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Tooth decay: how long teeth sit in acid
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In one pass The surface of a tooth carries a thin film made of bacteria and sticky material, called dental plaque, a kind of biofilm.
Educational content, not medical advice. See a clinician about your own case.
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Chapter 1
Plaque turns sugar into acid on the tooth
The surface of a tooth carries a thin film made of bacteria and sticky material, called dental plaque, a kind of biofilm. After you eat something sugary, the bacteria in this film break the sugar down for energy and give off organic acids as waste; the main one is thought to be lactic acid.
The acid collects in the liquid inside the plaque (plaque fluid), right against the tooth surface. Normally saliva and plaque fluid hold enough dissolved calcium and phosphate to be supersaturated with respect to tooth enamel, so the tooth does not dissolve; only when the pH falls below a certain line does the fluid start pulling mineral out of the tooth surface, which is called demineralization. That line is the critical pH. The often-quoted 5.5 is only an approximation: the more calcium and phosphate around, the lower the line sits, and it may be as low as about 5.1 or as high as 6.5.
Once the sugar has been swallowed and diluted by saliva, the buffering action of saliva can neutralize the acid, the pH climbs back toward neutral, and redepositing mineral onto the tooth surface gains the upper hand; this is called remineralization. Dental caries is these two processes alternating over and over through the day; damage shows only when demineralization wins out and enough mineral has been lost.
The acid collects in the liquid inside the plaque (plaque fluid), right against the tooth surface. Normally saliva and plaque fluid hold enough dissolved calcium and phosphate to be supersaturated with respect to tooth enamel, so the tooth does not dissolve; only when the pH falls below a certain line does the fluid start pulling mineral out of the tooth surface, which is called demineralization. That line is the critical pH. The often-quoted 5.5 is only an approximation: the more calcium and phosphate around, the lower the line sits, and it may be as low as about 5.1 or as high as 6.5.
Once the sugar has been swallowed and diluted by saliva, the buffering action of saliva can neutralize the acid, the pH climbs back toward neutral, and redepositing mineral onto the tooth surface gains the upper hand; this is called remineralization. Dental caries is these two processes alternating over and over through the day; damage shows only when demineralization wins out and enough mineral has been lost.
Numbers · One pH step down, about ten times more dissolves
The mineral in tooth enamel belongs to the hydroxyapatite family. The solubility of minerals such as table salt barely changes with pH; hydroxyapatite is different, becoming roughly 10 times more soluble for each 1-unit drop in pH. In pure water, only about 30 mg dissolves per litre at pH 7, against about 30 g at pH 4.These figures were measured in pure water, not in the mouth. Saliva and plaque fluid already carry dissolved calcium and phosphate, are normally supersaturated with respect to enamel, and dissolve it only once they fall below the critical pH, so the numbers cannot be read as how much of a tooth dissolves per litre inside the mouth. The critical pH values also need their conditions attached: the source states that it may be around 6.5 in people whose saliva is low in calcium and phosphate, about 5.5 in those whose saliva is high in them, and as low as about 5.1 in plaque fluid, which holds even more. These values come from early laboratory solubility studies; they are a plausible range, not measurements in populations.
Mechanism · Not the work of one germ
Early studies found that Streptococcus mutans and Streptococcus sobrinus were more abundant and more often detected at caries lesions than on sound tooth surfaces, and lactobacilli could be isolated from advanced lesions; this gave rise to the idea that specific bacteria cause caries. Later epidemiological studies found caries developing in the apparent absence of these bacteria, and found them persisting on surfaces that stayed sound; other bacteria that both make acid and tolerate it, such as Bifidobacterium, Actinomyces, Propionibacterium and Scardovia wiggsiae, are also associated with caries. These are associations and cannot simply be read as these bacteria causing caries.The explanation now widely accepted as the most plausible is the ecological plaque hypothesis: when dental plaque meets sugar again and again and spends repeated spells at low pH, acid-tolerant bacteria gain the upper hand, while beneficial bacteria that prefer a neutral environment are held back. One review divides the process into three stages. Normally plaque pH fluctuates between about 5.5 and 7.0 and the community stays in dynamic balance; as sugar arrives more often and for longer, acid-producing bacteria adapted to a pH of around 5.5 to 6 increase and demineralization begins; later still, the community's average pH settles between 4.5 and 5.5 and acid-tolerant bacteria such as Streptococcus mutans dominate. This is a hypothesis framework, and its pH figures were compiled by the authors from earlier studies rather than measured in the review itself.
