The end of tooth decay?

We’ve all had the importance of tooth-brushing drilled (sorry) into us from an early age, and it’s not hard to understand why: humans have been plagued by tooth decay for as long as we’ve been human, and had teeth.

Cro-Magnon skulls 25,000 years old show evidence of tooth decay, for instance, and as long ago as 5,000 B.C. the Sumerians were wondering what caused toothaches (their theory, found on clay tablets: small gnawing worms within the affected tooth).

The most common form of tooth disease is the “cavity,” more properly known as dental caries. Bacteria that live in the mouth react with carbohydrates to form acids that are strong enough to dissolve tooth enamel. Once acid has eaten a hole through this outer shell, other bacteria move into the next layer, the dentin, and if their progress isn’t stopped, can eventually infect the pulp cavity at the tooth’s center, then the root canal, and finally even the jaw itself, resulting in a pocket of pus: an abscess.

We brush and floss (those of us who do) in order to remove the bits of food bacteria feed on and even some of the bacteria themselves. This also prevents the build-up of plaque, which in this instance is not something you’re awarded for a singular achievement but a coating bacteria create to protect themselves from saliva. (Plaque can mix with salivary mucus and food residue to form something even nastier, called tartar.)

Wouldn’t it be nice if we could somehow negate all the nasty effects of the bacteria in our mouth without having to do all that physical labor of brushing and flossing, or suffering through the picking and scraping of a dental hygienist’s miniature (yet menacing) mechanisms?

We’re not there yet, but we’re getting closer.

Streptococcus mutans (S. mutans) has the ability to survive in a highly acidic environment, which is what makes it such a nasty tooth-decayer: remember, it’s the acid bacteria produce as they consume carbohydrates that eats away at tooth enamel. Take away a bacterium’s ability to survive in acid, and you don’t even have to kill it: it destroys itself with its own acidic waste.

Researchers have identified a bacterial enzyme that S. mutans produces, called fatty acid biosynthase M (FabM, mercifully, for short), that plays a key role in its acid-resistance. Interfere with the bacterium’s ability to produce FabM, and presto!, it becomes 10,000 times more vulnerable to acid damage.

FabM is thus a prime target for drug companies looking to produce an anti-tooth-decay medicine that could eliminate the need for crude brushing by making it impossible for tooth-decay-causing bacteria to produce enamel-dissolving acid.

But that’s just the tip of the iceberg. When you hear “streptococcus,” you probably don’t think of tooth decay right away anyway. Instead, you probably think of “strep” throat.

Well, it’s early days yet, but research suggests that FabM or something closely related may help all Streptococci (strep) and Staphylocci (staph) bacteria resist the natural defenses the human body throws at them, which include immune cells that, yes, attack the bacteria with acid.

And between them, strep and staph bacteria are responsible for meningitis, pneumonia, sepsis, “flesh-eating disease,” heart infections and much more. Not only that, they are evolving immunity to many of the antibiotics that have been used to successfully treat them up until now.

A research team at the University of Rochester Medical Center has received a $3.6 million grant from the National Institute of Dental and Craniofacial Research to attempt to create a catalogue of proteins that, along with FabM, may provide targets for new therapies for strep and staph infections, therapies that attack the bacteria in so many ways they won’t be able to evolve around them.

“Our first goal is to force the major bacterium behind tooth decay to destroy itself with its own acid as soon as it eats sugar,” says Robert G. Quivey, the principal investigator for the grant. “After that, this line of work could help lead to new anti-bacterial combination therapies for many infections that have become resistant to antibiotics.”

Or, to put it another way, today, the teeth—tomorrow, the world.

Permanent link to this article: https://edwardwillett.com/2008/01/the-end-of-tooth-decay/

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