < 0.05, t test).Conclusion: Re- and demineralization characteristics of enamel depended directly on baseline mineral loss and lesion depth. Treatment groups should therefore be well balanced with respect to baseline mineral loss and lesion depth. [ABSTRACT FROM AUTHOR]

The purpose of this clinical trial was to evaluate the effect of 1 year of daily application of 10% w/v CPP-ACP (casein phosphopeptide-amorphous calcium phosphate) paste in addition to regular toothbrushing with fluoridated toothpaste on the remineralization of enamel carious lesions in preschool children using quantitative light-induced fluorescence (QLF). A total of 103 Thai children (aged 21/2-31/2 years) with high caries risk who had at least 1 enamel carious lesion (ICDAS 1-3) on the labial surface of the upper anterior teeth were assigned to receive either CPP-ACP paste (n = 53) or placebo control (n = 50) following toothbrushing with fluoridated toothpaste after lunch at school. QLF measurement was performed at baseline, 6 months and 1 year. At 1 year, a significant reduction in fluorescence loss (ΔF), lesion area and lesion volume (ΔQ; p ≤ 0.001) of the lesions were found over time in both groups. However, no significant difference was observed between the groups (p = 0.79, 0.98 and 0.88, respectively). There was no statistically significant difference between the odds of ΔQ transition to a stage of regression or arrest compared with progression from baseline to 1 year between the two groups (OR = 1.03, 95% CI 0.31-3.39). The daily application of 10% w/v CPP-ACP paste on a school day for 1 year resulted in no improvement of enamel carious lesion remineralization in the primary upper anterior teeth as assessed by QLF. The lesion improvement was not superior to remineralization from regular toothbrushing with fluoridated toothpaste alone in these children. © 2015 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Demineralization in dentinal caries and erosion exposes dentine organic matrix. This exposed matrix, containing type I collagen and non-collagenous proteins, is then degraded by host collagenolytic enzymes, matrix metalloproteinases (MMPs) and cysteine cathepsins. The knowledge of the identities and function of these enzymes in dentine has accumulated only within the last 15 years, but has already formed a field of research called 'dentine degradomics'. This research has demonstrated the role of endogenous collagenolytic enzymes in caries and erosion development. In demineralized dentine, the enzymes degrade triple-helical collagen molecules, leading to the gradual loss of collagen matrix. Even before that, they can cleave off the terminal non-helical ends of collagen molecules called telopeptides, leading to the structural changes at the intramolecular gap areas, which may affect or even prevent intrafibrillar remineralization, which is considered essential in restoring the dentine's mechanical properties. They may also cause the loss of non-collagenous proteins that could serve as nucleation sites for remineralization. Here we review the findings demonstrating that inhibition of salivary or dentine endogenous MMPs and cysteine cathepsins may provide preventive means against the progression of caries or erosion. Furthermore, we also suggest the future directions for the new experimental preventive research to gain more knowledge of the enzymes and their function during and after dentine demineralization, and the pathways to find the clinically acceptable means to prevent the functional activity of these enzymes. © 2015 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

The possibility for remineralization of advanced root dentin lesions was investigated in vitro. Lesions were produced in acidic buffer solution with 0.1 and 0.5 ppm fluoride, for 3 and 5 weeks, respectively, using a single-section model. Next, the sections were immersed in a remineralization solution containing 0.1 ppm F (as NaF) for 20 weeks. Microradiographs were made after each 4-week-period. The lesions were around 500 μm deep, with mineral loss values between 11,000 and 18,000 vol%·μm. After 20 weeks of remineralization, the absolute amounts of deposited mineral ranged from 7,500 to 10,000 vol%·μm, corresponding to a repair between 50 and 85%. Lesion depth was, on average, reduced by 199 μm. This was not significantly different (at p < 0.05) between the four experimental groups. This study showed that remineralization of advanced dentinal lesions is possible in spite of the virtual absence of mineral in the lesion body after demineralization. The surface layer of the lesion was the preferred site for mineral deposition until mineral content values reached those of sound dentine. The mineral content in the lesion body increased with time, at a rate reflecting the initial severity of the lesion. We conclude that a remineralized surface layer does not inhibit transport of mineral ions to the body and that the remineralization in the lesion body reflected the number of sites for crystal growth. [ABSTRACT FROM AUTHOR]