Chapter 2
One sweet bite, how long the tooth sits in acid
Once sugar enters the mouth, plaque bacteria ferment it into acid, mostly lactic acid; the pH of the plaque fluid falls quickly, then slowly climbs back to where it was. This sharp-fall, slow-rise line is called the Stephan curve.
The climb back depends on saliva: once the sugar has been swallowed and diluted, saliva buffers the acid, the pH rises toward neutral, calcium and phosphate become plentiful again, and putting mineral back gains the upper hand.
Each time sugar is eaten during the day, a new acid period begins, so demineralization and remineralization keep alternating. One integrated hypothesis holds that the more often and the longer low pH occurs, the more readily demineralization starts. Following this mechanism, slowly sipping a sweet drink would push the curve down again and again, which is a reason frequency may matter; but that is an inference, not a measured result. In population data, frequency and total amount are tightly entangled and hard to separate; in adult data that adjust the two for each other, the link with amount is actually the steadier one.
The climb back depends on saliva: once the sugar has been swallowed and diluted, saliva buffers the acid, the pH rises toward neutral, calcium and phosphate become plentiful again, and putting mineral back gains the upper hand.
Each time sugar is eaten during the day, a new acid period begins, so demineralization and remineralization keep alternating. One integrated hypothesis holds that the more often and the longer low pH occurs, the more readily demineralization starts. Following this mechanism, slowly sipping a sweet drink would push the curve down again and again, which is a reason frequency may matter; but that is an inference, not a measured result. In population data, frequency and total amount are tightly entangled and hard to separate; in adult data that adjust the two for each other, the link with amount is actually the steadier one.
Evidence · Where the 30 minutes comes from
The shape of the curve comes from studies in the 1940s that measured plaque pH directly inside the mouth: after exposure to sugar, the pH falls sharply and then slowly returns to baseline. Those were early descriptive measurements; they show what the curve looks like but cannot support a precise recovery time.A 2019 review suggests the familiar 30 minutes was probably carried over from the early experiments of Stephan and Miller; the same review reports that telemetry experiments, which leave a probe on the tooth surface, saw the pH drop continue well beyond those 30 minutes. The author also raises the possibility that how sticky a food is affects the length of the acid period, though this is speculation. The available sources give no reliable number of minutes; 30 minutes is only a rough convention, and the real figure may be much longer.
Mechanism · Fluoride pushes the critical point down
Fluoride on the tooth surface reacts with enamel to form fluorapatite, which is less soluble than the original hydroxyapatite, and the effect is to lower the critical pH. Following this mechanism, the same curve spends less time below the critical line. Fluoride also speeds up and enlarges the remineralization of early lesions.Population data fit this picture: one review notes that when fluoride is used appropriately, the link between sugar and caries is very weak, and some studies cannot detect it at all; a Finnish adult cohort found that among people using fluoride toothpaste every day, the link between sugar amount and caries was weakened but not eliminated. Fluoride therefore blunts the harm of each acid period, but it does not make how much sugar is eaten irrelevant.
Chapter 3
How saliva puts mineral back
Once acid has drawn calcium and phosphate out of the enamel, saliva takes over: it dilutes the leftover sugar and carries it away as you swallow, and the bicarbonate it contains buffers the acid, so the pH of the plaque fluid climbs back toward neutral.
Most of the time, saliva and plaque fluid are supersaturated with calcium and phosphate relative to enamel: the liquid already holds so much mineral that the tooth surface has no reason to dissolve into it. A tooth only starts to dissolve when the pH drops below the critical pH. Once the pH recovers, the fluid is again saturated enough with calcium, phosphate and fluoride that dissolving stops and mineral settling back onto the tooth gains the upper hand. That is remineralization.
