| Summary: | Dental plaque is an oral biofilm that much like the rest of our microbiome has a role in health and disease. Specifically, it is the cause of very common oral diseases such as caries, gingivitis and periodontitis. The ideas about oral disease development have evolved over time with the techniques to analyze these changes. In the 19th century, scientists could not identify bacteria related to disease due to the lack of technology. This led to the Non-Specific Plaque Hypothesis or the idea that the accumulation of dental plaque was responsible for oral disease without discriminating between the levels of virulence of bacteria. In the 20th century these ideas evolved with the techniques to analyze the changes from health to disease. The first common hypothesis was the Specific Plaque Hypothesis (1976) proposing that only a few species of the total microflora are actively involved in disease. Secondly, the Non-Specific Plaque Hypothesis was updated (1986) and the idea that the overall activity of the total microflora could lead to disease, was enriched by taking into account difference in virulence among bacteria. Then, a hypothesis was considered that combines key concepts of the earlier two hypotheses: the Ecological Plaque Hypothesis (1994), which proposes that disease is the result of an imbalance in the microflora by ecological stress resulting in an enrichment of certain disease-related micro-organisms. Finally, the recent Keystone-Pathogen Hypothesis (2012) proposes that certain low-abundance microbial pathogens can cause inflammatory disease by interfering with the host immune system and remodeling the microbiota. In this comprehensive review, we describe how these different hypotheses, and the ideas around them, arose and test their current applicability to the understanding of the development of oral disease. Finally, we conclude that an all-encompassing ecological hypothesis explaining the shifts from health to disease is still lacking.
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