Efnisyfirlit

• Front Matter
  • Contributors
• Part I Dental caries: what is it and how widespread is it globally?
  • 1 Prologue
    • Introduction
    • The role of cariology in restorative dentistry
    • The content of this textbook
  • 2 Dental caries: what is it?
    • The disease
      • Figure 2.1 Schematic illustration of the determinants of the carious process. Those that act at the tooth surface level are found in the inner circle. With time, an ecological shift in the composition and metabolic activity of the biofilm (‘microbial deposit’) may result in an imbalance in the equilibrium between biofilm fluid and the mineral of the tooth. Thus, a net loss of mineral results in formation of a caries lesion (overlap of the two small circles). In the outer ring are listed more distant determinants that influence these processes at the individual and population levels.
    • Terminology
    • Background literature
    • References
  • 3 Clinical features of caries lesions
    • What do caries lesions look like clinically?
    • The deciduous dentition
      • Figures 3.1–3.8 Figure 3.1: A 3-year-old child with thick accumulations of dental plaque along the gingival margin of the buccal surfaces covering active caries lesions, some of which present with distinct cavities. Figure 3.2: Inactive/arrested caries lesions on buccal surfaces of upper central incisor teeth in a 5-year-old child. Note that the shape of the lesions indicates where the gingival margin was located at the time when these lesions developed. The oral hygiene has improved and the surfaces of these noncavitated opaque lesions are now smooth and shiny. Figure 3.3: Upper deciduous canine from a 5-year-old with an active, cavitated lesion along the gingival margin. On probing it would be soft, but there is no reason to probe such a lesion unless you wish to provoke a pain reaction! Figure 3.4: Upper incisors in a 5-year-old child. Several narrow, white opaque inactive caries lesions are located 1–2 mm from the gingival margins. One of the lesions exhibits a large cavity that is hard on probing. This is an example of an inactive, cavitated lesion. Figure 3.5: Deciduous first lower molar in a 2½-year-old child with two cavitated active caries lesions. Note the peripheral white, opaque rim of enamel surrounding the cavities. Figure 3.6: Lower first deciduous molars with active, cavitated lesions in the distal and disto-occlusal surfaces of a 6-year-old child. Figures 3.7 and 3.8: A 2-year-old child with extensive, active, partly cavitated caries lesions encircling the teeth. This is an example of so-called nursing bottle caries – or ‘bottle caries.’
      • Figures 3.9 and 3.10 Slightly discolored lesions on approximal and buccal surfaces of an exfoliated deciduous molar. Note that the shape of the lesions reflects the areas where dental plaque has been retained above the position of the gingival margin. Note also the opaque kidney-shaped part of the approximal lesion cervically to the brown-stained center of the lesion in Fig. 3.9.
    • The permanent dentition
      • The free smooth surfaces
        • Figures 3.11–3.14 Figure 3.11: Active, noncavitated carious lesion on lower second premolar. The shape is typical, as it follows the curvature of the marginal gingiva and corresponds to where a narrow band of dental plaque has been located in a stagnant area. The surface is dull and chalky. It is called a ‘white spot lesion,’ although it extends from the approximal amalgam filling all along the gingival margin. On the mesio-buccal surface of the lower first molar another noncavitated lesion has taken up brown stain. Note also the very thin lesion on the buccal surface of the first premolar along the gingival margin. Figure 3.12: Active, noncavitated carious lesion at lower second premolar with a typical banana-shape of the white, opaque lesion with the cervical border following the shape of the slightly inflamed marginal gingiva. A 1 mm rim of normal enamel between the lesion and gingiva indicates that the gingivitis, with swelling of the tissue, has been reduced as a result of attempts to control the oral hygiene. Note also the remains of a white opaque lesion on the lower first premolar along the mesial and distal margin of the amalgam filling. On the lower first molar a band of partly discolored, noncavitated lesion extends from an amalgam filling. This could be classified as secondary caries (recurrent caries), but is obviously the remains of a primary lesion. Figure 3.13: Arrested/inactive, noncavitated (‘white spot’) lesion on the lower first molar. The lesion exhibits a localized circular surface defect. The position of this lesion corresponds to where the marginal gingiva would have been at some stage during eruption of this tooth 30 years earlier. When viewing the lesion from different angles it is apparent that the surface is shiny and smooth, although the tip of a probe will clearly detect the defect (which is also hard). Figure 3.14: Extensive active, white, opaque and chalky buccal lesions which are noncavitated on the upper central incisors. A large superficial defect is seen on the upper right lateral incisor. Notice the obvious difference between the chalky, dull appearance of the carious lesion along gingiva and the creamy appearance of the white, opaque hypomineralized lesion of developmental origin (impaired enamel maturation) on the incisal third of this tooth. If a probe tip is moved gently across the surface, an obvious difference in surface texture is felt between the smooth (and shiny) surface of the developmental defect and the chalky texture of the carious lesion.
      • Approximal smooth surfaces
        • Figures 3.15–3.21 Figure 3.15 and 3.16: Active, noncavitated ‘early white spot’ lesions on mesial surfaces of upper and lower first molars are easily observed following shedding of primary teeth. The shape of each lesion indicates the stagnant areas where the biofilm (dental plaque) remained undisturbed. In the most demineralized areas in the center of the lesions, the porous enamel has taken up stain. The lesion in Fig. 3.15 was treated nonoperatively and has remained as an inactive, noncavitated lesion for almost 35 years! Figure 3.17: Active, discolored lesion on first molar with small cavity containing microbial deposits (dental plaque). Figure 3.18: Different stages of active, cavitated lesions in upper premolars. Note that undermined enamel in the second premolar is reflected by a yellow–whitish translucency of the enamel. Figures 3.19–3.21: Approximal lesions may be difficult to detect by direct visual inspection (Fig. 3.21), but inactive, severely discolored lesions can easily be diagnosed once the neighboring tooth is extracted (Figs 3.19 and 3.20).
        • Figures 3.22–3.26 Figures 3.22 and 3.23: In incisors, approximal lesions are easily discerned either directly or by reflected light, as shown in the distal surfaces of the incisors (Fig. 3.22). The cervical black rim of discoloration is a result of cigarette smoking and can be removed by polishing. Figures 3.24 and 3.25: In the premolar and molar regions it is much more difficult to see approximal lesions by direct inspection, even with careful training and experience. In this example the cavity in the first premolar came as a surprise, considering the relatively shallow enamel lesion recorded on the bitewing radiograph – a so-called iatrogenic damage when the dentist was drilling in the neighboring tooth. Figure 3.26: Even extensive active, cavitated lesions can remain difficult to detect until the adjacent tooth is lost. Such lesions may, however, reveal themselves by a bluish or yellowish discoloration of the undermined occlusal enamel ridge – compare with Fig. 3.18.
        • Figures 3.27 and 3.28 Dental caries is a local destructive lesion that, if not controlled or treated operatively, will continue to progress until the entire crown is destroyed and the lesions penetrate further into the root dentin.
      • Occlusal caries
        • Figures 3.29–3.36 Figure 3.29: Parts of the irregular occlusal surface in molars represent plaque stagnation areas and hence predispose to lesion development. Active, noncavitated lesions appear as chalky white, opaque lesions along the groove, fossa, pits and fissure systems. Figure 3.30: In the clinic the plaque must be removed gently from the occlusal surface either with a brush or explorer as otherwise this active, noncavitated lesion might not be seen. Figures 3.31 and 3.32: Arrested, noncavitated lesions often present as darkly stained pits and fissures. In Fig. 3.32, the cloudy, opaque areas in the premolars with a shiny enamel surface on cusps and enamel ridges represent dental fluorosis. Figures 3.33 and 3.34: Active carious lesions with small and large cavities. Note in Fig. 3.34 how the enamel appears bluish along the fissures as a result of the undermining nature of the occlusal caries lesions. When opened with a bur the occlusal surface is likely to show substantial destruction of the dental tissues. Figure 3.35: Active carious lesion with large cavity extending deep into dentin. Figure 3.36: Arrested occlusal caries lesion. The partly undermined enamel margins have been fractured and abraded away by mastication, and the dental plaque in the dentin cavity has been removed because the surface is in functional occlusion. The dark-brown dentin is hard and painless.
      • Occlusal caries lesions
        • Figures 3.37–3.43 The figures demonstrate lesions that clinicians had misdiagnosed as an arrested lesion and sound. The lesions might be easy to miss unless the tooth surface is absolutely well illuminated and dry. The radiographs in both cases demonstrate extensive radiolucent areas in the occlusal dentin indicative of rather deep carious lesions (Figs 3.38 and 3.40). The bluish appearance of the disto-lingual cusp in Fig. 3.37 should make the clinician aware of a possible undermining larger lesion. Likewise, there is an obvious cavity in the central fossa in Fig. 3.39. These cases represent examples of so-called hidden caries because the dentist had overlooked the clinical signs of lesions and the patient had not complained of any symptoms. The fact that these patients had otherwise very few fillings, and no other signs of active or arrested carious lesions despite being 18–20 years old, probably led the dentists to perform a more superficial dental examination. Figures 3.41–3.43: Example of an inactive occlusal lesion that the dentist assumed to be in need of operative treatment. The lesion in both enamel and dentin was hard on probing and in fact did not extend far into the dentin.
      • Root-surface caries
        • Figures 3.44–3.49 Anywhere on root surfaces where dental plaque accumulates (along the cervical margin at the enamel–cementum junction and along the gingival margin), active root surface lesions may develop with or without distinct cavities. Cavities may be soft (Fig. 3.46) or leathery (Fig. 3.47) and partly filled with microbial deposits. The color of the lesions may vary from yellowish to brownish or black. Figure 3.48: Meticulous oral hygiene can arrest root surface caries lesions and make the root surface appear shiny, although small surface cavities may remain. Arrested root surface lesions feel hard on gentle probing and show a brownish or black discoloration. Figure 3.49: Root surface lesions in the transition stage from active to arrested often exhibit a dull, leathery appearance. Lesion arrest is often a slow process that continues over years. The changes comprise surface abrasion and polishing, as well as mineral uptake (see Chapter 5).
        • Figures 3.50–3.53 These cases represent a dentist's nightmare! There are extensive active root surface caries lesions. Figs 3.50 and 3.51 show a patient who has undergone radiation of the head and neck. Although only very small amounts of biofilm can be seen, the lack of saliva results in extensive cervical and approximal active caries lesion. Note how the enamel is undermined along the cavity margins. The patient in Figs 3.52 and 3.53 had received antidepressants for a long time and presented with heavy soft microbial deposits on all exposed root surfaces. These teeth are very difficult if not impossible to restore. Figure 3.53 shows the patient at 4 months following intensive plaque control with a fluoride toothpaste. The lesions are now mostly arrested. The previously soft surface is leathery to hard, and from a biological point of view restorative dentistry has no role to play. Any restorative treatment would still be difficult, even using contemporary adhesive materials. Restorations might help the patient to improved cosmetics, but they would not contribute to better tooth survival – rather the opposite.
        • Figures 3.54–3.59 Examples of caries sequelae. The total destruction of the crown of a tooth may result in a local pyogenic granuloma of the gingiva (Fig. 3.54). In Fig. 3.55 the pulpal tissue has survived but is freely exposed to the oral cavity and covered by squamous epithelium (pulpal polyp). Most often, untreated dental caries results in necrosis of the pulp and development of a periapical abscess that may penetrate the bone to the oral cavity (Fig. 3.56) or in rare cases even directly to the surface of the skin (Figs 3.57, 3.58, and 3.59). The abscess from the lower central incisor has penetrated the mandible and pus is emptied regularly through a fistula. As long as the duct of the fistula remains open there is hardly any pain.
  • 4 How big is the problem? Epidemiological features of dental caries
    • Introduction
    • What? Defining the health issue at hand
      • Box 4.1 The five ‘W’ questions addressed by epidemiology
      • What counts as caries?
        • Validity and reliability of caries lesion detection systems
          • Box 4.2 Types of validity relevant to the ‘ideal’ caries lesion detection system
      • Grading the ‘severity’ of caries lesions
        • Table 4.1 Descriptors of the types of caries lesions detected using some of the major caries lesion detection systems currently in use
      • Expressing the extent of dental caries: the DMF count
        • Box 4.3 Some important limitations to the DMF index
          • General
          • M component
          • F component
          • D component
      • Summarizing the caries experience in groups of interest
        • Box 4.4 Central measures of disease frequency of relevance to dental caries
          • Occurrence measures
          • Incidence measures
      • Interpretation of caries data
        • Figure 4.1 The mean dmf/DMF counts in a cohort follow trend-lines. Upper left panel: Mean d3mfs counts according to school grade for cohorts of Danish children starting school between 1972 and 1985. Upper right panel: Mean D3MFS according to school grade for cohorts of Danish children starting school between 1972 and 1985. Lower left panel: Tracking of the mean d3mfs counts between ages 5 and 7 years for the Danish birth cohorts 1984–2005. Lower right panel: Tracking of the mean D3MFS counts between ages 7 and 15 years for the Danish birth cohorts 1984–2000.
    • Figure 4.2 There is a close relationship between the mean dmf/DMF count and the percentage of ‘caries-free’ children in a population. The two upper panels show the relationship between the d3mfs/D3MFS and the percentage ‘caries-free’ (d3/D3-threshold) children, and the two lower panels show that the relationship also holds for the d1mfs/D1MFS percentage ‘caries-free’ (d3/D3-threshold) children.
    • Figure 4.3 The frequency distribution of individuals according their individual D3MFS counts contracts as the mean D3MFS for the population decreases.
    • Who? The distribution of caries in populations
      • Variation and inequality in the distribution of caries
        • Figure 4.4 The relationship between the mean dmfs/DMFS and the mean dmft/DMFT.
        • Figure 4.5 The ratio of the d3mfs/D3MFS to d1mfs/D1MFS counts decreases with decreasing mean d3mfs/D3MFS counts.
        • Figure 4.6 The distribution of individual D1MFS counts among 12-year-old Lithuanian children, and the distribution for the same children 3 years later, when they had reached the age of 15 years. The left panel shows the simple frequency distribution of the D1MFS counts, whereas the right panel shows the cumulative frequency distribution of these counts.
        • Figure 4.7 The cumulative frequency distribution of individual D3MFS counts among 15-year-old Danes in 1980 and 1995 (left-hand panel), and the corresponding Lorenz curves (right-hand panel) illustrating the degree of inequality of the distribution of the caries burden in the population. Dividing the area (A) between the Lorenz curve for the year 1980 and the line indicating perfect equality by the total area under the perfect equality line gives the Gini coefficient.
      • Age and gender
        • Figure 4.8 The mean D3MFS among US adolescents, adults, and elderly in two national surveys, one in 1988–1994 and one in 1999–2004.
        • Figure 4.9 The mean DMFT and its components among adult and elderly Chinese examined 1984–1985.
        • Figure 4.10 The prevalence of any caries (D3 level), untreated caries (D3), and root caries among US adolescents, adults, and elderly in two national surveys, one in 1988–1994 and one in 1999–2004.
        • Figure 4.11 The mean D3MFS according to selected socio-demographic factors for the age groups 12–19 years, 20–64 years, and ≥65 years as recorded in 1999–2004.
        • Figure 4.12 The tooth-specific caries incidence rates (new lesions/1000 tooth-years at risk) for Danish boys and girls born 1980.
      • Race/ethnicity: genes or social class?
        • Figure 4.13 A comprehensive model of the global, national, and local structural drivers of the circumstances in which people are born, grow, live, work, and age, which in turn determine the biological processes that lead to dental caries in individuals and in populations.
      • The social gradient
        • Figure 4.14 The social gradient in oral health illustrated by the almost linear relationship between occupational classification and the prevalence of edentulousness.
    • Where? The geography of caries
      • Figure 4.15 The mean D3MFT counts for 12-year-olds in different countries as reported to the WHO Oral Health Country/Area Profile Programme Database (http://www.mah.se/capp/) in the 2000s.
      • Figure 4.16 The variation among the 267 Danish municipalities in the mean D3MFS counts for 15-year-olds in year 2003. Note the eightfold difference between the municipality with the lowest mean D3MFS (~1) and that with the highest mean D3MFS (~8).
    • When? Trends in caries
    • Why? The causes of caries
      • Figure 4.17 The mean D3MFT counts for 12-year-olds in different countries as reported to the WHO Oral Health Country/Area Profile Programme Database (http://www.mah.se/capp/) during the 1980s, 1990s and 2000s.
      • Proximal, strictly biological causes
        • Figure 4.18 The mean D1FS counts recorded among Swedish adults aged 20, 30, 40, 50, 60, 70, and 80 years in each of four surveys carried out in 1973, 1983, 1993, and 2003.
        • Figure 4.19 The trends in the mean d3mfs counts for Danish 5- and 7-olds-olds, and the trends in the mean D3MFS counts for Danish 7-, 12-, and 15-year-olds, as compulsorily reported to the Danish Health and Medicines Authority during the period from 1988 to 2012.
        • Figure 4.20 Keyes’ triad. Three overlapping circles indicate that concentricity in factors in host, microflora, and substrate is necessary for caries activity [101].
        • Figure 4.21 The Fejerskov and Manji model for caries causation. Adapted from [59].
      • Looking to the upstream causes of caries
    • References
• Part II The caries lesion and its biological determinants
  • 5 Pathology of dental caries
    • Introduction
      • Figure 5.1 Principal progress of mineral loss in relation to time. The slope of the line may vary depending on the caries challenge, and time may vary from weeks to months and years. The blue zone indicates that the mineral loss is not visible.
