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- Materials and methods
- Conflicts of interest
Understanding the mechanism of action of oral care active ingredients and technologies aids the long-term development of new and improved products. In the absence of this mechanistic understanding, research and development is generally limited to minor improvements in product performance over time. Although fluoride has long been recognised for its ability to help fight cavities[1, 2], understanding the specific mechanism(s) by which fluoride provides its benefits has been an ongoing topic of discussion over the past several decades[3-7]. In reality, most published studies, whether in vitro, in situ or full-scale clinical trials, have, in one way or another, provided insight into fluoride's mechanism of action. This knowledge has helped manufacturers significantly improve dentifrice stability, bioavailability and, importantly, overall anticaries performance[8, 9].
While caries is the result of acids generated by plaque bacteria, dental erosion, a more recently emerging oral care issue compared with caries, results from the excessive intake of acid-containing food and beverages – an unfortunate outcome of modern lifestyles. Widespread replacement of water and milk with acid-containing sports drinks, juices and carbonated beverages has the potential to dramatically reduce the life expectancy of exposed tooth surfaces. Exposure of tooth surfaces to excessive intake of acid-containing products can result in surface softening of the enamel, followed by rapid loss of the softened mineral when exposed to abrasive forces. Tooth abrasion can come from numerous sources, including the excessive ingestion of certain types of foods, such as raw foods, or even from the tongue because of its relatively constant movement over exposed tooth surfaces. While research has proven that subsurface mineral loss occurring during the early stages of caries can be replaced through the process of remineralisation[5-9] it is generally accepted that tooth surface loss resulting from erosive softening followed by abrasion is permanent. Although rehardening of surface-softened mineral is possible in the laboratory, it is far less likely to occur in vivo. Deposition onto the enamel surface of a protective barrier layer that is capable of protecting tooth-surface mineral against the initial softening that can lead to tooth surface loss may offer an effective approach for protecting teeth against erosive acid damage.
The current study focuses on the ability of the most commonly used fluoride sources in global dentifrices to deposit a barrier layer on the surface of pellicle-coated, acid-challenged enamel. Pellicle-coated enamel represents the natural condition of enamel in vivo[16, 17], and treatment with each of the fluoride-based products after an aggressive acid challenge provides a mechanistic insight into the ability of each of the commonly used fluoride sources to react with the acid-challenged substrate and create a protective barrier layer.
- Top of page
- Materials and methods
- Conflicts of interest
One mechanism that fluoride-containing products use to strengthen tooth mineral is through the process of remineralisation, substituting F in place of hydroxyl groups that have been removed from the enamel during the early stages of the caries process. Despite the widespread availability of fluoride dentifrices, and the confirmed ability of fluoride-containing dentifrices to strengthen enamel, the reported incidence of dental erosion is on the rise. Although protective against both the initiation and progression of caries, routine exposure to some of the commonly used fluoride sources does not appear to provide sufficient protection against the level of challenge that can be presented by dietary, erosive acids[19, 20].
Erosive acids attack tooth mineral by first softening the surface enamel, and this softening makes the enamel more susceptible than sound enamel to some of the abrasive forces at work in the mouth[11, 12]. There are a number of possible ways to help prevent both the initiation and progression of dental erosion:
- Reduce the level of acid intake
- Control how and where the acid is ingested
- Strengthen enamel to be more resistant to acid
- Coat exposed tooth surfaces with a protective barrier layer.
For oral care products, delivery of an agent that both makes enamel more acid-resistant and coats exposed tooth surfaces with an invisible, acid-resistant and retentive barrier layer capable of withstanding elevated levels of acid challenge would, in theory, have a clear advantage over agents that do not function via such a unique mechanism. This is especially true if the agent does not impede the delivery and penetration of fluoride into the enamel on exposed tooth surfaces.
