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The first ICNARA conference (International Conference on Novel Anticaries and Remineralizing Agents) was held in Chile in January, 2008, and the proceedings were published in Advances in Dental Research (Volume 21, 2009). That issue of Advances summarized the state of the science and set a research agenda for the future for two key components of caries management, namely, antibacterial agents and remineralizing agents. The second conference (ICNARA 2, January 2012) provided an update on science and new directions for research and clinical practice. Over the past decade, renewed efforts have been made across the world to establish proven methods of caries risk assessment and to provide direction for improved methods of caries management based upon risk levels. Evidence-based caries risk assessment tools are now available. The need for improved therapy to reduce the bacterial challenge that initiates the caries process, and to enhance remineralization, is now very clear. Fluoride therapy alone is insufficient to control the caries process in high-risk individuals. New remineralizing and anticaries products and new delivery systems are in development, and ICNARA 2 presents future technology for the management of dental caries.

Abstract Dental caries is a transmissible bacterial disease process caused by acids from bacterial metabolism diffusing into enamel and dentine and dissolving the mineral. The bacteria responsible produce organic acids as a by-product of their metabolism of fermentable carbohydrates. The caries process is a continuum resulting from many cycles of demineralization and remineralization. Demineralization begins at the atomic level at the crystal surface inside the enamel or dentine and can continue unless halted with the end-point being cavitation. There are many possibilities to intervene in this continuing process to arrest or reverse the progress of the lesion. Remineralization is the natural repair process for non-cavitated lesions, and relies on calcium and phosphate ions assisted by fluoride to rebuild a new surface on existing crystal remnants in subsurface lesions remaining after demineralization. These remineralized crystals are acid resistant, being much less soluble than the original mineral.

The science behind caries prevention and reversal is well understood. A recent clinical trial has confirmed that reducing caries risk results in a reduction in dental decay. Dental caries progression or reversal depends upon the balance between demineralization and remineralization and can be visualized for clinical purposes as the "caries balance." This balance is determined by the relative weights of the sums of pathological factors and protective factors. A structured caries risk assessment should be carried out based upon the concept of the caries balance. Following the risk assessment, a treatment plan is devised which leads to the control of dental caries for the patient. The balance between pathological and preventive factors can be swung in the direction of caries intervention and prevention by the active role of the dentist and his/her auxiliary staff.

This paper reviews the probable mechanism of dental caries and the role of fluoride in the inhibition or reversal of that process. The initial stages of root caries are comparable to enamel caries, being the acid dissolution of mineral resulting from acids generated by bacterial metabolism. The fermentation of carbohydrates by oral bacteria including mutans streptococci and lactobacilli initiate the root caries process, removing mineral from among the organic matrix which is primarily composed of collagen. Subsequent to this demineralization, the organic material can be further broken down by bacterial enzymes. Fluoride inhibits mineral loss during the acid dissolution process and enhances remineralization in a similar manner to that which occurs in dental enamel.

In situ models to assess the ability of oral care products or food components to enhance remineralization and/or inhibit demineralization of tooth enamel or roots must be very carefully designed to minimize the confounding effects of the many variables involved. Controlling these variables as closely as possible is essential if meaningful answers are to be obtained from the models. We have developed an in situ model which combines the experience of several groups. Detailed screening of subjects is essential. Selection criteria should include good general health, good dental health, mandibular partial denture, at least eight natural teeth, no active caries lesions, known fluoride history, normal salivary function, and no medications that affect salivary function. Each subject carries a sound enamel slab and an enamel slab with a pre-formed caries-like lesion (demineralized in vitro) in his/her denture on each side of the mouth for test periods of two or four weeks. The demineralization challenge is controlled by extra-oral immersion of the appliances in sucrose daily. Daily product exposure or daily food component exposure is used as desired. Compliance indicators and a diet diary are included. Whole saliva flow rate (unstimulated), plaque acidogenicity, and salivary fluoride are monitored during the test periods. At the end of the test period, the test slabs are assessed for mineral change, after being sectioned, by means of cross-sectional microhardness or microradiography. The mineral loss or gain (delta M, microns x vol%), compared with adjacent control sections retained in the lab, is calculated as change in delta Z (microns x vol%), namely, delta M = delta ZTEST - delta ZCONTROL.(ABSTRACT TRUNCATED AT 250 WORDS)

A pH cycling model which incorporated a severe demineralization component was used to evaluate fluoride uptake and lesion progression for each of a NaF-based dentifrice, NaF-based mouthrinse and a monofluorophosphate (MFP)-based dentifrice. Simultaneous transverse fluoride and calcium profiles across the resulting artificial lesions were obtained using a proton microprobe technique with a resolution of approximately 10 microns. Longitudinal microhardness testing and proton microprobe calcium profiles were used to determine the extent of lesion progression (delta Z) with respect to untreated controls. Under the pH cycling conditions of the present study, the NaF dentifrice and mouthwash were observed to have a considerably higher uptake of fluoride in the lesion than the MFP dentifrice. Although the mineral content profiles of the lesions differed for treatments with each of the fluoride products, the differences were not significantly different in this model.

