Caries Management - Science and Clinical Practice. Группа авторов

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.

      In-vitro experiments suggest that progress of enamel lesions is slowed by proteins derived from the tooth milieu,⁵⁰ which presumably adsorb to crystals surfaces and inhibit dissolution within the lesion.

       NOTE

      Demineralization is the central process in caries but varies at the tissue level and histological level. The relatively intact surface layer characteristic of enamel caries probably owes its existence to the effect of inhibitors of demineralization, especially fluoride. Quite low concentrations of fluoride in the tooth environment during a cariogenic challenge inhibit caries progression and during periods when pH is neutral can promote remineralization. Lesions can become arrested: a state which implies cessation of cariogenic conditions and inhibition of remineralization.

       BACKGROUND

       Mineral Precipitation in Caries

      Beside hydroxyapatite, there exist many other calcium phosphates, with different compositions and solubility properties, and some have, or might have, a role in caries. Brushite (CaHPO₄ · 2H₂O) is more soluble than hydroxyapatite at neutral pH but, because its solubility varies less with pH, it becomes less soluble than hydroxyapatite at approximately pH 4. It has been suggested as an intermediate in formation of the surface layer of the caries lesion but there is no direct evidence for this.⁴⁵ Two mixed calcium-magnesium salts—magnesium whitlockite [MWH; Ca₉Mg(HPO₄)(PO₄)₆] and magnesium-containing β-tricalcium phosphate [MTCP; (Ca, Mg)₃(PO₄)₂—are often referred to indiscriminately as whitlockite. MWH is more soluble than hydroxyapatite at neutral pH but in plaque fluid it becomes less soluble than either hydroxyapatite or brushite at about pH 5.5. During enamel lesion formation, small crystals, probably of MWH, are formed at the prism boundaries,⁴⁴ probably in association with release of magnesium, calcium, and phosphate from labile mineral at the advancing front. The intra-tubular mineral formed during dentin sclerosis may be needlelike hydroxyapatite or coarser crystals of MTCP or MWH.^51–53

      Fig. 2.16 Hypothesis for role of inhibitors (e.g., fluoride) in formation of a surface layer on caries lesions.⁴⁵ The mineral phase is patterned. Fluoride, dissolved in plaque fluid, diffuses into enamel pores and adsorbs to the mineral forming the pore walls (top), thereby reducing its solubility (depicted by heavy lines at the mineral surface). Because the concentration of available fluoride is low, it is depleted within the outer enamel (indicated by the shading within the pores), so the solubility of the inner enamel is not reduced. Consequently, during a cariogenic challenge, acid diffusing into the enamel dissolves only small quantities of mineral from the surface layer and more from the inner enamel, resulting in increased porosity.

      Dentin Lesion Formation

      In agreement with the higher concentration of impurities, lower crystallinity, and smaller crystal size of the mineral, in situ studies suggest that lesions in (root) dentin progress more than twice as fast as in enamel.⁵⁴ Demineralization of dentin exposes the abundant organic matrix and this then becomes vulnerable to the action of bacterial proteases and to nonenzymic chemical processes which alter dentin matrix irreversibly and impair its capacity to remineralize. Mineral usually precipitates within tubules in a narrow band between the lesion and the pulp: a phenomenon referred to as dentin sclerosis.^52,53 This plays a vital role in retarding the progression of bacteria from the lesion to the pulp. It is usually assumed that sclerosis is due to odontoblast activity but physicochemical dissolution–reprecipitation processes might play a large part⁵⁴ (for further elaboration, see Chapter 3).

      Fluoride and Lesion Formation

      Fluoride in the aqueous tooth environment diffuses into the lesion and slows down demineralization. In-vitro experiments show that the concentration required to affect mineral loss is inversely related to pH, but 2mg/L fluoride in the pH range 4.0–5.5 seems to be sufficient to prevent lesion formation