A review proposing an integrated hypothesis calls saliva the mouth's most important resilience factor. When there is less of it, sugar and acid are cleared more slowly, which for the plaque bacteria amounts to getting a larger dose from the same mouthful of sugar. A narrative review notes that saliva runs lower at night than by day; Sjögren syndrome, diabetes, and frequent use of some drugs that dry the mouth, such as antihistamines, can also impair salivary function and leave teeth more prone to decay.
Most of the time, saliva and plaque fluid are supersaturated with calcium and phosphate relative to enamel: the liquid already holds so much mineral that the tooth surface has no reason to dissolve into it. A tooth only starts to dissolve when the pH drops below the critical pH. Once the pH recovers, the fluid is again saturated enough with calcium, phosphate and fluoride that dissolving stops and mineral settling back onto the tooth gains the upper hand. That is remineralization.
A review proposing an integrated hypothesis calls saliva the mouth's most important resilience factor. When there is less of it, sugar and acid are cleared more slowly, which for the plaque bacteria amounts to getting a larger dose from the same mouthful of sugar. A narrative review notes that saliva runs lower at night than by day; Sjögren syndrome, diabetes, and frequent use of some drugs that dry the mouth, such as antihistamines, can also impair salivary function and leave teeth more prone to decay.
Evidence · Saliva at night
Saliva secretion follows a day-night rhythm. A 1972 physiology study had 8 volunteers collect unstimulated whole saliva at several fixed times of day for 4 to 26 days, and found a reproducible near-24-hour rhythm in flow rate. The study sampled only waking hours; it did not measure flow during sleep.That saliva runs high by day and low at night, and that the night-time drop favors the progression of decay, is the summary of a narrative review. The same review pooled a few small cross-sectional studies linking sweets before bed and late-night eating with more decay. These are associations, not cause and effect. Less saliva at night, with weaker rinsing and buffering, is the mechanistic reason people worry about sugar before bed, but the review cites no trial that directly compared eating sugar at night with eating it by day.
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Clinical · Why a dry mouth puts decay prevention first
An expert review of dental caries lists salivary dysfunction as a cause of decay and normal salivary function as a protective factor. Among the groups it singles out for focused prevention are people with Sjögren syndrome, people with diabetes, and people who often take medicines that dry the mouth, such as antihistamines. The chain is disease or drug → less saliva → teeth more prone to decay; it does not say that diabetes itself directly causes cavities, and the review gives no figure for how much the risk rises.Another review, which proposes an integrated hypothesis, describes what changes in the mouth when saliva falls: clearance slows, bicarbonate buffering runs short, the bacterial community shifts toward acid-tolerant species, and decay becomes more common. This is a mechanistic argument and comes with no effect size.
Evidence · Sugar-free gum: an effect, but a wide range
The idea behind sugar-free gum is that chewing stimulates more saliva, and saliva is the main source of calcium and phosphate ions around the teeth. In that review, though, this is the authors' assertion; it does not say how much the flow increases.The evidence for an effect comes from a 2020 systematic review and of 12 studies (11 and 1 before-after study), mostly in children aged 4 to 14. Groups chewing sugar-free gum developed on average about 28% fewer new cavities, but the 95% runs all the way from 7% to 48%. Study quality was moderate overall, the trials differed widely in how much gum was chewed, how often, and for how long participants were followed, heterogeneity (I²) was about 95%, and the authors themselves call the evidence tentative. The review was funded by the gum maker Mars Wrigley. Extending the result to adults calls for extra caution. For gums with added calcium and phosphate, the expert review's judgment is that the evidence has yet to build up.
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Chapter 4
A white spot can heal, a hole cannot
Early tooth decay loses the most mineral beneath the surface of the enamel: acid seeps in through the tooth surface and the net loss of mineral is greatest in the layer underneath, a process called demineralization, while the outermost skin, about 0.03 mm thick, stays almost intact. Once enough mineral has been lost underneath, the area shows on the tooth as a chalky white spot lesion.
