Caries Management - Science and Clinical Practice. Группа авторов

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      The Ecological Plaque Hypothesis

      Critics of the specific plaque hypothesis argue that mutans streptococci are also found in individuals who are clinically free of caries.^4,14 Contrastingly, S. mutans sometimes cannot be found in patients suffering from caries. Since the varied bacterial flora of the digestive system are essential to our body which continuously interacts with the environment, it is inappropriate to view a modification of the bacterial composition within our body as an infection. It is known that other factors are necessary to produce caries such as the regular supply of fermentable carbohydrates which promote the growth and metabolism of cariogenic bacteria. The presence of cariogenic microorganisms such as S. mutans therefore appears to be a necessary but not a sufficient factor for generating caries. These considerations have led the paradigm of the specific plaque hypothesis to be increasingly questioned.⁴

      In contrast to the specific plaque hypothesis, the ecological plaque hypothesis in favor today does not focus on infection with pathogenic microorganisms, but rather explains caries as a disturbance in the homeostasis of the oral microflora.¹⁵ This is caused by the selective favoring of (potentially) pathogenic microorganisms (such as S. mutans) by a sugar-rich diet. It is assumed that it is not an exogenous infection with pathogenic species that is responsible for caries. Rather, these species are a part of the physiological (endogenous) flora in healthy humans, and only the qualitative and quantitative changes are pathological.⁴ The increased consumption of fermentable carbohydrates favors microorganisms that efficiently metabolize these sugars into organic acids (acidogenic) and also tolerate the resultant low pH (aciduric).

      This ecological approach also influences therapy. Proceeding from the ecological plaque hypothesis, prevention no longer focuses on avoiding the transmission of germs. It is even probable that the transmission of a healthy bacterial oral flora from mother to child is preferable. Instead of avoiding the transmission of pathogens which is probably impossible, the development of a physiological bacterial oral flora in the mother is supported by appropriate interventions and recommendations. More recent approaches even seek to specifically reinforce a physiological bacterial flora through probiotic products.¹⁶ Avoiding the mother-to-child transmission of disease-promoting behaviors (sugar consumption) appears to be a more useful way to prevent caries. If caries and hence a pathogenic flora exist, the therapeutic goal is not to eradicate or decimate all bacteria, in contrast to earlier approaches, since this would harm the physiological flora. In addition, the decimation of a cariogenic species would probably enable another potentially pathogenic species to fill the ecological niche, which would lead to similar problems. Instead, the primary goal of therapy is to restore the physiological equilibrium (Chapters 9–12). If caries is not an infection, the necessity of complete excavation of infected dentin has to be put in question. The incomplete excavation of caries and creation of local conditions unfavorable to cariogenic bacteria (no room for the formation of a biofilm, cut off the source of nutrition with a sealant) can be sufficient to control the disease (Chapters 15–18).

       NOTE

      Based on our present knowledge, the ecological plaque hypothesis appears to be the most attractive and widely accepted theory on the etiology and pathogenesis of caries. The ecological plaque hypothesis focuses on the ecological equilibrium in the oral cavity as the source of caries which leads to therapeutic approaches that seek to control the different physiological factors of the process.