      • Figure 5.2 Schematic illustration of micro-events at a surface over time. The upper fluctuating line indicates pH fluctuations in a biofilm over time (minutes, hours, days). The three curves show three different examples of fluctuating mineral loss (up) or gain (down) in enamel as a result of innumerable fluctuations in pH. The horizontal dotted lines indicate where loss of mineral may be seen clinically as a white spot. See text for details.
    • Human dental enamel at time of eruption
      • Figures 5.3–5.5 The principal orientation of crystals in human enamel. Figure 5.3 is a schematic drawing showing that in the rods the long axes of crystals run in parallel with the long axes of rods (head), but in the interrod regions (tail) the crystals gradually bend in the cervical direction. This creates in a cross-section a fish-like figure consisting of a head and tail. Figure 5.4 shows this pattern in a fractured enamel surface examined by SEM. In Fig. 5.5 it is examined in a transmission electron microscope, where the section is cut perpendicular to the long axes of the rods. R: rod; IR: interrod.
      • Figures 5.6–5.8 Scanning electron micrographs showing an unerupted enamel surface at different levels of examination. Figure 5.6 shows an overview of perikymata and Tomes’ processes pits, and this is shown in detail in Fig. 5.7. Figure 5.8 shows at high magnification the ends of rounded crystals separated by distinct intercrystalline spaces. The surface is examined after removal of organic films.
      • Figures 5.9–5.11 Human enamel examined by scanning electron microscopy and transmission electron microscopy after removal of the mineral content (Fig. 5.11) just prior to eruption. In Fig. 5.9 the surface crystals are seen from a fractured surface. In Fig. 5.10 the surface shows rod (R) endings surrounded by periprismatic, arch-shaped gaps representing the openings of the interface between rod and interrod enamel (IR). The mineralized surface is highly irregular, occasionally with holes into the enamel filled by developmental proteins (Fig. 5.11). These proteins also occupy the gaps surrounding partly the rods and are part of the diffusion pathways throughout the enamel. E: enamel space; DP: developmental protein.
      • Figure 5.12 Drawing illustrating partly erupted premolar with microbial accumulations predominantly located along the gingival margin.
      • Figure 5.13 Enamel surface beneath the microbial plaque showing distinct signs of dissolution of rod (R) and interrod (IR) areas. These features are characteristic of active lesions at the subclinical level.
      • Figure 5.14 Enamel surface from the ‘clean’ cuspal region showing marked wear, particularly corresponding to the interrod areas (IR). These features are characteristic of inactive lesions at the subclinical level.
    • Enamel changes during early caries lesion development
      • How rapidly may changes be recorded (microscopically and clinically) in enamel covered by dental plaque?
        • Figure 5.15 Scanning electron micrograph of enamel surface prior to establishment of protected area by cementing orthodontic band. Note the rounding out of structural details by functional wear.
        • Figure 5.16 Scanning electron micrographs of enamel surface after 1 week with local protection against mechanical wear and biofilm allowed to form. Note initial dissolution of the outer enamel surface beneath the undisturbed plaque.
        • Figure 5.17 Diagram illustrating the distributions of enamel porosity at different stages of caries dissolution from the surface towards the enamel–dentinal junction. Parts (a) to (d) illustrate the gradual increase in pore volume after (a) 1 week to (d) 4 weeks of experimental caries in vivo.
      • Why does mineral loss predominantly occur underneath the enamel surface?
        • Figure 5.18 After 4 weeks of undisturbed biofilm the surface dissolution becomes more marked with loss of larger parts of perikymata overlappings.
        • Figure 5.19 Detail of eroded perikymata overlappings with exposed underlying rod and interrod enamel at different stages of dissolution.
      • How do such early lesions change when dental plaque is removed?
        • Figure 5.20 (a) Experimental tooth immediately after removal of the 4 week local protection by an orthodontic band. Note the typical appearance of an active enamel white spot lesion. (b) The same tooth 1 week after re-exposure to the oral environment. The inactive or arrested lesion appears less whitish due to wear and polishing of the external partly dissolved surface. (c) Experimental tooth immediately after cessation of 4 weeks of local protection. Note a typical opaque white, active enamel lesion. (d) The same tooth 2 weeks after re-exposure to wear in the oral environment. The arrested lesion is not readily visible in the clinic. Note the more shiny appearance of the surface.
    • The approximal white spot lesion
      • Figures 5.21–5.24 Scanning electron-micrographs of enamel caries lesions after removal of local protection. Overview (left) and high-magnification detail (right). Figure 5.21 shows typical features of active enamel lesion with partial and complete dissolution of outermost crystals immediately after removal of 4 weeks’ local protection. Courtesy of Scandinavian University Press. Figure 5.22 is after 1 week of exposure to the oral environment: multiple microscratches can be seen in the outermost partly dissolved crystal layer. Loosely bound crystals have been worn away (right). Courtesy of Scandinavian University Press. Figure 5.23 shows micro-wear after 2 weeks. Parts of the porous external micro-surface have been removed by wear. The exposed underlying crystals appear more tightly packed (right). Courtesy of Scandinavian University Press. Figure 5.24: After 3 weeks the surface appears smoother, with classical wear striation patterns owing to more complete removal of the eroded microsurface. The complete removal of loosely bound and partly dissolved crystals has exposed tightly packed crystals separated by a distinct network of intercrystalline spaces.
      • Surface features of the clinical white spot lesion
        • Figure 5.25 Clinical features immediately after removal of orthodontic appliances and cleaning. The orthodontic treatment had lasted for 2 years. Note the marked gingival reaction and the characteristic chalky surface appearance of the active enamel lesion.
        • Figure 5.26 After 3 months with careful oral hygiene the gingival tissues have recovered and the active lesion has been completely arrested. The white appearance of the lesion has diminished markedly due to polishing away of the eroded outermost enamel surface.
        • Figure 5.27 Scanning electron micrograph of replica of the active lesion. Note the distinct step between the eroded surface of the active lesion and the adjacent sound enamel (open arrows). A furrow has been made in the sound enamel area (arrows).
        • Figure 5.28 Scanning electron micrograph of replica of the arrested lesion. After 3 months, the furrow (arrow) has almost disappeared, and the step between the sound and arrested surface is slightly enhanced (open arrows).
        • Figure 5.29 Scanning electron micrograph of early surface dissolution cervical to contact facet (CF) in a natural, active enamel lesion.
        • Figures 5.30–5.32 Details of surface dissolution patterns seen in Fig. 5.29.
        • Figure 5.33 Scanning electron micrograph of part of an inactive enamel lesion with microcavity. At the bottom of the cavity, openings of striae of Retzius are seen. The rod pattern is clearly evident in the exposed enamel, in contrast to the abraded surface enamel.
      • Histology of the white spot lesion
        • Figures 5.34 and 5.35 Variations in surface features of rod (R) and interrod (IR) enamel in inactive lesions caused by variations in wear.
        • Figures 5.36 and 5.37 Ground section cut through the center of small enamel lesion examined in polarized light after imbibition in water (Fig. 5.36) and quinoline (Fig. 5.37): (1) surface zone; (2) body of the lesion; (3) dark zone; (4) translucent zone.
        • Figure 5.38 The principal pore volume distribution in the section examined Figs 5.36 and 5.37.
    • Progression of the enamel lesion
    • Arrest of the caries lesion
      • Figure 5.39 Microradiograph of ground section from enamel lesion demonstrating preferential subsurface loss of mineral. Note the variation in mineral loss, but the structure of prism pattern remains.
      • Figures 5.40 and 5.41 Scanning and transmission electron micrographs from body of the lesion showing partly dissolved enamel with enlarged gaps between rod (R) and interrod (IR) enamel. Note in Fig. 5.41 that the wide empty spaces represent artifacts caused by tissue preparation (sectioning).
      • Figure 5.42 Schematic illustration of progressive stages of lesion formation: (1) reactive dentin; (2) sclerotic reaction or translucent (transparent) zone; (3) zone of demineralization; (4) zone of bacterial invasion and destruction; and (5) peripheral rod direction. CT, central traverse line.
      • Table 5.1 Distribution of buccal surfaces of maxillary first permanent molars in three categories of diagnosis at age 8 and age 15 of the same surfaces. From [3]. Reproduced with permission of Sage Publications.
    • Occlusal caries
      • Figures 5.43–5.48 Histological sections through teeth exhibiting different stages of progression of occlusal caries lesions. By comparing these natural lesions with the diagram in Fig. 5.56 it will be appreciated why occlusal caries presents itself as undermining the enamel. If left ‘untreated’ a caries lesion stimulates the pulpo-dentinal organ to carry out reparative processes in the form of sclerotic (hypermineralized) dentin and at the pulpal interface reactive (tertiary) dentin. If the microbial mass is not removed then the final outcome will be necrosis of the pulp and periapical inflammatory reactions (Fig. 5.48).
      • Figures 5.49–5.51 Sections through occlusal fissures examined in polarized light. When examined dry in air an early subsurface caries lesion and surface porosities are seen in Fig. 5.49. The arrow shows a surface defect probably caused by vigorous probing. The dotted lines indicate prism direction. The bottoms of such fissures are having a structural complexity often with increased amount of developmental proteins which should not be considered as dental caries! In Fig. 5.50 a standard clinical probe is located at the entrance of a fissure. In Fig. 5.51 a caries lesion is confined to the enamel at both sides of the fissure. The section is examined dry in air and the lesion is thus reflecting areas where the pore volume exceeds 1%.
      • Figures 5.52 and 5.53 Microradiograms from two consecutive sections of the same fissure. Note the uneven distribution of demineralization.
      • Figures 5.54 and 5.55 Microradiogram and polarized light microscopic illustration of pattern of spread of a caries lesion. At sectioning the tissue was intact! In Fig. 5.55 a probe is located at the entrance to the fissure. Note the apparent undermining character of demineralization. See the text for explanation.
      • Figure 5.56 Schematic illustration of progressive stages of occlusal lesion formation in an occlusal fossa: (1) reactive dentin in the interface to the pulp; (2) sclerotic reaction or translucent (transparent) zone; (3) zone of demineralization; (4) zone of bacterial invasion and destruction; (5) dotted lines indicate the direction of the prisms.
    • Dentin reactions to caries progression
      • Figure 5.57 Ground section of active approximal lesion examined in transmitted light. The triangular enamel lesion reaches the enamel–dentin junction, with demineralization of the outer dentin (ZD) and sclerotic reactions (TZ) corresponding to the less advanced peripheral parts of the enamel lesion.
    • Pulpo-dentinal reactions
      • Pulpo-dentinal reactions before bacterial invasion into the dentin
        • Figures 5.58 and 5.59 Histological ground sections in the mesiodistal direction through human mandibular premolars and molars. In the approximal surfaces caries lesions extend at a varying depth towards the dentin. Note how sclerotic reactions in dentin (the translucent zone) and pulp may appear even at these stages of lesion development. Figure 5.59 is a higher magnification of the approximal space between the premolars. Note how the lesions penetrate in depth below the contact area. The approximal space appears partly empty because substantial shrinkage occurs during tissue preparation (the gingiva has been edematous and swollen) and some of the microbial deposits are lost.
        • Figures 5.60 and 5.61 Microradiographs of the border between the translucent zone (TZ) and normal dentin, with open dentinal tubules seen as dark lines. The dotted line in Fig. 5.60 indicates plane of view in Fig. 5.61.
        • Figure 5.62 Transmission electron micrograph from translucent zone showing two completely occluded dentinal tubules (ODT).
        • Figure 5.63 Figure 5.63: Transverse section of a dentin tubule showing advanced mineralization of the periodontoblastic space (PS). OP: Odontoblast process; ID: intertubular dentin.
        • Figure 5.64 Transverse section of odontoblast process (OP) and partly mineralizaed peri-odontoblastic space (PS).
        • Figure 5.65 Transverse section of mineralized odontoblast process (OP) and large, periodontoblastic space (PS) in which the majority of collagen fibers are mineralized.
        • Figure 5.66 Completely mineralized dentinal tubule (DT).
        • Figure 5.67 Four consecutive micro-computed tomography scans through deep caries lesion in a 2000-year-old tooth from Imperial Rome. The lesion had penetrated into the pulp where reactive dentin is indicated with an asterisk (a). Note the very pronounced sclerotic dentin reactions (hypermineralization) that delineate the base of the dentin caries cavity – indicated by arrows on (b), (c), and (d). The framed area in (b) shows an early caries lesion through enamel with a dentin demineralization at the enamel–dentin border.
      • Enamel destruction and bacterial invasion
        • Figure 5.68 Microradiograph of ground section through inactive approximal lesion that has been arrested for several years. The small cavity in the surface of the enamel may have facilitated some redeposition of mineral, but otherwise this degree of demineralization can remain unchanged lifelong.
        • Figure 5.69 Histological section of carious dentin from a deep, active lesion showing the zone of destruction (ZD) and zone of bacterial invasion (ZB).
        • Figures 5.70 and 5.71 Clusters of bacteria penetrating dentinal tubules and forming liquefaction focus.
        • Figure 5.72 Drawing showing the location of where two microradiograms are made along the walls of two different deep caries lesions that had never been interfered with. The teeth, originating from Tanzanians, exhibited dental fluorosis, which explains the hypermineralized Owens contour line (OL) in (a). It is striking that the zone of demineralization (ZD) is not very thick and delineated by the sclerotic zone (SZ) – compare with Fig. 5.67. RD: reactive dentin. In (b) the base of a very deep occlusal cavity is shown again with a relatively narrow zone of demineralization (ZD). It should be noted how the dentin towards the pulp shows ‘clouds’ of hypermineralization in the sclerotic zone (SZ).
        • Figure 5.73 Top: schematic drawing of the relationship between Knoop hardness, the outer carious dentin, the translucent zone, and the inner sound dentin. Bottom: the relation to bacterial invasion and mineralization phenomena in the dentinal tubules.
      • Pulp reaction
    • Root-surface caries
      • Clinical appearance of root caries lesions
        • Figures 5.74 and 5.75 Microradiograms of early stages of root-surface caries. Distinct demineralization is observed throughout the cementum but also extending into the underlying dentin deep to a relatively well mineralized cementum zone. Note the laminated appearance of the cementum in Fig. 5.75, which reflects variations in the mineral content of the imbrication lines.
      • Histopathological features of root-caries lesions
        • Figures 5.76–5.78 Microradiograms of sections through root caries lesions that have been developed experimentally in the oral cavity during 1, 2, and 3 months. Note how the mineral content in the surface zone increases with increased duration of the cariogenic challenge while there is a progressive subsurface loss of mineral in the dentin [38].
        • Figure 5.79 A 1 µm thick section through the surface layer of an active root surface caries lesion covered by microbial deposits. At this early stage, the microorganisms penetrate into the superficial layer of the cementum (arrows), which explains why the active root-surface caries lesion appears soft on probing. P: microbial plaque; C: cementum; D: dentin.
        • Figure 5.80 Approximal active root-surface caries lesion covered by dental plaque (inset). A microradiogram of a section through the center of the lesions shows loss of cementum (C) corresponding to the part of the surface where extensive loss of mineral has occurred. The body of the lesion is located deep to a surface zone which varies in mineral content. The dentinal tubules affected by the caries attack show the zone of sclerosis (SZ), and towards the pulp tertiary dentin (reactive dentin) has formed (TD) [36]. E: enamel.
        • Figure 5.81 (a) Section through an inactive root-surface caries lesion. When examined in transmitted light (b) and by microradiography (c), it is apparent that a considerable surface abrasion has occurred. Part of the lesion has been abraded away, but a localized radiolucent area remains, possibly reflecting a caries-active site [36].
        • Figure 5.82 Section through an arrested root-surface lesion where the microradiographic picture demonstrates extensive calculus formation extending into microcavities. Note the subsurface lesion cervical to the rim of calculus. E: enamel; CA: calculus.
    • Background literature
    • References
  • 6 Saliva and caries development
    • Introduction
    • Saliva and salivary glands
      • Figure 6.1 Location of the major salivary glands in humans: the parotid (strictly serous), the submandibular (seromucous), and the sublingual gland (mucoserous). The parotid gland (14–28 g), the largest salivary gland, is located bilaterally before and under the ear. The main excretory duct (parotid duct or Stenson's duct) ends in the cheek at the height of the upper molars. The submandibular gland (7–8 g) is located bilaterally under the jaw just medially of the mandibular angulus. The main excretory duct (Wharton's duct) has its orifice in the floor of the mouth, just behind the lower incisors. The sublingual gland (3 g) is located bilaterally in the floor of the mouth between the mandibular corpus and tongue. The sublingual gland secretes with numerous ducts directly to the floor of the mouth in the area where the gland is located and also via a main excretory duct (Bartholin's duct) that runs with the submandibular duct and also ends in the floor of the mouth at the level of the lower incisors. The minor salivary glands (<10 mg/gland), whose number is estimated at several hundred, are scattered among the oral mucosa of the palate (the palatinal glands that are strictly mucous), the lip (the labial glands), the cheek (the buccal glands), and tongue (the lingual glands). In the region of the papillae vallatae on the tongue are the von Ebner glands, which are strictly serous.