It is that intact surface that leaves a white spot a way back. The crystals left underneath act as scaffolding, and calcium and phosphate ions from saliva and plaque fluid can deposit back onto them; this is remineralization. If the conditions driving the decay change and preventive measures are added, a white spot can stop or even reverse, although the repair is mostly confined to the outer layer. Fluoride makes remineralization faster and more extensive; why it makes enamel more acid-resistant is covered in the fluoride story (see Fluoride).
If the surface caves in, the result is a visible hole, a cavity. The sources describe this stage as usually irreversible: under ideal conditions the hole may stop growing, but the missing structure does not grow back on its own; dental treatment is generally indicated once the lesion is irreversible and there are also symptoms or a functional need.
It is that intact surface that leaves a white spot a way back. The crystals left underneath act as scaffolding, and calcium and phosphate ions from saliva and plaque fluid can deposit back onto them; this is remineralization. If the conditions driving the decay change and preventive measures are added, a white spot can stop or even reverse, although the repair is mostly confined to the outer layer. Fluoride makes remineralization faster and more extensive; why it makes enamel more acid-resistant is covered in the fluoride story (see Fluoride).
If the surface caves in, the result is a visible hole, a cavity. The sources describe this stage as usually irreversible: under ideal conditions the hole may stop growing, but the missing structure does not grow back on its own; dental treatment is generally indicated once the lesion is irreversible and there are also symptoms or a functional need.
Mechanism · Why erosion does not grow back
Dental erosion and tooth decay take two different routes. In decay, the acid is made by bacteria in the plaque on the tooth; in erosion, the acid arrives directly from outside or from the stomach: many fruit juices and soft drinks have a pH below 3, and gastric juice is around 1.These acids dissolve enamel layer by layer, starting from the outermost surface, so no intact surface is left behind, and with it goes the matrix that new crystals could grow on. Once the dissolved surface meets saliva, it is quickly coated with an acquired pellicle made of salivary and bacterial proteins, and that coating actually inhibits mineral deposition. Dawes therefore concludes that erosion is irreversible.
He also notes that this view differs from some others held at the time. The safer reading is that enamel that has already dissolved does not grow back.
Clinical · Three paths for a white spot
A white spot can go one of three ways, depending on the local bacterial environment on the tooth, diet and fluoride: it can stop where it is but still leave a visible scar, because the optical properties of the enamel have changed; it can remineralize until it looks close to normal; or it can stay active and keep progressing deeper.Dawes lists the conditions under which remineralization can happen: an intact surface, a plaque-free tooth, enough saliva (or saliva stimulated by chewing sugar-free gum), and fluoride applied to the tooth. He calls the clinical evidence for this very good, but the reference he attaches to that sentence is an in vitro study of artificial lesions. These conditions are therefore better read as a mechanistic explanation than as a finding measured in clinical trials.
If a cavity keeps progressing after it forms, it eventually reaches the pulp, and at that point root canal treatment or extraction is usually needed. The sources describe dental treatment as indicated when the lesion has reached an irreversible stage and there are also symptoms, or a functional or aesthetic need.
Chapter 5
How often or how much: what the evidence says
Reasoning from the mechanism, the more often sugar is eaten, the more rounds of acid are produced. In the Swedish Vipeholm study, published in 1954, sticky sweets eaten between meals clearly increased new cavities, while sugar drunk in solution with meals did not noticeably increase them. But those groups changed not only how often they ate sugar but also its stickiness and timing, and they were not randomized.
In a Finnish adult cohort, once frequency and amount were adjusted for each other, only the amount was still linked to tooth decay. People who eat more sugar also tend to eat it more often, so the two are hard to pull apart. The most honest reading at present is that both frequency and amount matter, and dental prevention advice already limits both.
In a Finnish adult cohort, once frequency and amount were adjusted for each other, only the amount was still linked to tooth decay. People who eat more sugar also tend to eat it more often, so the two are hard to pull apart. The most honest reading at present is that both frequency and amount matter, and dental prevention advice already limits both.
