as people are getting older is that they wish to enjoy a well-functioning, painfree oral cavity. Therefore, tissue-saving procedures should be commonplace after caries prevention has failed, in order for the elderly to have a sufficient number of functioning teeth to assist them.
The idea for writing this monograph on the Evolution of Treating Cavitated Carious Lesions was born at the memorable congress of the European Organisation of Dental Research (ORCA) in Liverpool in 2014. It became operational first at the 2015 Leuven meeting, where the International Caries Consensus Cooperation (ICCC) was established. The ICCC published 4 papers in 2016 that form the basis of a number of chapters contained in the current monograph.
We wish the reader very many happy moments reading this work. We hope that this monograph finds its way to undergraduates in all dental schools and to postgraduate education courses around the world. The oral health profession has the knowledge and tools, as well as the duty to participate together with people/patients to “prevent restorations” and to “prevent root canal treatment and extraction on the basis of dental caries,” and to prolong a healthy dentition into older age. Let’s collectively do it.
Falk Schwendicke, Berlin
Jo Frencken, Nijmegen
Nicola Innes, Dundee
Schwendicke F, Frencken J, Innes N (eds): Caries Excavation: Evolution of Treating Cavitated Carious Lesions.
Monogr Oral Sci. Basel, Karger, 2018, vol 27, pp 1–10 (DOI: 10.1159/000487826)
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Pathophysiology of Dental Caries
aDivision of Oral Microbiology and Immunology, Department for Operative Dentistry, Periodontology and Preventive Dentistry, RWTH Aachen University Hospital, Aachen, Germany; bAix Marseille University, CNRS, ISM, Institute of Movement Sciences, Marseille, France
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Abstract
Carious lesion dynamics are dependent predominantly on the availability of fermentable sugars, other environmental conditions, bacteria, and host factors. Our current understanding of the microorganisms involved in the initiation and progression of caries is still rather incomplete. The most relevant acidogenic-aciduric bacterial species known to date are Streptococcus mutans, bifidobacteria, and lactobacilli. Whereas mutans streptococci are initiators, bifidobacteria and lactobacilli are more enhancers for progression. Boosters for microbial activity are specific environmental conditions, such as the presence of fermentable dietary sugars and the absence of oxygen. Based on these conditions, the necrotic and/or contaminated zone fulfils all criteria for disease progression and has to be removed. For those deep lesions where the pulp vitality is not affected, a selective removal of the contaminated leathery dentine should take place as this approach lowers the risk of regrowth of the few embedded microbial cells here. In repelling the microbial attack and repairing 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,