Caries Management - Science and Clinical Practice. Группа авторов

the prism core can be observed.

      • Enamel crystals dissolve either from the outside, getting shorter and smaller in diameter over time, or along the crystal c-axis, leading to hollow tubelike crystals.

      Dentin Caries

      Whether the caries process that started at the enamel surface will progress into deeper layers depends on the microenvironment at the enamel surface. Under cariogenic conditions the caries process continues and reaches the EDJ and the underlying dentin. As long as the caries is limited to enamel, the carious area located at smooth surfaces and interproximal areas is bigger at the outer enamel and decreases in size toward the EDJ (see Fig. 3.8).

      As soon as the EDJ is reached, the caries may spread along the EDJ to a certain extent and from there into the dentin (Figs. 3.13, 3.15, 3.16). The EDJ is known to have higher organic and lower mineral content than enamel and dentin.^31–33 Hence, its higher content of water and organic material may enable lateral spreading of cariogenic acids and assist demineralization of the EDJ area. The same may apply for the proteolytic action of certain bacterial enzymes (see later for more detail). However, the caries process does not extend evenly into underlying dentin from affected areas of the EDJ. The most prominent changes in dentin occur in the center where carious enamel reaches the EDJ. The width of the cariously affected dentin decreases from the EDJ toward the pulp during the advancement of the caries process. The spread of the caries process within dentin follows the direction of the dentinal tubules.

      However, lateral spreading of disease along the EDJ is observed more often at a more advanced stage of the caries process with breakdown of the enamel surface rather than with the latter still intact. The reason for this is not fully understood, and some authors have shown results indicating that the mineral content of the EDJ decreases continuously from enamel to dentin,^34,35 which casts doubt on the theory that the EDJ is more vulnerable to acids than the dentin.

      It is important to realize that there is a fundamental difference in reaction mechanisms between enamel and dentin. Enamel is a cell-free tissue which does not show any cellular response in the case of caries attack; enamel reaction is based on chemical dissolution and precipitation phenomena. Dentin is different, because it has to be considered as vital tissue, since it contains living cellular processes from the odontoblasts lining the pulpo-dentinal wall.^36,37 In dentin, the odontoblasts and the pulp are closely related to one another. Dentin shows reactions that are due to cellular mechanisms of the odontoblasts and therefore it is well justified to consider dentin and the pulp as a physiological unit (Chapter 1). The dentin–pulp unit is an organ in itself, consisting also of blood and lymphatic vessels, connective tissue, nerve tissue, stem cells, etc. This allows the dentin–pulp unit to react to stimuli, albeit physiological masticatory forces, traumatic injury (thermal, mechanical or chemical), or caries.^38,39 In that sense, the dentin–pulp unit can be compared with bone, whose inorganic fraction is modulated by osteocytes and osteoblasts, which also react to physiological or pathological stimuli.⁴⁰

      Fig. 3.15a–c Schematic illustration of caries into dentin with the enamel surface intact (a), enamel surface cavitated (b) and enamel completely broken in (c).

      a Appearance of dentin caries with an intact enamel surface layer (SL). Demineralized enamel (DE) has reached the enamel–dentin junction. Within dentin, the affected area has a broad base at the enamel–dentin junction, where the zone of demineralization (ZD) is often enclosed from the side by the sclerotic zone (SZ) that converges to a clearly visible zone deeper toward the pulp. Between the zone of demineralization and the sclerotic zone, a zone with “dead tracts” (DT) can be observed. Between the sclerotic zone and the pulp, dentin is hardly distinguishable from “normal” dentin, but it can be considered as affected dentin (AD), because the otherwise reactive or tertiary dentin (TD) would not be formed by the odontoblasts during the carious attack. Note that with the enamel surface intact, single bacteria may penetrate the porosities in enamel, but cannot be found within dentin.

      b With cavitated enamel (CE), bacteria (red dots) soon reach dentin and penetrate the dentinal tubules, referred to as the zone of bacterial penetration (ZP). As long as the bacteria are confined to the outer dentin, the characteristic zones within dentin persist: zone of demineralization (ZD), dead tracts (DT), sclerotic zone (SZ), “normal,” but affected dentin (AD), and tertiary dentin (TD). During the process of bacterial penetration, the zones spread toward the pulp, the dead tracts disappear, and the sclerotic zone becomes thinner.

      c In a widely cavitated caries lesion the enamel layer has partly gone (cavitated enamel, CE) and dentin is readily exposed to plaque accumulation (not shown). The superficial dentin layer, the zone of necrosis (NE), is heavily loaded with bacteria (red dots), is soft, and does not show the tubular structure of dentin any more. Underneath is the zone of bacterial penetration (ZP) that extends more and more toward the pulp. The demineralized zone advances in front of the zone of bacterial penetration at the expense of the sclerotic zone and the “normal” but affected dentin, but is overrun by bacterial penetration with time. Within the zone of bacterial penetration the dentin tubules are heavily loaded with bacteria. During the caries process the zone of bacterial penetration also widens laterally, shifting the sclerotic zone (SZ) sideways. The tertiary dentin (TD) is still present but is also penetrated by bacteria with time.

      Fig. 3.16a, b Histological mesiodistal section through the crown of a premolar tooth with an interproximal dentin lesion with light (left side of tooth section) and heavy enamel breakdown (right side of tooth section).

      a Transmitted light microscopic view. Within dentin the zone of demineralization (ZD, red-brown), the dead tracts (DT, dark), the sclerotic zone (SZ, bright), and “normal,” affected dentin (AD) can be seen in both lesions. The zone of bacterial penetration (ZP) is confined to the dark red-brown discolored area of the lesion on the right side, but its borders cannot be identified exactly. Tertiary dentin is hardly visible in this section.

      b Reflected light microscopic view of the same section as in (a). Other than in transmitted light, the dead tracts appear bright and the sclerotic zone is hardly visible.

      The histology of caries, as it extends into the dentin, reveals a sequence of different zones. While the order of these zones is always the same, the presence or absence of individual zones relates to the progress of the caries as it proceeds toward the pulp (Fig. 3.15).

      Early Signs of Dentin Reaction

      With continuing demineralization of the enamel layer and increasing enamel porosity, acids and toxins of bacterial origin are able to reach and penetrate the underlying dentin. This may be the case well before breakdown of the enamel surface integrity. At this stage, the bacteria are still organized within the plaque covering the enamel surface and do not penetrate the enamel or dentin just yet or only in small numbers.

      A first sign of dentin reaction is tubular sclerosis (see next paragraph). To avoid confusion, we start by looking at the changes within dentin from the pulpal side toward the EDJ. Usually, after the process of tubular