Applied Oral Physiology. Robin Wilding
enamel is clearly a dynamic process of dissolution and precipitation, it is not a vital process in the sense that living cellular reactions occur. In contrast, the pulp–dentin is a vital tissue capable of both a biomineralization process and a physical/chemical process providing some degree of repair to damaged dentin.
The caries process in dentin involves the demineralization of the mineral component and breakdown of the organic component, and so it is quite similar to the process of destruction which occurs in enamel, except that it progresses approximately twice as fast in dentin. This rapid progress is due to the ease with which organisms are able to migrate down the dentin tubules toward the pulp. These organisms may be seen in a section through a carious lesion. In the advancing front, just a few pioneer organisms are seen in contrast to the more established outer zones where the tubules are full of organisms (▶ Fig. 2.16).
Carious lesions in dentin consist of two distinct layers having different microscopic and chemical structures. The outer layer is heavily infected with bacteria, which are mainly located in the tubule spaces. The dentin collagen fibers are denatured, and so the structural organization disappears and there is no organic matrix to remineralize. The inner layer is more sparsely infected, but it has been demineralized by plaque acid. It still contains high concentrations of mineral salts and may be remineralized (▶ Fig. 2.17).
2.3.1 Bacterial Penetration
A large number of bacterial species have been isolated from dental caries but a few genera are commonly found and predominate (see Chapter 4.3 The Biofilms of the Oral Environment). The most frequently isolated from occlusal and smooth surface caries are the members of the Streptococcus species and in particular Streptococcus mutans, and Streptococcus sobrinus, collectively called the mutans streptococci. Actinomyces species are the dominant genus in root surface caries. Deep dentin caries has a predominance of lactobacillus organisms with several other gram-positive rods and filaments. Kidd and her coworkers took samples of carious dentin during cavity preparation and cultured the samples so as to count the number of bacteria.1 As the samples were taken, the dentin was assessed as either soft, medium, or hard, wet or dry, and pale or dark. The number of bacteria recovered diminished significantly as the caries became dryer and harder and the cavity became deeper. This reduction in numbers of bacteria was not marginal but of the order of 100 times less. There was no significant difference between the number of organisms cultured from medium as opposed to hard dentin. The color of the sample was not associated with the number of bacteria recovered. These findingssuggest that at the stage in cavity preparation, when the wet, heavily infected, soft dentin has been removed, further removal of medium, hard-stained dentin may not contribute to further reduction of infected material and may in fact be unnecessarily destructive. The question arises of the fate of slightly soft dentin when not removed, and whether it is a source of secondary caries.
Fig. 2.16 Histological sections of infected and affected dentin from a carious tooth. (a) A section of dentin (magnification × 1,000) toward the surface of a caries lesion with bacteria-like structures packed into the dental tubules. This dentin could be described as infected. (b) A section of dentin from the same tooth, closer to the pulp and partly visible in ▶ Fig. 2.12b. A few dentinal tubules are stained with bacterial debris. This zone of dentin could be described as affected.
Fig. 2.17 A diagrammatic representation of layers within a carious cavity. Dentin caries comprises two main layers. In the outer layer, the dentin is heavily infected with bacteria. Both organic matrix and mineral have been lost and the dentin is beyond repair. In the deeper layer, the dentin has been affected by plaque acids and demineralized. The number of colony-forming units (CFUs) of bacteria decreases (about 100 times) as cavity preparation proceeds into affected dentin. The damage in this layer is reversible if bacterial metabolism can be halted. A barrier of translucent (well-mineralized) dentin may be formed ahead of the advancing lesion. Reactionary (secondary) dentin forms to protect the pulp from acid irritation. (Adapted from Kidd and Joyston-Bechal 1987.)
2.3.2 Secondary Caries
Few dental restorations last a lifetime. Most eventually have to be replaced, either because they break down or because caries recurs. It used to be thought that recurrent or secondary caries was caused by the incomplete removal of all soft, infected dentin during the preparation of the cavity. The first indications that secondary caries may have other causes came from research studies which investigated leakage around the margins of restorations. According to Kidd, there is little evidence that leaving infected dentin behind after cavity preparation would result in caries progression.2 A review by Ricketts confirmed that the microflora left beneath restorations usually do not grow, although they may survive for several months. Their viability is determined by the degree to which nutrients are excluded by an effective restorative seal.3
2.3.3 Conservative Management of Deep Caries
A traditional goal in cavity preparation was to remove all soft dentin until hard dry dentin was reached. In the 1970s, Massler and Pawlak promoted the idea that this was unnecessarily destructive and could often lead to exposure of the pulp in deep cavities.4 They maintained that soft dentin was not necessarily infected but could be merely affected by plaque acids. They proposed a more conservative cavity preparation, which required the removal of infected dentin only, leaving behind soft but not infected, so-called affected dentin. Affected dentin could be remineralized if the acid production was halted. These suggestions were at the time supported by little experimental data, but there is now convincing evidence that the pulp–dentin has a significant ability to repair by the formation of reactionary dentin, provided that the heavily infected dentin is removed and the cavity is well sealed from the oral environment. The formation of reactionary dentin is the result of a cellular process involving the mineralization of a supportive extracellular matrix produced by the odontoblast. Demineralized (affected) dentin or enamel may also remineralize by a simple precipitation of mineral salts. The process may take place on the surface of an enamel or dentin cavity which is relatively free of bacteria but at some distance from the odontoblast.
2.3.4 Arrested Caries in Dentin
Arrested caries in dentin is clinically defined by hardness of the dentin surface and a yellow to dark brown color. Arrested carious lesions are found most commonly on lingual and labial aspects of teeth and less commonly in caries which has become arrested, the dentinal tubules in the area between the soft and hard dentin have been shown to be obstructed by large crystals. It has been suggested that this process appears to occur in a number of stages5 (▶ Fig. 2.18).
Fig. 2.18 A