Mechanism · Repeated acid shifts the bacteria
Frequent intake has a second consequence, and it plays out in the bacterial community inside the plaque. When plaque meets sugar regularly and keeps sitting at low pH, the environment favors the growth and metabolism of acid-tolerant bacteria, while holding back beneficial bacteria that prefer neutral conditions.This explanation is called the ecological plaque hypothesis. The review describes it as the currently accepted and most plausible explanation, but it is still a mechanistic model, based mainly on laboratory studies and on comparing the bacteria on healthy and decayed tooth surfaces, not a directly proven conclusion.
The same review also writes that changing the factors that drive this imbalance can control the disease. Its examples are reducing the amount and frequency of sugar intake, or switching snacks to sugar substitutes that mouth bacteria cannot turn into acid. Here, amount and frequency are named together.
Evidence · What the Vipeholm study saw
The Vipeholm study was carried out in an institution in Sweden and followed 436 long-term adult residents for 5 years; each group ate sugar in a different way.Sugar drunk with meals: a solution containing about 300 g of sucrose a day, taken with meals, more than twice the Swedish average intake at the time, did not noticeably raise caries activity.Sticky sweets between meals: the groups given toffees or caramels, specially made for the study and prone to cling to the teeth, ate them between meals, and their caries activity rose.After withdrawal: once these decay-promoting habits stopped, the rise disappeared, and the toffee and caramel groups went back to their earlier low level.
From this the authors concluded that the highest risk comes from eating sugar between meals in a form that lingers on the tooth surface.
Several limits belong with this result. Sticky food eaten with meals was not necessarily safe either: the group given sticky sweet bread with meals also showed a rise in the second year, and even with sugar held to a minimum, new caries still appeared. Nor was this a randomized trial: groups were assigned by ward, the participants were long-term residents with intellectual disabilities, there was no blinding, and applying the results to the general population calls for caution. In addition, the toffee groups changed not only how often they ate sugar but also its stickiness and timing, so the study supports the risk of a whole package of habits, eating between meals, sticky and often, and cannot isolate frequency on its own.
Evidence · Why adult data lean toward amount
The Finnish cohort included 1,702 adults who still had teeth and who took part in at least two of three rounds of national health surveys, spanning about 11 years. How much sugar they ate and how often were both self-reported on a food frequency questionnaire; the outcome was DMFT measured repeatedly, the number of teeth that were decayed, missing because of decay, or filled.After mutual adjustment: only the amount was significantly linked to DMFT; frequency was not.Shape of the dose response: risk rose roughly in a straight line with amount, and none of the curved shapes tried fit better than the straight line.Fluoride toothpaste: among people who used fluoride toothpaste daily, the link was weaker but did not disappear.
As van Loveren reports, the correlation between amount and frequency in these data was about 0.64. When two measures rise and fall together like this, and both are self-reported, adjusting each for the other makes it hard to tell their separate effects apart; frequency not reaching significance does not mean frequency is irrelevant.
Cross-sectional data from the US NHANES 2011–2016 on 10,514 adults point the same way: the amount of added sugar was consistently linked to tooth decay. The result for frequency depended on how it was counted: counted as the number of sugary items a day, it showed no link; counted as the number of eating occasions a day, it showed only a very weak link with DMFS (decayed, missing and filled tooth surfaces), about 5% higher per standard deviation, and no link with untreated decay. The authors also caution that the study did not measure how long each eating occasion lasted, which may understate the role of frequency, and that cross-sectional data cannot show cause and effect.
The van Loveren review weighed this evidence and still leaned toward frequency, on the grounds that frequency fits better with the mechanism of caries; he inferred that cutting the amount without cutting the frequency does not seem to be an effective way to prevent decay. This is the author's judgment reasoned from the mechanism, not something the data show directly.
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Numbers · Where the limit on amount comes from
In WHO's advice on sugars, the part on tooth decay rests on a 2014 systematic review by Moynihan and Kelly. From 5,990 papers it selected 55 studies: 3 intervention studies, 8 cohort studies, 20 population studies and 24 cross-sectional studies, with no ; the studies differed too much to be fully pooled in a .42 of the 50 studies in children, and all 5 studies in adults, reported at least one positive association between sugars and caries.Caries was lower when free sugars were below 10% of daily energy, with evidence rated moderate quality.An association was also seen below 5%, but the evidence was rated very low quality, and the authors' wording was that there may be benefit.