      • Table 6.1 Normal range for whole saliva flow rates and relative contribution of different gland types to whole saliva under various conditions [52]. Reproduced with permission of Thieme Publishing Group
      • Figure 6.2 Salivary gland structure showing both serous and seromucous end-pieces, intercalated ducts, myoepithelial cells, striated ducts, and excretory ducts and their relation to the autonomic nervous system afferents and efferents. The left-side schematic drawings show the main ion channels of the acinar and ductal cells. The ductal tissue has a low water permeability, as opposed to the highly water-permeable acinar tissue. Upon stimulation, neurotransmitters bind to specific receptors that activate cell signaling pathways, which result in an increase in intracellular calcium and opening of calcium-activated ion channels in the cell membrane. Average values for the ionic composition are given for primary saliva as well as unstimulated and stimulated whole saliva.
      • Stimulation and control of secretion
      • The glands
      • Formation of primary saliva
      • Modification of primary saliva
        • Figure 6.3 Concentrations of different inorganic constituents in saliva as a function of the saliva flow rate. Upper curves: parotid saliva; lower curves: submandibular/sublingual saliva. Note that the ordinates have logarithmic scales. The red line represents the saliva pH (−log [H+]).
    • Saliva and caries development: biological aspects
      • Figure 6.4 Functions of saliva and its components in relation to the age, thickness, and acid-producing capacity of the biofilm. The components shown in parentheses (mucins and amylase) increase the effect of the physical volume at various ‘stages’ of the caries process. All ‘stages’ may be present within the same dentition at the same time.
      • Formation of the pellicle
        • Figure 6.5 Development of the pellicle on a clean enamel surface showing the dentin, the enamel, the enamel surface with its negatively charged hydroxyapatite crystals having the phosphate groups nearest to the surface, the positively charged ionic double layer with much more calcium than phosphate, the first negatively charged proteins attached to this double layer, and whole saliva as the source of the pellicle proteins. The first proteins to form a pellicle are mainly the PRPs and statherin.
      • Important pellicle proteins
      • Functions of saliva on newly formed biofilms
      • Antimicrobial proteins and peptides
        • Table 6.2 Major antimicrobial proteins of human whole saliva
        • Figure 6.6 Glucose-stimulated acid production in dental biofilm of subjects with different concentrations of hypothiocyanite [OSCN−] in whole saliva. Gray circles show physiological levels of [OSCN−] in whole saliva and red circles show artificially increased [OSCN−] values obtained with oral hygiene products, in this case by enzyme-containing toothpaste.
      • Clearance and aggregation of oral bacteria
      • Functions of saliva on established biofilms
      • Amylase activity
      • Oral sugar clearance
        • Figure 6.7 Two subjects have rinsed with a sucrose solution. Owing to differences in saliva flow rates, the two subjects differ considerably in clearance rate (solid lines), causing a large difference in the decrease in plaque pH (hatched lines) by anaerobic bacteria within the plaque. Subject 1 had a higher salivary flow rate than subject 2, who had subnormal flow rates.
      • Saliva buffer capacity and pH regulation
        • The bicarbonate buffer system
          • Figure 6.8 (a) Titration of whole saliva with strong acid in a closed system. The upper curve shows stimulated saliva and the lower curve shows unstimulated saliva. Above pH 5.5 the buffering capacity is high owing to the buffering ability of the phosphate (1) and bicarbonate buffer system (2). At low pH values the slope of the curve becomes steeper, indicating a lower buffer capacity mainly from salivary proteins (3). (b) A typical Stephan curve of plaque pH in response to an oral sucrose rinse. In spite of the saliva buffer capacity the plaque pH can drop rapidly after a rinse to values below the critical pH of human saliva (red area), whereafter it slowly returns to baseline. The reason for this drop is that the saliva buffer capacity is only moderate. (c) Comparison with milk in the range from pH 4 to 7 (which is indicated by the circle and the arrow from (a)) shows the buffer capacity of whole saliva is much less than that of milk.
        • The phosphate buffer system
          • Figure 6.9 The phosphate buffer system as a function of pH (i.e., the Bjerrum diagram). Within the physiological pH range (6.0–7.5) most phosphate is on the and forms. The dark gray area represents the normal pH range of human saliva.
        • The protein buffer system
      • Saliva and caries lesion remineralization
      • Calcium and phosphate in saliva
      • Fluoride in saliva
      • Saliva saturation with respect to hydroxyapatite and fluorapatite
      • Critical pH values and remineralization
      • Other caries-related components in saliva
    • Saliva and caries development: clinical aspects
      • Dental findings in patients with low saliva flow rates
        • Figure 6.10 Clinical manifestations of dry mouth in a woman with Sjögren's syndrome: (a) multiple caries lesions; (b) dry mucosal surfaces and tongue in the same patient.
        • Figure 6.11 Dental caries related to subnormal flow rates and hyposalivation: (a) cervical lesions; (b) more generalized superficial erosion like defects of the crown.
      • Causes of subnormal saliva flow rates and hyposalivation
      • Medication
      • Sjögren's syndrome
      • Radiotherapy
        • Table 6.3 Influence of different conditions on salivary gland function. The three most important causes of a reduced salivary gland function are drugs, Sjögren's syndrome, and head and neck radiotherapy.
    • Evaluation of salivary gland function
      • Draining and spitting methods
        • Figure 6.12 Percentage reduction in flow rate of stimulated parotid and submandibular–sublingual (SM/SL) saliva as a function of time after start of radiotherapy (RT). Upper lines show parotid-sparing three-dimensional/intensity-modulated RT (IMRT) and lower lines conventional RT including the parotid, submandibular, and sublingual glands in the treatment area [54].
        • Figure 6.13 Measurement of the whole saliva flow rate by the draining method. Materials required are a plastic cup for collection and weight with two digits (a) and a stopwatch (b). During saliva collection the patient is placed in a relaxed hunched-over position with the face tilted slightly downwards (c). For stimulation, chewing on paraffin wax is a standard, which enables comparison of the results with normal values, and here the spitting method is used.
      • Suction and absorbent methods
      • Saliva flow rates and caries risk assessment
      • Compositional analyses of saliva
        • Figure 6.14 The effect of unstimulated whole saliva flow rates on the lesion depth (µm) in experimentally developed root caries lesions and the effect of unstimulated whole saliva flow rates on the mineralization level (percentage of a healthy root surface) in the surface layer of these lesions. Lesions were developed during a period of 2 months with undisturbed biofilm formation and without exposure to fluoride-containing oral hygiene products [6, 7].
    • Management of salivary gland hypofunction
      • Table 6.4 Management strategies for xerostomia and salivary hypofunction
    • Concluding remarks
    • Background literature
    • References
  • 7 Biofilms in caries development
    • Introduction
      • Figures 7.1 and 7.2 Figure 7.1: Microbial biofilms on teeth become clearly visible after staining with a disclosing solution. The biofilms are typically located at retention sites along the gingival margin and extend into the interproximal space. Figure 7.2: Occlusal surface of erupting third molar. Note that heavy microbial deposits (biofilms) are related to the fissures and partly cover the cuspal slopes. This is a freshly extracted tooth where a brown dye has been used to delineate the biofilm.
    • The resident microflora
      • Acquisition of the resident oral microflora
      • Benefits of the resident oral microflora
      • Site distribution of oral bacteria
      • Bacterial metabolism and ecological factors affecting the growth and metabolism of oral bacteria
        • Figure 7.3 The metabolism of oral bacteria, responsible for acid production, ESP production, ISP production, and alkali production: (1) glycosidases; (2) proteases/peptidases; (3) arginine deiminase; (4) urease; (5) sugar-binding proteins; (6) PEP–PTS; (7) lactate dehydrogenase; (8) pyruvate formate-lyase; (9) pyruvate dehydrogenase; (10) pyruvate oxidase; (11) PEP carboxylase/PEP carboxykinase; (12) proton-translocating ATPase; (13) glucosyltransferases; (14) fructosyltransferases.
    • Dental biofilms: development, structure, composition, and properties
      • Development and structure of young dental biofilms
        • Figures 7.4 and 7.5 Scanning electron micrographs demonstrating microbial colonization of human enamel 4 h after cleaning [70]. Figure 7.4: After 4 h exposure the enamel is covered by pellicle, which is a granular deposit, primarily located in Tomes’ processes pits (TP) and in perikymatal grooves (P). Figure 7.5: The first bacteria to colonize the tooth surface are of the coccobacillary type (B). Note that the granular deposit does not cover the tooth surface in a uniform layer (PE).
        • Pellicle formation
        • Pattern of early bacterial colonization (attachment and growth)
          • Figure 7.6 Simplified explanation of the principle of selective adherence of bacteria to enamel. Successful irreversible attachment is achieved when adhesins on the surface of a bacterium bind to a receptor in the pellicle (P).
          • Figures 7.7–7.9 Scanning electron micrographs demonstrating microbial colonization of human enamel 12 h after cleaning [70]. Figures 7.7 and 7.8: In 12-h-old biofilms the microorganisms spread in a monolayer along the perikymata (P). Figure 7.9: The monolayer of bacteria (upper part) is gradually replaced by a multilayer of cells (lower part) which is embedded in an intermicrobial matrix (M).
          • Figures 7.10–7.11 Distinct morphological changes may be recorded on the surface of the biofilms when comparing the microflora on teeth after 24 h (Fig. 7.10) and 48 h (Fig. 7.11). Whereas the 24-h-old biofilm comprises a mass of coccoid bacteria from which a few filaments extend, the 48-h-old microflora is almost entirely dominated by filamentous organisms [70].
        • Microbial succession
          • Figures 7.12 and 7.13 Forty-eight-hour-old biofilms on root cementum (Fig. 7.12) and enamel (Fig. 7.13) surfaces from the same individual. Note that the microbial biofilms are thicker and more densely packed on root cementum [67].
          • Figure 7.14 Proportions of various streptococci (%) from 4 h dental biofilm in caries-active and caries-inactive individuals [74].
          • Figures 7.15 and 7.16 Some bacteria in the surface of dental biofilms co-aggregate to form ‘corn cob’ structures (Fig. 7.15). Individual ‘corn cobs’ are composed of a central filament covered by spherical microorganisms (Fig. 7.16, cross-section) [72].
        • Microbial composition and structure of the climax community (mature biofilm)
          • Figure 7.17 Relative proportions of selected microorganisms in developing coronal biofilms (days 1–9) in relation to the atmospheric requirement.
          • Table 7.1 Composition of biofilms at distinct surfaces on sound teeth
          • Figure 7.18 Densely packed pleomorphic bacteria resembling Actinomyces form palisades along the tooth surface in 3-week-old dental biofilms [71].
          • Figure 7.19 Fluorescence in-situ hybridization of two-dimensional dental biofilm showing Actinomyces (blue), streptococci (green), and other bacteria (red). Note preferential colonization of Actinomyces in the inner layer of the biofilm.
          • Figures 7.20–7.22 Ultrastructure of 2-week-old dental biofilms from three individuals with different colonization patterns. Note that in addition to differences in thickness, the outer part of the biofilms varies in composition and structure [71].
      • Properties of dental biofilms
        • Table 7.2 Properties of biofilms and microbial communities
        • Figure 7.23 Telemetrically recorded pH changes of 2-, 3-, 5-, and 6-day-old interdental biofilms in a 62-year-old male volunteer during and after 2 min rinses with 10% sucrose solution. PC: paraffin chewing. Note that the rate and amount of acid formation increase with the age of the biofilm.
        • Table 7.3 Microbial interactions in dental plaque
    • Caries microbiology: a brief historical perspective
    • Methodological problems in microbiological studies of dental caries
      • Figure 7.24 Distinction between cross-sectional and longitudinal study designs to investigate the role of dental biofilm bacteria in caries. Cross-sectional studies are relatively quick and easy to perform on different population groups, but they only show associations between the microflora and caries because each site is sampled only at a single time point. Longitudinal studies provide more insights into the microbial etiology of dental caries because the microflora can be compared (a) before and after the diagnosis of a lesion and (b) between sites that developed caries and those that remained caries free. All sites to be investigated are clinically caries free at the start of sampling.
    • Microbiology of caries
      • Enamel caries
        • Table 7.4 Mean proportions of mutans streptococci (MS) and lactobacilli (L) on teeth in schoolchildren (7–8 years old) who remained caries free or who developed a caries lesion during a longitudinal study [51]
      • Root-surface caries and infected dentin
        • Table 7.5 Mean proportions of selected bacteria from biofilms developing on root surfaces with and without caries [8]
    • Cariogenic features of dental biofilm bacteria
    • The ‘ecological plaque hypothesis’ to explain the role of dental biofilm bacteria in the etiology of dental caries
      • Figure 7.25 Velocity of acid production by six oral streptococcal species at different pH values. The bold line represents the median, and the box and error bars the 95% and 75% confidence intervals respectively [19].
      • Figure 7.26 The ecological plaque hypothesis and the etiology of dental caries. The diagram depicts a dynamic relationship whereby an environmental change in the biofilm (e.g., low pH) drives a shift in the balance of the resident microflora, thereby shifting the balance towards enamel demineralization. Caries could be controlled by inhibiting the putative pathogens (MS or other acid producers) or by interfering with the environmental changes driving the ecological shift; for example, by reducing the acid challenge by the use of sugar control, saliva stimulation, and/or biofilm removal. MS: mutans streptococci.
      • Figure 7.27 The caries process according to the extended ecological caries hypothesis Adapted from Takahashi and Nyvad, 2008 and 2011 [87, 88] In this hypothesis environmental acidification acts as the main driving force for acid-induced adaptation and acid-induced selection of the microbial community as it passes form the dynamic stability stage via the acidogenic stage to the aciduric stage. Concurrently, caries lesion dynamics shifts towards net mineral loss. Note that reactions may be reversed by elimination of the acid stress.
      • Figure 7.28 Acid-induced adaptation of non-mutans streptococci (data adapted from [89]). (a) Acidogenicity (final pH values) after the glucose addition at pH 7.0. The bacteria were grown at pH 7.0 until the logarithmic phase of growth and further grown at pH 5.5 for 0, 0.5, 1.0, and 1.5 h. (b) Acidurance (survival rate) after 1 h at pH 4.0. The bacteria were grown at pH 7.0 until the logarithmic phase of growth and further grown at pH 5.5 for 0, 0.5, 1.0, and 1.5 h. The treated bacterial cells were plated on blood agar and counted for colony-forming units after anaerobic incubation.
      • Figure 7.29 Acid-induced selection of oral bacteria. (a) Bacterial growth rate at acidic pH (data adapted from [34]). Bacteria were grown at various pH values with pH control by periodic addition of alkali, and bacterial growth rates were calculated from the logarithmic growth phase. Data are the means of two strains of mutans streptococci, two strains of non-mutans streptococci, and two strains of Actinomyces. (b) Bacterial survival at pH 4.0 (data adapted from [66]). The bacterial cells grown at pH 7.0 were exposed to pH 4.0 for 0, 0.5, 1, 1.5, and 2 h in buffer solution. The treated bacterial cells were plated on blood agar and counted for colony-forming units after anaerobic incubation.
    • Concluding remarks
    • Background literature
    • References
  • 8 Diet and dental caries
    • History
    • Early ecological studies
    • Experimental human studies
      • Figure 8.1 Information from the Vipeholm study: average DMFT per person relative to the type and time of eating various sugars and sugar-containing products. Solid lines represent experimental periods with increased consumption between meals; dashed lines represent control periods or increased consumption only during the meals.
      • Figure 8.2 Increase in decayed, missing, filled tooth surfaces (DMFS) in the three groups in the Turku experiment based on clinical and radiographic findings including white spots.
    • Influence of fluoride on the diet–caries relationship
      • Figure 8.3 Sugar consumption (kilograms per year per person) in Denmark and caries experience (DMFT) in 12-year-old schoolchildren between 1974 and 1997.
    • Measuring cariogenicity
      • Plaque pH measurements
        • Figure 8.4 Stephan and Miller, in 1943, measured the course of the pH on buccal surfaces of the first permanent incisors after a glucose rinse. They repeated the experiment after the left tooth had been cleaned.
        • Figure 8.5 An example of the Stephan curve as used in health promotion materials.
        • Figure 8.6 pH course in dental plaque up to 15 min rinsing with human milk, cow milk, 7% lactose, and 7% sucrose.
        • Figure 8.7 The Stephan response curves obtained from sound occlusal surfaces, inactive occlusal caries lesions, and deep, active occlusal caries lesions following a sucrose rinse. Mean values.
        • Figure 8.8 Examples of the pH course in 5-day-old undisturbed interproximal dental plaque measured with pH-telemetry under various rinsing conditions. PC: paraffin chewing; H2O: water rinsing; U: urea rinsing [50].
      • In-situ caries models
      • Clinical experiments
    • Sweeteners
      • Cariogenic sweeteners
        • Monosaccharides and disaccharides
        • High-fructose corn syrup
          • Table 8.1 Different types of carbohydrates and sugar substitutes grouped according to potential cariogenicity and type and number of saccharides
        • Starches
          • Table 8.2 The composition and relative sweetness of the disaccharides
      • Noncariogenic carbohydrate bulking agents
      • Sucrose substitutes
        • Cariogenic oligosaccharides
        • Likely low cariogenic and noncariogenic mono- and disaccharides
          • Monosaccharides
          • Disaccharides
      • Noncariogenic sucrose substitutes
        • Noncaloric intense sweeteners
          • Steviolglycosides
        • Caloric sweeteners
          • Sugar alcohols
          • Sorbitol
            • Figure 8.9 The main routes of manufacturing sugar alcohols.
            • Table 8.3 Properties and applications of various sugar alcohols
          • Xylitol
            • Figure 8.10 The course of pH in interproximal plaque after a 10% sucrose rinse, 10% xylitol rinse, and 10% sorbitol rinse. PC: paraffin chewing; H2O: water rinsing; U: urea rinsing [103].
