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Chapter 6: The Problem with Scorched Earth

In which we examine what antiseptic mouthwashes actually do to your mouth, retract two claims I made too confidently, and follow the argument into an intensive care unit where it was settled by a toothbrush

The Tooth Fairy does not love the scorched earth approach!

I want to be careful here, because I'm about to criticize products that millions of people use daily, that are recommended by many dental professionals, and that do have some legitimate therapeutic applications. I'm not trying to tell you that everyone who has ever used Listerine has been poisoning themselves. That would be alarmist and inaccurate.

But I am going to present evidence that regular, long-term use of antiseptic mouthwashes for daily maintenance—as opposed to therapeutic use for specific conditions—may not be doing what you think it's doing. And it may be doing some things you would never have expected.

Let's look at the data.

The Efficacy Question

First, do antiseptic mouthwashes actually prevent oral disease in healthy people who are already brushing and flossing?

This turns out to be a surprisingly difficult question to answer definitively, because most studies are short-term (weeks to months) and measure intermediate outcomes like plaque indices and gingival bleeding rather than long-term outcomes like cavity development or tooth loss.

What we can say:

Chlorhexidine is genuinely effective at reducing plaque and gingivitis over the short term. Multiple systematic reviews confirm this.1 However, chlorhexidine has significant side effects—tooth staining, taste disturbance, increased calculus formation—that make it unsuitable for indefinite daily use. It's typically recommended for short-term therapeutic courses (post-surgical, during periodontal treatment) rather than ongoing maintenance.

Alcohol-based mouthwashes (like traditional Listerine) show more modest effects. A 2006 meta-analysis of six-month studies found that antiseptic mouthwashes reduced plaque by about 33% and gingivitis by about 26% compared to placebo or no treatment.2 But the studies in that review were short-term, and the clinical significance of a 26% reduction in a gingivitis index isn't entirely clear.

Cetylpyridinium chloride (CPC) mouthwashes have weaker antimicrobial activity than chlorhexidine. Evidence of meaningful clinical benefit is less robust.

Here's the critical gap: very few studies have examined whether long-term antiseptic mouthwash use prevents actual dental disease—cavities, periodontal destruction, tooth loss—in people who are already performing mechanical oral hygiene. We have abundant evidence that antiseptics kill bacteria in the short term. We have limited evidence that this translates to better long-term oral health outcomes in the general population.

The assumption that killing bacteria must help has been doing a lot of work.

The Microbiome Disruption Problem

Even if antiseptic mouthwashes don't cause direct harm, they may cause indirect harm by disrupting the oral ecosystem in ways that don't favor health.

A 2020 study in Scientific Reports put 36 healthy adults through seven days of placebo rinsing and seven days of 0.2% chlorhexidine, and compared their own mouths to themselves.3 After the chlorhexidine week:

  • Bacterial diversity fell and the proportions of major taxa shifted
  • Nitrate-reducing species declined specifically
  • Saliva became more acidic, with more lactate and glucose in it
  • Salivary and plasma nitrite fell

Read that third point again. A product marketed for oral health made the mouth more acidic—which is the condition enamel dissolves in.

What that study could not tell us is whether the shift recovers, because it never looked after people stopped. A 2024 study did.8 Twenty patients rinsed with chlorhexidine twice daily for four weeks after periodontal surgery, then were followed for four weeks after stopping. Diversity fell in both saliva and plaque, and Streptococcus in plaque went from 8.2% to 25.8%—a shift toward the community associated with caries. Four weeks after stopping, saliva had returned to baseline. Plaque had not. The habitat that matters most for cavities was the one that didn't bounce back.

That study also looked for antibiotic-resistance genes and, to its credit, didn't find a significant change. A couple of tetracycline efflux-pump genes drifted upward without reaching significance. I mention it because you will eventually read a headline claiming mouthwash is breeding superbugs, and the honest state of that evidence is: a non-significant trend in twenty people, plus laboratory work showing chlorhexidine-adapted bacteria becoming harder to kill with colistin.9 In a petri dish. Nobody has shown that happening in a person's mouth.

Now, an altered microbiome isn't necessarily a harmful microbiome. But given what we know about the benefits of certain oral bacteria (alkali production, pathogen competition, nitrate reduction), a less diverse community with fewer of these beneficial species seems unlikely to be an improvement.

The "kill 99.9% of germs" claim that appears on so many products is technically true for the moments after use. But that 0.1% that survives, plus recolonization from surfaces the mouthwash didn't reach (deep in biofilms, in crypts of the tongue), means the mouth repopulates within hours. The question is what repopulates—and there's no guarantee it's a healthier community than what was there before.

