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Fluoride’s Mechanism of Action
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.16
The hydroxyapatite of tooth enamel is primarily composed of phosphate ions (PO43–) 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.16‑18
Point of Interest: When the pH on the tooth surface becomes acidic, phosphate in oral fluids combines with hydrogen ions (H+) to form hydrogen phosphate species (see below.) Under these conditions, phosphate is “pulled” from tooth enamel to restore phosphate levels in the saliva, and the hydroxyapatite dissolves. As pH returns to normal, the calcium and phosphate in saliva can recrystallize into the hydroxyapatite, remineralizing the enamel.
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.2,9,19
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 3). In fact, the presence of fluoride increases the rate of remineralization.
Figure 3. Fluorapatite Formation.
Adapted from: Posner, 1985.20
(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.
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 4).
Figure 4. Fluoride Reactivity.
Adapted from: Cury, 2009.19
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.
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 5). Even when available at very low concentrations, fluoride is effective as an anticaries agent.2,19,21
Figure 5. Demineralization/Remineralization.
(A) Plaque acids cause a demineralized, sub-surface lesion. (B) Fluoride treatments remineralize the lesion with a more acid resistant fluorapatite mineral.
Video 1. Demineralization/Remineralization with Fluoride.