Caries Management - Science and Clinical Practice. Группа авторов

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      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 in enamel.^47,48 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.

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