Caries Management - Science and Clinical Practice. Группа авторов

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СКАЧАТЬ lower estimate of critical pH indicates the increasing severity of the challenge with falling pH (see Fig. 2.7).

      Fig. 2.14 Clearance of H⁺ ions from plaque during the second phase of the Stephan curve. H⁺ ions released from fixed (nondiffusible) buffers associated with bacterial cell walls (left) diffuse out slowly (dashed arrow, bottom). Clearance is accelerated by diffusible buffers from saliva—bicarbonate (top) and phosphate (middle)—which act as H⁺-transporters.

      Fig. 2.15 Release of calcium ions bound to bacteria during a cariogenic challenge. At neutral pH, Ca²⁺ ions are bound to carboxyl groups (top left) and phosphate groups (bottom left), associated with bacterial cell walls. When plaque pH falls, Ca²⁺ ions are displaced by H⁺ ions (top right, bottom right). The resulting fall in H⁺ ion concentration and the rise in Ca²⁺ concentration raise the degree of saturation of the plaque fluid and hence ameliorate the cariogenic challenge. Some Ca²⁺ ions act as bridges between neighboring plaque bacteria (middle) and increase plaque cohesion; these bridging Ca²⁺ ions are also released under acidic conditions.

      The overall severity of a cariogenic challenge is influenced by several factors. It is mainly the overall concentration of sugar in a food item that determines how far the pH will fall in a single exposure, so high-sugar foods pose a greater challenge (see Fig. 2.2). Similarly, the more frequently sugar is consumed, the longer the plaque pH can remain below neutrality, so that the potential for remineralization is reduced (see Fig. 2.2). As predicted by the ecological plaque hypothesis, frequent exposure to sugar causes selection for acidogenic, aciduric bacteria and for bacteria producing intracellular polysaccharides, which will intensify the cariogenic challenge (greater, more prolonged pH fall). If the main sugar to which the plaque is exposed is sucrose (the most abundant sugar in sweetened foodstuffs), the plaque cariogenicity will be increased as explained above. Although complex dietary carbohydrates, such as starch, are thought to be relatively noncariogenic, starch probably increases the stickiness of sugar-rich foods, thereby retaining them close to the tooth surface and prolonging the cariogenic challenge.⁴⁰

      Some members of the plaque flora mitigate the effects of lactic acid production. Veillonella, which is consistently found in plaque, derives energy from metabolizing lactic acid to acetic and propionic acids. As these are weaker acids than lactic acid, they will remove H⁺ from the plaque fluid and thus tend to raise pH.³ Other bacteria can produce ammonia from nitrogen-containing substances—amino acids, for example—and this will tend to raise the pH. Plaque bacteria bind appreciable quantities of calcium⁴¹ and when the pH falls, Ca²⁺ ions are released (Fig. 2.15; Table 2.2) in exchange for H⁺ ions. This will increase the degree of saturation.

      The main host factors influencing the cariogenic challenge are the flow rate and buffering capacity of saliva.^1,38 The pH rise in the second phase of the Stephan curve is facilitated by good salivary flow, as this helps to clear H⁺ ions away from the plaque. A mitigating factor in the caries process is that consumption of foods stimulates salivary flow and this is accompanied by increased salivary bicarbonate concentration: both enhance H⁺ ion removal from the plaque.

       NOTE

      The presence of dental plaque, made up of densely-packed bacteria, on sheltered regions of the tooth prevents flow of oral fluids over the tooth surface, so exchange of substances between the tooth surface or plaque and the oral fluids occurs by the slow process of diffusion. Consequently, metabolism of sugar by plaque bacteria results in accumulation of acid, and a fall in plaque pH, followed by a pH rise as H⁺ ions are cleared into the saliva. The pattern of rapid pH fall and slower pH recovery in plaque is called the “Stephan curve.” An episode when plaque pH is below the “critical pH” (~5.2–5.5 for enamel) constitutes a cariogenic challenge, when the tooth can lose mineral. The severity of the cariogenic challenge is influenced by many factors, including diet (especially sugar consumption), the plaque flora, the flow rate and buffering properties of saliva.

      Chemistry of Caries

      Lesion formation is controlled by two processes: dissolution of mineral and diffusion of acid into the hard tissues (and of mineral ions outward).

      Enamel Lesion Formation

      The solubility, and therefore the rate of dissolution, increases from the surface to the enamel–dentin junction^27,42 (see also Chapter 3), in correlation with a similar gradient in the concentrations of carbonate and magnesium.⁴³ At a smaller scale, the mineral at the prism boundaries (intraprismatic mineral) is significantly more soluble than that in the prism cores²⁷ and is the first part of the enamel structure to be attacked at the advancing front of a lesion (translucent zone). The prism boundaries contain the largest enamel pores, and they are further enlarged by this loss of mineral to form preferential pathways of diffusion during further lesion progress, when demineralization occurs within the prisms.⁴⁴

      The overall rate of lesion advance is governed by diffusion, which means that the lesion progresses more slowly the further it penetrates into the tissue,⁴⁵ although this may be modified by the inward gradient of increasing solubility. Lesions progress faster in enamel of deciduous teeth than in that of permanent teeth⁴⁶ (Table 2.3). This seems to be due mainly to quantitative differences in pore structure (Table 2.3) rather than to differences in mineral solubility.^27,46

      A prominent feature of caries lesions of enamel is a surface layer which retains much more mineral than the underlying body of the lesion. Numerous mechanisms by which the surface layer could retain so much mineral have been proposed.⁴⁵ The theory that seems to be best supported by the available evidence, is that inhibitors dissolved in the aqueous environment of the tooth adsorb to crystals in the surface layer and inhibit dissolution, so that this layer is spared while underlying tissue remains vulnerable and continues to dissolve (Fig. 2.16). The inhibitors involved could include such substances as proteins and pyrophosphate but fluoride is likely to play an especially important part.^45,47 In-vitro experiments under reasonably realistic conditions suggest that in the absence of fluoride enamel surfaces are simply demineralized, whereas in the presence of fluoride at low concentrations, for example, 0.1mg/L, a surface layer is formed instead.^47,48 Fluoride ions probably also promote precipitation of fluorhydroxyapatite on crystals in the surface layer and this would account for improved crystallinity observed in this layer.⁴⁹ In vivo, a surface layer does not form immediately, possibly because of the low fluoride concentrations available.

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