> in fact, it forms less than 2% of all the bacteria that cause caries<p>I tracked down the chain of citations here. The directly cited article (<a href="https://www.nature.com/articles/sj.bdj.2018.81" rel="nofollow">https://www.nature.com/articles/sj.bdj.2018.81</a>) says the following:<p>"These caries ecological concepts have been confirmed by recent DNA- and RNA-based molecular studies that have uncovered an extraordinarily diverse microbial ecosystem, where S. mutans accounts for a very small fraction (0.1%–1.6%) of the bacterial community implicated in the caries process.[20]"<p>Note the sudden conversion of "implicated in the caries process" to "cause caries".<p>The next step in the citation chain is <a href="https://www.cell.com/trends/microbiology/abstract/S0966-842X(14)00225-X" rel="nofollow">https://www.cell.com/trends/microbiology/abstract/S0966-842X...</a>.<p>"In recent years, the use of second-generation sequencing and metagenomic techniques has uncovered an extraordinarily diverse ecosystem where S. mutans accounts only for 0.1% of the bacterial community in dental plaque and 0.7–1.6% in carious lesions[14,15]."<p>Now the claim is merely one of prevalence!<p>The next steps in the citation chain, <a href="https://karger.com/cre/article-abstract/47/6/591/85901/A-Tissue-Dependent-Hypothesis-of-Dental-Caries" rel="nofollow">https://karger.com/cre/article-abstract/47/6/591/85901/A-Tis...</a> and <a href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0047722" rel="nofollow">https://journals.plos.org/plosone/article?id=10.1371/journal...</a>, do seem to plausibly provide evidence that there are other mouth-colonizing bacteria which would perform the same function as S. Mutans when it comes to causing caries, such that fully eliminating S. Mutans probably wouldn't eliminate caries entirely.<p>But, importantly, the citation in the McGill article doesn't much support the original claim, and this citation chain could easily have bottomed out in a completely different set of results which didn't happen to lend some (weak) evidentiary support to the high-level claim.<p>Also importantly, this article is committing the sin of figuring out some reasons why a treatment might not be perfectly effective in all cases, and implicitly deciding that justifies ignoring any non-total benefits (i.e. cases where S. Mutans would have been counterfactually responsible for causing caries, that could be prevented). Questions that would have been appropriate, but were apparently uninteresting:<p>"Does this intervention also happen to chase out other acid-producing bacteria that fulfill a similar ecological niche as S. Mutans?"<p>"What percentage of caries cases would be prevented by chasing out just S. Mutans with this intervention, while leaving other acid-producing bacteria untouched?"<p>Likely this is because answers to those questions would not really have changed the bottom line. That bottom line was written by the "unanswered" safety concerns (reasonable in the abstract, less obviously reasonable in this specific case). All of the listed safety concerns have evidence pointing in various directions. Very little of that evidence is listed, probably because it's not in a format that's legible to scientific institutions. The article does note, earlier on, "The toxicity of this Mutacin-1140 compound had not been tested. What would be the consequences of millions of bacteria in the mouth releasing this compound? The answer wasn’t clear, even though the archetypal compound in the family Mutacin-1140 belonged to was known to be very safe." This is obviously relevant evidence about the safety of Mutacin-1140. _How much_ evidence? Unasked, unanswered. (I have no idea how predictive the safety of other compounds in the same family is of another unstudied compound in that family, I'm not a biologist. But this is not an _unanswerable_ question.)<p>(Marginal conflict of interest: I know the Lumina founder socially. I have no financial interest in that venture or any of his other ventures. I have not taken Lumina myself.)