There is one more study worth your attention here, and I'm going to hand you its weakness along with its finding. In 2024, researchers reported that three months of daily Listerine Cool Mint left participants with more Fusobacterium nucleatum and Streptococcus anginosus in the throat—two species that keep turning up in the cancer literature.10 It was a proper randomized, placebo-controlled crossover trial, which is more than most microbiome studies can say. The weakness: the placebo mouthwash shifted the community about as much as the Listerine did. Fifty-nine people, no dietary or smoking data, and a narrow study population. The authors themselves wrote that they were reluctant to draw substantial conclusions, which is a rarer kind of honesty than it should be, and I'd rather quote it than bury it.

I'll tell you what that study is not, because a great deal of noise has been made about it: it is not a cancer finding. It measured bacteria. Nobody in it developed anything. The leap from "these species became more abundant" to "this product causes cancer" is precisely the leap this book refuses to make on its own behalf, and I'm not going to make it just because the conclusion would flatter my argument.

The Blood Pressure Connection — and Why I've Had to Soften It

This was, for years, the finding that changed how I think about antiseptic mouthwash. I have to walk part of it back, and I'd rather do it here in the open than quietly edit the page and hope you didn't notice.

Remember the nitrate-reducing bacteria we discussed earlier? The ones that convert dietary nitrate to nitrite, which then becomes nitric oxide—a vasodilator that lowers blood pressure? Those bacteria live in your mouth. When you use antiseptic mouthwash, you kill them along with everything else.

The mechanism holds up. A 2013 study in Free Radical Biology and Medicine had 19 healthy volunteers use chlorhexidine twice daily for seven days.4 Oral nitrate-reducing capacity dropped substantially, plasma nitrite fell, and systolic blood pressure rose by roughly 2–3.5 mmHg. A 2019 study found antibacterial mouthwash blunted the blood-pressure-lowering effect of exercise, which also runs through nitric oxide.5 A prospective cohort found frequent over-the-counter mouthwash use associated with developing hypertension.6 The 2024 chlorhexidine-versus-propolis work sharpened the picture further: chlorhexidine left the nitrite-producing species present while impairing their nitrite-producing activity.11 The bacteria were there. They'd been silenced.

The blood pressure number does not hold up—or at least, not yet. When researchers pooled those trials, the effect dissolved. A 2024 meta-analysis of five controlled crossover trials found systolic pressure up 1.59 mmHg and diastolic up 0.46 mmHg, neither statistically significant, with a trial sequential analysis concluding the evidence base is simply too small to settle the question.12 A 2026 meta-analysis focused specifically on chlorhexidine reached the same place: two individual studies showed real increases, the pooled result showed none, and the authors landed on "moderate confidence that any change is insignificant or very small."13

Science Note — what the evidence actually supports

  • Antiseptic rinses impair oral nitrate reduction. Well documented. Repeatedly measured. Not in dispute.
  • That impairment raises your blood pressure enough to matter. Unsettled. Individual trials found 2–3.5 mmHg. Two meta-analyses pooling those same trials found nothing significant.
  • The distinction is between no demonstrated effect and demonstrated absence of an effect. We are in the first, not the second — the studies are small, short, and few.

Here is what I want you to take from this. The mechanism is real and measured: your mouth participates in your cardiovascular system, and sterilizing it interrupts a pathway that matters. Whether that interruption moves the number on the cuff is a question five small trials cannot answer, and I was wrong to write as if they had. I'd rather hand you an argument with a hole in it than one I've patched with confidence I haven't earned.

The ecological case against daily sterilization never rested on blood pressure. It rests on the fact that we adopted the habit without ever demonstrating it helps healthy people.

The Alcohol Controversy

Traditional antiseptic mouthwashes contain substantial amounts of alcohol—up to 27% in some formulations, higher than wine. This alcohol serves as a solvent for the active ingredients, as a preservative, and as an antimicrobial agent in its own right.

There has been long-running controversy about whether alcohol-containing mouthwashes increase the risk of oral cancer.

The mechanism would be plausible: alcohol is a known carcinogen, the oral mucosa is directly exposed, and some people use these products multiple times daily for years or decades. Acetaldehyde, the first metabolite of alcohol and a confirmed carcinogen, is produced in the mouth from alcohol by oral bacteria.