A root dentin single-section model was developed to compare the efficacy of different fluoride treatments on the remineralization of lesions. Shallow (~170 μm) and deep (~400 μm) lesions were produced in acetic acid buffer solutions (pH 5.0) with 0.1- and 0.5-ppm fluoride for 3 days and 2 weeks, respectively. Next, the sections were pH-cycled for 4 weeks. Following the pH cycling, all sections were first remineralized for 5 weeks, then subjected to 10 days of demineralization. The treatments were (1) no treatment (control), (2) daily 1,450-ppm NaF toothpaste, (3) weekly 4,000-ppm fluoride solution, (4) a combination of treatments 2 and 3. In the shallow lesions, the 4,000-ppm fluoride solution and the combination treatment enhanced mineral deposition at the lesion front, producing a second, slightly hyperremineralized layer. Similarly, in the deep lesions a second remineralized layer was detected. In all lesions, the fluoride solution treatment showed significantly more remineralization compared to the control and the toothpaste treatment (p<0.05), most of which was formed during the pH cycling. In the demineralization period, the control showed significantly higher mineral loss than all other treatments. These results indicate that a 4,000-ppm fluoride solution might be effective for remineralization of root dentin lesions even over 400 μm depth. [ABSTRACT FROM AUTHOR]

Though the mineral distribution of the dentine carious lesion varies largely from tooth to tooth and from patient to patient, there are two main distribution profiles that characterize natural carious lesions in dentine. These profiles include softened and subsurface lesion types. The mineral distribution relationship between the starting profile and the profile after remineralization is not known. In order to study the relational aspects, we have produced demineralized dentine samples in vitro with mineral profiles similar to those of typical natural carious lesions, and subsequently remineralized the samples in a remineralizing solution with various fluoride concentrations (0, 2 and 10 ppm F). The mineral distributions were obtained by using an improved microradiographic technique. In addition, the nature of deposited mineral was analyzed by diamond-coupled total internal reflectance spectroscopy. Definite relationship was observed between the original lesion mineral distribution and the mineral distributions following remineralization. The amount of mineral present in approximately the first 50 μm of the lesion influenced the overall mineral profile after remineralization, possibly through influencing ion transport. If the amount was high (> approximately 10 vol%), the deposited mineral was confined to the surface (0-50 μm). The original mineral at those depths acted like a nucleus of mineral regrowth when the amount of residual mineral was intermediate, and like a transport barrier when the surface layer was well mineralized. If a surface barrier was not present, mineral was deposited at deeper depths in the lesion. Fluoride effect on dentine remineralization was dependent on the original mineral content and its distribution in the lesion. Although a high concentration of fluoride was very effective in low-mineral lesions, it produced hyperremineralization on well-mineralized subsurface lesions so that it prevented effective remineralization especially in deeper lesions. [ABSTRACT FROM AUTHOR]

The remineralization of whole human dentine treated with a neutral EDTA solution was investigated: the treatment periods were 15, 30 and 120 min. From the literature it is known that EDTA removes noncollagenous proteins (NCPs) from dentine powders. In order to extract more phosphoproteins from dentine lesions, in part of this work samples were also treated with 1 M NaCl or 4 M guanidine chloride solutions. All the dentine samples after the treatments mentioned were immersed subsequently in a remineralizing solution without fluoride for 2 weeks and microradiographed. To investigate the effects of fluoride, samples treated with EDTA for 120 min were also remineralized with 2ppm fluoride in solution. The results presented show that: (1) Measurable remineralization did not occur when fluoride was free in the remineralizing solution. Because remineralization occurred neither at the lesion front nor in the nonmineral part of the surface-softened tissue, presumably the NCPs (inhibitors) of underlying dentine diffused into the tissue during the remineralization period. (2) 2ppm fluoride caused remineralization at the lesion front. In this case we assume fluoride either acted as nucleating agent or overcame the NCP effects at the lesion front. [ABSTRACT FROM AUTHOR]