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 can spread deeper and in large numbers into both enamel and dentin. Usually, the demineralized areas within a well-developed dentin caries lesion precede the bacterially infected areas. Among the histological techniques used to investigate enamel and dentin caries lesions, light microscopy can be used to reveal different zones within enamel and dentin caries that correspond to different pore volumes and size distribution of such porosities. Microradiographic techniques are able to analyze exactly the mineral content as a function of lesion depth. Scanning electron microscopy shows changes at the enamel surface at early lesion states and within a lesion at the enamel prism level, while transmission electron microscopy provides insight into changes at the crystal level. Even when a caries lesion progresses, demineralization is interrupted by phases of remineralization. Net remineralization can be achieved only when the biological and chemical conditions at the surface of such a lesion change toward a less cariogenic environment. Clinically, this means successful regular plaque removal and administration of fluoride. Under these conditions, the caries process can come to halt and remineralization of the outer layers of enamel or exposed dentin is possible. However, the result of lesion remineralization can be considered to be a “scar,” because complete remineralization in the sense of a “restitutio ad integrum” does not occur. Remineralization of deeper lesions most likely leaves behind a less mineralized area. Both caries and erosion cause loss of mineral from a tooth, but the etiology and the histology are considerably different. Erosion is not caused by bacteria, but by the direct dissolution of enamel and dentin due to acids that originate from the nutrition, the stomach, or other environmental sources. Erosion leads to immediate irreversible loss of calcium and phosphate from the enamel or dentin surface and creates only a shallow softening of the surface. This softened surface is prone to abrasive loss, but may be remineralized when left mechanically undisturbed for some time.
Acknowledgments. The author would like to thank Prof. Dr. Hans Ulrich Luder, University of Zurich, Center for Dentistry, Institute for Oral Biology for kindly providing Figs. 3.9, 3.10, 3.13, 3.16,