The evidence has firmed up considerably since this argument started, and it does not go the way you might expect from someone with my opinions about mouthwash.

The largest pooled analysis of the question gathered twelve case-control studies—8,981 people with head and neck cancer, 10,090 without—and adjusted for the things that actually cause oral cancer: pack-years of smoking, drinks per day, education.7 Ever having used mouthwash versus never: odds ratio 1.01. That is a fancy way of writing nothing at all.

A 2023 systematic review and meta-analysis of fifteen studies found the same.14 Any mouthwash versus none: 1.00. Alcohol-containing mouthwash specifically: 1.20, not statistically significant. Once or twice a day: not significant.

The signal only appears at the extremes. Three or more rinses a day carried an odds ratio of 2.58. More than forty years of use, 1.44. Use for more than thirty-five years in the pooled analysis, 1.15. And those are exactly the numbers where I trust the evidence least, because the person rinsing four times a day for forty years is disproportionately the person with something in their mouth they're trying to cover up—which is often tobacco or alcohol, and those confounders are notoriously hard to fully adjust away.

So let me be plain, and let me be plain in the direction that costs me something: if you use alcohol-containing mouthwash in ordinary amounts, the evidence does not support a meaningful oral cancer risk. The 2008 review that started this fight,21 and the mixed-evidence framing I used to give you, have both been overtaken.

The alcohol is still doing something I object to—it's contributing to the antimicrobial effect, it dries the mucosa, and dryness is its own problem. But I'm not going to let you believe it's giving you cancer, because that isn't where the evidence landed, and a field guide that shades the data toward its own conclusions isn't a field guide. It's an advertisement with better vocabulary.

Local Tissue Effects

Beyond systemic effects, antiseptic mouthwashes can cause local irritation:

  • Mucosal irritation and desquamation: High-alcohol mouthwashes can damage the oral mucosa, especially with frequent use
  • Dry mouth: Alcohol is a drying agent; paradoxically, a product meant to improve oral health may reduce the saliva that provides natural protection
  • Taste disturbance: Particularly with chlorhexidine, but to some degree with other antiseptics
  • Tooth staining: Chlorhexidine is notorious for this, but other agents can also contribute
  • Altered taste sensation: Some users report persistent taste changes even after discontinuing use

These effects are usually described as "minor" or "cosmetic," but they're not trivial for people who experience them. And the dry mouth effect is particularly counterproductive given how important saliva is for oral health.

When Antiseptics Are Appropriate

I've been making the case against routine antiseptic mouthwash use, but I want to be clear: there are legitimate therapeutic applications.

Post-surgical use: After oral surgery, including extractions, the risk of infection is elevated and normal oral hygiene may be difficult or impossible. This is the strongest evidence antiseptics have, and I won't undersell it: a Cochrane review found chlorhexidine rinse around extraction cut the risk of dry socket by about 42%, and chlorhexidine gel placed directly in the socket by about 58%.15 If you have ever had dry socket, you already know why that matters.

Active periodontal disease: When periodontitis has been diagnosed and professional treatment is ongoing, antiseptic rinses may help control bacterial populations while the inflammatory condition is being addressed. Be clear-eyed about the size of the benefit, though: chlorhexidine chips placed in the pocket after scaling and root planing buy about 0.77 mm of probing depth and 0.57 mm of attachment.16 Real, worth having, measured in fractions of a millimeter—and delivered locally into the pocket, which is a different thing from swishing antiseptic across your whole mouth twice a day.

Patients at very high caries risk: In some cases—severe dry mouth, high S. mutans counts, history of rampant decay—more aggressive antimicrobial approaches may be justified.

Immunocompromised patients: Those with reduced immune function may benefit from antiseptic protection that healthy individuals don't need.

Pre-procedural rinses: A brief rinse before dental procedures reduces bacterial aerosols and may reduce post-operative infection risk.

The pattern here is that antiseptics are useful for specific therapeutic situations, typically short-term, where the benefits clearly outweigh the disruption costs. What's questionable is extending these products to daily maintenance in healthy individuals.

The Intensive Care Unit Changed Its Mind

I've saved this for last because it is the closest thing to a controlled experiment that anyone has run on my entire argument, and it wasn't run by dentists. It was run by hospitals, on the sickest people in them, over two decades.

If you put a person on a ventilator, bacteria from their mouth can travel down the tube into their lungs and cause pneumonia. The response, adopted across the developed world beginning in the early 2000s, was the most logical thing imaginable: swab the mouth with chlorhexidine. Sterilize the source. It became standard of care, written into hospital bundles, audited for compliance.