On this basis, WHO in 2015 recommended that adults and children keep free sugars below 10% of daily energy, a strong recommendation, and that going further, below 5%, is a conditional recommendation. Free sugars are the monosaccharides and disaccharides added to foods and drinks, plus the sugars naturally present in honey, syrups, fruit juices and fruit juice concentrates; the sugars in fresh fruit, vegetables and milk are not included.
After that guideline, a 2022 ten-year update combined the studies of the original review with those newly included from 2011 to 2020, 78 in all; 64 showed at least one positive association, while 20 also reported results with no association. New cohort data confirmed the 10% line, and the quality of evidence for the 5% line rose from very low to low.
All of these figures concern amount, not how often sugar is eaten; there are no randomized controlled trials and the studies are mainly observational, so they show associations. They sit on the side of amount mattering too.
moynihan-2014-sugars-caries-whomoores-2022-sugars-caries-update
In practice · Fluoride toothpaste changes the question
Fluoride toothpaste does not wipe out the effect of sugar; it weakens it. On the tooth surface, fluoride makes early lesions remineralize faster and take back more mineral. In the Finnish cohort, among people who used fluoride toothpaste every day, the link between sugar and tooth decay was weaker but still present. The van Loveren review puts it more strongly: when fluoride is used appropriately, the relation between sugar and caries is very weak or cannot be detected at all. The two sources agree in direction and differ in strength.The review describes individual prevention in the dental clinic as built around two things: limiting the amount and frequency of sugar, plus frequent use of fluoride toothpaste, with stronger measures such as fissure sealants added according to caries risk. When assessing risk, the dentist asks how much sugar is eaten a day, how many times, how many snacks come between meals, and what kind of toothpaste is used.
Putting these sources together: eating sugar in smaller amounts and less often both sit on the side of fewer cavities; eating sticky sweets again and again between meals is the high-risk pattern the Vipeholm study points to, while whether stickiness is the key factor is still speculation; regular fluoride toothpaste weakens this link, but in the Finnish cohort it did not make it disappear. This is a general science summary, and the state of anyone's teeth is for a dentist to judge.
Chapter 6
The tool: how long teeth sit in acid each day
To judge what sugar does to teeth, besides counting how many grams were eaten, count how many acid spells the tooth surface goes through each day, and how long each one lasts. After sugar, plaque pH falls sharply and then climbs back slowly; one spell is often said to last about 30 minutes, but continuous monitoring reported in a review shows it can run longer. Following that mechanism, every snack or sweet drink between meals opens a new acid spell, and sipping slowly amounts to topping up the sugar again and again; eating at bedtime meets a mouth with less saliva at night, so rinsing and buffering are both weaker. The sugar in honey and fruit juice also counts as free sugars.
Counting acid spells is reasoning from mechanism, not a replacement for total amount: in population data, frequency and total amount travel closely together, and amount counts as well. Fluoride toothpaste speeds up the remineralization of early lesions and is widely seen as the foundation of preventing decay. A hole you can see usually cannot grow back, and toothache or a darkening tooth belongs with a dentist.
Counting acid spells is reasoning from mechanism, not a replacement for total amount: in population data, frequency and total amount travel closely together, and amount counts as well. Fluoride toothpaste speeds up the remineralization of early lesions and is widely seen as the foundation of preventing decay. A hole you can see usually cannot grow back, and toothache or a darkening tooth belongs with a dentist.
In practice · Counting a day in acid spells
The unit being counted is the acid spell, not the gram. Reasoning from the way pH falls and then recovers after sugar, a glass of juice finished in one go is one spell, while the same glass sipped across an afternoon is an afternoon of repeated top-ups. Sugar in honey, syrups, fruit juice and juice concentrates counts as free sugars, just like sugar added to food; sugar that occurs naturally in fresh fruit, vegetables and milk does not. The World Health Organization guideline makes keeping free sugars below 10 percent of energy a strong recommendation, and going below 5 percent a conditional one, with very low-quality evidence behind the latter.For infants and young children, the American Academy of Pediatric Dentistry (AAPD) policy stresses in dietary counseling: avoiding frequent intake of sugary drinks and foods, avoiding on-demand bottle or breastfeeding at night after 12 months of age, and no juice for children aged 6 to 12 months.
