The Disease: 4 Paradigm Shift in Cariology
The previous chapters have addressed the etiology, pathogenesis, and clinical appearance of caries. This brief chapter will discuss the effects of scientific caries models and paradigms as well as approaches to treat the disease. Furthermore, pathogenesis will be illustrated in a model that will allow us to categorize the various options for intervention in Chapter 9. This chapter addresses the following topics:
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The influence of scientific paradigms on dentists’ approaches to treat caries
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The specific and ecological plaque hypotheses
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A current model of the pathogenesis of caries
Scientific Paradigms
Paradigms are understood to be the generally accepted scientific concepts and the worldview in a particular era. Paradigms are based on theories and models and form the scientific framework in which the scientists work. Abstract, idealized, and simplified models are frequently used to make the complex phenomena and interrelationships of nature comprehensible, explicable, and predictable. Of course, simplifications, idealizations, and abstractions can be problematic. Paradigms as well as the models and theories that underlie them come up against limits in certain situations. A paradigm, with its associated theories and models, is always accepted by the scientific community within a particular field as long as it is capable of satisfactorily explaining the relationships in nature and making reliable predictions. Once a paradigm meets its limits, it needs to be modified or replaced by a competing paradigm with its own theories and models. The new paradigm is then gradually accepted by more and more members of the scientific community, and the old one is finally abandoned. This process is termed a “scientific revolution.”1,2
Dentistry and medicine are also influenced by scientific paradigms. For example, the dentistry that is practiced in many countries, and which is represented in this book, is based on what is generally termed “Western academic medicine.” Contrastingly, “traditional Chinese medicine” avails itself of different paradigms which are mostly incompatible with Western academic medicine. The various medical paradigms naturally influence the ways in which we treat illnesses. Consequently, the therapeutic approaches in “Western academic medicine” are completely different from those in traditional Chinese medicine.
Paradigms and theories also reflect the scientific and social experiences of the scientists who created them. For example, the specific plaque hypothesis and the forms of therapy that are derived from it (see below), which were created during the beginning of the second half of the last century, reflect the widespread concept of human domination, scientifically and technologically, of a specific (hostile) environment. The ecological plaque hypothesis that was developed in recent decades arose during a period in which people, particularly in industrialized nations, became aware that fighting the environment has negative consequences. Hence protecting the environment and species is recommendable from both ethical and pragmatic points of view. In medicine, it was revealed that microorganisms are not harmful per se, and that they have irreplaceable, positive functions in our body.3 Consequently, the ecological plaque hypothesis does not point to the environment (infection with certain bacteria) as the primary cause of caries, but rather to our own behavior.
The present abandonment of the specific plaque hypothesis and embracing of the ecological plaque hypothesis is a classic paradigm shift that is bringing about a sustainable change in treatment concepts in dentistry.4
How Paradigms Influence Our Clinical Approach
The Specific Plaque Hypothesis
The chemo-parasitic theory that was founded by Miller in the beginning of the last century5 described the metabolic activity of bacteria as the main cause of caries. Later experiments with gnotobiotic (germ-free) rodents identified certain specific types of bacteria such as mutans streptococci and lactobacilli as essential factors in the etiology of caries.6–8 It was revealed that gnotobiotic hamsters did not develop caries even when they consumed sugar-containing food, whereas hamsters infected with Steptococcus mutans developed caries when they consumed cariogenic food. The resulting specific plaque hypothesis describes the infection of a host with specific pathogenic germs (e.g., S. mutans or Lactobacillus spp.). Consequently, caries was, and is, described frequently as a “transmittable infectious disease.”9 This view has influenced dentistry for many years.
If caries is considered an infectious disease, the most attractive preventive measure, as is the case with other classic infectious diseases, is to avoid contact with the pathogen. This consequentially led to preventive methods for avoiding the transfer of germs, for example, from the mother to the child. It was frequently recommended that the mother and child avoid the exchange of saliva.10 This led to recommendations that young mothers not put pacifiers or their children′s spoons in their mouth.11 Parents however, found that it was almost impossible to prevent the transfer of colds between the parent and child and vice versa. How was this to be prevented with mutans streptococci? Where else should children acquire their physiological oral flora if not from their closest contact person? Whether it is in fact possible or even desirable to consistently avoid the transmission of bacteria from parents to children is hence questionable. After an individual acquires a classic infectious disease, the therapy focuses on fighting the pathogen (if possible) with, for example, antimicrobial substances. In caries therapy, this means mechanically or chemically removing the pathogen, or at least decimating the bacterial plaque. Attempts were even made to regularly deliver antibiotics in toothpaste.12 The complete excavation of caries in the dentin is based on the belief that the disease can only be stopped by completely eradicating the pathogen. Also immunological approaches such as the development of vaccines against S. mutans are an extension of the specific plaque hypothesis.13
NOTE
The specific plaque hypothesis views caries as primarily originating from an infection with specific bacteria and leads to therapeutic approaches that seek to completely eradicate the pathogenic germs.
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