The anti-caries activity of fluoride is contributed to in several ways. Two major aspects of fluoride action are (i) the inhibition of demineralization at the crystal surfaces within the tooth, and (ii) the enhancement of subsurface remineralization resulting in arrestment or reversal of caries lesions. Fluoride present in the aqueous phase at the apatite crystal surface may play a determining role in the inhibition of enamel or dentin demineralization. In one part of the present study, the initial dissolution rate of synthetic carbonated-apatite in acetate buffers was measured with fluoride present in the buffer in the 0-2.6 mmol/L (0-50 ppm) range. Inhibition of demineralization was shown to be a logarithmic function of the fluoride concentration in solution. In the second part of the present study, an in vitro pH-cycling model was used for determination of the effect on net de/remineralization of enamel by treatment solutions containing fluoride in the 0-26 mmol/L (0-500 ppm) range. The net mineral loss was shown to be negatively related to the logarithm of the fluoride concentration. These studies have demonstrated an exponential quantitative relationship between fluoride concentration and inhibition of apatite demineralization or enhancement of remineralization. The clinical implications are (i) that simply increasing fluoride concentration may not necessarily give increased cariostatic benefit, and (ii) that improving the means of delivery of relatively low fluoride concentrations for longer times should be more appropriate for enhancing clinical efficacy.

The aim of the present study was to examine a sodium fluoride anticalculus dentifrice product containing soluble pyrophosphate for its ability to promote remineralization and/or inhibit demineralization of dental enamel in a pH cycling model in vitro. Enamel crowns with windows were subjected to 14 days of alternating demineralization and remineralization periods at 37 degrees C. Teeth were immersed 5 min daily in one of the test dentifrice systems (1:3 slurry in deionized water) between the demineralization and remineralization cycles. Test dentifrices included (1) sodium fluoride (NaF; 1,100 ppm F)/silica abrasive (Crest) and (2) NaF (1,100 ppm F) with 3.3% soluble pyrophosphate/silica abrasive (Crest Tartar Control). Controls included a placebo dentifrice (silica abrasive) with no added fluoride and a group which received no treatment at all, i.e., demineralization/remineralization only. Overall, both of the NaF dentifrices were very effective in limiting in vitro caries progression and were not significantly different from each other. Inclusion of pyrophosphate in the NaF dentifrice did not affect the net outcome of the cycling demineralization/remineralization processes which is in agreement with recent clinical and in situ studies of these products.

The presence of clinically detectable areas of decalcification (observable as whitened areas) following the removal of orthodontic appliances is well recognized. The aim of the present study was to determine quantitatively the amount of demineralization and the ability of commercially available products to inhibit or reverse orthodontically related demineralization. Twenty orthodontic patients scheduled to have premolars extracted were randomly divided into four groups--one control and three test groups. The extracted premolars (numbering 58) were bracketed using an acid-etch composite system; each patient was given precise oral hygiene instructions and supplied with a sodium fluoride (1,100 ppm fluoride) dentifrice and an orthodontic toothbrush. The control group brushed only with the supplied dentifrice. In addition to brushing with the dentifrice, those in test group I rinsed once each night with a sodium fluoride (0.05%) mouthrinse; group II received a weekly topical APF treatment (1.2% fluoride); and Group III received a weekly topical APF treatment and rinsed once each night with the sodium fluoride mouthrinse. All premolars were extracted after 1 calendar month. Mineral profiles were determined on cross-sectioned teeth 50 to 75 micron occlusal and cervical to the brackets, directly underneath the brackets, and 500 micron away from the brackets. The control teeth (dentifrice only) demonstrated up to 15% demineralization to a depth of 50 micron. All of the test teeth produced rehardening and/or inhibition of demineralization (P less than 0.01). Those in test group III showed a particularly hard outer layer. The study demonstrated that measurable demineralization occurred around orthodontic appliances after only 1 month and this demineralization can be completely inhibited and/or reversed by the use of commercially available fluoride products.