          • Other sugar alcohols
          • Clinical trials with sorbitol
          • Clinical trials with xylitol
          • Chew or polyol effect
    • Protective factors in foods
      • Dairy products
      • Probiotics
    • Diet and dental erosion
    • Conclusion
    • References
  • 9 Demineralization and remineralization: the key to understanding clinical manifestations of dental caries
    • Introduction
    • Enamel mineral
    • Stability of calcium phosphates
      • Figure 9.1 (a) Cross-cut enamel crystal from outermost highly mineralized human enamel. The hexagonal crystal exhibits a dark central line and a lattice striation with an interval of 0.817 nm (~8.2 Å) between the lines which intersect each other at an angle of 60° reflecting the unit cell of hydroxyapatite. (b) Schematic drawing of a ‘typical’ enamel crystal. These crystals are about 350 Å in thickness and 1000 Å in width. Ions in the hydration shell can easily be exchanged. Once ions are bound in the hydroxyapatite lattice (e.g., fluoride) it is not easily exchanged unless the crystal is dissolved. For an explanation of the drawing, please see the text.
      • Figure 9.2 Phase solubility diagram at 25 °C for salts of calcium phosphates that may form under physiological conditions.
    • Crystal dissolution
    • Why is apatite solubility increased by acid?
      • Table 9.1 Calcium and phosphate concentrations, activities, and activity products with respect to hydroxyapatite for the same solution at pH 5, 6, and 7 and at a temperature of 37 °C
      • Figure 9.3 Transmission electron micrographs of part of the body of a caries lesion that is severely demineralized (a). The arrows in (a) and (c) indicate crystals with central dissolution. In (b) and (d) so-called caries crystals are shown. Some of these are in fact partly dissolved crystals with redeposition of minerals in the centers of crystals indicated with arrow heads.
    • Effect of carbonate and fluoride on apatite dissolution and growth
      • Figure 9.4 Calcium output from enamel during demineralization in solutions initially containing 2.2 mmol/L calcium chloride and 2.2 mmol/L potassium phosphate, adjusted to the pH and fluoride [F] levels indicated. For original figure, refer to [27, 28].
    • Demineralization and remineralization of the dental hard tissues
      • Figure 9.5 Degrees of saturation with respect to various calcium phosphates and to calcium fluoride in parotid saliva [14]. The degrees of saturation are given by log n(ion product in saliva)/(solubility product), in which n is the number of ions in the actual salt. The salts may all at least occasionally occur in the oral cavity as part of teeth or calculus, or as a precipitate after topical fluoride application. Saliva is highly supersaturated with respect to the apatites, which is the basis of the integrity of the teeth in the mouth. The saturation with respect to the other calcium phosphates explains their occurrence in calculus, while the undersaturation with respect to calcium fluoride shows that saliva invariably dissolves that salt.
      • Figure 9.6 Solubility of hydroxyapatite as a function of pH. Salivary concentrations of calcium and phosphate are indicated by the horizontal line. The solubility of apatite increases considerably as pH decreases. It should be noted that caries develops in the pH range around 4.0–5.5, while teeth are eroded in the pH range 2.5–4.0.
      • Figure 9.7 Microradiogram of a white spot lesion showing the subsurface, demineralized lesion deep to a relatively well mineralized surface layer. Note the preferential loss of mineral along the striae of Retzius whereby these and the prism pattern become clearly visible.
      • Figure 9.8 Microradiogram of an erosion of a human tooth. No subsurface demineralization is seen as the enamel is dissolved layer by layer.
      • Figure 9.9 Scanning electron micrograph of an enamel surface after a conditioning etching with phosphoric acid. The prism pattern is clearly seen, with accentuated arcade-shaped prism boundaries.
    • Caries demineralization
      • Figure 9.10 Solubility of hydroxyapatite (HAp) and fluorapatite (FAp) as a function of pH in the range 4–7. Above the solubility line for HAp, solutions will be supersaturated with respect to both HAp and FAp. In saliva, formation of calculus and remineralization of caries lesions may occur. Between the two solubility lines solutions will be undersaturated with respect to HAp and saturated with respect to FAp. In saliva, HAp tends to dissolve and FAp may form; that is, a caries lesion may develop. Below the solubility line for FAp, both apatites may dissolve and erosions develop.
      • Figure 9.11 A schematic drawing showing the effect of the numerous pH fluctuations in the biofilm on the dental enamel. This diagram reflects the solubility of hydroxyapatite and fluorapatite as a function of pH in the range of 4.5–5.5 as demonstrated in Fig. 9.10. While hydroxyapatite dissolves in the subsurface region, the fluoridated apatite can build up in the surface layer of the tooth.
      • Figure 9.12 Microradiogram of a caries lesion in enamel with a highly varying loss of mineral in the body of the lesion. Both the Retzius lines and the prism pattern with cross-striation of several prisms are clearly visible. Note how the apparently greater degree of well-mineralized surface layer exhibits obvious surface dissolution along the very surface that gives a moth-eaten appearance. Clinically, this will be apparent as surface roughness when moving the tip of an explorer across the surface – and the lesion will have an opaque appearance.
      • Figure 9.13 (a) Microradiogram of a caries lesion with a well-mineralized surface layer, under which the subsurface demineralization extends to and further into the dentin. (b) The graph demonstrates a high fluoride content in the surface layer and very little fluoride in the subsurface lesion body, despite a high exposure to fluoride. A slight increase at the border between the enamel and dentin can be distinguished.
    • Remineralization of enamel
      • Figure 9.14 Laboratory attempt to take teeth with natural active caries lesions (a) and (c), and expose these consecutively to solutions saturated with respect to phosphate and calcium respectively in order to fill up the pores of the lesions with these ions followed by elevating the pH in the solutions to create a supersaturation within the enamel lesions. The only result was mineral deposition on the tooth surface (b).
      • Figure 9.15 Transmission electron micrographs from the very surface of inactive, remineralized caries lesions. In addition to irregular mineral deposits between hexagonal enamel crystals (a), numerous small hexagonal crystals form onto partly demineralized larger crystals (b, c), ending within the dissolved crystals (d).
      • Figure 9.16 Scanning electron micrographs of replicas from an enamel surface before (a) and after acid conditioning (b). After 3 weeks the typical etch pattern of the prisms can be discerned. The enamel scratch (from brushing with an abrasive toothpaste) in (a) can be seen also in (b) and (c), whereas the small scratches has been eliminated.
      • Figure 9.17 Active enamel caries lesions following removal of orthodontic brackets (a) and after 1 month of proper oral hygiene (b). The lesions have diminished a little in degree of opacity (partly mineral uptake, but in particular surface polishing) and are inactive but remain from then on as scars in the enamel.
      • Figure 9.18 In-situ experimental caries lesion development and remineralization. (a) An example of how small enamel samples can be inserted in a device and placed in the mouth of volunteers for month. (b) Caries lesions created in the laboratory are exposed to proper oral hygiene and followed for 3 months (c). Note that even a very standardized subsurface artificial caries lesion cannot be totally eliminated by mineral uptake and extensive tooth polishing with a fluoride-containing toothpaste.
      • Figure 9.19 Scanning electron micrographs of the lesions shown in Fig. 9.18b and c. Note how the etched surface in (b) is partly polished away after 3 months (c).
    • Remineralization of dentin
      • Figure 9.20 Microradiographs of three inactive caries lesions that had been arrested for several years. Note that the demineralization extends throughout the enamel. The surface zone varies extensively in mineral content both between different lesions (a, b) and within lesions (c–e).
      • Figure 9.21 Microradiograph of a caries lesion remineralized for years in vivo (a). The surface layer of this third molar has been abraded away, giving the saliva access to the lesion body and resulting in a considerable uptake of mineral. The graph of the fluoride scan (b) shows uptake of extraordinary amounts of fluoride in the remineralized zones of the lesion.
      • Figure 9.22 Microradiograph of an experimental root caries lesion in situ after (a) 3 months with daily plaque removal, followed by (b) 3 months with daily plaque removal and topical fluoride treatment. (c) The mineral content as a function of depth corresponding to the dotted lines in (a) and (b). The treatment resulted in an overall mineral gain because of an increase of the mineral content in the surface layer and formation of a mineral zone in the body of the lesion 125 μm deep to the surface. Scale bar: 100 μm. For original figure, refer to [18].
      • Figure 9.23 Microradiographs of experimental root caries lesion in situ after (a) 3 months and (b) 6 months without plaque removal. (c) The mineral content as a function of depth corresponding to the dotted lines in (a) and (b). Note that the lesion depth increased and that the mineral content in the surface layer decreased over time. Scale bar: 100 μm. For original figure, refer to [18].
      • Figure 9.24 Transmission electron microscopic pictures of normal cementum not exposed to the oral environment (a, b) and exposed root surface (c, d). Note the difference in crystal size showing evidence of crystal growth when apatite crystals in cementum had been exposed to the oral cavity. For original figure, refer to [31].
    • Background literature
    • References
• Part III Diagnosis
  • 10 The foundations of good diagnostic practice
    • Introduction
    • The making of a dentist
      • The ‘art of dentistry’ and caries scripts
      • Variation in clinical decisions
      • Can caries scripts be changed?
    • The dental examination: in the best interest of our patients
      • The symptom-driven dental visit
      • The routine (screening) check-up visit
    • What are we looking for? What is caries?
      • Figure 10.1 Essentialistic versus nominalistic caries concepts. The essentialistic concept holds that a caries truth exists interposed between the causes and the signs and symptoms. The nominalistic concept holds that dental caries is no more than a label attached to tooth surfaces sharing certain defining characteristics; that is, a convenient and succinct way of describing the signs and symptoms.
      • Figure 10.2 The ‘caries process’ – a schematic illustration of the causes of caries lesions (=signs and symptoms). Those causes that act at the tooth surface level are found in the inner circle, while the more distant determinants are found in the outer circle. Adapted from [43].
      • Essentialistic versus nominalistic caries concepts
      • The elusive truth about caries
        • Figure 10.3 Schematic illustration of microevents at a surface over time. The upper fluctuating line indicates pH fluctuations in a biofilm over time (minutes, hours, days). The curves show different examples of fluctuating mineral loss (up) or gain (down) in enamel as a result of innumerable fluctuations in pH. The horizontal dotted lines indicate where loss of mineral may be seen clinically as a white spot.
    • The wealth of caries diagnostic methods and criteria
    • The evolution in caries diagnostic methods
    • Diagnostic test assessment in the essentialistic gold-standard paradigm
      • Diagnostic accuracy: sensitivity and specificity
        • Table 10.1 Examples of measurement scales used in caries diagnosis
        • Table 10.2 The diagnostic test matrix for a dichotomous test result (T) in the diagnosis of caries
      • Predictive values positive and negative
      • Receiver operating characteristic curves
    • Evaluating caries diagnostic methods
      • Figure 10.4 The ROC curve connecting points determined by (1 − specificity, sensitivity). The test is a hypothetical caries test with nine threshold values (the end-points (0, 0) and (1, 1) do not count as threshold values because they respectively correspond to never declaring caries present or always declaring caries present). See text for explanation of points A and B (p.183).
    • Leaps in the essentialistic gold-standard reasoning
      • Which is the caries gold standard?
      • Spectrum bias and transferability
      • Problems in interpreting sensitivity and specificity
      • Caries lesion: ruled in or ruled out?
        • Table 10.3 Number of errors resulting from the application of three caries diagnostic methods used to detect cavitated lesions
      • Problems interpreting receiver operating characteristic curves
      • Caries diagnostic correctness: a blind alley
    • Diagnostic test evaluation in the nominalistic caries paradigm
      • Long-term health outcomes: the management options?
    • Inter- and intra-examiner errors in caries diagnosis
      • Table 10.4 Example of data-table arising when assessing the intra-examiner reliability of caries diagnoses made at the cavity level
    • How do we deal with the unavoidable diagnostic uncertainty?
    • The additional diagnostic yield argument
      • In the land of the blind the one-eyed is king
      • Different diagnostic methods tell different stories
        • Figure 10.5 Undemineralized section of lower first molar and second premolar both showing caries lesions with complications in the pulpo-dentinal complex. Only the first molar shows a cavity and the premolar might be recorded as sound. Hanagawa Collection. Ciba University, Japan.
    • Concluding remarks
    • References
  • 11 Visual–tactile caries diagnosis
    • Introduction
    • The diagnostic process
      • The medical perspective on diagnosis
      • The dental perspective
      • Caries scripts
    • Why do we diagnose caries?
    • Diagnosis from a dental caries perspective
      • Achieving the best health outcome for the patient by classifying caries lesions corresponding to the best management options for each lesion type
        • Cavitated caries lesions
        • Noncavitated and microcavitated caries lesions
        • Active lesions
          • Figure 11.1 Decision-making tree for dental caries, including activity assessment as a key factor in the decision process. The flow diagram promotes the concept that active lesions – cavitated and noncavitated as well as recurrent lesions – need professional management, whereas inactive lesions do not need treatment besides self-performed toothbrushing with fluoride toothpaste. The flow diagram does not consider individual factors that may influence the modality or intensity of the professional treatment. See text for further explanation. Modified after [52].
        • Inactive lesions
      • Informing the patient
      • Longitudinal assessment of the caries process
    • How early should caries lesions be detected?
    • What are the best visual–tactile caries diagnostic criteria?
      • The concept of validity
        • Table 11.1 The 2 × 2 table that might arise if we attempted to verify our approximal cavity diagnoses in 200 consecutively examined first molars by means of subsequent extraction and inspection of the teeth
      • The concept of reliability
        • Table 11.2 The hypothetical 2 × 2 table that might arise if we evaluate the inter-examiner reliability of cavity diagnoses in 6000 surfaces in 50 consecutively examined patients
    • Commonly used visual–tactile criteria
      • Recording of cavities only
        • Figure 11.2 The caries profile of 12-year-old Lithuanian children exemplified by three different visual–tactile caries lesion classifications. Note differences in the clinical outcome with regard to total number of lesions, cavitated and noncavitated lesions, and active and inactive lesions.
      • Recording of cavitated and noncavitated lesions
      • Lesion depth assessment
      • Lesion activity assessment: Nyvad criteria
        • Figure 11.3 Typical clinical manifestations of active and inactive caries lesions according to [53]. Active noncavitated lesion on smooth surface (a) and occlusal surface (b). (c, d) Inactive noncavitated lesion on smooth surface (c) and occlusal surface (d). (e) Active noncavitated lesion with microcavity on approximal surface. (f) Inactive noncavitated lesion with microcavity on smooth surface. Active (g) and inactive (h) cavitated lesions. See text for further explanation. (a), (b), and (d) from [53].
        • Figure 11.4 Typical clinical manifestations of active and inactive caries lesions in the primary dentition. (a) Active noncavitated lesion on buccal surface. (b) Active noncavitated lesion with microcavity in occlusal surface. (c) Active cavitated lesion on approximal surface. (d) Inactive noncavitated lesion on occluso-lingual surface. (e) Inactive noncavitated lesion with microcavity on occlusal surface. (f) Inactive cavity on lingual surface.
        • Figure 11.5 Polarized light microscopic images of noncavitated enamel caries lesion showing subsurface loss of mineral responsible for the opaque appearance of the lesion in the clinic. The white contour at the surface layer of the lesion indicates the principal difference between a rough/dull active lesion (a) and a smooth/shiny inactive lesion (b).
        • Figure 11.6 Symbols for indicating lesion activity in the dental diagram. Active lesions are marked by filled circles (noncavitated) and filled boxes (cavities), whereas inactive lesions are marked by empty circles and boxes respectively.
      • Root-surface caries
        • Figure 11.7 (a) Active root surface caries lesion in upper canine presenting a softened surface. (b) Inactive root surface caries lesion in upper incisor showing a smooth discolored surface.
      • Recurrent (secondary) caries
    • Differential diagnosis
      • Figures 11.8–11.16 Figure 11.8: Active recurrent root surface caries lesions on lower canine and premolar next to composite fillings with overhangs (arrows). These lesions should be treated by nonoperative intervention (site-specific improved hygiene and application of topical fluorides) in conjunction with refurbishing of the lesions to facilitate biofilm removal. Note also dark shadow on the buccal surface of the premolar reflecting underlying amalgam filling. Figure 11.9: Inactive recurrent root surface lesion next to amalgam filling on lower incisor. No treatment is needed. Figure 11.10: Active recurrent caries lesion next to composite filling on the occlusal surface. The lesion needs operative treatment because the cavity cannot be cleaned properly. The cavity is soft on probing. Figure 11.11: This filling has fractured across the isthmus and part of the restoration is loose. Biofilm forms beneath the loose amalgam resulting in an active recurrent caries lesion that needs operative treatment. The cavity is soft on probing. Figure 11.12: Ditching along margins of amalgam restoration which most likely developed because of overfilling. No caries is detected. No treatment is needed. Figure 11.13: Gingival amalgam fillings with stained margins and inactive recurrent caries. Refurbishing of the fillings may facilitate oral hygiene. Figure 11.14: Buccal amalgam with overhang and inactive recurrent caries. The filling should be refurbished to make cleaning easier. Figure 11.15: Old amalgam fillings in patient with erosion. Note that the normal anatomy of the teeth has gone and that the fillings are elevated above the eroded enamel/dentin surface. In spite of defective margins, no caries is present. No treatment is advocated. The filling in the neighboring premolar was lost due to progression of erosion. Figure 11.16: Stained margins of composite filling in upper premolar. The stain may be due to incomplete removal of previous amalgam filling. No need for replacement if the margins of the filling are clinically intact.