It did not work.

In 2014, a systematic review found that chlorhexidine oral care was associated with increased mortality in patients who hadn't had cardiac surgery.17 That finding was alarming enough to be re-tested directly. A stepped-wedge randomized trial across six Toronto ICUs then removed chlorhexidine from oral care for 3,260 ventilated patients and measured what happened to mortality.18 Nothing happened to mortality. The harm signal did not reproduce—which I report because the honest version of this story includes the part where the scary finding failed to replicate.

But the benefit didn't show up either. A 2024 network meta-analysis pooled 22 trials and 5,314 patients across three different chlorhexidine concentrations and found no reduction in pneumonia, no reduction in time on the ventilator, no reduction in ICU stay, no reduction in death—at any concentration.19 In 2022, the infection-control guidelines had already reversed the recommendation. Routine chlorhexidine oral care in ventilated patients: no longer advised.

And what replaced it?

A toothbrush.

A 2024 meta-analysis of fifteen studies and 10,742 hospitalized patients found that daily toothbrushing reduced hospital-acquired pneumonia by a third, and reduced ICU mortality by about a fifth.20 Shorter time on the ventilator. Shorter ICU stays. Mechanical disruption of biofilm, performed with the oldest tool in this book, outperformed the chemical that had replaced it.

Tooth Fairy Note

I want to sit with you in this for a moment, because I have been making this argument for a very long time and I did not expect the proof to arrive from an intensive care unit.

In the one setting where the case for sterilization was strongest — where the patients are sickest, the stakes are highest, and the money and attention were all pointed at the problem — medicine spent twenty years on an antiseptic that never delivered. Then it went back to brushing the teeth, and the pneumonia rate fell.

Not because the antiseptic was evil. Because disrupting the biofilm was always the thing that mattered, and killing things in the water above it was never a substitute for that.

If it didn't work there, in the hardest case, with everyone watching — what exactly do you suppose it's doing in your bathroom at eleven at night, after you've already brushed?

The Marketing Reality

The Tooth Fairy deals with a snake oil salesman.

Why do people use antiseptic mouthwash daily despite the limited evidence of benefit and the emerging evidence of harm?

Partly because of marketing. Listerine's famous campaigns—"Kills Germs That Cause Bad Breath," "Kills 99.9% of Germs"—have been extraordinarily successful at equating antibacterial action with oral health. The burning sensation, which might otherwise be perceived as irritation, has been reframed as evidence that "it's working."

Partly because of authority. When dental professionals recommend mouthwash without specifying that they mean therapeutic use, patients reasonably interpret this as an endorsement of daily use.

Partly because of intuition. The germ theory is so deeply embedded in our cultural understanding that "killing germs" seems obviously good. The idea that killing germs might be harmful—that some germs are helpful—requires a more sophisticated understanding than most people have been given.

And partly because alternatives haven't been clearly presented. If you're told that brushing and flossing aren't enough, and the only additional measure you know about is antiseptic mouthwash, that's what you'll reach for.

The Bottom Line

Let me summarize what the evidence supports:

  1. Antiseptic mouthwashes do kill bacteria in the short term. This is not in question.

  2. Whether this killing prevents oral disease in healthy people who brush and floss is less clear than commonly assumed.

  3. Antiseptic mouthwashes disrupt the oral microbiome, reducing diversity and beneficial species. In plaque—the habitat that matters most for cavities—that shift had not recovered four weeks after stopping.

  4. Antiseptic mouthwashes impair nitrate reduction. This is measured and repeated. Whether that impairment meaningfully raises your blood pressure is unsettled: individual trials found 2–3.5 mmHg, and two meta-analyses pooling those trials found no significant effect.

  5. They do not appear to cause oral cancer at ordinary use. Pooled evidence finds no association. A signal appears only at three-plus rinses daily or several decades of use, where confounding by smoking and drinking is hardest to exclude.

  6. Local effects including irritation, dryness, and taste disturbance are documented.

  7. Specific therapeutic applications (post-surgical, active periodontal disease, high-risk patients) remain appropriate—and for dry socket prevention, genuinely valuable.

  8. In the setting where sterilization had its best case—ventilated ICU patients—it failed. Guidelines reversed. Toothbrushing won.

If you're a healthy person using antiseptic mouthwash twice daily because you think it's helping your oral health, the evidence suggests you should reconsider. Not because it will give you cancer, and not because it will certainly raise your blood pressure—I've just spent this chapter taking both of those claims down to what the data actually supports. Reconsider because the benefit was never demonstrated in people like you, and because you are paying money to reduce the diversity of an ecosystem you depend on.

