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.
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