Caries Management - Science and Clinical Practice. Группа авторов

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СКАЧАТЬ 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. Upon re-entry after typically 6 or 12 months following temporary restoration with a sub-base of Ca(OH)₂, clinically it can be observed that the former soft dentin close to the pulp becomes harder due to remineralization in most cases. To date there is no clear proof where the minerals come from, but most likely both the calcium reservoir from Ca(OH)₂ and pulpal tubular fluid (calcium and phosphate) are involved.

      Cervical caries lesions with dentin (or cementum) at the surface show a significant potential for remineralization. However, remineralization of dentin is mostly attributed to mineral deposition in the dentinal tubules. In-vitro experiments of remineralization of dentin with artificially created carieslike lesions showed hypermineralization (Fig. 3.25). In this case the mineral content of the remineralized dentin at the dentin surface showed a higher mineral content than sound dentin. The body of the lesion within the dentin, however, remained hypomineralized.

      Fig. 3.24a–c TMR from artificial enamel caries following demineralization and remineralization.

      a Microradiograph (detail of a TMR x-ray exposure) of a surface-perpendicular cut through an artificial early enamel caries lesion directly after the demineralization regimen. Surface layer (SL) and lesion body (BL) are clearly visible.

      b Microradiograph of the same specimen as in (a), but after 14 days remineralization in situ. The lesion body is less pronounced than in (a), indicating remineralization.

      c Microradiogram of the microradiographs of (a) and (b) shows a mineral uptake throughout the entire lesion body of this shallow carious lesion of the enamel.

      In addition to successful plaque removal, presence of fluoride facilitates remineralization of caries lesions by shifting the chemical balance from net-demineralization to net-remineralization.

       NOTE

      Caries arrest can be observed clinically quite often. To turn the caries process round from net-demineralization to net-remineralization the local conditions at the tooth surface must change. Specifically, the overlying biofilm needs to be completely removed or at least significantly reduced. Arrestment influences in particular the surface zone and the dark zone in enamel caries lesions. Even deep parts of dentin caries can remineralize when the overlying caries process is interrupted, a mechanism that is used during stepwise excavation.

      Correlation of Histology with Radiography and Clinical Appearance of Caries

      The correlation between histology, and clinical and radiographic appearance of caries much depends on the circumstances. These include the development of the actual caries lesion, lesion site, and how well radiography and clinical observation can be performed. However, there is some correlation between histology, clinical appearance and radiography.⁶⁷ In Table 3.1 the typical correlation between histology, clinical radiography, and clinical appearance is provided, but it is important to recognize that some variation is possible.

      Fig. 3.25a–d TMR from artificial dentin caries following remineralization with intermittent fluoride exposure.

      a Microradiograph (detail of a TMR x-ray exposure) from a former 60μm deep dentin lesion after 1day of remineralization with three exposures by a 1500ppm fluoride solution for 5min every 8h. Within the lesion body two distinct layers of mineral accumulation can be seen (arrows).

      b Microradiogram of the microradiograph in (a) shows the same two mineral-rich layers (black arrows) with almost the mineral content of sound dentin (50vol%).

      c Microradiograph (detail of a TMR x-ray exposure) from a former 60μm deep dentin lesion after 5days of remineralization with exposure to 1500ppm fluoride solution for 5min every 8h (experiment from 3.24a continued). Within the lesion body a wide hypermineralized layer has formed that is delineated toward sound dentin by a demineralized layer (black arrow). Note that the lesion (demineralized layer) has shifted deeper into the dentin.

      d Microradiogram of the microradiograph in (a) shows the same wide hypermineralized layer and the demineralized layer that has travelled deeper into the dentin.

      Erosion—a Noncarious Defect

      Noncarious defects, if not caused by direct traumatic injury, are due either to wear (attrition, abrasion, abfraction, and erosion) or defects that were established during tooth development (molar-incisor-hypomineralization, trauma, fluorosis). In particular, erosive defects have come under scrutiny in the last decade.

      The etiology of dental erosion is different from caries (Chapter 2), and so is the histology. Erosion, however, is not caused by bacteria, but by the direct dissolution of enamel and dentin due to acids.⁶⁸ Those acids may originate from the nutrition (acidic food and drinks) or stomach (by reflux or vomiting). In some cases, environmental reasons (e.g., poorly maintained swimming pools or frequent exposure to acidic vapors in industry) or individual habits may account for dental erosion. Under erosive conditions calcium and phosphate dissolved from enamel or dentin are immediately detached from the enamel or dentin surface and not “parked” in a reservoir like dental plaque for some time, and for this reason they become immediately and irreversibly lost.

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