Fluoride toothpaste is the base. A Cochrane review pooling around 70 trials in children and adolescents found that, compared with non-fluoride toothpaste, it cut the three-year increase in decayed permanent tooth surfaces by about 24 percent, with twice-daily brushing doing better than once. One review holds that when fluoride is used properly, the link between sugar and caries becomes very weak or undetectable; yet in Finnish adults, daily fluoride toothpaste only weakened the link between total sugar and caries rather than removing it.
Saliva is the main source of calcium and phosphate ions around the teeth, and chewing sugar-free gum increases its flow. One estimated that sugar-free gum lowered caries increment by about 28 percent, but the interval was wide (7 to 48 percent), study quality was moderate, results varied a lot between trials, most participants were children, and the funder was the gum maker Mars Wrigley.
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Red flag · When it is time to see a dentist
An early lesion sits beneath the enamel surface and looks like a white spot. At this stage, changing the conditions that drive it or adding preventive measures can stop it or even reverse it; repair, though, mostly happens at the surface, so a halted lesion may leave a visible scar, or it may remineralize until it is barely noticeable.Once the surface collapses into a hole you can see, the damage has usually passed the point of return; under ideal conditions the hole may stop growing, but the hole itself does not grow back. If there are symptoms or functional needs at that point, it usually takes dental treatment to deal with it; if decay keeps going it reaches the pulp, and root canal treatment or extraction may then be needed.
So toothache, a visible hole, or a tooth turning dark or discolored all call for a dentist's examination, and changing how often sugar is eaten cannot stand in for that. What is described here is mechanism; it does not replace a dental examination or treatment.
References · 9
- Pitts, N. B., Zero, D. T., Marsh, P. D., Ekstrand, K., Weintraub, J. A., Ramos-Gomez, F., Tagami, J., Twetman, S., Tsakos, G., & Ismail, A. (2017). Dental caries. Nature Reviews Disease Primers, 3, Article 17030. 10.1038/nrdp.2017.30
- Dawes, C. (2003). What is the critical pH and why does a tooth dissolve in acid? Journal of the Canadian Dental Association, 69(11), 722–724. jcda.ca/sites/default/files/back_issues/vol-69/issue-11/722.pdf
- Stephan, R. M. (1944). Intra-oral hydrogen-ion concentrations associated with dental caries activity. Journal of Dental Research, 23(4), 257–266. 10.1177/00220345440230040401
- Nyvad, B., & Takahashi, N. (2020). Integrated hypothesis of dental caries and periodontal diseases. Journal of Oral Microbiology, 12(1), 1710953. 10.1080/20002297.2019.1710953
- van Loveren, C. (2019). Sugar restriction for caries prevention: Amount and frequency. Which is more important? Caries Research, 53(2), 168–175. 10.1159/000489571
- Bernabé, E., Vehkalahti, M. M., Sheiham, A., Lundqvist, A., & Suominen, A. L. (2016). The shape of the dose-response relationship between sugars and caries in adults. Journal of Dental Research, 95(2), 167–172. 10.1177/0022034515616572
- Kurtović, A., Talapko, J., Bekić, S., & Škrlec, I. (2023). The relationship between sleep, chronotype, and dental caries—A narrative review. Clocks & Sleep, 5(2), 295–312. 10.3390/clockssleep5020023
- Gustafsson, B. E., Quensel, C.-E., Lanke, L. S., Lundqvist, C., Grahnén, H., Bonow, B. E., & Krasse, B. (1954). The Vipeholm dental caries study: The effect of different levels of carbohydrate intake on caries activity in 436 individuals observed for five years. Acta Odontologica Scandinavica, 11(3–4), 232–364. 10.3109/00016355308993925
- World Health Organization. (2015). Guideline: Sugars intake for adults and children. Geneva: WHO. www.who.int/publications/i/item/9789241549028
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