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href="#ulink_29344990-dc38-52a2-8372-94e999cf6e86">7]), and the discussion still goes on [8]. As a matter of fact, S. mutans is detected in a few cariesfree and found absent in several caries-active individuals, impairing its outstanding caries indicatory potential. Furthermore, most relevant acidogenic-aciduric bacterial species are: (i) S. mutans relatives (called mutans streptococci or MS) with a similar virulence potential, namely S. sobrinus; (ii) bifidobacteria, including Bifidobacterium dentium and other closely related oral Bifidobacterium spp., but also the more distantly related species Scardovia wiggsiae, and (iii) lactobacilli, especially those with pellicle-adhesive potential [9].

A number of epidemiological and in vitro studies suggested that S. sobrinus – under circumstances yet to be determined – may be even more cariogenic than S. mutans [8–11]. In addition, targeted clinical studies have suggested that preschool and 15-year-old school children harbouring both S. mutans and S. sobrinus had a higher incidence of dental caries than those with S. mutans alone (for a review see Conrads et al. [10]).

      Unlike MS, the highly aciduric bifidobacteria, especially B. dentium, do not colonise hard surfaces per se, since denture plaque associated with denture stomatitis harboured high levels of MS, lactobacilli, and yeasts, but not B. dentium. This indicates that B. dentium does not simply colonise intact dental hard surfaces but instead suggests that it is the lesion initiated by other species that facilitate the attachment and proliferation of B. dentium. In contrast to MS, the presence of this species might therefore be more a result than the cause of initial lesions. Clearly, B. dentium and MS are significant independent indicators [9].

      A similar role (more profiteer than initiator) was recently proposed for lactobacilli, with Lactobacillus fermentum, L. rhamnosus, L. gasseri, L. salivarius, L. plantarum, and the L. casei-paracasei group as the most abundant species. According to this concept, precaries lesions become a retentive, low pH niche for lactobacilli accumulation, which take advantage of their proclivity for making and surviving in an increasingly reduced pH environment. In some cases, the lactobacilli can even outcompete and exclude the MS that created the retentive niche, which might explain why caries lesions are sometimes free of MS but not or very rarely free of lactobacilli [9].

Other less investigated but interesting cariesindicator candidates are Atopobium spp., Slackia exigua and a few others [11, 12]. The entire network of microbial organisms involved, which are not only bacteria but also saccharolytic yeasts (e.g., Candida albicans), Archaea (enhancer of fermentation processes by consuming end products such as CO₂ and H₂), or bacteriophages (enhancer of lateral gene transfer and thus of evolution), is extremely complex and diverse.

      Taken together, every cavity might have its own demineralising consortium of active organisms and genes, but the following simple principles are universal:

      1 Presence of acidogenic-aciduric microorganisms and their ability to attach to the pellicle-coated tooth surface, either directly (pioneers such as MS) or indirectly (beneficiaries such as bifidobacteria and lactobacilli; for a review see Conrads et al. [10]).

      2 Environmental conditions favouring the multiplication and metabolism of such species: access to low-molecular sugars, especially sucrose, and low redox potential at the same time. High sugar and low oxygen leads to rapid fermentation and acid production.

      With these simple principles, it is possible to identify (constitute) what a carious tissue actually is and how much tissue must or should be removed or excavated to stop further decay.

      Histology of a Carious Tissue – The Microbiological Perspective

The degree of success in eliminating bacteria during cavity preparation and prior to the insertion of a restoration may increase the longevity of the restoration and therefore the success of the restorative procedure. The complete eradication of bacteria in a caries-affected tooth during cavity preparation is considered a difficult clinical task and – from the perspective of a microbiologist – almost impossible, and also not required anymore, as is discussed in the chapter by Bjørndal [this vol., pp. 68–81]. Attempts to excavate completely extensive carious tissue may affect the vitality of the pulp and weaken the tooth structure. In principal, disinfection of the cavity preparation after caries excavation can aid in the elimination of bacterial remnants, reducing the risk for recurrent caries and failure of the restoration. However, the side effects of chemical disinfectants (e.g., chlorhexidine or benzalkonium chloride) on the restorative treatment, including reduced dentine bond strength, have been a major concern for both dental clinicians and researchers [13], and therefore alternatives still have to be found and their efficacy proven.

As shown in Figure 1, the carious tissue consists of 4 different zones, but only 3 clinically noticeable layers. The outer layer, clinically the soft dentine, consists of the necrotic zone with the microbial biofilm attached, and the contaminated zone. The soft dentine is characterised by a gradient of microorganisms with cell-numbers between 10¹ and 10⁸ per mg (measured from the inside to outside, pulpal to coronal), including aciduric, facultative anaerobic bacteria. Comparing the conditions here with the principles mentioned above, this necrotic and/or contaminated zone fulfils all criteria for disease (demineralisation) progression as it is anaerobic (low redox potential demanding a fast substrate turnover for sufficient energy resourcing) and, at least temporarily, fed by high concentrations of fermentable dietary carbohydrates. This layer has to be removed.

Fig. 1. Histology of carious tissue. Note the correlations between cross-section, ultrastructure zones, and clinical (tactile) manifestations. modified from Innes et al. [14] and Ogawa et al. [15]. Reprinted by Permission of SAGE Publications, Inc.

The next layer is the demineralised zone, which correlates clinically with leathery dentine. This zone is characterised by few microorganisms per milligram, very little nutrients (since already consumed by the bacteria and yeasts in the outer layer), and a strictly anaerobic atmosphere. While the latter condition favours demineralisation by acid production, the sheer low number of fermenting bacteria and the very low nutritional source prohibits substantial multiplication and metabolism. It is the consensus that for deep lesions, extending beyond the inner (pulpal) third or quarter of dentine radiographically, selective removal (incomplete excavation to protect the pulp) should be limited to soft dentine, excluding the removal of contaminated leathery dentine [14]. From the microbiological point of view, this approach is tolerable as electron transport within, and acid production by, the few cells is also very low in this zone. However, bacteria have several strategies to overcome harsh conditions and – after preparation, disinfection if applicable, infiltration if applicable, and restoring – might still be alive although in a dormant state [16, 17]. This means the lesion and the bacteria are arrested, but only temporarily. If there is gap formation at the tooth-restoration

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