Caries Management - Science and Clinical Practice. Группа авторов

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СКАЧАТЬ 3.1 Correlation between histological, radiographical, and clinical appearance of developing caries. For radiography and clinical appearance ideal conditions are assumed (approximal caries for radiography but directly accessible to the naked eye regarding its clinical appearance)

Histology	Radiography	Clinical appearance
–	–	Sound
Surface etching	–	–
Shallow (approx. <100µm) enamel subsurface lesion with intact surface layer	–	White (brown) spot, visible only under dry conditions
Enamel subsurface lesion extending halfway to the EDJ with intact surface layer	Hardly visible, maybe slightly in outer enamel	White (brown) spot, visible only under dry conditions (no cavitation)
Caries lesion extending to the EDJ with enamel surface still intact. Dentin reactions comprising development of different zones and tertiary dentin	Translucency in enamel	White (brown) spot, visible under dry conditions, but often also visible under wet conditions (no cavitation)
Dentin reactions comprising different zones and build-up of tertiary dentin. Within localized areas of enamel breakdown, bacteria penetrating the enamel can be found	Translucency in outer third of dentin	White (brown) spot, visible under dry and wet conditions. Small, localized breakdown of the enamel surface may be visible
Following enamel breakdown, bacteria can be found within dentin tubules. Dentin reactions comprising different zones and tertiary dentin	Translucency in middle third of dentin	Well developed macroscopic cavitation, usually within a white (brown) spot. Possibility of discomfort or pain
Dentin is exposed further. The exposed dentin surface starts to disintegrate (necrotic zone) and the zone of penetration reaches deeper into dentin. In an advanced state bacteria can have penetrated up to the pulp	Translucency in inner third of dentin	Well developed cavity with increased likelihood for discomfort or pain

      With respect to erosive mineral dissolution of enamel, two different types of dissolution occur that are relevant to the further destiny of the damaged enamel. Consider a single exposure to an acidic solution under laboratory conditions: a certain amount of material, a layer of ca. 0–1μm, is completely lost and cannot be remineralized in any way. (Under harsh laboratory conditions—not comparable to the clinical situation—this can exceed 1μm.) The newly exposed surface is softened and porous up to about 10μm, showing some similarity to the acid-etch pattern after exposure to 35%–40% phosphoric acid that is used prior to placing an adhesive restoration (Fig. 3.26). The softened surface zone is not homogeneously soft, but shows a gradient of increasing hardness from a more softened surface to the sound enamel underneath. This gradient extends to a depth of up to 10μm, but usually is less than that. For this reason, surface microhardness measurements (such as Vickers and Knoop) may not work reliably, because the tip of the indenter rests on harder material, probably sound enamel already, indicating microhardness values harder than the actual hardness of the outermost layer.⁶⁹

      The softened layer is highly vulnerable to mechanical forces, such as attrition, abrasion or toothbrushing.^70,71 While erosion leads to irreversible tooth substance loss of the outermost layer of enamel, the softened layer may be remineralized, at least to a certain extent and hereby regain its mechanical resistance toward toothbrushing and other mechanical forces. It has been shown in situ that saliva takes much longer than one hour to remineralize softened eroded enamel to restore its original mechanical resistance.⁷¹ In an effort to combat enamel erosion, timing of toothbrushing (i.e., before or after erosive meals) may be crucial (Chapter 10), but also fluoride has been found to be effective, to a limited degree.^72,73

      In the clinical situation, the acquired pellicle seems to have an important protective effect against erosion, particularly when the erosive attack is not too severe. Most studies on enamel erosion to date have been performed under laboratory conditions without enamel protected by an acquired pellicle. Due to the protective effect of the pellicle, the loss from erosive substance in the mouth is far less than that predicted from experiments on polished yet unprotected enamel surfaces. This may explain why people of older age with “normal” eating habits still have their own teeth in function, despite regular consumption of acidic fruit, vegetables, and beverages.

      An erosive attack on dentin leaves collagen fibers at the surface, a phenomenon that is also known from acid etching in adhesive dentistry. It is known that the exposed collagen network on the surface of dentin acts protectively toward further erosion of the surface, but may be damaged by proteolytic enzymes, such as pepsin in the case of esophageal reflux or vomiting as the cause of erosion.⁷⁴ Newer strategies against dentin erosion consider particularly the collagen matrix of dentin. The role of metallo-matrix proteinases (MMPs) present in dentin seem to play a role in dentin degradation due to caries and erosion,⁷⁵ and hence ways of reducing the MMP-activity are currently under investigation.⁷⁶

       NOTE

      Erosion is loss of dental hard tissue due to direct dissolution by acids from the nutrition, the stomach, or the environment that are not of bacterial origin. During an erosive attack, calcium and phosphate are lost irreversibly and the remaining enamel or dentin surface is demineralized up to a few micrometers. Areas covered by plaque are protected from erosion. The acquired pellicle seems to play an important role in prevention of erosive substance loss.

      Fig. 3.26 Section through enamel after 1min of erosion in citric acid (false colors). The enamel specimen was embedded in acrylic (PMMA) following erosion and sectioned perpendicularly to the surface through eroded (E) and noneroded (NE) enamel. The green band on top of the enamel surface in the eroded area represents a layer of demineralized, but at this stage not completely lost, enamel of 10μm thickness.

       SUMMARY

      The cause of caries lesion development—the accumulation of dental plaque—is facilitated at specific, mechanically protected areas. Caries lesions typically initiate at these so-called predilection sites/plaque stagnation areas. The development of a caries lesion starting at the enamel surface and spreading toward dentin and further toward the pulp follows the same mechanisms, independently of the site of such a lesion. Histology reveals different zones within a caries lesion, depending on the depth of the lesion, but also on whether and to what extent the enamel surface has broken down. With a caries lesion that is limited to enamel, the outer layer of the enamel is less mineralized than sound enamel, but more mineralized than the subsurface lesion. As long as the enamel surface is macroscopically intact, only a few bacteria can be found within the enamel. With breakdown of the intact enamel surface, lesion development is accelerated and bacteria СКАЧАТЬ