Caries Management - Science and Clinical Practice. Группа авторов

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СКАЧАТЬ human salivary proteins on the precipitation kinetics of calcium phosphate. Calcif Tissue Int 1979;28(1):7–16

      26. Lendenmann U, Grogan J, Oppenheim FG. Saliva and dental pellicle—a review. Adv Dent Res 2000;14:22–28

      27. Zahradnik RT, Moreno EC, Burke EJ. Effect of salivary pellicle on enamel subsurface demineralization in vitro. J Dent Res 1976; 55(4):664–670

      28. Nederfors T. Xerostomia and hyposalivation. Adv Dent Res 2000;14:48–56

      29. Bardow A, Lagerlöf F, Nauntofte B, et al. The role of saliva. In: Fejerskov O, Kidd E, eds. Dental Caries. The Disease and its Clinical Management. Oxford: Blackwell Munksgaard; 2008: 190–207

      30. Brudevold F. Aldersforandringer I tandnemaljen. Nor Tandlægeforen Tid 1957;67:451–458

      31. Mjør IA. Changes in the teeth with aging. In: Holm-Pedersen P, Löe H, eds. Textbook of Geriatric Dentistry. Copenhagen: Munksgaard; 1996:94–102

      32. Scott J. Degenerative changes in the histology of the human submandibular salivary gland occurring with age. J Biol Buccale 1977;5(4):311–319

      33. Baum BJ. Changes in salivary glands and salivary secretion with aging. In: Holm-Pedersen P, Löe H, eds. Textbook of Geriatric Dentistry. Copenhagen: Munksgaard; 1996:117–126

      34. Marsh PD, Martin M. Oral microbiology. 3rd ed. London: Chapman and Hall; 1992

      35. Marsh PD. Microbial ecology of dental plaque and its significance in health and disease. Adv Dent Res 1994;8(2):263–271

      36. Sibley CG, Ahlquist JE. The phylogeny of the hominoid primates, as indicated by DNA-DNA hybridization. J Mol Evol 1984;20(1): 2–15

      37. Smith M. Nobel lecture. Synthetic DNA and biology. Biosci Rep 1994;14(2):51–66

      38. de Soet JJ, Nyvad B, Kilian M. Strain-related acid production by oral streptococci. Caries Res 2000;34(6):486–490

      39. Gibbons RJ. Bacterial adhesion to oral tissues: a model for infectious diseases. J Dent Res 1989;68(5):750–760

      40. Nyvad B, Kilian M. Microbiology of the early colonization of human enamel and root surfaces in vivo. Scand J Dent Res 1987;95(5):369–380

      41. Thylstrup A, Bruun C, Holmen L. In vivo caries models—mechanisms for caries initiation and arrestment. Adv Dent Res 1994; 8(2):144–157

      42. Ekstrand KR, Bjørndal L. Structural analyses of plaque and caries in relation to the morphology of the groove-fossa system on erupting mandibular third molars. Caries Res 1997;31(5): 336–348

      43. Carvalho JC, Thylstrup A, Ekstrand KR. Results after 3 years of non-operative occlusal caries treatment of erupting permanent first molars. Community Dent Oral Epidemiol 1992;20(4): 187–192

      44. Ekstrand KR, Kuzmina IN, Kuzmina E, Christiansen ME. Two and a half-year outcome of caries-preventive programs offered to groups of children in the Solntsevsky district of Moscow. Caries Res 2000;34(1):8–19

      45. Wakita M, Kobayashi S. The three-dimensional structure of Tomes’ processes and the development of the microstructural organisation of tooth enamel. In: Suga S, ed. Mechanisms of Tooth and Enamel Formation. Berlin: Quintessenz;1983:165

      2 Etiology and Pathogenesis of Caries

      Peter Shellis

       Microbiology of Caries

       Chemistry of Dental Minerals

       Solubility, Dissolution, and Crystal Growth

       Minerals of Dental Tissues

       Fluoride and Calcium Phosphate Chemistry

       The Cariogenic Challenge

       Chemistry of Caries

       Enamel Lesion Formation

       Dentin Lesion Formation

       Fluoride and Lesion Formation

       Remineralization and Lesion Arrest

       Dental Erosion

As described in Chapter 1, teeth are continuously bathed in saliva, one of the main functions of which is to minimize mineral dissolution and precipitation within the mouth^1,2: both can be harmful to the teeth and other oral tissues. Saliva can ameliorate the effects of challenges that tend to dissolve tooth tissue, such as consumption of acidic foods, because it has an approximately neutral pH, is reasonably well buffered, and contains mineral ions. In dental caries, this homoeostasis is overcome by acid-generating metabolic processes in localized accumulations of bacteria. This in turn causes loss of mineral from the hard tissues, which destroys their integrity and eventually impairs their function.

      Most of the surface of a tooth is kept free of bacteria by friction from the tongue, cheeks, and foodstuffs. However, bacteria colonize areas of the surface protected from these frictional forces (plaque stagnation areas) and form a film of closely packed bacteria known as dental plaque^3,4 within which is created a unique microenvironment, partly isolated from the saliva and immediately adjacent to the tooth surface. The human diet includes a variety of easily-fermentable carbohydrates: monosaccharides such as glucose and fructose; disaccharides such as sucrose and maltose; and oligosaccharides such as those found in honey. In this chapter, these will be collectively referred to as ‘sugar’ and specific carbohydrates will be named. On each occasion when sugars are ingested, they are metabolized by plaque bacteria and this results in the accumulation of organic acid end products and hence causes a temporary reduction in plaque pH. Such an episode can pose a “cariogenic challenge” since, if the plaque pH falls low enough, mineral within the underlying dental hard tissue can dissolve. The progressive loss of mineral through dissolution by plaque acid (demineralization) during repeated cariogenic challenges is the primary process in dental caries.

      This basic etiology is summarized by the well-known Venn diagram of Keyes⁵ (Fig. 2.1), which illustrates СКАЧАТЬ