Although we understand a lot about gum disease, there are still a number of mysteries that we have had difficulty unraveling. For example, why do some people with relatively poor oral hygiene remain at the gingivitis stage of gum disease without having it ever evolve into periodontitis, while other people seem to suddenly vault into periodontitis without much time for us to prevent it?
A new understanding of gum disease may change the way we prevent the condition, and possibly the way we treat it as well.
The Current Model of Gum Disease
The current model of gum disease works something like this: there are good bacteria, bad bacteria, and very bad bacteria, and even some heroic bacteria called probiotics that can fight gum disease. Good bacteria can live in our mouths harmoniously, never causing us health problems. Bad bacteria, on the other hand, cause us to develop minor forms of gum disease as well as dental cavities. Very bad bacteria, on the other hand, infect our gums aggressively, attacking our tissues and causing periodontitis. This leads to receding gums, bone loss, and, ultimately, tooth loss.
There is some allowance for genetic susceptibility, but, overall, the impact of two factors: whether you have the bad or very bad bacteria, and how many of them you do have.
Polymicrobial Synergy and Dysbiosis (PSD)
The emerging model of gum disease is sometimes described as polymicrobial synergy and dysbiosis (PSD). In this model, multiple different types of bacteria work together to create a dysfunctional state in your mouth and create new opportunities for themselves.
In this model, it isn’t just bad or very bad bacteria that can cause problems. Instead, bacteria like Porphyromonas gingivalis act as keystone organisms. A keystone organism doesn’t just attack and damage your tissues. Instead, it organizes destructive activities among many different bacteria in your mouth, including some of the so-called good organisms. In this model, a relatively small population of keystone bacteria can cause extreme damage because it can leverage the population of other bacteria to perform its attacks. Sometimes, our own cells may even turn against us.
We’ve already talked about some of the partnerships between good bacteria and bad ones. The new model says that’s actually the norm and not the exception, and it points to some triggers in our own biochemistry that might contribute to the development of these partnerships.
We’ll have to see how this new understanding alters our approach to treatment and prevention.