b Detail from the same tooth. Transversal clefts filled with bacteria have formed perpendicular to the dentinal tubules, most likely along incremental dentin growth lines.
Fig. 3.19 Cross-sectional microhardness (Knoop) profiles from sound and carious dentin. Sound dentin reaches its hardness maximum a few hundred micrometers from the enamel–dentin junction and shows decreasing hardness from there on, toward the pulp. Carious dentin is very soft to start with at the bottom of the cavity. From there on, hardness increases and may reach hardness values at or above those of sound dentin—if a sound dentin layer is still present under the carious dentin lesion. Further toward the pulp within sound dentin, the hardness values decrease again (redrawn after Fusayama et al.49).
Fig. 3.20 Comparison of nanohardness values (Berkovich, right y-axis) with mineral content (TMR, left y-axis) of an artificially created enamel caries lesion. Both methods show some similarity in the shape of the profiles. The intact surface layer can be seen with both methods, as well as the body of the lesion. Mineral content of 50vol% or less causes severe tissue softening, with nanohardness values below 5GPa. Mineral content increases faster toward the end of the lesion. In this case, the end of the lesion concerning mineral content can be found at ca. 110μm where nanohardness has not yet reached “sound” values. The scattering of the measured values is bigger for nanohardness than for mineral content, which is partly attributed to the small probing diameter of the Berkovich indenter.
NOTE
Within carious enamel, hardness and mineral content show some correlation, but not to an extent that allows calculation of exact values for one method from the other. Within carious dentin, hardness increases from demineralized dentin, which is soft, toward sclerotic dentin, which in some parts is a little harder than sound dentin. Between the sclerotic zone and the pulp, hardness decreases again, in a similar way as if no caries were present.
Fluorescence Properties of Carious and Healthy Dental Hard Tissue
Although fluorescence of human and animal tissue was discovered many years ago,52 the use of native autofluorescence of teeth for diagnostic purposes53–57 and caries therapy58 became valued only recently. Figure 3.21 shows a fluorescence image of a slice (100μm) prepared through differently developed carious areas of two teeth. When excited with violet light, healthy enamel and dentin fluoresce yellow-green, but dentin yellow-green autofluorescence is markedly brighter. The noncavitated interproximal caries (Fig. 3.21a) shows a demineralized zone within enamel that does not reach the EDJ. Nevertheless, within the underlying dentin a “darker zone” extends two-thirds of the way toward the pulp, which is identical to the zone of sclerotic dentin found in transmitted light microscopy.59 On the other hand, red autofluorescence is emitted from bacterially infected enamel of the interproximal lesion. Note that the infected, red fluorescing zone is limited to enamel, while the underlying dentin already shows signs of reaction due to diffusion of acids and other metabolites. The occlusal lesion present in this tooth slice shows bacterial activity (red autofluorescence) at the bottom of the fissure, but has not penetrated the dentin. However, the dark-appearing sclerotic dentin zone surrounds a bright yellow-green fluorescing zone. This is the demineralized zone, which is brighter due to dequenching of yellow-green fluorophores.60 A fluorescence image of a slice through a more advanced occlusal lesion with enamel breakdown (Fig. 3.21b) shows penetration of bacteria into the dentin (red autofluorescence), a zone of demineralization (bright yellow-green zone), and a less fluorescent zone (darker appearance) of sclerotic dentin.
The cause of the red autofluorescence is porphyrin compounds which are produced by bacteria.61 These porphyrins, mainly coproporphyrin and protoporphyrin IX,62 are immobilized within the dental hard tissue and constitute an excellent marker for areas with heavy bacterial infection. Single bacteria scattered within dentinal tubules do not produce sufficient amounts of porphyrin compounds. Therefore, it has been suggested to use the contrast between red-fluorescing, heavily infected dentin and yellow-green fluorescing, healthy dentin as a means for caries detection during caries excavation58,63
Fig. 3.21a, b Fluorescence images from tooth sections using an excitation wavelength of 405nm viewed though a 530-nm high-pass filter. Generally, healthy dentin fluoresces more strongly than does enamel. Sound enamel and sound dentin fluoresce green. Bacterially contaminated areas fluoresce red due to the presence of bacterially synthesized porphyrin compounds. The cracks through enamel and dentin are artifacts due to the preparation procedure.
a Oral and occlusal carious lesion with macroscopically intact enamel of a bucco-oral cut through a lower molar tooth. The less developed oral lesion shows a bright green fluorescence of the demineralized enamel, and red fluorescence (RF) in the outer demineralized enamel which is contaminated with bacteria. Although the bacteria and enamel demineralization has not reached the inner third of the enamel layer, within the underlying dentin an area fluorescing less than sound dentin can be traced, stretching toward the pulp. This area is identical with the sclerotic zone (SZ). The increased mineral depositions within the dentinal tubules cause a quenching of the fluorophores, which are most likely organic in nature. The occlusal fissure lesion shows bacterial activity (red fluorescence, RF) in the fissure just starting to penetrate the dentin. The sclerotic zone (SZ) appears less fluorescent (dark) around the demineralized zone (ZD) which fluoresces brighter green than sound dentin. The bright green fluorescence of demineralized dentin is caused by dequenching of the green fluorophores.
b Within the dentin, two thin fluorescent horizontal lines are present, which may resemble two less mineralized incremental lines (IL), although tetracycline intake during the respective growth phase cannot be fully excluded as being the cause. From the occlusal plane two differently severely cavitated lesions have caused histological changes within the dentin. The bigger lesion (left hand side) shows bacterial penetration (BP; red fluorescence, RF) mainly into the enamel and just beginning into the dentin. Within the dentin the brightly green fluorescing zone of demineralization (ZD) and the underlying less fluorescing sclerotic zone (SZ) can be identified. The smaller cavitated lesion on the right hand side shows a narrow zone of demineralization (ZD) all the way through the pulp.
NOTE
Carious enamel and dentin exhibit a strong red autofluorescence which is different from the green autofluorescence emitted from healthy teeth when excited with violet light. This can be differentiated with the naked eye.
Caries of the Exposed Root
Caries of the exposed root has shown increased prevalence over the past few years, particularly among the elderly.64 Development of root caries relies on the exposure of root areas, mostly due to gingival recession, and the accumulation of plaque (Fig. 3.22). With regard to plaque accumulation, the development of root caries is not so much different from caries development at other sites, e.g., interproximal, occlusal, and smooth surfaces. The cementum layer may cover the outer surface of the exposed root. This layer can be removed with