Caries Management - Science and Clinical Practice. Группа авторов

Much higher fluoride concentrations (5–10 times) are required to obtain equivalent inhibition of lesions in dentin.⁵⁵ In vivo, dissolved fluoride in the oral environment is derived mainly from fluoride toothpaste, mouth rinses, or fluoridated water but the immediate source for the lesion is the plaque. Fluoride diffusing into plaque—for example, after tooth-brushing—is bound by two mechanisms: by binding to bacterial surfaces by way of Ca²⁺ ions⁵⁶ (Fig. 2.17), and possibly by precipitation of calcium fluoride-like mineral. Both reactions are reversible and provide a source of F⁻ ions as the plaque fluoride concentration falls. Release is accompanied by release of Ca²⁺ ions and is greater at lower pH. These processes exert a considerable caries-preventive action. Fluoride is also taken up by other intraoral “reservoirs,” for example, the oral mucosa and the tooth surfaces. However, the special effectiveness of the plaque fluoride storage is demonstrated by the fact that one hour after a fluoride rinse (1000mg/L, ~1000ppm), the concentration of dissolved fluoride in the plaque fluid is not only higher than in saliva but is still at a level which in-vitro experiments indicate can prevent lesion formation⁵⁷ (Fig. 2.18).

      Remineralization and Lesion Arrest

      The progression of a caries lesion can be slowed or halted if the severity or frequency of cariogenic challenges is reduced, for example, by plaque control or restriction of sugar intake, by a reduced frequency of ingestion of sugar, or by loss of an adjacent tooth, which exposes a previously inaccessible approximal surface to the cleansing and buffering action of saliva. Such changes favor remineralization over demineralization, especially when fluoride is available. However, in-situ experiments suggest that, even when the cariogenicity of the tooth environment is reduced, not all lesions remineralize and some continue to progress. The fate of a lesion seems to depend on intraoral factors such as saliva flow rate and composition.⁵⁸

      Fig. 2.17 Fluoride binding and release in plaque. A: Before exposure to fluoride, plaque bacteria bind calcium ions, some of which act as bridges between adjacent cells (cf. Fig. 2.15). B: After exposure to high concentrations of fluoride (e.g., dentifrice, mouth rinse) fluoride ions form complexes with bound calcium ions. Because each fluoride ion uses only one of the calcium valencies, further sites for calcium and fluoride binding are created. With time, the reverse process occurs, fluoride and calcium being slowly released, so that the fluoride concentration in plaque fluid remains elevated for a prolonged period. C: A rapid fall in pH, as during a cariogenic challenge, causes calcium ions to be displaced from binding sites on bacterial surfaces. This results in a rapid release of both calcium and fluoride ions to the plaque fluid.

      Fig. 2.18 Fluoride in plaque fluid and saliva at baseline and at 30 and 60 minutes following a rinse with 1000mg/L sodium fluoride. (Data from ref.⁵⁷.)

      Lesions take up proteins from the oral fluids⁵⁹ and these tend to inhibit crystal growth.^1,2,60 Under some circumstances, such protein might actually enhance the effect of fluoride, by inhibiting mineral crystal growth in the surface layer of enamel lesions, so that remineralization can occur in the subsurface part of the lesion.⁶⁰ However, continuing accumulation of protein would eventually inhibit remineralization in all parts of a lesion. Sealing of a lesion by complete remineralization of the surface layer, or inhibition of crystal growth within the lesion by proteins could explain the observation that lesions that have been in existence for a long time (6 months or more) seem to be resistant to fluoride treatment.⁶¹

       NOTE

      Remineralization is a fundamental part of pH cycles (pH drop and a subsequent rise) and happens primarily when the pH returns, say, from 5.5 to 7.0. Caries arrest is when no nett loss of ions happens over time.

      Dental Erosion

      In erosion there is a direct effect on all exposed tooth surfaces by acidic substances, without the mediation of bacteria, so the damage extends over a wide area and is not localized as in caries lesions. However, approximal and gingival areas seem to be spared, probably because of the high buffer capacity of plaque. The acids responsible for erosion can be endogenous or exogenous.⁶² Endogenous acid consists of gastric juices entering the mouth by reflux, as in bulimia or in gastro-esophageal disorders. Exogenous acid may be industrial or occupational in origin, for example, acidic industrial vapors, or may be contained in foods (e.g., pickles) or drinks (e.g., wines, soft drinks, fruit juices).

      The challenge posed to the tooth surface by exposure to an acidic substance is typically much more severe than a cariogenic challenge. In a cariogenic challenge, the milieu (plaque fluid) is partly saturated with respect to tooth mineral and the pH rarely falls as low as 4.0, whereas erosive substances typically contain little or no calcium or phosphate and the pH can be as low as 2.4.⁶³ The pH/solubility curve for HA (see Fig. 2.7) shows that at such low pH values dissolution is extremely high. Moreover, whereas transport of dissolved mineral away from the tooth during a cariogenic challenge is diffusion-controlled and slow, clearance is much faster in erosion, especially where the erosive agent is a liquid. Thus, even though an erosive challenge is typically short (1–2 minutes for a soft drink⁶⁴), the rate of demineralization is very much faster than in caries.

      Fig. 2.19a–c Softening and abrasion in erosive tooth wear. a: Cross-section of sound enamel with prism boundaries marked as oblique lines. b: Enamel after exposure to erosive liquid. At the outermost surface, some enamel has been dissolved completely (original surface marked by dashed line). Beneath this zone, acid has diffused into the enamel and produced a “softened” zone (stippled), in which there is partial demineralization. Demineralization extends deepest along the prism boundaries (marked by heavy lines), because of the raised solubility of the mineral at these sites. c: If the surface in b is exposed to abrasive forces (e.g., toothbrushing), the outer, more heavily demineralized, part of the softened layer is worn away, resulting in further loss of tooth surface.

      The primary lesion in enamel erosion is partial demineralization (“softening”) of a layer extending some micro-meters below the surface, created by acid diffusing into the submicroscopic pores of the tissue (Fig. 2.19). Softened enamel is vulnerable to mechanical forces that would have no effect on sound enamel, for example, friction from the tongue or toothbrushing.⁶⁵ Consequently, the softened tissue can be lost quite soon after the erosive challenge (Fig. 2.19), and repeated challenges eventually result in visible loss of tissue.⁶⁵ Erosion of dentin creates a superficial layer of demineralized dentin matrix which is vulnerable to the action of bacterial proteases and then to abrasion.⁶⁶

       SUMMARY

      Dental caries consists of the loss of mineral from dental hard tissues, as a result of the conversion of dietary sugars to acid within a bacterial biofilm (dental plaque) formed in sheltered locations on the tooth surfaces.