The current model of periodontal disease indicates that the presence of a large quantity of periodontal pathogens is necessary to initiate periodontal disease development. This model is favorable because the time it takes for the accumulation of sufficient numbers of perio bugs gives us a fighting chance to prevent disease development. The new model, however, indicates that low-abundance bacteria critical for dysbiosis are now known as keystone pathogens, the best-documented example of which is Porphyromonas gingivalis. This is definitely not welcome news, as it reduces the wiggle room between health and disease.
Another fundamental difference between the current and new models is the participation of the entire microbial community in tissue destruction, rather than just the periodontal pathogens. This is another unwelcome research finding, and it represents a seismic shift in knowledge. How is it that what we understood to be benign bystanders are now known to be pitching in with gum tissue breakdown?
This brings us to the next fundamental difference. P. gingivalis elevates the virulence of the entire community following interactive communication with accessory pathogens. What type of interactions? Changes to the genetic expression of the entire microbial community. Does this mean that every single microbe is involved? We are not sure yet, but at the minimum, many more bacterial species are virulent participants. The elevation of the entire community by P. gingivalis is why it is called a keystone pathogen in the new model, rather than a periopathogen.
There are more details to PSD that are also critically important to understand. My next blog post will fill in more information.
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