Caries Management - Science and Clinical Practice. Группа авторов

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СКАЧАТЬ 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 sclerosis has begun, the odontoblasts start building a layer of reactive dentin, also referred to as reparative or tertiary dentin (Fig. 3.15; see also an advanced lesion in Fig. 3.17a). Since odontoblastic processes and nerve fibers extend well into the dentinal tubules, it is conceivable that the advent of toxins into dentin tubules already triggers the synthesis of reactive dentin by the odontoblasts. Reactive dentin can be found when the caries process reaches deeper into dentin, but it is absent in some cases (Fig. 3.16). When the caries process develops slowly over a long time, reactive dentin has a more regular structure with dentinal tubuli, which may be very similar to normal primary or secondary dentin. Under highly cariogenic conditions—that is, rapidly evolving caries which imposes a strong stimulus on the pulp, particularly on the odonto-blasts—the expression of reactive dentin is accelerated and its structure may be poorly organized (dysplastic) with lack of dentinal tubules, and is called osteodentin or fibrodentin. Mature tertiary dentin consists of type I collagen, as normal dentin does, while its predentin also comprises type III collagen.⁴¹ In the earlier state of dentin affected by the caries process, a layer of normal, unaffected dentin remains below the reactive dentin.

       NOTE

      Dentin reacts to caries before the demineralization process reaches the enamel–dentin junction (EDJ) and long before the enamel surface breaks down. The first sign of dentin reaction is tubular sclerosis. At this stage no bacteria can be found in the dentin and, as long as the enamel surface is macroscopically intact, hardly any bacteria penetrate the enamel owing to the small size of the enamel porosities at the surface.

      Further on, in the direction of the EDJ, a layer of sclerotic dentin (earlier referred to as the translucent zone) is visible in thin sections using transmitted light microscopy. It is broadest (in the centripetal direction) close to the underlying layer of normal, unaffected dentin, but has “wings” extending almost parallel to the dentinal tubules toward the EDJ. This zone appears bright in transmitted light microscopy, but dark in reflected light microscopy, because the dentin is more translucent due to a better match of the refractive indices of the sclerotic tubules and intertubular dentin. Sclerotic dentin shows occluded tubules with a thick peritubular layer, and a calcified tubular lumen that contains predominantly highly organized apatite crystals and, to a lesser degree, crystals of the Whit-lockite type.⁴² Keep in mind that these properties are true for a state of caries development where the enamel surface is porous, but still intact, and the dentin itself is hardly demineralized. The properties and shape of the sclerotic zone change with the progression of demineralization.

      The next zone toward the outside of the tooth appears relatively dark in transmitted light microscopy. Formation of this zone, referred to as “dead tracts,” is a consequence of tubular occlusion in the underlying zone consisting of sclerotic dentin. The dead-tract zone is ideally completely enclosed within the sclerotic zone (Fig. 3.15). Due to tubular occlusion within the sclerotic zone and retraction of the odontoblastic cellular processes, the dentinal tubules in the dead-tract zone appear empty and cut off from the living odontoblast; that is why it is commonly termed “dead tract.” This term comes from experiments in which a dye was placed in the pulp chambers of extracted teeth with dentinal caries and its penetration back into dentin was observed in sections using transmitted light microscopy.⁴³ It was observed that the dye penetrated into the dentinal tubules of healthy dentin. In areas at the border of carious lesions, dye penetration came to a halt at the sclerotic dentin and could not penetrate further. Dead-tract dentinal tubules easily fill with air in thin sections. They may contain remnants of the odontoblastic processes and are typically more permeable for incoming acids and proteolytic enzymes than tubules within healthy dentin. Therefore, this zone is less resistant toward further progression of the caries process. At later stages of the caries process involving enamel cavity formation, bacteria are well able to penetrate the dentinal tubules within the dead-tract zone.

      Between the dead tracts and the EDJ the so-called demineralized zone can be found, usually when carious enamel demineralization reaches the EDJ. It is caused by the penetration of organic acids of bacterial origin into the dentin. Although this zone is considerably demineralized, it appears rather similar to healthy dentin in transmitted and reflected light microscopy. The zone of demineralization contains less mineral (approximately down to 25% and less) and has lower hardness (approximately down to as low as 10KHN and less) than the sclerotic dentin. As long as the enamel has not collapsed, it is unlikely that bacteria penetrate the underlying dentin. This means that the cariogenic acids, enzymes, and toxins of bacterial origin are synthesized in the dental plaque covering the enamel surface and, consequently, travel deep into the dentin by diffusion as long as the enamel surface has not broken down.

       NOTE

      With the enamel surface still intact, the caries process reaches the EDJ. With further caries development the following zones can be seen using transmitted light microscopy (from the enamel–dentin junction toward the pulp):

      • Zone of demineralization

      • Dead tracts

      • Sclerotic zone

      • Normal, but affected dentin

      • Tertiary dentin

      Continuing Caries Progression into Dentin

      Collapse of the (pseudo-) intact enamel surface means a significant change in caries progression and prognosis. As long as the enamel surface is macroscopically intact, penetration of dental plaque, bacteria, or their components is very much limited. Collapse of the intact enamel surface not only means that the enamel porosities have become so big that they no longer support mechanical stability, it also means that huge numbers of bacteria are able to penetrate the enamel lesion. Consequently, removal of bacteria and dental plaque from the porosities and the enamel crater by mechanical means is not possible any more for most occlusal and interproximal lesions. From this point on, depending on the available nutritional conditions, further lesion development is most likely to occur. With invasion of huge numbers of bacteria into the porous enamel, bacteria soon reach the EDJ and invade the dentin, forming the zone of penetration, which takes over the former zone of demineralization. Still at this point, the zone of demineralization precedes the bacterial invasion. This is of some clinical relevance, because it means that demineralized dentin does not necessarily contain bacteria and may be left during excavation (Chapter 18). Also, irreversible pulpal inflammation is typically seen only at later stages, with the bacteria advancing as close to the pulp as around 0.5mm.⁴⁴

      With penetration of bacteria deeper into the demineralized zone, the demineralized zone itself moves toward the zone of sclerotic dentin at the expense of the dead-tract zone (Fig. СКАЧАТЬ