Caries Process and Fluoride’s Mechanism of Action

Dental caries is an infectious disease caused by the complex interaction of cariogenic (caries-causing) bacteria with carbohydrates (i.e., sugars) on the tooth surface over time. Cariogenic bacteria metabolize carbohydrates for energy and produce organic acids as byproducts. The acids lower the pH in the plaque biofilm.²²

The hydroxyapatite of tooth enamel is primarily composed of phosphate ions (PO₄^3–) and calcium ions (Ca²⁺). Under normal conditions, there is a stable equilibrium between the calcium and phosphate ions in saliva and the crystalline hydroxyapatite that comprises 96% of tooth enamel. When the pH drops below a critical level (approximately 5.5 for enamel, and 6.2 for dentin), it causes the dissolution of tooth mineral (hydroxyapatite) in a process called demineralization. When the natural buffer capacity of saliva elevates pH, minerals are reincorporated into the tooth through the process of remineralization.^22-24

Caries is simply the result of a series of demineralization/remineralization cycles where, over time, demineralization conditions prevail. The caries process can be affected in several ways. One of the most effective methods to prevent caries is by promoting remineralization and slowing down demineralization. This can be accomplished with fluoride therapy.^4,15,25

When fluoride is present in oral fluids (i.e., saliva), fluorapatite, rather than hydroxyapatite, forms during the remineralization process. Fluoride ions (F-) replace hydroxyl groups (OH–) in the formation of the apatite crystal lattice (Figure 6). In fact, the presence of fluoride increases the rate of remineralization.

Figure 6. Fluorapatite Formation. (A) Fluoride ions (F–) replace hydroxyl groups (OH–) in hydroxyapatite to form fluorapatite in the tooth enamel. (B) A portion of the apatite crystal lattice is depicted showing the replacement of hydroxide for fluoride

Figure 6. Fluorapatite Formation. (A) Fluoride ions (F–) replace hydroxyl groups (OH–) in hydroxyapatite to form fluorapatite in the tooth enamel. (B) A portion of the apatite crystal lattice is depicted showing the replacement of hydroxide for fluoride

Adapted from: Posner, 1985.²⁶

Fluorapatite is inherently less soluble than hydroxyapatite, even under acidic conditions. When hydroxyapatite dissolves under cariogenic (acidic) conditions, if fluoride is present, then fluorapatite will form. Because fluorapatite is less soluble than hydroxyapatite, it is also more resistant to subsequent demineralization when acid challenged (Figure 7).

Figure 7. Fluoride Reactivity.

Figure 7. Fluoride Reactivity.

Adapted from: Posner, 1985.¹⁹

FIGURE 8. pH mapping image reveals acid pocket underneath the biofilm on the tooth surface despite exposure to pH 7 buffer.

FIGURE 8. pH mapping image reveals acid pocket underneath the biofilm on the tooth surface despite exposure to pH 7 buffer.

Under cariogenic conditions, carbohydrates are converted to acids by bacteria in the plaque biofilm. When the pH drops below 5.5, the biofilm fluid becomes undersaturated with phosphate ion and enamel dissolves to restore balance. When fluoride (F–) is present, fluorapatite is incorporated into demineralized enamel and subsequent demineralization is inhibited. Under pH conditions 4, the fluoride is unavailable for remineralization.

Caries is a sub-surface phenomenon. With fluoride treatment, a noncavitated lesion can be remineralized with fluorapatite and have greater resistance to subsequent demineralization than hydroxyapatite (Figure 9). Even when available at very low concentrations, fluoride is effective as an anticaries agent.^4,25,27

Figure 9. Demineralization/Remineralization. (A) Plaque acids cause a demineralized, sub-surface lesion. (B) Fluoride treatments remineralize the lesion with a more acid resistant fluorapatite mineral.

Figure 9. Demineralization/Remineralization. (A) Plaque acids cause a demineralized, sub-surface lesion. (B) Fluoride treatments remineralize the lesion with a more acid resistant fluorapatite mineral.