by cementum, which continues to form throughout life. It may not be obvious exactly where the apex is when examining a periapical radiograph because of this cementum, and accessory canals may not be visible (▶ Fig. 2.15).
Fig. 2.14 The partially formed root of an unerupted third molar. The root apices do not close until the roots are fully formed.
Fig. 2.15 An SEM image of the apex of a fully formed root shows a number of accessory canals. (Magnification × 100). The main apical foramen is not quite at the apex of the tooth but emerges to one side of it. In this example, it is on the left, slightly hidden by an overhang of cementum.
Key Notes
Cavity preparation opens thousands of dentinal tubules. As the preparation approaches the dental pulp, the tubules become wider and the fluid flow in response to mechanical, thermal, or chemical irritation increases. Conservative cavity preparations reduce pulpal irritation and postoperative pain.
2.3 Response of the Pulp–Dentin to Caries
The unhindered progress of caries with irreversible damage to the pulp–dentin and periodontium, which has been outlined above, is relatively unusual except in rapidly progressing carious lesions. More commonly, the caries process is gradual, and the pulp–dentin has time to mount some defense. While caries of 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
