Tooth enamel lesions

LeGeros, R.Z., Silverstone, L.M., Daculsi, G. and Kerebel, L.M. (1983) In vitro caries-like lesion formation in F-containing tooth enamel. Journal of Dental Research, 62, 138-144. 

Fig. 9.10. Artificial caries lesion in human tooth enamel by the ten Cate method (a) z = 0 (b) z = —14 m 370MHz (Peck and Briggs 1986).

Fig. 9.13. Quantitative analysis of the contrast from a white spot lesion in human tooth enamel (i) micrograph, 370 MHz (ii) V(z) curves of selected points along the line in the micrograph (iii) Rayleigh velocity and attenuation calculated from V(z) measured at each of the points on the line in (i) (Peck et al. 1989).

In the absence of therapeutic agents, tooth minerals are continually being exchanged between saliva and tooth enamel. Under the above acidic conditions enamel dissolves, which leads to the formation of a carious lesion. However,... 

Edmunds DH, Whittaker DK, Green RM Suitability of human, bovine, equine, and ovine tooth enamel for studies of artificial bacterial carious lesions. Caries Res 1988 22 327-336. 

White spot lesions are the earliest macroscopic evidence of enamel caries [37], The lesions are caused by acids formed by bacterial fermentation of dietary sugars. This leads to a fall in plaque pH and dissolution of the mineral component of the tooth enamel. Under normal conditions, the demineralization process is balanced by remineralization due to diffusion of ions (Ca, P and hydroxyl) from saliva into the enamel when plaque pH returns to neutrality. However, if demineralization extent exceeds that of remineralization, then an incipient lesion is formed. 

From a mechanistic viewpoint it is reasonable to anticipate an inverse clinical relationship between calculus and caries. Calculus formation is essentially a mineralisation process. The development of a caries lesion is the result of the net demineralisation of tooth enamel by plaque acid. These processes both involve crystalline calcium phosphate phases in contact with liquid, saliva and/or plaque fluid, containing their constituent ions. The oral environment also contains other salivary constituents and bacteria, which either inhibit or promote crystal growth or dissolution. 

In coronal caries, the enamel of the tooth crown is affected. With lasting caries, the lesion deepens and acquires a conical shape. In polarized light microscopy, zones with different mineral densities can be distinguished, such as the lesion body and the mineralized surface layer... 

Early dental caries (incipient lesions) are non-cavitated and limited to the outer enamel surface. Clinically, these lesions are identified as visible white spots when the tooth is air-dried (Fig. 11.1). The incipient lesion is known as a subsurface lesion since the surface appears intact. However, histological investigations have shown that below the surface, there are zones that vary in porosity (voids from mineral loss) as well as biochemical composition (e.g. fluoride, water and carbonate content) [29]. The enamel caries can vary from a depth of 100-250 J.m (for incipient caries) to entirely through the enamel ( 1.5mm deep), at which point the cavitated lesion has extended into the underlying dentin [35]. The diagnostic challenge remains early caries detection and the focus has been on caries lesions that form on the tooth crown affecting the enamel. The remainder of the discussion will therefore concentrate on enamel caries. 

Fig. 11.7. A Mesial surface of an extracted human premolar containing an early carious lesion. Dashed lines mark the regions scanned to produce the OCT images in (B) and (C). B OCT depth image from a region of sound enamel. C OCT depth image from a region of the carious lesion. Inset photomicrograph of a thin tooth section revealing the subsurface lesion.

Chapter 5 concerns the mechanical properties of tooth mineral, with particular emphasis on the use of nanoscale hardness measurements to elucidate the variations across the tooth surface and how they may be associated with tooth function. The influence of environmental factors, such as those described in Chapter 4, are also discussed. In addition, the authors present very recent studies, employing a variety of state-of-the-art techniques, on pellicle-coated enamel and on the early carious lesion, which complements the work described in Chapters 2 and 4, respectively. 

Early non-cavitated carious lesions only may be repaired by remineraUzation processes. However partly because of the uncertainty in outcome, and partly because results are more reliable, the method of choice for the repair of a tooth damaged by caries is surgical removal of the carious region, followed by repair with some sort of synthetic material. The act of cutting out damaged tooth material (enamel and dentine) is known to compromise the mechanical properties of the tooth [43], as shown by the results in Table 1.1. In this study, a set of 10 non-carious teeth was used per experimental set. They were mounted in dental stone and tested in compression, with the load at failure in kilograms recorded. 

Non-carious cervical lesions of the tooth are typically wedge-shaped and show loss of tooth tissue mainly on the buccal surfaces of the tooth close to the cemento-enamel junction. This is the case, regardless of the tooth affected [72]. When the tooth is loaded asymmetrically, there are typically flexing stresses, and these produce tension on one side of the tooth and compression on the other. Both types of force are located close to the cemento-enamel junction [86], The result is that tooth mineral fractures in this region, and falls away, causing a non-carious lesion to develop. These lesions typically involve exposure of the dentine [72]. 

It has been suggested that erosion of this type may contribute to the development of non-carious cervical lesions because erosive agents enter the surface of the enamel through internal channels. Having done so, they would weaken the enamel by chemical attack from within. The resulting affected enamel would then be more susceptible to wear (tooth brush erosion) and fracture when loaded than unaffected enamel. This erosion might influence the formation of cervical lesions without having a primary role in their occurrence. 

There are a certain number of options to control and reduce dental caries, the biggest problem in tooth care. The use of fluoride salts is one of the most effective methods to prevent or slow down demineralization that causes tooth decay [16,17]. The action of fluoride can be explained by its antimicrobial action, its interaction with enamel to form a fluorinated hydroxyapatite compound (hydroxyfluorapa-tite or fluorapatite Ca5(P04)3F) by substitution of an hydroxyl ion in hydroxyapatite Ca5(P04)3(0H), which is more resistant to add than enamel on its own, and its repairing effect by formation of calcium and phosphate, which ranineralize the tiny lesions in which caries begin. 

The permanence of bacterial plaque on the tooth surface will lead to loss of minerals constituents of the dental enamel, promoting the installation of the caries disease [42,43]. The carious lesion is characterized by the tooth structure (hydroxyapatite) di-mineralization by the production of organic acids, such as lactic acid, resulting from bacterial (dental biofilm) metabolism [42,43]. This results in loss of calcium and phosphate ions, which subsequently diffuse out of the tooth. In this complex process, the microorganism, particularly streptococcus species, have an important role in its etiology [43]. 

As for the future, methods to prevent or cure tooth decay are likely to involve a biochemical approach. The role of fluoride is now well established, and means of remineralizing a carious lesion or chemically modifying the tooth, the enamel surface and its bacterial population offer scope for further investigation. 

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