Recently researchers at the University of Alabama at Birmingham School of Dentistry published a very interesting article summarizing their research. Though this most certainly is not my field of expertise, I’ve been asked to provide my thoughts regarding this very interesting article.
It seems that a number of media authors have gotten hold of this article, and in typical journalistic fashion so common today (aka Fake News), have presented it as being right on the cusp of eradicating tooth decay very soon. No, it’s not. It is simply another step toward that goal.
To understand the potential for benefit, you first need to understand the basics of the problem. There are over 700 different types of bacteria found in the mouth. But only one (Streptococcus mutans) is the primary culprit in causing tooth decay (cavities). I will refer to Streptococcus mutans as simply S. mutans.
S. mutans is the primary bacteria that, after ingesting sugar, gives off lactic acid. It’s this lactic acid that softens and eats holes in teeth, which are commonly called “cavities”. These holes and softened tooth structure not only damage our teeth, but they serve as incubators to grow more and more S. mutans, resulting in higher and higher numbers of S. mutans in the mouth, and more and more cavities occurring.
S. mutans bacteria extrude a sticky glue called dextran (technically something called a “glucosyl glucan polymer”) that sticks to the tooth surface, creating a layer of biofilm. Though a Waterpik type device will remove food debris and most of the thickness of biofilm, even these oral irrigators cannot fully remove the bottom microscopic layers of S. mutans biofilm because the dextran glue is so strong. This is why brushing and flossing has always been so very important – because it takes the physical brush bristles and floss to “scrape” off the glued-on microscopic bottom layers of Strep mutans.
So a word to the wise – if you’re going to use a Waterpik type oral irrigator, use it AFTER you’ve brushed and flossed. Your brush and floss will scrape off and loosen all of the biofilm, and then the oral irrigator will flush it all out.
So, is this new research (discussed below) the real deal? Well, from a 30,000 feet view, it certainly sounds promising. But I can’t tell ya how many claims like this that I’ve read about over the past 40+ years that never really went anywhere. So I wouldn’t hold my breath… but you may want to consider keeping your fingers crossed.
Computers – love ‘em or hate ‘em. In this case, definitely, love ‘em. This research was made possible by performing “in silico” tests. This means that the original tests were done with computer simulation. How cool is that?
They entered the chemical structure of 500,000 drug-like small molecule compounds into the computer to see which may affect the S. mutans biofilm. From there they selected 90 compounds to perform computer simulations of how these 90 compounds would affect the three S. mutans enzymes that form dextran biofilm.
This entire idea of preventing the formation of dextran by S. mutans isn’t new. Previously, scientists have found ways to reduce the biofilm – but never enough to really help. Through those previous scientific studies, scientists found out more about the structure of the enzymes that form the biofilm. This knowledge about the structure of enzymes is what allowed the computer simulations to work. The computer simulations pointed out one compound, that seemed to work better than the others. They named this compound #G43.
Rats seem to have the same type of susceptibility to cavities as humans, but (like humans) only when the rats are fed a diet with sugars. The result was that the rats treated with #G43, shown in computer simulations to reduce formation of S. mutans biofilm by more than 95%, showed major reductions in cavity formation than rats fed with the same sugary diet without the treatment with the compound.
The Best Laid Plans of Mice (in this case Rats) and men (in this case Researchers)…sometimes turn out screwy!
But here’s the really strange part that nobody’s talking about. In the tests on the rats, there was absolutely no statistically significant difference in the amount of S. mutans biofilm created between the test group and the control group of rats. In other words, the rats treated with #G43 still had as much biofilm, but they had 95.6% less cavity formation.
Do you have any idea why? I certainly don’t…and neither do those research scientists.
So what they thought would happen is, the rats treated with #G43 would form almost no S. mutans biofilm, and therefore not cause cavities in response to the sugar in the diet. But it didn’t work that way. Those rats treated with #G43 still formed just as much S. mutans biofilm…but didn’t form cavities.
So What Does This Mean?
Obviously, they’re still a long way from figuring this out. But we’ve learned a lot of good stuff here through science. Most important discoveries have taken a long time, and have resulted from mistakes and simply stumbling onto things during the research. Hey, we’ll take whatever we can get.
Here are some of the important things regarding the article from my personal perspective:
- Though the simple formation of S. mutans biofilm, compared to what they originally thought, turned out not to be the key, we can be pretty sure that the three S. mutans enzymes that make up biofilm have something to do with the results.
- They were able to compare the two compounds that resulted in the most affect on the three S. mutans enzymes that form biofilm. By doing that, they were able to find what these two compounds had in common. So now they’ve got a pretty good idea what part of these molecules have the beneficial effect. This could lead to some great things.
- Why not just try to find a way to KILL S. mutans? That’s not a good idea. Our mouths have a normal “balance” of over 700 types of bacteria and fungal organisms. We need that balance to keep our mouths healthy. All the various bacterial and fungal organisms keep each other in check. If you kill all of the S. mutans bacteria, this would result in an imbalance in the bacterial flora of the mouth, causing other problems.
- The #G43 didn’t kill or damage the S. mutans bacterial at all. Just as many of these bacteria grew, and appeared to grow normally. So there will be nothing to make these bacteria “adapt” to #G43 and any compounds created later. So resistant strains of S. mutans should not develop in the future.
I’d like to say this is a great beginning, but that would take away from all of the very important previous research that has led to this study. So I’ll say this is a great finding in the “steps” toward a cure to cavities.
This most recent study has now discovered more definitive information, giving more “direction” to follow in future studies. So again, don’t hold your breath, but keep your fingers crossed.