That's a quieter argument than the one I used to make. It also happens to be the one that survives contact with the evidence.

There are better approaches. They're older approaches, in many cases. They work with your mouth's ecology rather than against it.

Which brings us to the paradigm shift that's underway—from warfare to stewardship, from scorched earth to ecosystem management.

  1. James, P., et al. (2017). Chlorhexidine mouthrinse as an adjunctive treatment for gingival health. Cochrane Database of Systematic Reviews, 3, CD008676. ↩

  2. Gunsolley, J. C. (2006). A meta-analysis of six-month studies of antiplaque and antigingivitis agents. Journal of the American Dental Association, 137(12), 1649-1657. ↩

  3. Bescos, R., Ashworth, A., Clarke, C., et al. (2020). Effects of chlorhexidine mouthwash on the oral microbiome. Scientific Reports, 10, 5254. DOI: 10.1038/s41598-020-61912-4. Single-blind crossover intervention, 36 healthy adults, seven days placebo then seven days 0.2% chlorhexidine. Note this was an intervention in which participants served as their own controls, not a comparison of habitual users against non-users. ↩

  4. Kapil, V., et al. (2013). Physiological role for nitrate-reducing oral bacteria in blood pressure control. Free Radical Biology and Medicine, 55, 93-100. PubMed ↩

  5. Cutler, C., et al. (2019). Post-exercise hypotension and skeletal muscle oxygenation is regulated by nitrate-reducing activity of oral bacteria. Free Radical Biology and Medicine, 143, 252-259. ↩

  6. Joshipura, K., et al. (2020). Over-the-counter mouthwash use, nitric oxide and hypertension risk. Blood Pressure, 29(2), 103-112. DOI: 10.1080/08037051.2019.1680270. Prospective, but modest: 540 participants analyzed, mean follow-up under three years, mouthwash use self-reported. ↩

  7. Boffetta, P., et al. (2016). Mouthwash use and cancer of the head and neck: a pooled analysis from the International Head and Neck Cancer Epidemiology Consortium. European Journal of Cancer Prevention, 25(4), 344-348. DOI: 10.1097/CEJ.0000000000000179. Twelve case-control studies, 8,981 cases and 10,090 controls, adjusted for pack-years, drinks per day, and education. Ever use versus never: OR 1.01 (95% CI 0.94–1.08). Use exceeding 35 years: OR 1.15 (1.01–1.30). More than once daily: OR 1.31 (1.09–1.58). ↩

  8. Bartsch, S., et al. (2024). Chlorhexidine digluconate mouthwash alters the oral microbial composition and affects the prevalence of antimicrobial resistance genes. Frontiers in Microbiology, 15, 1429692. DOI: 10.3389/fmicb.2024.1429692. Twenty post-surgical patients, four weeks of use with four weeks of follow-up after stopping. Small and single-arm, but the only study to date that looked at what happens after you quit. ↩

  9. Kampf, G. (2023). Chlorhexidine resistance or cross-resistance, that is the question. Antibiotics, 12(5), 798. DOI: 10.3390/antibiotics12050798. In vitro only. Chlorhexidine-adapted Gram-negative bacteria showed reduced colistin susceptibility without ever having been exposed to colistin. No clinical study has shown this arising from oral mouthwash use in people. ↩

  10. Laumen, J. G. E., Van Dijck, C., Manoharan-Basil, S. S., et al. (2024). The effect of daily usage of Listerine Cool Mint mouthwash on the oropharyngeal microbiome: a substudy of the PReGo trial. Journal of Medical Microbiology, 73(6), 001830. DOI: 10.1099/jmm.0.001830. Randomized, placebo-controlled crossover; 59 participants, three months per arm. Crucially, community composition shifted significantly from baseline after both the Listerine and the placebo arms, which the coverage of this study almost universally omitted. No dietary or smoking data. The authors describe themselves as reluctant to draw substantial conclusions. ↩

  11. Comparative effects of propolis and chlorhexidine mouthwash on the oral microbiome and blood pressure (2024). Journal of Oral Microbiology. DOI: 10.1080/20002297.2024.2439636. Chlorhexidine increased the relative abundance of nitrite-producing species while impairing their nitrite-producing activity—the taxa present, the function silenced. ↩