      • Figure 11.17 (a) Dental fluorosis (TF1) in the gingival part of upper canine and premolar. Note the fine white horizontal lines which reflect the perichymatal pattern of enamel. This clinical manifestation is distinctly different from the arcade-shaped inactive noncavitated caries lesions shown in (b) reflecting the retention of plaque along the former gingival margin.
      • Figure 11.18 Well-demarcated opacities of non-fluoride origin in incisal part of lower incisors [55]
      • Figure 11.19 MIH in the primary (a, b) and permanent dentition (c, d). Note that MIH-associated hypoplastic enamel defects are easy to differentiate from caries when they appear in areas of the tooth that are commonly not affected by caries, such as cusps. (d) Active cavitated caries lesion with undermined enamel has developed in central occlusal fossa. At this advanced stage of lesion development it is not possible to say whether caries was accelerated because of the presence of a hypoplastic defect in the fissure. Note also areas of opaque enamel in all the MIH-affected teeth.
      • Figure 11.20 (a) Clinical manifestation of invasive cervical root resorption on lower canine. Note the sharp occlusal border of the lesion and the presence of reddish granulation tissue. (b) It is obvious from the radiograph that the lesion is subgingival. There is a small opening to the periodontal membrane.
    • Visual–tactile caries examination: a systematic clinical approach
      • Good lighting and clean, dry teeth
        • Figure 11.21 Making ready for a visual–tactile caries examination after isolation of the teeth with cotton rolls and a suction device.
      • Sensible use of the probe
        • Figures 11.22–11.24 Figure 11.22: Reflected light from the mouth mirror reveals a dark shadow on the mesial approximal surface of upper first molar (arrow). Note also the presence of a noncavitated lesion on the mesio-oral part of the same surface (arrow). Figure 11.23: Transmitted light from the operating lamp allows detection of approximal lesions in upper anterior teeth. Figure 11.24: Inactive noncavitated lesion on the mesial surface of lower molar detected after careful inspection using a mouth mirror (arrow).
        • Figure 11.25 Lower canine and incisor (a) before and (b) after plaque removal. Note the presence of typical active noncavitated lesions after plaque has been removed with the side of a probe.
      • Caries predilection sites
        • Figures 11.26–11.27 Figure 11.26: Examination of noncavitated caries lesion using the tip of a sharp probe that is moved gently across the surface of the lesion at an angle of 20–40° to assess lesion texture. Figure 11.27: Forceful poking with the probe perpendicular to the lesion should be avoided in order not to cause irreversible damage to the surface of the lesion!
    • Additional aids in visual–tactile caries diagnosis
      • Fiber-optic transillumination
        • Figure 11.28 Caries lesion detected by FOTI on the mesial aspect of upper second premolar (arrow). The lesion is seen as a dark shadow.
      • Tooth separation
        • Figure 11.29 (a) An orthodontic elastic separator has been placed between upper premolar and molar. To insert the separator the elastic is stretched between two surgical forceps and one half of the elastic is worked down through the contact point. (b) After 2–3 days the separator is removed. It is now possible to see and ‘feel’ the surface texture of the lesion with the tip of a probe.
      • Magnification
    • Benefits and limitations of visual–tactile caries diagnosis
      • Figure 11.30 Relative diagnostic yields of clinical and radiographic examinations of approximal and occlusal surfaces at the cavitated and noncavitated levels respectively. The data were obtained from children examined at 12 and 15 years of age. Note that at the noncavitated/enamel level of diagnosis, the clinical examination (only) revealed a higher number of lesions than did the radiographic method (only). Only for approximal lesions at the cavity/dentin level of diagnosis did the radiographic method (only) perform better than the clinical examination (only). Age of the individuals did not influence the results [44, 45].
    • References
  • 12 Additional caries detection methods
    • Introduction
    • Radiography
      • Indications for radiography
      • What does the dental radiograph show?
        • Figure 12.1 Bitewing radiograph showing radiolucencies in nearly all approximal surfaces due to caries.
      • Radiographic technique
        • Intraoral bitewing technique
          • Figure 12.2 (a) A 25-year-old presenting with toothache in the lower right first molar (46). The bitewing radiograph reveals a deep occlusal dentin lesion in 46. (b) Bitewing radiograph taken less than 2 years previously. It is far too light, without contrast, and useless for caries diagnosis.
          • Figure 12.3 A bitewing radiograph is being taken. A film holder supports the film lingually and the patient closes together on a part of this holder. A beam-aiming device helps the operator to position the tube so that the beam is directed at right angles to the film.
          • Figure 12.4 A bitewing radiograph on a size 2 image receptor covering as many surfaces as possible when the receptor is placed with its middle behind the upper first molar. Dentin caries is present in the distal surface of the upper right first premolar. Note also lesion in enamel.
          • Image receptors
          • Conventional film
          • Digital receptors
            • Sensors
            • Phosphor plates
        • Extraoral bitewing technique
      • Radiographic detection of caries lesions
        • Figure 12.5 Bitewing radiographs obtained with a panoramic unit. Note distinct radiolucencies in the upper right second molar and premolar.
        • Figure 12.6 The shape and extent of a lesion influence its radiographic depiction. A superficial lesion with a great extent along a proximal surface may seem both deeper and darker than a lesion that is smaller in the direction of the X-rays but actually deeper.
        • Approximal surfaces
          • Figure 12.7 Magnified radiograph of approximal caries lesions in enamel in lower left premolar and molar. The enamel lesions are depicted as radiolucent triangles with their bases towards the tooth surface. Note also ‘cervical burnout’ in the cervical part of the premolar.
          • Figure 12.8 Magnified radiograph of approximal caries lesions in enamel and outer dentin in lower left molars.
          • Figure 12.9 (a) Magnified radiograph showing dentin caries lesion in mesial surface of upper right molar and enamel caries lesion in distal surface of neighboring premolar. (b) Stepwise drilling of the dentin lesion revealed the presence of a micro cavity (arrow). This case illustrates that micro cavitation cannot be detected by radiography.
        • Occlusal surfaces
        • ‘Hidden caries’
          • Table 12.1 Percentages of cavitations in permanent teeth with radiographic approximal enamel and dentin caries found in in vivo studies [28]
          • Figure 12.10 Magnified radiograph of deep occlusal dentin caries lesion in lower left first molar. The lesion appears as a semicircular radiolucency in dentin. No radiolucency is seen in enamel.
      • Radiographic detection of recurrent caries lesions
        • Figure 12.11 Recurrent caries on the distal surface of an upper left second molar (arrow).
      • False-positive caries diagnoses in radiographs
        • Figure 12.12 Bitewing radiograph of a patient with active caries lesions diagnosed clinically. The radiograph shows several radiolucencies in enamel in approximal surfaces of lower molars and premolar. Large radiolucency in dentin in distal surface of upper right first premolar resembling caries appeared clinically to be a composite filling without detectable caries (false-positive radiographic diagnosis). Note also the radiolucent area in the distal part of the occlusal surface of lower right second molar that might be caries.
      • Diagnostic validity of radiography for caries lesion detection
        • Accuracy
          • Table 12.2 Expression of diagnostic accuracy for diseased and healthy surfaces
        • Reliability
      • Factors determining the progression of caries in radiographs
        • Approximal caries
          • Figure 12.13 Number of caries lesions in enamel and dentin reported from 336 bitewing radiographs by three dentists [29].
          • Post-eruptive age of teeth
          • Previous caries experience
          • Primary vs. permanent teeth
          • Tooth and surface types
            • Figure 12.14 Annual caries rates (number of new lesions/100 tooth-surface-years) of (a) upper and (b) lower posterior approximal surfaces from 12 to 22 years of age by tooth surface From [60].
          • Lesion depth at baseline
          • Risk of cavitation
            • Figure 12.15 Annual caries rates (number of new lesions/100 tooth-surface-years) of posterior approximal surfaces from 12 to 22 years of age. Median values of all surfaces.
          • Caries/restoration status of neighboring surfaces
            • Table 12.3 Risk of approximal caries development in relation to caries status of the neighboring surface in 11/13–21/22-year-olds [85]
            • Figure 12.16 Two magnified radiographs showing caries lesion progression over 4 years in the same patient. (a) Dentin caries lesion in the distal surface of lower right primary second molar – a condition that increases the risk of caries development in the neighboring surface. (b) Four years later the second premolar had erupted and the mesial surface of the permanent first molar showed dentin caries.
            • Table 12.4 Risk of development of new lesions in occlusal surfaces in relation to tooth types [61]
        • Occlusal caries
      • Timing of radiographic follow-up
    • Methods based on light and electrical current
      • Methods based on light
        • Physico-chemical principles
          • Table 12.5 Overview of diagnostic methods based on light and electrical current
        • Devices based on fluorescence (semi-quantitative)
          • DIAGNOdent
            • Table 12.6 Sensitivities and specificities of different additional caries diagnostic devices when used in occlusal surfaces, compared with visual–tactile caries examination (data retrieved from [11, 69]). Data reported for enamel level, except for QLF (dentin level)
            • Figure 12.17 (a) The DIAGNOdent pen with the tip for detection of occlusal caries. (b) Close-up of the tip for approximal detection and the knob for turning it around.
          • VistaProof
            • Figure 12.18 Procedure for occlusal detection with the DIAGNOdent pen. The tip has to be rotated around the vertical axis (a, b). This ensures that the tip picks up fluorescence from the slopes of the fissure walls where the carious process may start. The position shown in (b) gives no signal.
            • Figure 12.19 Procedure for approximal detection with the DIAGNOdent pen. (a) Measurement of the fluorescence (zero value) of a sound spot on the coronal part of the facial surface. (b) Measurement at the approximal site. The approximal space is carefully penetrated.
          • SOPROLIFE and SOPROCARE
        • Quantitative light-induced fluorescence
          • Figure 12.20 Clinical use of QLF.
          • Figure 12.21 Principles of the QLF method for quantification of an enamel caries lesion. (a) The actual fluorescence image of a caries lesion; (b) the reconstructed image, in which fluorescence radiance of the original sound enamel at the lesion site was reconstructed by interpolation of values indicating sound enamel around the lesion. (c) The difference between the measured and the reconstructed values gave the resulting fluorescence loss in the lesion.
        • Digital imaging fiber-optic transillumination
          • Figure 12.22 DIFOTI for the detection of occlusal caries.
      • Methods based on electrical current
        • Electrical conductance measurements
          • Figure 12.23 (a) ECM. The electrical caries monitor with its tip. (b) Air flows through the tube to dry the tooth surface. (c) The measurement of a spot. To prevent the current from ‘leaking’ through a superficial layer of moisture to the gingiva, an airflow is applied to dry the occlusal tooth surface around the probe.
        • Electrical impedance measurements
    • Are the additional methods suitable for use in clinical practice?
    • Can the methods serve as adjuncts to a visual–tactile caries examination?
    • References
• Part IV Controlling dental caries
  • 13 The caries control concept
    • Why the caries control concept should replace caries prevention
      • Figure 13.1 Schematic illustration of the caries control concept. Because of continuous exposure to the metabolically active biofilm, disease control must be maintained lifelong. Both nonoperative and operative treatments are part of the caries control concept, but operative treatments should never be the only treatment provided for patients with active caries lesions. See text for a detailed explanation.
    • How caries control was managed in the past
    • Arrest of active enamel caries
    • Arrest of active root caries
      • Figure 13.2 Nonoperative control of caries progression on occlusal surface of erupting first molar. (a) Thick biofilm before and (b) after plaque removal. Note the presence of active noncavitated lesions in the groove–fossa system after plaque removal and drying. (c) After 3 months of nonoperative treatment the translucency of the enamel in the central part of the groove–fossa system appears normal, but opaque lesions are still visible next to gingiva distally.
      • Figure 13.3 Arrest of root-surface caries. (a) Active root-surface caries lesion in upper canine presenting a softened surface. (b) Same lesion after 1 year of nonoperative caries control by improved toothbrushing with fluoride toothpaste. The lesion has turned into an inactive stage as evidenced by the hard and shiny surface. (c) After 4 years the lesion is still inactive and has taken up stain. Note also the inactive lesion in the gingival part of enamel.
      • Figure 13.4 Consecutive stages of nonoperative treatment of active noncavitated root-surface caries lesion on the buccal surface of upper left canine. The figure shows changes in the clinical appearance of the lesion after 3, 6, and 18 months. Note that, within the observation period, improved oral hygiene leads to gradual changes in color and surface structure of the lesion, from soft and yellowish to hard and darkly discolored. Also note changes in the topography of the marginal gingiva.
    • Arrest of active cavitated caries
      • Figure 13.5 Consecutive changes of nonoperative treatment of active cavitated root-surface caries lesions on the buccal surfaces of lower first and second premolars. The illustrations show the clinical appearance of the active lesions after (b) 2, (c) 4, and (d) 10 years. The successful treatment was achieved through careful daily plaque removal with a fluoride toothpaste. After 4 years an overhanging rim of unsupported enamel at the occlusal aspect of the lesion was removed to facilitate cleaning. Although cosmetically a problem to most patients, these lesions did not need operative treatment, which may weaken the teeth substantially and, in the long run, reduce their survival.
      • Figure 13.6 (a) Active cavitated lesions filled with microbial deposits in anterior teeth. The dark brown appearance of the lesions is a result of discoloration of the softened dentin. This is obvious when most of the dental plaque is removed with a toothbrush, as seen in (b). Such cavitated lesions can be converted into arrested lesions by nonoperative interventions using a fluoride-containing tooth paste. In this patient, after 2–3 weeks of plaque control, the lesions were no longer sensitive to cold and sweet, and 4 months later they were hard on probing.
      • Figure 13.7 Sequential stages of nonoperative caries control in active cavitated primary teeth. The cavity in the first molar had previously been filled, but the filling was lost. (a, b) Active carious cavities before and after ‘slicing’ of unsupported enamel to make the cavities cleansable with a toothbrush. (c, d) Successive stages of lesion arrest in the second molar after 3 months and 6 months respectively. The floor of the dentin cavity became harder and darker over time. Note that the first permanent premolar erupts into a clean environment!
    • Role of fluoride in lesion arrest
    • Benefits and limitations of the caries control approach – and some recommendations
    • References
  • 14 Fluorides in caries control
    • Introduction
    • Fluoride in caries prevention and control
      • Figure 14.1 Prevalence and severity of mottled enamel in 21 cities in the USA with varying levels of F− in their drinking water [46]. (Public domain.)
      • Figure 14.2 Mean number of decayed, missing, and filled teeth (DMFT) and F− concentration of the drinking water from the 21 city study [46]. (Public domain.)
      • Figure 14.3 Dental caries in Grand Rapids children after 10 and after 15 years of fluoridation (– – – – –), in Grand Rapids before fluoridation (––––) and in the natural fluoride area Aurora (––––).
      • Figure 14.4 Dental caries in Grand Rapids before water fluoridation and in Aurora with fluoride in the water supply. The dashed line indicates caries progression in a boy moving from the non-fluoride to the fluoride area on his 11th birthday [107].
      • Figure 14.5 Log transformation of the fluoride level in the drinking water and the prevalence and severity of mottled enamel in 21 cities in the USA with varying levels of fluoride in their drinking water [46].
      • Figure 14.6 Log transformation of the fluoride level in the drinking water and caries prevalence in 21 cities in the USA with varying levels of fluoride in their drinking water [46].
      • Figure 14.7 Caries experience of children from England and Wales in 1973, 1983 and 1993 [131].
    • Cariostatic mechanisms of fluoride
      • Figure 14.8 Schematic representation of the effect of F− available in oral fluids on the dynamics of caries progression over time.
      • Table 14.1 F− concentration in dental plaque from schoolchildren according to the status of water fluoridation (Piracicaba, SP, Brazil, 1986–1987).
      • Figure 14.9 Mean F− concentration in whole saliva after various topical F− treatments. (1) Toothbrushing with NaF dentrifice (0.50 mg F−) followed by 10 s mouth rinse with water. (2) Chewing of chewable F− tablets (0.42 mg F−). (3) Chewing of plain F− tablets (0.50 mg F−). (4) Chewing of F−-containing chewing gum (0.50 mg F−) for 15 min. (5) A 2 min mouth rinse with 0.2% NaF solution. (6) Topical application of APF (1.2% F−, pH 3.2). (7) Topical application of neutral 2% NaF solution. Figures in parentheses denote initial F− concentration after 1–3 min [23].
      • Table 14.2 F− concentration in cariogenic dental biofilm formed in situ, according to the toothpaste used (mean ± SD, n = 14).
    • Dental fluorosis and metabolism of fluoride
      • Figure 14.10 Ground sections of teeth examined in transmitted light. Notice how the early stages of dental fluorosis (a) exhibit a porous zone in the outermost enamel. With increasing severity this zone of porosity extends deeper into the enamel (b), and in very severe cases the porosity extends deep into the enamel tissue along the entire tooth crown (c) and in the cervical areas extends to the enamel–dentin junction.
      • Figure 14.11 Microradiograph showing extensive hypomineralization of fluorosed enamel deep to a well-mineralized surface zone. Note incremental lines of Retzius. This represents a score of 4 according to the TF index.
      • Figure 14.12 TF score 4 represents entirely white opaque enamel (see lower canine). As a reflection of the extension of subsurface hypomineralization, part of the surface enamel may break away posteruptively, creating TF scores 5–7. Brown discoloration of the porous enamel, which has occurred posteruptively, is also visible.
