A1 Dental caries

Topic

Dental caries is a chronic infectious disease that develops when the balance between the demineralization and remineralization of tooth enamel and dentin is disrupted. Tooth enamel is the mineral structure that normally resists the loss of its components as long as this balance remains stable; when demineralization exceeds remineralization, the enamel begins to experience a net loss of mineral, and this sustained imbalance is what gives rise to dental caries.

Dental biofilm forms on the surface of the enamel; this is a bacterial community harboring acidogenic bacteria—primarily *Streptococcus mutans* and *Lactobacillus*—capable of metabolizing fermentable dietary carbohydrates. These acidogenic bacteria within the biofilm convert fermentable carbohydrates into organic acids, and the accumulation of these acids lowers the biofilm's pH, acidifying the immediate environment of the enamel.

When the biofilm pH drops below the critical pH specific to the enamel mineral—close to a pH of 5.5 for the original mineral—dissolution is triggered: the hydroxyapatite crystal that makes up the enamel releases calcium and phosphate ions into the biofilm solution, driven by the concentration gradient established between the crystal and the solution. As long as the biofilm pH remains above the critical pH, the hydroxyapatite crystal remains stable and does not release ions; it is only upon crossing this threshold that dissolution is initiated.

The speed at which the hydroxyapatite crystal releases calcium and phosphate—the dissolution rate—does not depend on the biofilm pH in a simple manner, but rather on the degree of saturation of the biofilm solution with respect to that mineral: the lower the degree of saturation, the higher the dissolution rate. This relationship is strongly non-linear, governed by a sensitivity that, depending on the conditions of the hydroxyapatite crystal, can become either more or less pronounced. Consequently, even slight further drops in the degree of saturation can result in disproportionate increases in the dissolution rate.

Within the dental enamel, the cumulative mineral loss resulting from hydroxyapatite crystal dissolution gives rise to the carious lesion, which begins in the subsurface enamel and progresses toward the surface. The depth of the carious lesion increases in proportion to the square root of the elapsed time, as its progression is governed by the diffusion of ions and acids through the enamel rather than by the rate of the chemical reaction itself. When cumulative mineral loss exceeds a structural threshold of the enamel, the carious lesion ceases to be subclinical and manifests as clinical cavitation.

Fluoride present in the oral environment is incorporated into the enamel; by reacting with the mineral, it promotes the formation of fluorapatite rather than pure hydroxyapatite. Since fluorapatite is less soluble than hydroxyapatite, its presence shifts the enamel's critical pH to even more acidic values—approximately one to one-and-a-half units below the original critical pH, reaching a level near 4.5. This allows the enamel to withstand acid dissolution at acidity levels that would have previously triggered mineral loss. Thus, fluoride enhances the enamel's resistance to the very organic acids produced by dental biofilm.

The net result of this process determines the clinical fate of the enamel: if demineralization driven by organic acids from dental biofilm consistently outweighs the resistance conferred by mechanisms such as fluoride, mineral loss progresses to cavitation and the enamel becomes structurally compromised, resulting in the dental caries condition described earlier. Conversely, when the resistance of the tooth enamel succeeds in containing that dissolution, the balance between demineralization and remineralization is maintained, and dental caries does not manifest clinically.

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