The Microbiome: Linking Bacteria, Health, and Disease

Robert C. Rickert, PhD; Scott Peterson, PhD

Disclosures

June 19, 2013

Editorial Collaboration

Medscape &

In This Article

Why We Develop Dental Caries

Dr. Peterson: My first experience and what attracted me to the microbiome project to begin with was that of the dental caries problem. There was a very clear cause-and-effect relationship that has been established for that particular disease. It's about pH.

Maybe I can illustrate here for you to make it clear. If we draw an axis here, with this being time and this being pH, we have a microbiome on the tooth surface that has a pH just about neutral. I'm going to draw another mark here at a pH of 5.5. The significance of this particular pH is that we know that when the pH of the tooth surface goes below 5.5, you start to have enamel erosion. That's what a cavity really is -- the reduction of calcification on the tooth.

So within minutes after consuming a meal, the microbiome goes to work eating furiously. That reduces the pH of the environment immediately, and it will dip down. Over the course of time, it will come back up to its original state. This all transpires in about 60 minutes.

Now, we know what the healthy profile looks like -- notice that it doesn't go below this 5.5 pH range. But when a person is starting to develop caries or actually has an active caries lesion, their basal pH before eating a meal is reduced. As they eat, it dips under this line. The time that it spends under this line, of course, influences the rate at which you might develop disease. In extreme examples, a person may live at a baseline level that's very close to this and spend a significant amount of time following a meal below this key pH.

Dr. Rickert: This, of course, is greatly affected by the diet one chooses.

Dr. Peterson: That's part of it. Your mother knew best. She told you to brush your teeth after a meal and to avoid sugar. All of these things are very much related to what we understand now about the disease.

It's through this that I became so impressed by the extraordinary power of the microbiome to influence something as simple as pH. It gives one a very clear way of approaching a problem, because we know it's about that.

This is quite different from infectious agents, where we think of an etiologic agent being a single entity. Here, we're talking about a community. This particular community is made up predominantly of organisms that really know how to utilize sugar. It's through that utilization of sugar that the pH is so tremendously affected and how it can cause disease.

What we're trying to do is make use of twins -- both monozygotic and dizygotic twins -- who were reared in the same homes eating the same diet (for the most part, these are children) in areas where there's no fluoride in the water system.

Dr. Rickert: Why would that be important -- that there's no fluoride in the water system?

Dr. Peterson: In general, the most informative studies that one can do in any kind of microbiome are longitudinal studies, because one wants to track the progression of the microbiome as an individual transitions from a state of health to a state of disease. Many human diseases can't be captured in the time frame of typical funding. Without fluoride in the water, it's very common that, if you enroll 100 kids into a study, 25 of those kids will develop caries over the time of your study. So the longitudinal aspect of our studies gets greatly powered by that reality.

On top of that, we're including twins. By controlling for the genetics of your host environment, as well as environmental factors, such as diet, we can narrow the number of confounding effects and study the impact of the microbiome and how it changes from the state of health to that of disease.

These kids are discordant -- one twin pair is caries-free, and the other one is caries-active. They're remarkably similar when they're both caries-free or both caries-active, but when they diverge their phenotypes, that's when we see differences in their microbiomes and how we can start to attribute relationships between particular species in the microbiome and disease.

Dr. Rickert: That's a very good example. Could you give us some other examples of your current research that address that topic?

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