      • Figure 14.13 TF score 1: the earliest clinical sign of dental fluorosis appears as thin, white, opaque lines running across the tooth surface corresponding to the position of the perikymata.
      • Figure 14.14 In addition to the thin, white, opaque lines, the earliest signs of dental fluorosis may include small, opaque, white areas along cusp tips, incisal edges, or marginal ridges.
      • Figure 14.15 In TF score 2 the opaque white lines are more pronounced and frequently merge to form wider bands.
      • Table 14.3 The Thylstrup–Fejerskov index.
      • Figure 14.16 Diagrammatic illustration of the clinical features of dental fluorosis from the mildest form (TF 1) to the most severe (TF 9). Compare with Table 14.3.
      • Figure 14.17 In TF score 3 the entire tooth surface exhibits cloudy, white, opaque areas between which accentuated perikymata lines are evident.
      • Figure 14.18 Another example of TF score 3 with the addition of posteruptive staining of the porous enamel.
      • Fluoride dose and dental fluorosis
        • Figure 14.19 Relationship between Fci and daily F− dose pooling data.
        • Figure 14.20 Diagram showing the percentage of teeth exhibiting dental fluorosis according to the TF classification. The tooth types are ranked from left to right in the order of mineralization. The data originate from children born and raised in an area of Denmark with less than 0.1 ppm F− in the drinking water [101]. +: maxillary teeth; −: mandibular teeth.
        • Figure 14.21 Daily amounts of toothpaste (grams) required to be ingested to constitute an intake of 0.1 mg F−/kg for 12 and 20 kg children for three different F− levels in toothpaste (1500, 1000, and 500 ppm F−).
        • Table 14.4 Amount of dentifrice used per brushing (grams) or F− per brushing (milligrams)a by age.
        • Table 14.5 Percentage ingestion of dentifrice fluoride by age.
        • Figure 14.22 Bioavailability of F− ingested from toothpastes, depending on the content of the stomach.
        • Table 14.6 Estimated dose of F− (mg F−/kg body weight per day) to which a sample of Brazilian children were subjected during toothbrushing with MFP/CaCO3 or NaF/silica formulations, based on total or soluble F− concentrations in toothpastes (mean ± SD).
        • Table 14.7 Estimated median weights of children [54] and fluoride intake according to age estimated from twice daily use of a 1000 ppm F toothpaste [86].
      • Where is fluoride found in nature?
      • Fluoride absorption, distribution, and elimination in the body
      • Fluoride concentrations in teeth
        • Figure 14.23 Schematic representation of the F− concentration in enamel and dentin from the outer surface of the enamel to the dentin–pulp interface for subjects with a low and higher F− intake.
        • Figure 14.24 Enamel F− concentrations in the outer 300 µm of the enamel for erupted teeth with different degrees of fluorosis. See Fig. 14.16 for explanation of the TF index [146].
        • Figure 14.25 F− concentration measured in surface enamel in vivo in upper central incisors at the age of about 7 years (shortly after eruption). The concentration is the same in central and cervical enamel. However, after 7 years in the oral environment it is apparent that F− in the cervical enamel (where plaque accumulates) increases, whereas it remains unchanged or gradually drops in central parts that have been exposed to attrition/toothbrushing [144].
        • Figure 14.26 Fluoride concentrations in sound and carious enamel. The lowest concentrations are found in body of the lesion and then the sound bulk enamel. The surface enamel layer covering the lesion has picked up considerable amounts of F− from the surrounding fluids.
      • Pathogenesis of dental fluorosis
        • Figure 14.27 F− concentrations in the surface enamel of deciduous canines and dental caries prevalence in the deciduous dentition. No relationship between the two is apparent [143].
    • The effectiveness of fluorides in the control of dental caries: evidence from systematic reviews
      • Systematic reviews as objective summaries of the best evidence from research in informing decisions in health care, and the importance of Cochrane reviews
        • Table 14.8 Hierarchy of evidence about effectiveness (for therapeutic interventions).
      • Systematic reviews on the effectiveness of fluorides, with a special focus on the Cochrane fluoride reviews
      • Measuring treatment effect in systematic reviews of caries trials
      • Systematic review of evidence on the effects of water fluoridation
      • Systematic review of evidence on the effects of topically applied fluoride modalities (toothpastes, mouthrinses, gels, varnishes)
        • Table 14.9 York review on water fluoridation [118]. Summary of main results (for dental caries and fluorosis).
        • Table 14.10 Cochrane reviews of topically applied F− treatments (TFTs). D(M)FS/d(e)fs pooled estimates of effect measured as prevented fractions (PFs).
        • Table 14.11 Cochrane reviews of topically applied F− treatments. Factors potentially influencing effectiveness; results from random effects meta-regression analyses of D(M)FS prevented fractions (PFs).
        • Table 14.12 Cochrane reviews of topically-applied F− treatments. Comparative effect on caries increment from direct comparisons between F− treatments (used against each other and against a combination) – D(M)FS pooled estimates measured as prevented fractions (PFs).
        • Table 14.13 Comparative effect on caries increment from direct comparisons of toothpastes of different F− concentrations. D(M)FS pooled estimates measured as PFs (placebo comparisons only) – Cochrane review.
        • Table 14.14 Cochrane reviews on the effects of fluoridated milk, slow-release F− devices, and F− supplements.
      • Systematic review of evidence on the effects of fluoride supplements (tablets, drops, lozenges), slow-release fluoride devices, fluoridated milk, and salt fluoridation
      • A summary of the main evidence from systematic reviews: relevant implications for practice and research
    • Rational use of fluorides in caries control in different parts of the world: recommendations
    • Background literature
    • References
  • 15 The role of oral hygiene
    • Introduction
    • Some theoretical considerations
    • The biological effect of tooth cleaning
    • The clinical effect of tooth cleaning
      • Figure 15.1 Mean pH (blue) and standard deviation (red) of approximal plaque following a 2 min rinse with 10% sucrose solution (a) before and (b) after plaque removal with dental floss (n = 8). PC: paraffin chewing.
      • The tooth/site level
        • Figure 15.2 Mineral distribution curves of enamel specimens after different experimental toothbrushing regimens in situ. The mineral content is plotted versus the distance from the outer surface. P: no toothbrushing for 3 months; NF: brushing with a non-fluoride toothpaste for 3 months; F: brushing with a fluoride toothpaste for 3 months; D: artificially demineralized control specimen.
        • Figure 15.3 Mineral loss of root-caries specimens after different treatments in situ. The red and green lines indicate periods with and without plaque removal respectively. The solid data points (A–D) and error bars give the mean values and standard error of the mean for the amount of mineral removed in each group (n = 9). E and F indicate the mean amount of mineral removed from sound root surfaces after a 3-month period without and with tooth cleaning respectively. The mean mineral content value for sound control surfaces (blue horizontal line) is included for comparison (n = 5).
      • The level of the individual
        • Table 15.1 Caries increment (decayed surfaces) during the final year of a 3-year experiment of different preventive measures.
      • The population level
        • Figure 15.4 Demonstration of how useful the mswaki can be in maintaining proper oral hygiene. Look at this gentleman's clean oral cavity. He has never used anything but the mswaki. He cuts a thin branch of a tree and peels the bark. Then he chews the end to form a small brush which is easy to use throughout the oral cavity when used gently with small rotating movements. The other end can be cut to be used as a tooth pick approximally.
        • Figure 15.5 Relative risk (RR) of caries at different levels of plaque accumulation and sugar consumption in terms of unit risk for teeth with plaque index PI = 0–0.9, 1.0–1.9, and 2.0–3.0 and low (I), middle (II), and high (III) sugar exposures. Primary teeth; 5-year-olds.
    • The effect of professional tooth cleaning
      • Figure 15.6 The Karlstad studies (1973–1978): annual caries increments at different professional tooth-cleaning frequencies.
    • The effect of dental flossing
    • Concluding remarks
    • References
  • 16 Are antibacterials necessary in caries prophylaxis?
    • The biofilm lifestyle and the rationale for antibacterial intervention
    • Biological activity and mode of action
      • Figure 16.1 Oral delivery, binding, release, and clearance of antibacterial agents in the oral cavity. The agent binds to oral mucosa, tooth surfaces, pellicle, and dental biofilm bacteria according to its affinity Kb and released from its binding site depending on its dissociation constant Kd and salivary clearance rate. The oral mucosa represents the major reservoir for substantive agents. After [50].
      • Figure 16.2 Dose curves of (a) an agent with high substantivity and (b) an agent with low substantivity. The horizontal dotted lines represent the effective dose levels. The effective dose–time area (circumscribed between the curves and the dotted lines) may be similar if the low substantivity agent is applied frequently. After [37].
      • Figure 16.3 Modification of biofilm biochemistry.
      • Table 16.1 Stages and mechanisms of biofilm formation as targets for interference.
      • Inhibition of bacterial adhesion and colonization
      • Inhibition of bacterial growth and/or metabolism
      • Detachment and disruption of dental biofilms
      • Modification of dental biofilm biochemistry and ecology
    • Vehicles for caries prophylactic agents
      • Mouthrinses
      • Sprays
      • Dentifrices
      • Gels
      • Chewing gums and lozenges
      • Sustained-release vehicles
    • Specific agents
      • Figure 16.4 The molecular formula of chlorhexidine.
      • Figure 16.5 The molecular formula of triclosan.
      • Figure 16.6 The molecular formula of xylitol.
      • Chlorhexidine
        • Mode of action and clinical use
        • Caries-prophylactic effect
      • Triclosan
        • Mode of action and clinical use
      • Xylitol
    • Other agents proposed for caries prophylaxis, but without documented anticaries effects
      • Cetylpyridinium chloride
      • Delmopinol
      • Hexetidine
      • Essential oils
      • Sanguinaria extracts
      • Metal ions
      • Sodium dodecyl sulfate
      • Enzymes
    • Risk of antibacterial resistance development?
      • Intrinsic resistance
      • Acquired resistance
    • Concluding remarks and future approaches
    • Background literature
    • References
  • 17 The principles of caries control for the individual patient
    • Introduction
    • How are current caries activity and risk of future caries progression assessed?
      • How should the visual–tactile activity assessments be made?
      • Identifying caries risk factors
        • Table 17.1 Checklist of biological and environmental caries risk factors.
        • Medical history
          • Table 17.2 Causes of dry mouth.
        • Dental history
        • Caries risk assessment systems
          • Figure 17.1 Rapidly progressing caries in 28-year-old male who had ignored oral hygiene and who had been sipping sugared coffee regularly during the day for 5 years. The patient visited the dentist because it was difficult for him to get a new job! This is a “yellow” patient in whom all risk factors can be modified in conjunction with the operative treatment.
      • Identifying social and demographic risk factors
    • How is the information used to categorize patients into risk groups?
      • What can and what cannot be modified by the patient?
      • Categorizing caries-activity status and caries-risk status
        • Figure 17.2 Guideline for categorizing patients into caries-activity/caries-risk status and for setting the recall interval for caries control. OH = oral hygiene.
    • What nonoperative treatments are available?
      • Plaque control
        • Toothbrushing
        • Interdental cleaning
        • Professional tooth cleaning
      • Use of fluoride
        • Table 17.3 Clinical procedure of professional tooth cleaning.
        • Figure 17.3 Diet analysis form.
      • Dietary modification
        • Recording the diet
        • Analysis of the dietary record
        • Dietary advice
        • Age and diet
    • How is the individual helped to control disease progression?
    • When should the patient be recalled?
      • Setting the recall interval
      • Examining the mouth at recall
      • Assessment of compliance at recall
        • Recording changes in oral health behavior and caries lesion activity at recall
      • Resetting the recall interval
        • Figure 17.4 Recording sheet used to monitor caries lesion activity and maintain an overview of the nonoperative treatments given.
    • Caries control in children and adolescents
      • What is special about caries control in children and adolescents?
      • When to start caries control in children
        • Early childhood caries (ECC)
          • Figure 17.5 Caries has ruined the upper incisors in a 20-month-old child who sipped a bottle of sugar-containing liquid during the night. Note the whitish and chalky border of enamel that indicates very high caries activity.
        • Achieving behavior change
        • Effective caries control in children
        • Orthodontic treatment
          • Figure 17.6 (a) Active caries with and without cavity formation caused by frequent snacking and poor oral hygiene in combination with fixed orthodontic treatment. (b). Excessive plaque formation seen at a previous visit before the appliance was removed.
    • Patients with a dry mouth
      • Radiotherapy
      • Plaque control and fluoride
        • Figure 17.7 (a) The patient has been irradiated in the region of the salivary glands for the treatment of a malignant tumor. Heavy plaque deposits are obvious over the lesions [27]. Reproduced with permission of Oxford University Press. (b) A typical pattern of caries attack on occlusal surfaces in a patient with a dry mouth, in this case caused by radiotherapy in the region of the salivary glands. The cusp tips and incisal edges are attacked because the dentin is often exposed by tooth wear in these areas. Plaque may stagnate in the concave areas [27].
        • Figure 17.8 Cancer patient who has mastered caries control subsequent to resection of the left mandible and radiation therapy of the head and neck. The patient received regular professional tooth cleaning and topical fluoride therapy in conjunction with meticulous self-performed oral hygiene.
      • Dietary advice for patients with dry mouth
      • Conservative measures to relieve the symptoms
      • Salivary stimulants
      • Saliva substitutes
        • Sprays or mouthwashes to give viscosity
        • Products containing antimicrobial proteins
        • Viscous or ropy saliva
    • Failure
    • References
  • 18 Caries control for frail elders
    • Introduction
    • A conceptual model of oral health
      • Figure 18.1 A model of oral health [55, 57].
    • Frailty
      • Figure 18.2 Numbers (×1000) of people >85 years by percentage of the total population in 2013 [104].
      • Figure 18.3 Percentage of people over 65 years of age in institutional care by country [48].
    • Physical characteristics of caries in elderly mouths
    • Incidence of caries in frail adults
      • Figure 18.4 Rampant caries in a man consuming multiple anticholinergic medications and frequent sugar.
    • Recognizing the risk of caries
      • Number of teeth
      • Multimorbidity
      • Polypharmacy and dry mouth
      • Diet
      • Oral hygiene
      • Socioeconomic status
      • Prostheses
      • Previous caries
    • Impact of caries in frailty
      • Figure 18.5 Recurrent caries at the margin of a crown in a patient with a history of recurrent root caries.
      • Figure 18.6 An elderly patient with a clean mouth managed successfully with a shortened dental arch and tooth restorations in the mandible, and a complete denture in the maxilla.
    • Management of caries in frailty
      • General principles of management
      • Managing dementia
      • Environment and oral hygiene
      • Oral care plans
        • Table 18.1 Example of an oral care plan for the patient shown in Fig. 18.6.
      • Dry mouth
      • Diet
      • Restorative dentistry
    • Summary
    • References
• Part V Operative intervention
  • 19 Classical restorative or the minimally invasive concept?
    • Operative dentistry and caries control
      • What constitutes the treatment of caries?
      • Why and when are operative treatments (restorations) required?
        • Cavitated occlusal lesions
        • Approximal surfaces
          • Table 19.1 Clinical studies relating radiographic appearance to cavitation in permanent teeth.
        • Free smooth surfaces
          • Figure 19.1 Diagrammatic representation of approximal demineralization as seen on bitewing radiographs.
      • G.V. Black and the classical restorative concept
        • Figure 19.2 (a) Cervical lesions covered by plaque. (b) Same cavities 14 days later after removing overhanging enamel with a diamond finishing bur and instruction in cleaning. Teeth were brushed twice a day with a toothbrush and toothpaste with fluoride. From a cariological point of view these teeth are now stable, but to improve their appearance they are to be restored with composite. (c) Completed restorations. The small color difference is due to the teeth being dry and will disappear after some hours when they are wet with saliva.
        • Figure 19.3 Green Vardiman Black, 1836–1915.
      • Minimal intervention concept
        • Figure 19.4 Restoration is not required in this second premolar. The lesions will not be cavitated and can be arrested by cleaning alone.
        • What were the factors behind the change of approach?
      • What is happening in your dental school?
    • Sealants
      • Occlusal sealants
        • Introduction
          • Figure 19.5 Distribution of 12-year-old Danish children according to caries severity 1974–1991. Note the caries decline over these years and how occlusal caries has not declined as much as approximal and incisor caries.
        • Materials
          • Figure 19.6 Glass–ionomer sealant in an erupting tooth: (a) demineralized enamel in tooth 2.6 of a 7-year-old girl; (b) occlusal surface sealed with Fuji IX GP Extra®.
        • Techniques for resin-based sealants
        • Technique for glass–ionomer sealant
        • Outcomes
          • Figure 19.7 (a) Etching the occlusal surface with 37% orthophosphoric acid gel. (b) Etched enamel after rinsing and drying showing chalky white surface before placing a resin-based sealant. (c) Application of fissure sealant to whole occlusal surface. (d) Sealant being light-cured. (e) The occlusion is checked with articulating paper, which will locate areas of occlusal contact with a colored mark.
          • Figure 19.8 Differences between a sealed and an infiltrated caries lesion. While an approximal sealant, colored yellow, covers the surface (a) caries infiltration aims to fill the microporosities within the caries lesion (b) [39].
        • How long should sealants last?
      • Approximal sealing and infiltration
        • Figure 19.9 Approximal sealing of a D2 lesion on distal surface of tooth 24: (a) radiograph; (b) application of a rubber ring for separation; (c) removal after 4-5 days, cleaning and inspection of the lesion to insure noncavitation; (d) rubber dam isolation, etching of proximal surface and application of sealant or adhesive patch; (e) final polish.
