Название: Caries Management - Science and Clinical Practice
Автор: Группа авторов
Издательство: Ingram
Жанр: Медицина
isbn: 9783131693815
isbn:
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. The loss of mineral can be reversed by crystal growth driven by precipitation of mineral ions derived from the oral fluids (remineralization). Caries lesions progress when demineralization outweighs remineralization and ultimately break down to form cavities, with consequently impaired tooth function. The rate of progress is influenced by the plaque flora, diet, salivary biochemistry, oral hygiene, and numerous behavioral and socioeconomic factors. Fluoride is perhaps the most important factor, because it both reduces demineralization and enhances remineralization. Fluoride reduces solubility of tooth mineral through reactions at the crystal surfaces. It is thus considered that topical application to maintain low but effective fluoride concentrations in the tooth environment is more effective than systematic routes of fluoride delivery. Dental erosion is less localized than caries, is caused by more severe acid challenges, and poses difficult problems of prevention.
REFERENCES
1. Edgar WM, Dawes C, O'Mullane D, eds. Saliva and Oral Health. 3rd ed. London: BDJ Books; 2004
2. Hay DI, Moreno EC. Macromolecular inhibitors of calcium phosphate inhibition in human saliva. Their roles in providing a protective environment for the teeth. In: Kleinberg I, Ellison SA, Mandel ID, eds. Saliva and Dental Caries. New York: IRL Press; 1979:45–58
3. Marsh PD, Martin M. Oral Microbiology. 3rd ed. London: Chapman Hall; 1992
4. Marsh PD, Nyvad B. The oral microflora and biofilms on teeth. In: Fejerskov O, Kidd, EAM, eds. Dental Caries. The Disease and its Clinical Management. Oxford: Blackwell Munksgaard; 2003: 29–48
5. Keyes PH, Jordan HV. Factors influencing the initiation, transmission, and inhibition of dental caries. In: Harris RS, ed. Mechanisms of Hard Tissue Destruction. New York: Academic Press; 1963:261–283
6. Fejerskov O, Kidd EAM, eds. Dental Caries. The Disease and its Clinical Management. Oxford: Blackwell Munksgaard; 2003
7. ten Cate JM, Featherstone JD. Mechanistic aspects of the interactions between fluoride and dental enamel. Crit Rev Oral Biol Med 1991;2(3):283–296
8. Harris R, Nicoll AD, Adair PM, Pine CM. Risk factors for dental caries in young children: a systematic review of the literature. Community Dent Health 2004; 21(1, Suppl):71–85
9. Shellis RP, Duckworth RM. Studies on the cariostatic mechanisms of fluoride. Int Dent J 1994; 44(3, Suppl 1):263–273
10. Lussi A, ed. Dental Erosion. Basel: Karger; 2006. Monographs in Oral Science; vol 20
11. Tanzer JM. Dental caries is a transmissible infectious disease: the Keyes and Fitzgerald revolution. J Dent Res 1995;74(9): 1536–1542
12. Tanzer JM, Livingston J, Thompson AM. The microbiology of primary dental caries in humans. J Dent Educ 2001;65(10): 1028–1037
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