The Fluoride Question

Part III: Dental Caries Is Not a Fluoride-Deficiency Disease

Whenever concerns about fluoride are raised, the response is almost automatic: But fluoride prevents cavities.

That statement deserves a closer look.

There is an important difference between saying that fluoride can alter mineral chemistry at the surface of a tooth and saying that adding fluoride to an entire community’s drinking water meaningfully prevents dental caries. Those are not the same question.

As I discussed in Part I of this series Fluoride and the Developing Brain, the 2024 Cochrane review found that in contemporary studies, starting community water fluoridation was associated with an average difference equivalent to approximately 0.24 fewer decayed, missing, or filled primary teeth per child. The evidence was rated low certainty, and the confidence interval included the possibility of no benefit. For permanent teeth, Cochrane described the contemporary evidence as very uncertain.

That is approximately one-quarter of one primary tooth. This estimate suggests a small average additional benefit in primary teeth, with uncertainty that includes no benefit. It deserves careful consideration, especially when older estimates of effectiveness are used to justify present-day policy.

And that leads me to a much bigger question:

What disease are we actually trying to treat?

In Part II, “Fluoride in the Water: Who’s Measuring Your Dose?”, I examined why a water concentration is not an individual dose. Here, I want to examine the other side of that equation: individual need. Just as people differ in how much fluoride they ingest and retain, they differ in the conditions driving their tooth decay. A meaningful discussion of prevention must consider both.

One of the most persistent fluoride messages is that children need to ingest fluoride while their teeth are developing so that fluoride can become incorporated into enamel and make those teeth stronger. Yet even the CDC’s own detailed review of fluoride mechanisms says something quite different. As early as 2001, the CDC explained that fluoride’s predominant cavity-preventing effect occurs after teeth erupt, through topical action in the mouth: posteruptive and topical. In other words, its principal action occurs primarily after the tooth has erupted, when fluoride is present in saliva and plaque fluid at the tooth surface.

The CDC also acknowledges that simply having a high concentration of fluoride incorporated into sound enamel cannot, by itself, explain fluoride’s caries-preventive effect. Fluoride present around the tooth can influence mineral loss during an acid challenge and may facilitate remineralization when conditions improve. It can also affect bacterial metabolism under certain conditions. But these are primarily surface-level interactions occurring within the saliva-biofilm-enamel environment.

That distinction matters enormously. Fluoride may change how the tooth surface responds to disease. It does not explain why the disease is occurring.

Dental Caries Is Not a Fluoride-Deficiency Disease

I keep coming back to this:

Dental caries is not a fluoride-deficiency disease.

When a patient presents with repeated decay, I do not believe the most important question is, How can I get more fluoride onto or into this patient?

My question is: Why is this patient developing decay?

Current decay and a history of decay are among the strongest predictors of future decay. To help my patient stop getting cavities, I need to answer these questions:

• What does the oral biofilm look like?
• How frequently are fermentable carbohydrates entering the mouth?
• How much saliva is the patient producing?
• What is the quality of that saliva?
• How effectively does it buffer an acid challenge?
• What is the resting oral pH?
• Is the patient experiencing medication-induced xerostomia?
• Are they mouth breathing?
• Is reflux present?
• What is happening nutritionally and metabolically, including blood glucose control and diabetes?
• Could digestive conditions, dietary restrictions, or impaired nutrient absorption be relevant to this patient’s oral health?
• Are hormonal changes contributing to oral dryness or changes in the oral environment?
• What does the patient’s individual oral microbiome tell us?

These factors will not be identical in every patient, and not every factor will contribute to every case. That is precisely why prevention must be individualized. Caries is a biological disease process with multiple interacting contributors.

When a patient keeps developing cavities, we need to ask more than, “Are you brushing and flossing?” We need to investigate what is allowing the disease process to continue—and work with the patient and, when appropriate, their medical team to address it.

