Caries Management - Science and Clinical Practice. Группа авторов

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.

      A Current Model of Caries

      The etiology of caries has been described in various models and ways.^17–20 The famous Venn diagram by Keyes (see Fig. 2.1, p. 22) shows the three essential etiological factors for caries: “bacteria,” “tooth,” and “sugar.”¹⁷ Later, König suggested including “time” as a fourth essential factor.¹⁸ Both models are based on the specific plaque hypothesis and—for reasons of simplicity—ignore other influencing factors. The model introduced by Fejerskov and Manji (see Fig. 21.1, p. 307) in contrast, shows caries as a multifactorial disease.

      Figure 4.1 shows a pathogenesis model of caries based on the ecological plaque hypothesis: According to our present understanding, a sugar-rich diet plays a primary role in the etiology and pathogenesis of caries.²¹ A greater role has been assigned to sugar because caries is a disease of civilizations that consume a greater amount (or excess?) of sugar, which was not the case throughout most of human history.²² The excessive consumption of fermentable carbohydrates appears to be less physiologically normal than the regular existence of small numbers of potentially cariogenic bacteria in the physiological flora. The frequent consumption of fermentable carbohydrates causes a pathological shift in the oral microflora and promotes acidogenic and aciduric species.¹⁵ Consuming fermentable carbohydrates also causes potentially cariogenic bacteria such as S. mutans to produce organic acids that demineralize the enamel and dentin. This finally causes the characteristic signs and symptoms of caries. Protective factors also influence the development of caries. Both the host's defenses and the patient's oral hygiene limit the growth and metabolism of the oral biofilm and hence the production of acids. With its buffering properties and minerals, saliva promotes the remineralization of the enamel. The remineralizing effect of saliva can be supported by the application of fluorides and calcium compounds.²³ In addition to these local, direct factors, other behavioral and socioeconomic factors are associated with caries as revealed by epidemiological investigations.²⁴ However, these only indirectly influence the caries process through the local factors.⁴

      Fig. 4.1 The pathogenesis of caries. The primary causal pathogenic factor (dark red) for caries is the frequent consumption of fermentable carbohydrates (sugars). This causes an ecological shift in the oral biofilm favoring acidogenic and aciduric species (pathogenic flora). The increased metabolic activity of the biofilm, which is also triggered by sugar consumption, causes the formation of organic acids. This leads to demineralization of dental hard tissues, which consequently results in the characteristic signs and symptoms of caries. On the contrary there are several protective factors (dark green): the host defense (immune system) and the oral hygiene limit the number of microorganisms. By oral hygiene the biofilm can be completely removed at least locally, and thus acid formation can be avoided. In addition, the components of saliva as well as locally applied fluorides and calcium enhance the remineralization of dental hard tissues, which may alleviate the signs and symptoms of caries. Besides these (local) direct factors there are several indirect (distant) factors, which only indirectly influence the caries process but may be strongly associated with caries. For simplicity, not all associations are marked.

      With the exception of the consumption of fermentable carbohydrates that is shown in Fig. 4.1 as a pathogenic factor (dark red), all of the other factors that locally influence the caries process are shown as protective factors (dark green). However, the minimization or elimination of protective factors can have a significant influence on the caries process. For example, the elimination of saliva's protective function in patients with hyposalivation frequently causes caries to progress extremely fast, even though other factors are scarcely modified.²⁵ The risk factors for caries are accordingly increasing the pathogenic factor of fermentable carbohydrates as well as eliminating or reducing protective factors.

      According to our present understanding, caries is a multifactorial disease. If and how fast caries develops depends on the complex interrelationships between the various pathogenic and protective factors. If the protective factors predominate, caries does not develop, or existing caries is arrested or healed. However, if the pathogenic factors predominate, the disease progresses.²⁰ This dynamic character of the caries process enables the disease to be influenced in every stage. Approaches for preventing caries therefore seek to minimize the pathogenic factors and support the protective factors.

       SUMMARY

      Scientific paradigms guide our understanding of diseases and therefore also influence our preventive/therapeutic approaches. The paradigm of the specific plaque hypothesis leads to preventive approaches for avoiding infection with cariogenic microorganisms and forms of therapy to eliminate all cariogenic microorganisms. Contrastingly, the ecological plaque hypothesis is based on environmental and behavioral influences and consequently leads to interventions for reducing pathogenic factors and/or promoting protective factors.

      REFERENCES

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      10. Caufield PW, Cutter GR, Dasanayake AP. Initial acquisition of mutans streptococci by infants: evidence for a discrete window of infectivity. J Dent Res 1993;72(1):37–45

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