Reports of the death of dental cavities are greatly exaggerated

From the article:

In 1924, an Irish bacteriologist by the name of James Kilian Clarke isolated a bacterium he found in a dental cavity. It looked like some sort of mutated version of a streptococcus, so he named it Streptococcus mutans, or S. mutans for short.

A few decades later, S. mutans had established itself in the minds of the scientific community as the great culprit behind dental caries, what experts call its etiology, meaning its cause. The bacterium was able to stick to the surface of our teeth and, in processing the sugars in our mouth, it would produce large amounts of acid, specifically lactic acid. Normally, our saliva is able to neutralize a lot of this acid, but S. mutans secretes complex sugars that create a sort of film over our teeth called plaque, trapping its acid underneath. Over time, the tooth, eroded by the acid, would cavitate and develop a hole.

In the late 1970s, however, a chance event would promise to change the game. Dr. Jeffrey Hillman, a dentist and researcher then based in Boston, had found a version of S. mutans that had a very specific mutation, which meant that it produced less acid when metabolizing sugars. This opened the door to replacement therapy. A destructive approach to the problem of dental carries would be to use an antibiotic to kill the culprit; with replacement therapy, the idea is to replace the culprit with a version of it that is harmless. An example of this has been explored recently with genetically engineered mosquitoes that do not bite and that can only produce male offspring in an attempt to reduce the spread of diseases like Zika and yellow fever. Could we colonize the human mouth with this naturally mutated S. mutans and thus bid goodbye to cavities?

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For a few decades, they laboured to find (or engineer) a strain of S. mutans that apparently checked all of the right boxes. Eventually, they arrived at strain BCS3-L1. It did not produce the dreaded lactic acid but instead metabolized sugars into ethanol and a molecule called acetoin, which is responsible for the flavour of butter. It also secreted a compound called Mutacin-1140 which kills other strains of S. mutans but which, importantly, does not destroy BCS3-L1. In rats, it colonized the mouth easily and the animals looked fine after six months. A strain that preceded BCS3-L1 was also tested in five human volunteers in the 1980s and the bacterium stuck to their teeth for many years (at least 14 in two cases).

It was time to see if BCS3-L1 could be sold to Americans as a novel drug.

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By 2014, the company admitted that the only possibility moving forward was to partner with someone else. Otherwise, the work would have to be abandoned.

Around that time, the patent they had for this bacterial strain expired. Aaron Silverbook, who founded a company called Lantern Bioworks, saw a way to rescue this technology from the regulatory red tape: what if it wasn’t filed as a drug but as a probiotic? He made a deal with Oragenics to acquire the recipe and aimed to get it approved by the FDA through its much less stringent probiotic pathway. He first sold it in Próspera, a libertarian charter city on a Central American island where any biotech product can be sold as long as the buyer signs a waiver, and now the product, renamed Lumina, is gaining hype on social media among cryptocurrency enthusiasts and DIY experimenters. You can even preorder the product for USD 250, to be shipped in June of this year.

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Only, there is a slight problem.

This whole technology is predicated on the assumption that dental caries are caused only (or, at the very least, mostly) by S. mutans. That was, after all, the accepted theory in the 1970s when Hillman got the ball rolling. Our understanding of dental caries, however, has greatly advanced in the interim.

We went from calling caries an infectious disease that was specifically caused by S. mutans—much like how the influenza virus causes the flu—to gaining a more ecological perspective on the disease. S. mutans is not the only acid-producing oral bacterium that can cause caries: in fact, it forms less than 2% of all the bacteria that cause caries, and a little over one in seven people with caries do not have S. mutans in their mouth. There is even a scientific paper on dental caries literally titled “Beyond Streptococcus mutans”!

Caries occur because of a catastrophic shift in the balance of our mouth’s bacterial and fungal ecosystem. It is not due to any one bacterium, and any bacterium capable of releasing acid after ingesting sugars can contribute to this. Even if you could reliably stop S. mutans from producing acid, you could not guarantee the absence of future dental caries. The reason why S. mutans became the Big Bad of the 1970s dentistry world is because researchers were stuck studying the mouth bacteria they could grow in the laboratory, and S. mutansgrows well in the conditions scientists were selecting back then. But now, with DNA technology, scientists have been able to detect 800 different species of bacteria in the human mouth.

We are thus left with a product, Lumina, that cannot guarantee the prevention of future caries and whose safety can be summarized by a giant question mark.