Role of Streptococcus mutans in human dental decay.

Dental caries is a highly prevalent diet-related disease and is a major public health problem. A goal of modern dentistry is to manage non-cavitated caries lesions non-invasively through remineralization in an attempt to prevent disease progression and improve aesthetics, strength, and function. Remineralization is defined as the process whereby calcium and phosphate ions are supplied from a source external to the tooth to promote ion deposition into crystal voids in demineralized enamel, to produce net mineral gain. Recently, a range of novel calcium-phosphate-based remineralization delivery systems has been developed for clinical application. These delivery systems include crystalline, unstabilized amorphous, or stabilized amorphous formulations of calcium phosphate. These systems are reviewed, and the technology with the most scientific evidence to support its clinical use is the remineralizing system utilizing casein phosphopeptides to stabilize and deliver bioavailable calcium, phosphate, and fluoride ions. The recent clinical evidence for this technology is presented and the mechanism of action discussed. Biomimetic approaches to stabilization of bioavailable calcium, phosphate, and fluoride ions and the localization of these ions to non-cavitated caries lesions for controlled remineralization show promise for the non-invasive management of dental caries.

New Approaches to Enhanced Remineralization of Tooth Enamel

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.

The chemistry of enamel caries.

Since 1935, various mechanisms have been suggested for the formation of subsurface lesions and, in particular, the surface layer covering enamel lesions. The relatively intact mineral-rich and porous surface layer is most likely caused by kinetic events. The suggested mineral-rich outer layer in sound enamel, the organic matrix, the pellicle, or a non-uniform ion distribution have all been shown to be non-essential for surface layer formation; they may, however, influence the rate of surface layer formation. Models based on outer surface protection by adsorbed agents, the dissolution-precipitation mechanism, and combinations of these two models, as well as models based on porosity or solubility gradients, are discussed in this paper together with their advantages and disadvantages. Most models have not explained some important recent experimental observations on initial in vivo caries lesion formation: e.g., initial enamel lesions formed in vivo do not have a surface layer initially but develop this mineral-rich layer later on; and the fact that the F- level in the solid sound enamel is not determining the subsurface lesion formation. Furthermore, the observations that in vitro fluoride ions in the liquid at very low levels (approximately equal to 0.02 ppm) determine surface layer formation are difficult to explain. A new kinetic model for subsurface lesion formation is described, in which inhibitors such as F- or proteins play an important role. The model predicts that if lesions depth and demineralization period are denoted by df and t, lesion progress can be described by: dfp = alpha t + c, where alpha and c are constants with 1 less than or equal to p less than or equal to 3, depending on the lesion formation conditions. If lesion progress is entirely diffusion-controlled, p = 3, corresponding to low inhibitor concentrations; if the inhibitor content is so high that the progress is controlled by processes at the crystallite surface, p = 1. A kinetic mechanism for surface layer formation in vivo is proposed, based on the assumption that F- is a main inhibitor in the plaque-covered acidic in vivo situation. The inhibiting fluoride, adsorbed onto the crystallite surfaces at OH- vacancies, originates from the so-called fluoride in the liquid phase (FL) between the enamel crystallites. Under acidic conditions (plaque), we have, due to an influx of fluoride from the saliva or plaque as FL, an aqueous phase in the enamel supersaturated with respect to the mineral for a small distance (x*) only.(ABSTRACT TRUNCATED AT 400 WORDS)

The nature of early caries lesions in enamel.

Aim: This in vitro study was conducted on enamel blocks of human premolars with the aim of evaluating the remineralization potential of fluoride and ACP-CPP and the combination of ACP-CPP and fluoride on early enamel lesions. Materials and Methods: Fifteen intact carious free human premolars were selected. The coronal part of each tooth was sectioned into four parts to make 4 enamel blocks. The baseline SMH (surface microhardness) was measured for all the enamel specimens using Vickers microhardness (VHN) testing machine. Artificial enamel carious lesions were created by inserting the specimens in demineralization solution for 3 consecutive days. The SMH of the demineralised specimens was evaluated. Then the four enamel sections of each tooth were subjected to various surface treatments , i.e. Group 1- Fluoride varnish, Group 2- ACP-CPP cream, Group 3- Fluoride + ACP-CPP & Group 4- Control (No surface treatment). A caries progression test (pH cycling) was carried out, which consisted of alternative demineralization (3hours) and remineralization with artificial saliva (21 hours) for five consecutive days. After pH cycling again SMH of each specimen was assessed to evaluate the remineralization potential of each surface treatment agent. Then, to asses the remineralization potential of various surface treatments at the subsurface level, each enamel specimen was longitudinally sectioned through the centre to expose the subsurface enamel area. Cross-sectional microhardness (CSMH) was evaluated to assess any subsurface remineralization Results: Statistical analysis using one-way ANOVA followed by multiple comparisons test was applied to detect significant differences at P ≤ 0.05 levels between various surface treatments at different phases. Conclusions: With in the limits, the present study concludes that; ACP-CPP cream is effective, but to a lesser extent than fluoride in remineralizing early enamel caries at surface level. Combination of fluoride and ACP-CPP does not provide any additive remineralization potential compared to fluoride alone. Fluoride, ACP-CPP and their combination are not effective in remineralizing the early enamel caries at the subsurface level.

Remineralization potential of fluoride and amorphous calcium phosphate-casein phospho peptide on enamel lesions: An in vitro comparative evaluation.

Tooth enamel remineralization

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Tooth enamel remineralization