  12. Farook, F. F., Alnasyan, B., Alhamid, R., et al. (2024). Association between mouth rinse use and changes in blood pressure: a systematic review and meta-analysis with trial sequential analysis. International Journal of Dental Hygiene, 22(1), 65-77. DOI: 10.1111/idh.12714. Five controlled crossover trials. Systolic +1.59 mmHg (95% CI −0.15 to 3.33), diastolic +0.46 mmHg (−0.72 to 1.64), neither significant. The trial sequential analysis concluded the evidence base is too small to settle the question in either direction. ↩

  13. Toonen, L. S. J., Van Swaaij, B. W. M., Vagevuur, M. L., et al. (2026). The effect of chlorhexidine mouthwash on blood pressure: a systematic review and meta-analysis. International Journal of Dental Hygiene, 24(3), 390-403. DOI: 10.1111/idh.70035. Two of the five included studies found significant increases; pooled, there was no significant difference from control. See also the accompanying commentary: Mutahar, M., et al. (2026). Evidence-Based Dentistry. DOI: 10.1038/s41432-026-01233-z. ↩

  14. de Araújo, J. S. S., et al. (2023). Mouthwash use and oral cancer: a systematic review and meta-analysis. Revista de Saúde Pública, 57, 90. DOI: 10.11606/s1518-8787.2023057004752. Fifteen case-control studies, 6,515 cases and 17,037 controls. Any mouthwash: OR 1.00 (0.79–1.26). Alcohol-containing: OR 1.20 (0.93–1.55), not significant. Three or more times daily: OR 2.58 (1.38–4.82). Over forty years of use: OR 1.44 (1.10–1.90). ↩

  15. Daly, B., et al. Local interventions for the management of alveolar osteitis (dry socket). Cochrane Database of Systematic Reviews. Chlorhexidine rinse before and after extraction: RR 0.58 (95% CI 0.43–0.78). Chlorhexidine gel placed in the socket: RR 0.42 (0.21–0.87). Moderate-certainty evidence. ↩

  16. Effectiveness of chlorhexidine gels and chips in periodontitis patients after scaling and root planing: a systematic review and meta-analysis (2023). BMC Oral Health, 23, 684. DOI: 10.1186/s12903-023-03241-2. Probing depth reduction −0.77 mm (−1.0 to −0.55); clinical attachment gain −0.57 mm (−0.86 to −0.27). ↩

  17. Klompas, M., et al. (2014). Reappraisal of routine oral care with chlorhexidine gluconate for patients receiving mechanical ventilation: systematic review and meta-analysis. JAMA Internal Medicine, 174(5), 751-761. ↩

  18. Dale, C. M., Rose, L., Carbone, S., et al. (2021). Effect of oral chlorhexidine de-adoption and implementation of an oral care bundle on mortality for mechanically ventilated patients in the ICU (CHORAL): a multi-center stepped wedge cluster-randomized controlled trial. Intensive Care Medicine, 47(11), 1295-1302. DOI: 10.1007/s00134-021-06475-2. 3,260 patients across six ICUs. Removing chlorhexidine did not reduce mortality (23.5% versus 21.2%), though oral health scores improved. The cleanest test of the harm hypothesis, and it came back null. ↩

  19. De Cassai, A., Pettenuzzo, T., Busetto, V., et al. (2024). Chlorhexidine is not effective at any concentration in preventing ventilator-associated pneumonia: a systematic review and network meta-analysis. Journal of Anesthesia, Analgesia and Critical Care, 4, 30. DOI: 10.1186/s44158-024-00166-2. Twenty-two RCTs, 5,314 patients, three concentrations. See also the 2022 SHEA update (Infection Control & Hospital Epidemiology), which withdrew the recommendation for routine oral chlorhexidine and recommended toothbrushing instead. ↩

  20. Ehrenzeller, S., & Klompas, M. (2024). Association between daily toothbrushing and hospital-acquired pneumonia: a systematic review and meta-analysis. JAMA Internal Medicine, 184(2), 131-142. DOI: 10.1001/jamainternmed.2023.6638. Fifteen studies, 10,742 patients. Hospital-acquired pneumonia RR 0.67 (0.56–0.81); ICU mortality RR 0.81 (0.69–0.95). ↩

  21. McCullough, M. J., & Farah, C. S. (2008). The role of alcohol in oral carcinogenesis with particular reference to alcohol-containing mouthwashes. Australian Dental Journal, 53(4), 302-305. The review that opened this argument. Superseded by the pooled analyses above, and cited here for the history rather than the conclusion. ↩