Читать книгу Caries Excavation: Evolution of Treating Cavitated Carious Lesions - Группа авторов - Страница 14

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 interface, possibly further supported by the microleakage of fluids and salivary proteins to the gap, this leads to inevitable microbial colonisation from saliva, but also to the possible regrowth of dormant cells and, ultimately, secondary caries formation. Therefore, for less deep lesions, selective removal should take place down to firm dentine, which not only has clinical advantages (more depth for a solid restoration), but also lowers the risk of regrowth of surviving microbial cells.

Finally, pulpally the translucent zone of firm softer dentine is characterised by demineralisation since acids, but not the bacterial cells, penetrate to this depth. Here, the plate-form apatite crystals apparently dissolve and recrystallise into a rhomboid form, defined as whitlockite [Ca₉(MgFe)(PO₄)₆PO₃OH]. This crystalline form seems to be softer and less resistant to cutting and acids [15]. This layer might not be absolutely sterile, but metabolism of aciduric microorganisms is almost impossible and thus negligible. For repelling and combatting the microbial attack and repairing damages, the host has developed several ingenious strategies.

Fig. 2. a Histology of sound dentine in a premolar. b Dentine tubules are numerous and wide open on the pulp side. c They are less numerous and appear more narrow at mid-distance between the pulp and the dentine-enamel junction. d Dentine tubules are very narrow and many of them appear completely obliterated upon approaching the dentine-enamel junction.