Fluoride alone does not resolve all the conditions driving decay. It does not restore inadequate salivary flow or poor buffering capacity, change frequent sugar exposure, or address medication-induced dry mouth and mouth breathing during sleep.

When I see decay, I want to understand the terrain that allowed it to develop.

If saliva is inadequate, why? If buffering is poor, why? If the oral environment remains acidic for prolonged periods, what is contributing to that acidity, including possible silent reflux or GERD? If the biofilm is highly acidogenic, what is feeding it?

If a patient brushes beautifully but continues developing decay, what have we missed? If someone suddenly develops new cavities after decades without decay, what changed? A medication? Mouth breathing? Menopause-related dryness? Diet? Hydration? Metabolic health?

There is no single answer for every patient. Lasting prevention means identifying the contributors relevant to that person and helping address them.

Stop guessing. Start testing.

That means examining the biofilm and its behavior, assessing saliva and buffering capacity, and reviewing diet, medical history, medications, and the daily oral hygiene routine. Testing should help answer a specific clinical question and guide what we do next.

Helping a tooth resist an unhealthy environment is valuable. But my goal reaches further: to help create an oral environment that supports health and gives that patient a better chance of staying cavity-free.

Fluorosis Is Not “Just Cosmetic”

There is another part of this discussion that dentistry too often minimizes: dental fluorosis.

The American Dental Association currently describes dental fluorosis as “primarily a cosmetic concern.” The ADA explains that it occurs when excessive fluoride is ingested while permanent teeth are developing and that changes can range from white flecks or striations to brown discoloration and pitting in more severe disease.

I have a problem with the ADA phrase in another of their articles calling fluorosis just cosmetic. My concern is what can be overlooked when fluorosis is framed primarily as a cosmetic issue. Severity matters, and so does the experience of the person living with it.

Certainly, very mild fluorosis can consist of faint white markings that may never bother the individual, and we should not claim that every person with mild fluorosis has structurally weak teeth or experiences psychological distress.

But fluorosis exists on a spectrum.

It is a developmental alteration of enamel caused by excessive systemic fluoride exposure while enamel is forming. With increasing severity, enamel can become more porous and hypomineralized, and severe fluorosis may involve staining, pitting, and post-eruptive enamel breakdown. That is not merely a paint-color problem.

And appearance matters too. Our teeth are front and center when we smile, laugh, speak, interview for jobs, date, take photographs, and interact with the world. A 2024 systematic review examined 16 studies involving more than 16,000 children and adolescents. Nine of those studies reported an adverse association between dental fluorosis and oral-health-related quality of life. The researchers appropriately described the evidence as heterogeneous, but the findings certainly do not support dismissing every psychosocial effect as meaningless.

Fluorosis should therefore be discussed honestly. Not every case is consequential. But neither is every case “simply cosmetic”.

Cochrane’s earlier fluorosis analysis estimated that at approximately 0.7 mg/L, about 40% of people may have fluorosis of some degree, while approximately 12% may have fluorosis considered aesthetically concerning. Those estimates were based on older evidence and were not newly updated in the 2024 review, so they need to be interpreted with appropriate caution.

Still, place those figures beside the contemporary caries findings.

The possible average benefit in primary teeth is approximately 0.24 of one tooth.

The earlier fluorosis estimate at 0.7 mg/L was approximately 40% with fluorosis of some degree and approximately 12% with fluorosis of aesthetic concern.

These figures come from different analyses and should not be treated as a simple head-to-head calculation. But they absolutely belong in the same risk-benefit discussion.

Especially when the intervention is population-wide.

There is one more reason fluorosis matters to me. Dental fluorosis is visible evidence that systemically ingested fluoride reached a developing tissue and altered the way that tissue formed. That does not mean fluorosis proves neurological injury. It does not. But Part I of this series examined emerging concerns about prenatal fluoride exposure and neurodevelopment. Fluorosis should remind us of a fundamental biological principle:

Dose, timing, and developmental vulnerability matter.

We already accept that principle when discussing developing enamel. We should be willing to investigate it rigorously when discussing other developing tissues as well.

