damage, the host has developed several ingenious strategies. A major resistance to carious lesion progression is mounted by the dentine-pulp tissues. The signalling molecules and growth factors released upon dentine demineralisation upregulate the odontoblast activity and act as sensor cells. After carious stimulation, odontoblasts initiate an inflammatory reaction by producing chemokines and synthesise a protective tertiary dentine. After the destruction of these cells, the pulp still has a high capacity to synthesise this tertiary dentine thanks to the presence of adult stem cells within the pulp. Also, in addition to the systemic regulation, the pulp which is located within the inextensible confines of the dentine walls has a well-developed local regulation of its inflammation, regeneration, and vascularisation. This local regulation is due to the activity of different pulp cell types, mainly the fibroblasts, which secrete soluble molecules that regulate all these processes.
© 2018 S. Karger AG, Basel
Microbiology of Tooth Decay
Dentistry dates as far back as 5,000 BC when people in India, Egypt, Japan, and China thought dental caries were a result of a “tooth worm.” The term “dental caries” first appeared in the literature around 1634 and is derived from the Latin word cariēs for decay and from ancient Irish ara-chrinn, it decays. The term was originally used simply to describe holes in the teeth with little knowledge of the aetiology and pathogenesis of the disease [1].
Concepts and beliefs about the cause of dental caries have evolved over many centuries, with the involvement of microorganisms recognised since the late 1800s. Readers interested in the concepts in caries microbiology and their development over time can find comprehensive literature on the topic [2, 3]. Despite thousands of publications, however, the central question of the relative importance of different bacteria in the disease remains unanswered.
With technical advances in our ability to identify, cultivate, and count different microorganisms, our views have evolved regarding the contribution of particular species of plaque bacteria to the caries process [4]. But it might take another 20–50 years, as a rough estimate, before deep-sequencing technologies and the gene databases have reached such a quality that the entire gene repertoire and interactions within a carious tissue can be determined. The limits so far are the length of an ambiguity-free sequence read (which is currently as short as 500 bp applying the leading Illumina sequencing technology) and, as a consequence, the need to select a short but taxon-representative region, usually a variable region, e.g., V1-V3, V3-V4, or V3-V5 of the 16S rDNA (total length 1,545 bp) or – even better – of the 23S rDNA (total length 2,905 bp). For instance, V3-V4 sequence results will leave many saccharolytic Streptococcus and Actinomyces species as “unclassified.” That means our current picture about the microorganisms involved in the initiation and progression of caries or other especially polymicrobial diseases is still rather incomplete. However, the species known to be involved so far and the correlated pathomechanisms of dental caries can be taken as a draft model and are thus discussed below.
In dental caries, we see an ecologic shift within the dental biofilm environment, driven by frequent access to fermentable dietary carbohydrates. This leads to a move from a balanced population of microorganisms of low cariogenicity to a consortium of high cariogenicity and to an increased production – and correlated tolerance – of organic acids promoting dental hard tissue net mineral loss. That is why we call this consortium acidogenic and acidophil (synonym aciduric). Besides the presence of fermentable dietary carbohydrates and selection of acidogenic-aciduric bacterial species, the host susceptibility, which is a rather simplified term for a multifactorial complexity, is the third major player.
The acidogenic-aciduric bacterial species Streptococcus mutans is recognised as being eminently involved in cariogenic processes, including early childhood caries, enamel carious lesions, cavitated lesions, or carious dentine. However, over time its attributed role changed from that of a true pathogen (specific plaque hypothesis [5]) to enhancer (active role) and/or indicator (passive role) of a sugar-triggered cariogenic vicious circle (extended caries ecological hypothesis [6, 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
