Caries Management - Science and Clinical Practice. Группа авторов

or dental therapeutic removal of tartar, polishing, or periodontal treatment (scaling and root planing). It is known that dentin is more vulnerable to demineralization than enamel, and the same applies to the cementum layer (see Chapter 2). In most cases root caries spreads across the cementum or dentin surface to a certain extent, while initially its depth is limited. The dentin of the root has fewer dentinal tubules than coronal dentin and it is already in a “mature” state when root caries develops, due to a history of external stimuli following root exposure, or simply age, with a high degree of sclerosis.⁶⁵ It has been observed that bacteria are already able to penetrate the cementum layer in an early state of root caries development, while bacteria penetrate into the underlying dentin at a later state of lesion development. A well-mineralized surface zone forms at the surface of the cementum or dentin (when cementum is absent). The body of the lesion underneath this mineral-rich surface zone is heavily demineralized with about 50% or less of the natural mineral content of sound dentin⁶⁶ (see Fig. 3.23). The histological layering within root dentin is similar to coronal dentin. However, a cross-section through a root caries lesion shows that root caries lesions are rather shallow, and saucer-shaped in most cases.

      Fig. 3.22a, b Cervical caries lesions of different activity from two different patients.

      a Active root caries in a lower molar of an elderly patient. The cavitated caries lesion is partly filled with plaque. The gingiva is inflamed in the area of the lesion and reaches into the cavity.

      b Arrested root caries lesion in a lower molar of a middle-aged patient. The lesion was arrested following a change in toothbrushing habits. The surface is shiny and hard and acquired a pattern of toothbrushing abrasion. The discoloration of arrested root caries lesions tends to get darker with time.

      Fig. 3.23a, b Microradiography of a carious cervical lesion of a lower molar cut just above the cemento-enamel junction.

      a Due to the severe carious circumstances the enamel layer in the area of the caries lesion has been lost. The exposed dentin shows a remineralized layer at the surface.

      b Microradiogram showing the mineral content of the cervical caries lesion along the dashed arrow in (a). The high mineral content of the mineralized zone at the surface, the low mineral content at the center of the caries lesion, and a continuous increase in mineral content toward the end of the lesion can be seen. Also, in the sound part of the microradiogram, a decrease in mineral content toward the pulp is visible.

       NOTE

      For development of root caries the same principles apply as for coronal caries, but there are a few points that facilitate the development of caries within cementum and dentin at the cemento-enamel margin. Two major factors contribute to root caries: the exposure of the cervical region in conjunction with the fact that cementum and dentin are more vulnerable to demineralization than enamel; and patient age, which is associated not only with root exposure, but also with lower salivary flow and reduced tooth-cleaning capabilities.

      Caries Arrest and Remineralization

      The caries process is driven by carbohydrate-consuming, acid-producing bacteria, organized in a biofilm, that is, the dental plaque (Chapters 1 and 2). The caries process will continue as long as the microenvironment at the tooth surface does not change its cariogenicity. In other words, caries arrest is possible only when the surface conditions change, owing to sufficient plaque removal. If a patient is able to significantly improve the microenvironment at the tooth surface of a formerly progressing caries lesion, there is a good chance that the caries process may be halted. As soon as the improvements to the microenvironment wear off, the caries process most likely will continue.

      Daily dental practice provides many examples of caries arrest. A prime example is the band-shaped enamel white spot lesion at the buccal side of molars and other teeth that developed during tooth eruption along the gingival margin due to lack of plaque removal in this area. Quite often, with further eruption of these teeth, lesion progression stops. What remains is a “scar,” a shiny band-shaped white spot parallel to, but clearly above, the gingival margin (see Fig. 3.7).

      Another example is cervical caries lesions in dentin or cementum, which do not necessarily need operative treatment and filling therapy. In an active state these lesions are covered by plaque. Following plaque removal, in most cases a (light-) brownish, soft (“leathery”) surface appears. As to the degree of discoloration, a wide range of brownish hues is possible. If the patient is able to avoid plaque accumulation by daily cleaning of the respective area, such lesions will arrest (Fig. 3.22); the surface becomes harder and, in most cases, the lesion becomes darker in color. This process usually takes months.

      It is widely accepted that primary caries lesions, as soon as the overlying plaque is removed, do not progress further. The situation is not that simple in case of secondary caries (caries adjacent to restorations). In some cases of secondary caries there is a gap between the restoration and the enamel or dentin wall. Most likely, this gap is filled with plaque, but daily removal of dental plaque from this gap is not practically possible. To avoid complete removal of the restoration, sealing of this gap is an option (Chapter 19). By sealing the marginal gap, progression of a secondary caries lesion can be avoided and the lesion becomes arrested.

      So far we have seen that lesion arrest is possible under clinical conditions. However, beyond lesion arrest, complete lesion remineralization would be desirable. Complete remineralization seems possible only for very shallow (a few micrometers deep only), artificially created, carious enamel lesions. Natural caries lesions limited to enamel show mineral accumulation in the outer layers, but deeper areas of the lesion seem not to remineralize properly. The reasons for this are not exactly known, but the presence of incorporated protein within the lesion as well as reduced diffusion due to blocked diffusion channels within the remineralized surface layer may play a role. Under the respective clinical conditions (e.g., regular plaque removal, provision of fluoride) the surface zone (pseudo intact surface layer) that is less mineralized than sound enamel, but more mineralized than the body of the lesion, gains mineral and widens (Fig. 3.24). Under ideal circumstances it can contain almost as much mineral as sound enamel. The body of the lesion may accumulate mineral but always stays less mineralized than sound enamel. Particularly under the influence of fluoride, a layering (intermittent zones of more-mineralized enamel) within the body of the lesion forms. In in-vitro experiments using artificially created carieslike enamel lesions, the lesions gained mineral, but the depth of the lesion increased further, albeit to a small extent.

      Caries lesions extending into dentin with macroscopically intact enamel have a chance to remineralize, limited to the enamel as described above. In those lesions it is highly unlikely that the dentin will undergo significant remineralization. However, caries lesions very deep into dentin show a tendency toward remineralization if they are cut off from caries attack from outside of the tooth. This can be seen during a stepwise excavation procedure, where bulk caries is removed, but close to the pulp carious, soft dentin is left behind to avoid pulp exposure.