What Are We Really Protecting?

So now I come back to the argument I hear repeatedly:

But fluoride prevents cavities.

Perhaps the better question is:

What is causing this patient’s cavities, and are we addressing that?

Fluoride’s principal caries-preventive action is predominantly topical and occurs after teeth erupt. Fluoridated water supplies that topical exposure as it passes through the mouth, while swallowed fluoride also contributes to systemic exposure. The question is whether the additional benefit of delivering fluoride through drinking water justifies that exposure, considering contemporary evidence, other preventive options, and differences in individual vulnerability.

One patient may have excellent saliva, stable pH, low carbohydrate frequency, a healthy biofilm, and no history of decay. Another may have severe xerostomia, frequent snacking, reflux, mouth breathing, and rampant caries. Those are not the same patient. They do not have the same biology. They do not have the same risk. And yet, community water fluoridation treats them as though they require the same intervention. That is precisely the kind of thinking I believe dentistry needs to reconsider.

• Preventing dental caries.
• Looking at the biofilm.
• Measuring saliva.
• Evaluating buffering.
• Assessing pH.
• Talking honestly about carbohydrate frequency.
• Recognizing medication-induced dry mouth.
• Addressing nasal breathing and airway issues where appropriate.
• Investigating reflux.
• Looking at nutrition, hormones, metabolic health, and individual susceptibility.
• Stop assuming that every cavity represents a need for more fluoride.

Is reflux contributing to acid exposure in the mouth? Although reflux-related erosion and dental caries are different processes, both belong in a thorough investigation of tooth damage. When reflux is suspected, appropriate medical evaluation and testing can help us address the source of that exposure alongside protecting the teeth. My goal is to improve the oral environment from both directions: within the mouth and through care for the conditions affecting it.

Better Questions. Better Prevention.

Dental caries is not a fluoride-deficiency disease. It is a biological process with multiple interacting contributors. If we truly want to prevent it, we need to understand the biology—and investigate what is allowing decay to develop in each patient.

We have much to assess, measure, and improve: saliva, buffering capacity, biofilm, diet, medications, breathing patterns, and medical conditions that influence the oral environment. Our goal should reach beyond treating the next cavity to helping the patient change the conditions that keep allowing cavities to form.

Medicine has changed recommendations before. Dentistry has changed recommendations before. Public health has changed recommendations before. Reconsidering a recommendation when the evidence changes is not a failure of science. That is science doing exactly what science is supposed to do.

Our patients deserve prevention guided by evidence, thoughtful investigation, and their individual needs.

Stop guessing. Start testing.

Test. Teach. Treat. Repeat.

Coming Up: Fluoride Part IV

And there is one more question I want to explore next.

If community water fluoridation is as essential to preventing dental decay as we have been told, what should happen when a community stops fluoridating? Cavities should increase—right? Several communities and countries have actually given us the opportunity to look. In Part IV of this series on fluoride, we will examine what happened when communities stopped fluoridating their water. Did decay increase, remain stable, or decline—and what else changed during those years? These studies offer an opportunity to examine outcomes, while considering differences in diet, dental care, other fluoride exposure, and study design.

Barbara Tritz

Queen of Prevention

References

Iheozor-Ejiofor Z, Walsh T, Lewis SR, et al. Water fluoridation for the prevention of dental caries. Cochrane Database Syst Rev. 2024;10:CD010856. doi:10.1002/14651858.CD010856.pub3.

Centers for Disease Control and Prevention. Recommendations for Using Fluoride to Prevent and Control Dental Caries in the United States. MMWR Recomm Rep. 2001;50(RR-14):1–42.

American Dental Association. Toothpastes: Fluoride and Dental Fluorosis. ADA Oral Health Topics.

Montanher PL, et al. Impact of dental fluorosis on the oral health-related quality of life: a systematic review. Clin Oral Investig. 2024;28(11):599. doi:10.1007/s00784-024-05991-x.