        • Figure 19.10 Resin infiltration after etching and drying. A foil applicator is in place to allow accurate placement of the etchant and protect the adjacent tooth. This is removed after etching, the tooth washed, ethanol applied, and thoroughly dried. Now a new foil applicator is inserted and the infiltrate applied. The foil is now removed, the tooth dried with compressed air, and the infiltrate light-cured.
        • Indications and reservations
    • Atraumatic restorative treatment
      • Definition and history
      • Fissure sealing and minimal operative intervention
        • Atraumatic restorative treatment sealants
        • Atraumatic restorative treatment restorations
        • Cavity cleaning
          • Figure 19.11 ART sealant step by step using a high-viscosity glass–ionomer (Fuji IX, capsulated). (a) Tooth 46 with a pit and fissure system that required a sealant protection. (b) Remove debris from the pits and fissures with a sharp probe. (c) Condition the occlusal surface and pits and fissures with a cotton wool pellet, dipped in polyacrylic acid. (d) Wash the occlusal surface and pits and fissures with a wet cotton wool pellet. (e) Dry the occlusal surface and pits and fissures with a dry cotton wool pellet. (f) Press the glass–ionomer mixture into the pits and fissures with the index finger. (g) Remove finger after 10–15 s. Mixture has been pushed towards the periphery of the occlusal surface. (h) Check the bite. (i) Remove excess glass–ionomer material with hand instruments. (j) Apply a layer of petroleum jelly over the ART sealant. (k) Ask the patient not to eat for at least 1 h.
          • Figure 19.12 A small cavity opening with partly demineralized enamel. The destruction at the enamel–dentin junction is wider than at the cavity opening, giving the lesion a pyramid shape.
          • Figure 19.13 A cavitated dentin lesion in the occlusal surface of the first molar. Note the whitish coloring around the lesion opening. This is a sign of partly demineralized enamel that will easily fracture off after slight pressure with a dental hatchet (see lines of cleavage, Fig. 19.12). In doing so, the cavity opening will increase in size and will allow easy access to the excavator for removal of infected dentin. Also note the cavitated lesion in the buccal surface.
          • Figure 19.14 Further opening of a cavitated dentin lesion using a hatchet. (a) Look at the enamel buccal to the lesion; it is demineralized and very thin. (b) Place the dental hatchet at the edge of the cavity opening and press slightly. (c) The enamel has now fractured. Continue removing enamel that is demineralized.
          • Figure 19.15 Small cavitated dentin lesion in a lower first molar. (a) The enamel access cutter is used to further open the cavity. (b) The end of this pyramidal-shaped instrument is placed in the cavity opening and the instrument is turned anticlockwise several times, grinding down the thin enamel that forms the opening.
      • Atraumatic aspects
        • Table 19.2 Overview of studies that compared dental anxiety and dental pain between the ART and the conventional treatment approach [59].
        • Dental anxiety and dental pain with atraumatic restorative treatment
        • Local anesthesia with atraumatic restorative treatment
        • Tooth tissues saving with atraumatic restorative treatment
      • Restorative materials used with atraumatic restorative treatment
      • The atraumatic restorative treatment approach step by step using high-viscosity glass–ionomer
        • Equipment required
        • Dental instruments and consumable materials
          • Figure 19.16 A set of ART instruments consists of a mouth mirror, an explorer, a pair of tweezers, an enamel access cutter, a dental hatchet, excavators (small and medium size), and an applier/carver.
        • Atraumatic restorative treatment sealant and restoration protocols
        • Operators
          • Figure 19.17 ART restoration of a dentinal lesion, step by step. (a) Notice the discoloration around the cavity opening, which indicates that the caries has extended under the enamel. This unsupported enamel is demineralized and will break off easily under slight pressure (see Chapter 5 and Fig. 19.12). (b) Opening of cavity further for improved access with the blade of the hatchet. (c) Caries removal using a small excavator. (d) The conditioner is applied to the cleaned cavity and pits and fissures with a cotton wool pellet. (e) Carefully dried cavity before placing the filling. (f) Incremental cavity pits and fissures are filled with glass–ionomer cement. (g) Firm finger pressure is applied over the occlusal surface. This is called ‘press-finger technique.’ (h) Excess filling material visible at the outer margins of the occlusal surface. (i) ART restoration after the bite has been adjusted. The filling material is not yet covered with petroleum jelly. (j) Completed restoration. The cavity is filled and the pits and fissures are sealed.
      • Effectiveness of atraumatic restorative treatment sealants and restorations
      • Causes of failure of atraumatic restorative treatment restorations
      • Atraumatic restorative treatment in the elderly
      • Atraumatic restorative treatment and people with a disability
      • Atraumatic restorative treatment in the public services
      • Atraumatic restorative treatment and dental education
      • Concluding remarks on atraumatic restorative treatment
    • Conventional minimal intervention methods
      • Materials available
      • Amalgam, composite resin, and glass–ionomer restorations
      • Relevant technical aspects of minimally invasive management
        • Preservation of tooth structure
          • Figure 19.18 (a) Cavitated lesions visible in the occlusal surface. (b) The preparation after excavation; note distinct differences in lesion extension between the active lesion in the central fossa compared with the slowly progressing microcavitated lesion in the mesial fossa. The lesion on the mesial surface was not included in the preparation because it was arrested.
          • Figure 19.19 Examples of damaged enamel surface in molar adjacent to preparation in premolar. Due to a low caries activity, this damage did not subsequently result in cavity formation.
        • Protection of the surface of an adjacent tooth
          • Figure 19.20 A band is placed around the second premolar to protect its approximal surface, while the carious lesion on the distal surface of the second premolar is opened with a diamond bur.
          • Figure 19.21 Phases in a preparation technique for protecting the adjacent tooth surface. (a) A wedge is placed and initial opening of the lesion is made using the bur. (b) Gingival beveling after using the the Sonysis device (Kavo). (c) The Sonysis tip in use. This instrument only cuts on one side. The side next to the adjacent tooth is smooth and can do no damage.
          • Figure 19.22 (a) Cavity preparation in the second premolar has scored the mesial surface of the amalgam in the first molar. (b) The scored surface has now been polished and the anatomy of the proximal surface established before placing the new restoration. However, the mesial surface may now be too flat to acquire an appropriate approximal contact point to avoid food impaction.
        • Establishing a contact point
        • Seal and cleansability of the margins
          • Figure 19.23 Examples of different types of separation rings. In each, the principle is the same. The spring-loaded ring forces the teeth apart. The thin metal matrix is carefully burnished to the adjacent tooth, the cervical margin of the band is firmly wedged to ensure a tight fit, and the restoration placed. When the ring is removed, the separated teeth move together and a tight contact results.
          • Figure 19.24 The ‘snow-plough’ technique: (a) inserting the flowable composite after applying a sectional matrix; (b) flowable composite in place; (c) inserting the hybrid composite; (d) restoration after curing; (e) finished restoration.
        • Clinical examples
          • Figure 19.25 Occlusal sealant restoration. (a) Cavitated lesions in molars in a 12-year-old girl (1997). Rubber dam applied. (b) Preparations after opening the lesions with a diamond bur. Opening of the distal fossa in the molars might not have been needed because the lesions were inactive. (c) Lesions after excavation. (d) Restored lesions – a three-step etch-and-rinse adhesive was used together with a hybrid composite. A white sealant was placed on the rest of the occlusal surfaces. The sealants might not have been needed, since there was no active caries. (d) The restorations after 15 years; the patient is now 28 years old. Note that the sealants have partly been abraded away. (e) A clinical picture from the buccal aspect, shows darkly stained arrested lesions, the scars of previous periods of active caries.
          • Figure 19.26 ART occlusal sealant restoration. (a) Cavity cleaned according to ART in tooth deciduous molar of a 4-year-old girl. (b) Not only the cavity is restored, but also the adjacent pits and fissures have been sealed using Ketac Molar Easymix®, providing extra protection.
          • Figure 19.27 Approximal box restoration. (a) Deep cavitated caries lesion distally in the first upper premolar extending close to the pulp; see radiograph in (kii). (b) Dentin lesion after opening and removal of enamel with a diamond bur. (c) After removing soft dentin at the enamel–dentin junction using a round bur and water coolant. A 2 mm zone is created along the enamel–dentin junction to provide sound dentin for bonding. The central soft caries has not yet been removed. (d) The cavity after careful removal of most of the soft dentin, leaving a layer centrally covering the pulp, aiming at indirect pulp capping. In this case the central carious dentin was not protected by a liner. (e) Matrix, wedge, and separation ring applied. The etchant is in place. (f) The first layer of flowable composite is inserted but not cured. (g) The first layer of hybrid composite is inserted and both layers are cured together. (h) The first two layers have been cured. (i) The restoration after removal of the matrix. (j) The restoration after finishing. (k) Three radiographs: (ki) 3 years before treatment, (kii) just before treatment, and (kiii) after treatment.
          • Figure 19.28 Cervical composite restoration. (a) Clinical examination of 32-year-old male shows cervical lesions covered by biofilm, in spite of 1 year of nonoperative treatment focusing on improved cleaning with fluoride toothpaste. It was decided to place restorations to aid cleaning. (b) Cavity preparation with minimal loss of dental hard tissues. (c) Restoration with three-step total etch technique and direct composite resin.
          • Figure 19.29 Restoration of root caries with glass ionomer cement: (a) caries lesion in upper canine, poor plaque control; (b) after excavation; (c) after injection of the cement, a special matrix is placed and surplus is removed; (d) after 5 min waiting, the matrix is removed; (e) finishing using a fine-grit diamond bur; (f) application of the protective varnish; (g) finished restoration; (h) restoration after 3 years.
          • Figure 19.30 The larger lesion. (a) Amalgam restoration with clinically defective margins occlusally and distally before treatment. (b) After amalgam removal. (c) After excavation with a round bur and water coolant. Note wooden wedges in place preventing bleeding of the interdental gingivae. (d) This shows a typical problem when a wide box is present and an attempt is made to place a separation ring. The ring forces the matrix out of position. (e) and (f) The solution is to place the distal sectional matrix first without a separation ring while leaving the separation ring and sectional matrix mesially. (g) Etching the cavity. (h) Filling the mesial box and shaping the buccal and palatal walls of the distal box. (i) After curing this, the separation ring can easily be placed. (j) The finished restoration.
      • Replacement or repair of failed restorations
        • Figure 19.31 Lingual crack caused by polymerization shrinkage of composite. Therapy? None, as long as the patient does not have complaints.
        • Figure 19.32 Marginal breakdown of composite restorations. Therapy? No cavity preparation required, just local cleaning, etching, adhesive application, and composite completion.
        • Figure 19.33 (a) The distobuccal cusp is fractured. (b) A bevel is placed in the enamel and the cusp replaced with composite. (c) The completed and polished restoration.
        • Figure 19.34 (a) The enamel has fractured on the lingual side of the proximal box. (b) The defect is cleaned, etched, bonded, and filled. (c) The completed repair.
        • Figure 19.35 Tooth 14 has a 12-year-old mesial–occlusal–distal composite restoration. On the radiograph a cervical recurrent carious lesion is present. (a) Note the small fracture of the marginal ridge of the composite restoration in tooth 15 mesially. (b) A distal box is prepared and the mesial contour of 15 is reshaped. (c) Placement of sectional matrix, wooden wedge, and separation ring results in tight approximal contact. (d) A syringeable hybrid composite was used to complete the restoration.
    • Minimal intervention and the deciduous dentition
      • Function and longevity of deciduous teeth: do they matter?
        • Table 19.3 Eruption times and lifespan of deciduous teeth.
      • Anatomical considerations
        • Figure 19.36 Anatomical differences between a deciduous (left) and a permanent (right) molar. Dentin (a) and enamel (b) thickness is less in deciduous teeth partly due to voluminous pulp horns in deciduous teeth.
        • Figure 19.37 The radiograph shows an interradicular radiolucency (arrow) indicating irreversible inflammation of the pulp and subsequent necrosis. Pulpal treatment or extraction is required. The radiograph does not reveal inflammation but indicates that conservative treatment alone will not suffice in this case.
      • Minimal intervention approaches
        • Inactivation of lesions without caries removal
          • Figure 19.38 (a) ECC (early childhood caries) is a severe problem with heavy plaque, gingivitis, and active white spot and cavitated lesions. (b) Another case has been inactivated by the introduction of toothbrushing with fluoridated toothpaste.
          • Figure 19.39 NRCT. (a) The NRCT method, direction of cleaning, and the brush. (b) After slicing. The marginal ridges have been partly removed on the second molar mesial and completely removed on the first molar mesial/distal, allowing respectively access to the secondary caries lesion (second molar) and the primary caries lesions (first molar). Note the loss of contact has been limited (V-shaped sliced surfaces). Now the parents need to learn how to brush. (c) Half a year after slicing. The same case 6 months later, brushing is not perfect, plaque is still present, but the lesions are arrested.
          • Figure 19.40 Ultraconservative treatment protocol. Small-sized cavities are treated according to the ART approach, medium-sized cavities are enlarged using a hatchet, and medium- and large-sized cavities are cleaned with toothbrush and toothpaste daily. The picture shows the situation 1 year after treatment. Note that the ART restorations perform well and that the caries process in the open cavities has been arrested.
          • Figure 19.41 The Hall crown. (a) Before cementation; no caries removal and no occlusal or proximal reduction. (b) The crown directly after cementation. Inevitably the bite is ‘high.’ (c) Six weeks later. The bite has nearly reestablished.
        • Sealing techniques with no caries removal
        • Partial caries removal and restoration
      • Complete caries removal and restoration
      • Choice of treatment
    • References
  • 20 Caries ‘removal’ and the pulpo-dentinal complex
    • Introduction
    • The pulpo-dentinal complex and caries
    • Pulpitis and its clinical diagnosis
    • Why are pulpo-dentinal reactions important to the choice of operative management?
    • The infected dentin concept and its clinical consequence
      • Figure 20.1 (a) Extracted molar with a cavitated occlusal lesion. The dotted line shows the plane of section. The tooth is wet, which is why there is no change in translucency around the cavity. Compare this appearance with the clinical picture in Fig. 20.2a, where on a dried tooth the translucency is obvious. These two pictures emphasize the importance of drying teeth during a clinical examination. (b) The cut face after sectioning the extracted tooth. Note the undermined enamel (arrow). Sites A, B, C, and D are histologically detailed in (c)–(f). The histological pictures show the relationship of the microorganisms (m) to the dentin and enamel–dentin junction. (c) Site A. The microorganisms penetrate the dentinal tubules superficially in the center of the cavity. (d) Site B. Microbial growth along the enamel–dentin junction gap, but not into dentin tubules. (e, f) Sites C and D. The microbial accumulation and size of the gap decrease towards the periphery of the open cavity. Arrows show a pattern of demineralized rod structure.
      • Figure 20.2 The cavitated coronal lesion with accumulations of microorganisms, and with a change in enamel translucency around the cavity (a) demonstrating that enamel demineralization at this stage develops along enamel–dentin junction and creates a retrograde pattern of enamel demineralization (b, c). The clinical removal of overhanging and undermined enamel is here guided by the retrograde pattern of enamel demineralization (d). The opening of the closed ecosystem along the enamel–dentin junction reveals a brown discolored demineralized dentin related to the exposed central and oldest part of the lesion, whereas the peripheral and outermost area has a more light yellow discoloration. A probe penetrates with easy fragment loss of the tissue, which is very soft and oozing moisture (d–e). Note the gap is visible in the clinic between the enamel and the dentin due to extensive dentin demineralization (e, f). Clinically recorded by Bjørndal in 2006.
      • Figure 20.3 The current clinical practice of mechanical excavation combines a peripheral dentin excavation, carried out using a round bur (a, b), with elimination of the centrally infected tissue using an excavator (c, d). The probe is used to assess clinical consistency; and here, dentin that is hard to touch has not yet been obtained (e). Note that the deeper and soft carious dentin is a fragmented tissue (f). An excavation close to the pulp represents a risk, because cracks along the fragments may lead to pulp exposure. Clinically recorded by Bjørndal in 2006.
    • Studies placing fissure sealants over carious dentin
      • Figure 20.4 An old restoration has been removed and stained; soft, friable, dry dentin is present beneath. This does not require vigorous excavation, although exposure is unlikely because reactionary (tertiary) dentin will be present. The cervical margin must be made hard prior to placing a new restoration to ensure a good bond and seal.
    • Stepwise excavation studies
      • Figure 20.5 Deep caries lesion in a lower premolar during sequences of caries excavation (a–d). Undermined enamel along the enamel-dentin junction can be noted as a white zone around the cavity (a). During removal of the undermined enamel a clear pattern of demineralized enamel (b) is noted along the enamel–dentin junction. In the first excavation procedure the superficial and central part of demineralized dentin is removed, including the peripheral parts of the lesion. The exposed soft dentin is light brown (c). Following temporary filling and a treatment interval of 6 months, and before final excavation, the central exposed dentin is dark brown (d).
      • Figure 20.6 A deep lesion treated with stepwise excavation in a lower second molar (a). Note remnants of the roots of the first molar indicating a very rapid caries progression. The second molar was permanently restored with a composite inlay. After 1 year, pulp vitality was confirmed, and a new radiograph showed no apical radiolucency (b). A 4-year recall confirmed the vitality of the pulp as well as the absence of apical radiolucency (c). However, complete arrest of caries activity has not been achieved; a new proximal lesion has progressed in the third molar.