There is a growing body of evidence, using a range of dental erosion models, that stannous fluoride provides an enhanced level of protection against erosive acid challenges compared with other F sources commonly used in oral care products[15, 21-25]. Clearly, not all models are alike and each model must stand on its own merit. However, when widely different models consistently provide similar outcomes, the collective data tend to point to similar conclusions. As we began to investigate the effects of different fluoride sources on the prevention of dental erosion, we made use of several models to understand not only if stannous fluoride consistently provided enhanced protection compared with other commonly used sources of fluoride but also why and how.
Using a variety of performance-based models, both in vitro and in situ, we have consistently demonstrated enhanced performance for stabilised SnF2 dentifrices compared with other marketed, fluoride-based formulations[15, 22, 23, 26, 27]. Additional studies, using models focused on understanding mechanisms related to performance, have demonstrated that:
- Stannous fluoride deposits onto powdered hydroxyapatite (HAP) surfaces, and this deposition occurs either from aqueous treatments or from fully formulated, stabilised SnF2 dentifrice. In each case, deposition of SnF2 resulted in enhanced protection to the HAP surfaces against acid challenges.
- Stannous fluoride deposits onto pellicle-coated enamel surfaces, beginning with the first treatment, and remains on the tooth surface for at least several hours after treatment. Additional treatments result in deposition of a more intense barrier layer.
The present study was designed to demonstrate how a barrier layer might attach to enamel surfaces, particularly pellicle-coated surfaces subjected to an erosive acid challenge before treatment with product. The method clearly demonstrates that a protective layer has been deposited onto pellicle-coated, acid-challenged tooth enamel. The results of the study highlight the mechanistic ability of the SnF2 to deposit onto the type of surface that is likely to occur in vivo, in a way that is different from other types of fluoride. This is important, because this difference in surface reactivity may help explain why stabilised stannous-containing products have routinely demonstrated an ability to provide a different level of protection against erosive acid challenges.
Alizarin red S (See Figure 3), an anthraquinone, has been used for many years as a calcium-selective dye. It was first noted as a biological stain in 1567, when it was observed that when fed to animals, it stained their teeth and bones red. When exposed to reactive calcium-containing surfaces, an alizarin red S–calcium complex is formed through a chelation process, and the end product is a clearly visible red stain. This is the result of reaction between the alizarin red S and calcium via its sulfonate and hydroxyl groups. When certain elements are present in sufficient quantities, and are strongly attached to enamel surfaces, such as SnF2, deposition of alizarin red S onto the enamel surface is blocked. Unpublished studies from our collaboration have suggested the level of stain can be generally associated with the level of protection measured in both in vitro[15, 22, 26] and in situ erosion clinical trials[23, 27], with higher levels of stain associated with agents delivering lower levels of protection. Although not included in this study, placebo (0 ppm F toothpaste) treatment results in a score of 4 on this scale, which is associated with 0% protection. While fluoride from all of the test products would be expected to react with free calcium sites on the acid-challenged enamel, only the treatment from the stabilised SnF2 dentifrice was able to attach with a sufficient level of retention that it was not displaced by exposure to the calcium-selective alizarin red S dye. This result suggests that either the bond between F and Ca resulting from treatment with the other F salts tested was weaker than that of the SnF2-treated enamel, or that the bond between the stabilised SnF2 and the enamel surface is more than simple attachment between F and exposed Ca sites on the tooth surface. The literature suggests that stannous-containing products are capable of forming metal-rich precipitates on the enamel surface, most likely Ca(SnF3)2, SnOHPO4 or Sn3F3PO4. All of these have been shown to provide enamel with high acid resistance. Results of the current study suggest the barrier layer deposited on enamel after treatment with stabilised SnF2 is likely linked to both calcium and phosphate sites on the enamel surface, providing the overall complex a more secure means to remain attached to the acid-challenged surface. This result would suggest that the barrier layer associated with the use of the stabilised SnF2 treatment is likely composed of more than one of the proposed metal-rich precipitates. Further studies are needed to confirm specifically which of the precipitates are present after treatment with the stabilised SnF2 product.