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.
Table 3.1 Correlation between histological, radiographical, and clinical appearance of developing caries. For radiography and clinical appearance ideal conditions are assumed (approximal caries for radiography but directly accessible to the naked eye regarding its clinical appearance)
| Histology | Radiography | Clinical appearance |
| – | – | Sound |
| Surface etching | – | – |
| Shallow (approx. <100µm) enamel subsurface lesion with intact surface layer | – | White (brown) spot, visible only under dry conditions |
| Enamel subsurface lesion extending halfway to the EDJ with intact surface layer | Hardly visible, maybe slightly in outer enamel | White (brown) spot, visible only under dry conditions (no cavitation) |
| Caries lesion extending to the EDJ with enamel surface still intact. Dentin reactions comprising development of different zones and tertiary dentin | Translucency in enamel | White (brown) spot, visible under dry conditions, but often also visible under wet conditions (no cavitation) |
| Dentin reactions comprising different zones and build-up of tertiary dentin. Within localized areas of enamel breakdown, bacteria penetrating the enamel can be found | Translucency in outer third of dentin |
White (brown) spot, visible under dry and wet conditions.
|