    • Randomized controlled clinical trials on stepwise excavation outcome
      • Table 20.1 Exposure rates in randomized clinical trials of stepwise excavation.
    • Do we need to reenter?
      • Figure 20.7 Indirect pulp capping. (a) Deep carious second lower deciduous molar before indirect pulp treatment. (b) Same tooth on bitewing. (c) After excavation of the dentin–enamel junction. The biomass is still present in the center of the cavity. (d) Removing biomass with a rotating prophy brush and fluoride toothpaste only. (e) After removing the biomass. Next the cavity was dried, a resin-modified glass–ionomer liner (Vitrebond/3 M Espe) was applied, and the cavity was restored with a compomer (Dyract/Dentsply Caulk). (f) Clinical result after 2 years and 4 months. (g) Radiographic result after 2 years and 4 months.
    • What happens if we do not remove caries at all but seal it in the tooth permanently?
    • Further consideration of deciduous teeth
    • Conclusion on caries removal and the pulpo-dentinal complex
    • References
  • 21 Longevity of restorations: ‘the death spiral’
    • Introduction
    • Clinical assessment of restorations
    • Assessment of restoration longevity
      • Table 21.1 Clinical assessment of restorations.a
      • Table 21.2 Criteria for clinical assessment of restorations.a
      • Figure 21.1 Detailed assessment of occluso-distal, class II amalgam restoration in the lower second molar. The 28-year-old male patient complains about occasional pain from the region. Fracture and loss of distal part of restoration. Probably minor fracture of disto-lingual cusp, too. Plaque covered active caries in the cavity. Gingivitis in adjacent gingiva. Overall assessment and intervention. Damage is occurring in the tooth and the surrounding tissues. The restoration is not acceptable. Replace restoration immediately.
      • Figure 21.2 Detailed assessment of occluso-distal, class II amalgam restoration in the first upper premolar: (a) clinical photograph; (b) plaster model. Minor fracture of buccal part of marginal ridge. No evidence of plaque or caries in the cavity. No evidence of gingivitis in adjacent papilla. No complaints of pain or food impaction. Overall assessment and intervention. There is no damage of tooth or surrounding tissues. The restoration is acceptable. No intervention needed.
      • Figure 21.3 Detailed assessment of 2-year-old, distal, class III composite resin restoration in the upper lateral (a). Fracture of disto-incisal corner of the tooth beneath otherwise optimal restoration. Overall assessment and intervention. The restoration is not acceptable. Repair or replace restoration sooner or later. However, the 46-year-old female patient did not want the restoration to be repaired! She attended 4 years later with the same unrepaired but now worn restoration, which she still did not want to be repaired! (b) Illustration that restoration of the incisal tooth fracture would require reduction of the incisal edge of the lower canine to protect the class IV restoration against fracture and/or loss during occlusion/articulation.
      • Figure 21.4 Detailed assessment of 12-year-old, mesial, class III composite resin restoration in the upper canine. Obvious deep and extended marginal staining along the periphery of the restoration. No evidence of secondary or recurrent caries. Overall assessment and intervention. The restoration is objectively acceptable. However, the patient may find the restoration not acceptable and in that case it has to be replaced sooner or later.
    • The amalgam debate and its consequences for restoration longevity
      • Figure 21.5 Annual number of amalgam restorations, tooth-colored restorations, endodontic treatments, and extractions performed in adults in general dental practice in Denmark from 1980 to 2011.
    • Longevity of restorations in the primary dentition
      • Figure 21.6 Median values and ranges for annual failure rates obtained in longitudinal studies of class I/II restorations in posterior primary teeth using different types of restorative materials. The number of studies n is given for each material.
      • Figure 21.7 Cumulative survival distribution of 2025 class II restorations in primary teeth performed in amalgam (AM), conventional glass–ionomer (GI), resin-modified glass–ionomer (RMGI), and compomer (COM). The curves are drawn as long as at least 10 restorations remained in function. The points at which the curves cross the horizontal quartile lines are indicated by arrows on the abscissa. It appears that the median or 50% longevity for GI restorations was around 3 years, while more than 75% of the AM, RMGI, and COM restorations would still be in function at that time, provided that the teeth have not been exfoliated before then. The difference is highly significant (p = 0.000). The vertical bars represent standard errors of the survival rates [72].
      • Figure 21.8 Bar graph showing 3-year survival rates (mean, standard error) for class II restorations in primary teeth made in amalgam, conventional glass–ionomer (GI), resin-modified glass–ionomer (RMGI), and compomer by eight dentists with at least 15 restorations in each type of material. The figure also illustrates that GI resulted in the lowest 3-year survival rate for all eight dentists, while one dentist received the highest 3-year survival rate with amalgam, four with RMGI, and five with compomer, and two dentists got equally superior results with RMGI and compomer [69–71].
      • Figure 21.9 Cumulative survival distribution of 1341 unrestored approximal surfaces adjacent to class II restorations in primary teeth performed in amalgam (AM), conventional glass–ionomer (GI), resin-modified glass–ionomer (RMGI), and compomer (COM). The curves are drawn as long as at least 10 surfaces remained unrestored and under observation. The points at which the curves cross the horizontal quartile lines are indicated with arrows on the abscissa. It appears that the median or 50% longevity for surfaces in contact with AM restorations was around 3.5 years, compared with 4.5 years and 5.5 years for surfaces in contact with COM and RMGI respectively. The GI curve followed the RMGI curve, but the surfaces could only be followed for 4.5 years owing to short longevity of GI restorations. The difference is highly significant (p = 0.008). The vertical bars represent standard errors of the survival rates [73].
    • Longevity of restorations in the permanent dentition
      • Figure 21.10 Median values and ranges for annual failure rates obtained in longitudinal studies of class I/II restorations in posterior permanent teeth using different types of restorative materials. The number of studies n is given for each material.
      • Figure 21.11 Bar graph showing median recorded age of failed amalgam and composite resin restorations in adults in relation to type of restoration.
    • Longevity of fissure sealants
      • Figure 21.12 Bar graph showing median recorded age of failed amalgam and composite resin restorations in adults in relation to type of failure.
      • Figure 21.13 Cumulative survival distribution of 153 resin restorations and 368 resin sealants placed in teeth with manifest occlusal enamel and dentin caries lesions in children and adolescents. The 4-year survival rates were around 90% for the restorations, but just 60% for the sealants (p = 0.000). The vertical bars represent standard errors of the survival rates [74].
    • Longevity of atraumatic restorative treatment restorations
      • Figure 21.14 Examples of ART restorations: (a) 3-year-old occlusal restoration in the upper second primary molar and (b) 4-year-old occlusal–distal restoration in the lower second primary molar.
    • Factors influencing restoration longevity
      • Figure 21.15 Variables of significance for overall survival of restorations in the primary dentition and for occurrence of the three most frequent types of failure; i.e. bulk fracture of restoration, loss of retention, and endodontic complications.
    • Consequences of restoration longevity for dental health and cost
      • Figure 21.16 Cumulative cost of restorative treatment using amalgam, composite resin, or cast gold/ceramic for class II restorations over a 65-year period. The calculations are based on actual Danish costs (1× for amalgam, 2.5× for composite, and 8× for gold/metal-ceramic restorations) and today's expectations as to their median longevity: 8 years for composite, 12 years for amalgam, and 18 years for gold/metal-ceramic class II restorations.
      • Figure 21.17 Illustration of the detrimental long-term consequences for the dental health of the restorative cycle – ‘the death spiral.’ Over the years, the initially sound first lower premolar (a) has been restored with a localized (b) and then an extended occlusal amalgam restoration (c), a two-surfaced (d) and a three-surfaced occluso-proximal amalgam restoration (e), and because of gingival caries (f) or abrasion (g) a facial composite (h) and amalgam restoration (i), a cast gold crown (j), and eventually a bridge has been made (k) after extraction of the premolar (l).
    • Concluding remarks
    • References
• Part VI From chair-side to population caries control
  • 22 Caries prevention and control in low- and middle-income countries
    • Introduction
      • Table 22.1 World Bank country grouping according to GNI per capita.
    • Caries: a public health problem in low- and middle-income countries
      • Figure 22.1 Movement of population income groups 1990–2011 [40].
      • Social determinants and risk factors of caries in low- and middle-income countries
      • Caries burden in low- and middle-income countries
        • Figure 22.2 New conceptual model for oral health inequalities [90].
        • Table 22.2 Average caries experience expressed as DMFT in the permanent dentition of 12-year-olds in LICs, LMICs, UMICs, and HICs (data from 2000 onwards, WHO CAPP).
        • Figure 22.3 Proportion distribution of DMFT components in the permanent dentition of 12-year-olds in LICs, LMICs, UMICs, and HICs
      • Early childhood caries in low- and middle-income countries
    • Health and oral health systems in low- and middle-income countries
      • Table 22.3 Essential activities in PHC [93].
      • Barriers to the integration of oral health care into primary health care
        • Table 22.4 Possible reasons why oral health care has not been included in PHC.
      • Workforce planning for oral health care
        • Box 22.1 Does the dentist-to-population ratio matter?
        • Figure 22.4 Global density of dentists in 2009.
      • Illegal oral care: symptom of a bigger problem
        • Figure 22.5 Street ‘dentists’ in India.
    • Public health approaches to address caries in low- and middle-income countries
      • Policy options to reduce risks to oral health and promote prevention
        • Table 22.5 Selected policy options for reducing dietary risk factors.
        • Box 22.2 The Fit for School Approach
      • Fluoride strategies as public health tools in low- and middle-income countries
        • Water fluoridation
        • Salt fluoridation
        • Milk fluoridation
        • Professionally applied fluorides
        • Fluoride toothpaste
          • Table 22.6 Criteria and guiding principles for the selection of a fluoride intervention according to the FLINT.
          • Table 22.7 Possible challenges for implementing water fluoridation.
      • Considerations specific to the promotion of fluoride toothpaste in low- and middle-income countries
        • Affordability of fluoride toothpaste as an essential commodity
        • The use of fluoride toothpaste in areas with high levels of natural fluoride in water
        • Ensuring the quality of fluoride toothpaste
          • Figure 22.6 Number of days of household expenditure required to pay for one annual dosage of toothpaste at the lowest price by country and population group. The 30%, 50%, and 70% percentiles of the poorest sector of the population in a country are presented.
          • Table 22.8 Options for policy and action related to promotion of AFT.
      • Integrating basic oral health care into primary health care
        • The Basic Package of Oral Care
        • Reviewing the Basic Package of Oral Care
          • Table 22.9 Examples of partial implementation of the BPOC.
          • Table 22.10 Possible barriers to implementing the BPOC.
        • The future for the Basic Package of Oral Care
      • Strengthening surveillance and research in low- and middle-income countries
      • Measuring caries matters for advocacy and planning
      • The PUFA index to assess dimensions of untreated caries
      • Urgent need for health services research
      • Integration, advocacy, and a supportive policy context
    • Conclusions and recommendations
      • Figure 22.7 (a, b) Pulpal involvement (P/p); opening of pulp chamber is visible or coronal tooth structures are destroyed by caries. (c, d) Ulceration (U/u); traumatic ulceration in the soft tissues (tongue and mucosa) caused by tooth or root fragments. (e, f) Fistula (F/f); a sinus tract releasing pus originating from an abscess and opening into the oral cavity. (g, h) Abscess (A/a), dento-alveolar abscess.
      • Table 22.11 Scoring criteria of the PUFA/pufa index.a
      • Figure 22.8 Relation between efficacy and effectiveness in different settings [55].
    • References
  • 23 How accurately can we assess the risk for developing caries lesions?
    • Introduction
      • Figure 23.1 Percentage distribution of 12-year-olds according to D3MFS counts in Kuopio (n = 161) and in Jyväskylä (n = 154) in 1998.
      • Figure 23.2 Cumulative percentage distribution of 12-year-olds in Kuopio and Jyväskylä in 1998 plotted against the cumulative distribution of their D3MF counts (Lorenz curve). If all children had had the same number of D3MF surfaces, the curves would have coincided with the diagonal.
      • Figure 23.3 A graphical look at the high-risk strategy.
    • The risk of developing caries lesions cannot be observed directly for an individual patient
    • The course of a typical study for evaluating the accuracy of a prediction
      • Figure 23.4 Outline of a typical follow-up study for evaluating the predictive power of a dichotomous predictor of caries risk.
      • Table 23.1 A 2 × 2 table for evaluating the accuracy of a dichotomous prediction and formulae for selected measures of accuracy.
      • Sensitivity, specificity, false-positive rate, and false-negative rate
      • Positive and negative predictive values
      • Crude hit rate, the Youden index, and diagnostic odds ratio
      • Positive likelihood ratio and negative likelihood ratio
    • A real-life example of using a single, dichotomous predictor
      • Table 23.2 A summary of the results of a study where visible plaque on the labial surfaces of maxillary incisors at the age of 19 months was used for predicting the onset of at least one caries lesion by the age of 36 months.
    • Interpretation and use of the measures of prediction accuracy
      • Other types of predictors and their combinations
      • Single predictors with multiple possible threshold levels
        • Figure 23.5 The percentage distribution by the number of new D3MFS surfaces in a 3-year period among subjects for whom the risk of developing caries lesions was considered high and for whom it was considered low in a cohort of 384 initially 13-year-old children living in Vantaa, Finland. For the criteria of high and low risk, see text.
        • Figure 23.6 The percentage distribution of subjects according to D3MFS counts at baseline in a cohort of 384 initially 13-year-old children living in Vantaa, Finland.
        • Table 23.3 Prediction of 3-year D3MFS increment ≥5 (n = 104) by baseline D3MFS score in a cohort of 384 initially 13-year-old children living in Vantaa, Finland.
      • The receiver operating characteristic curve
        • Figure 23.7 ROC curves illustrating the relationship of the true- and false-positive rates at different threshold levels of baseline D3MFS count. For D3MFS, the figures are the same as in Table 23.3 where this count was used as a predictor of 3-year D3MFS increment ≥5.
        • Figure 23.8 ROC curves for baseline D1aMFS, salivary lactobacilli (LB), mutans streptococci (MS), and buffer capacity score (BC) in a cohort of 384 initially 13-year-old children living in Vantaa, Finland.
        • Table 23.4 Prediction of 3-year D3MFS increment ≥5 (n = 104) by baseline lactobacilli score (LB) in a cohort of 384 initially 13-year-old children living in Vantaa, Finland.
        • Table 23.5 Prediction of 3-year D3MFS increment ≥5 (n = 104) by a logistic risk function in a cohort of 384 initially 13-year-old children living in Vantaa, Finland.
        • Figure 23.9 ROC curve for the logistic risk function (Table 23.5) including all four predictors (LogReg). The ROC curve for baseline D1aMFS (Figs 23.7 and 23.8) has been repeated for comparison.
      • The coin has two sides
        • Figure 23.10 Percentage distribution of subjects according to 3-year D3MFS increment among those with baseline D1aMFS counts of 0–13 and ≥14 respectively in a cohort of 384 initially 13-year-old children living in Vantaa, Finland.
    • What level of accuracy would be sufficient in everyday practice?
      • Figure 23.11 Percentage distribution of subjects with no baseline DMFS according to D3MFS increment in a cohort of 384 initially 13-year-old children living in Vantaa, Finland.
    • What level of accuracy can be achieved?
      • Signs of past caries experience
      • Microbiological tests
        • Salivary lactobacilli
        • Salivary mutans streptococci
        • Salivary yeasts
        • Other salivary factors
      • Dietary habits and oral hygiene
        • Social factors
      • Joint predictive power of multiple predictors
    • Clinical caries risk assessment: is it possible?
    • How valuable are the proposed measures?
    • Concluding remarks
    • Background literature
    • References
  • 24 Caries control in low-caries populations
    • Introduction
    • A low caries frequency entails the polarization of the caries problem
    • Are effective and feasible measures available for protecting the high-risk individuals from dental decay?
      • Figure 24.1 Mean approximal DMFS increment in 2 years among initially 13-year-old participants of a caries trial performed in Kuopio, Finland, in the late 1980s.
      • Figure 24.2 Mean DMFS increment in 3 years among initially 12-year-old participants of a caries trial performed in Vantaa, Finland, in the middle 1990s.
    • Noninvasive treatment of early caries lesions among teenagers exposed to community-wide oral health promotion
      • Figure 24.3 Mean DMFS increment in 3.4 years among initially 11–12-year-old participants of a caries trial performed in Pori, Finland, in the early 2000s.
    • A model for controlling caries in low-caries child populations
      • Figure 24.4 A model for controlling dental caries in cooperation between people, health professionals, and the society.
    • A demonstration case in 0–18-year-old Danes
      • The public dental health care for children and adolescents in Denmark
      • The Odder municipality dental health-care program
        • Figure 24.5 Mean DMFS for all 18-year-olds in the Odder municipality from 1999 to 2012 compared with the national average for 18-year-olds in Denmark.
        • Figure 24.6 Mean DMFS for all 15-year-old children in Odder municipality from 1999 to 2012.
      • Is this model also applicable in low-caries populations in less-privileged populations around the world?
        • Figure 24.7 Mean DMFS among 18-year-olds in Odder municipality from 1999 to 2012.
        • Figure 24.8 The frequency distribution of 18-year-olds in Odder municipality according to their caries experience from 1999 to 2012.
    • Concluding remarks
    • References
  • 25 Epilogue. Controlling the global burden of dental caries: the evidence calls for a reorganization of the oral health-care system
    • References
• Back Matter
  • Index
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