Dental caries

Dental caries is a progressive disease of the hard tissues of teeth, in which acids produced by microorganisms in the dental biofilm dissolve the mineral of enamel and dentin. Caries is best understood as a dynamic process rather than a single event: early lesions can be arrested or reversed when the local pH returns to neutral and minerals are redeposited, but repeated acid attacks can produce cavities that require restoration. Its basic causes are a cariogenic biofilm, frequent intake of fermentable carbohydrates, and host factors such as saliva, tooth structure, and genetics acting over time. The disease is strongly shaped by nutrition, social conditions and access to care.

The condition matters because it is extremely common. Untreated decay in permanent teeth is among the most prevalent health conditions globally, and the burden falls unevenly across income groups and countries. Caries is therefore a central topic in public-health, epidemiology and health-promotion, as well as in clinical dentistry. This entry covers the tooth tissues involved, the microbiology and chemistry of lesion formation, the risk factors and classification of lesions, diagnosis and global burden, prevention (especially fluoride and its policy debates), restorative and non-surgical treatment, complications, the history of how the disease was understood, and current research directions.

Definition and the demineralization–remineralization balance

Dental caries is a chronic, multifactorial condition. It is mostly characterized by structural mineral loss of the enamel beneath an apparently intact surface layer. Because the process runs in both directions, a lesion reflects a balance rather than a single event. Acid is produced when sugars from food and drink interact with bacteria in the dental biofilm (plaque). Mineral is removed during each acid episode and returned when saliva neutralizes the acid. Demineralization and remineralization occur many times throughout the day, and caries progresses only when demineralization exceeds remineralization. This is why the disease is considered potentially reversible: in some instances, when demineralization is limited to a shallow surface, remineralization can halt or even reverse the caries process.

The threshold separating these two directions is the critical pH. It is defined as the highest pH at which there is a net loss of minerals from tooth enamel. For enamel it is generally placed at 5.5, but it can be a little higher or lower depending on individual factors. Above this value, a stable equilibrium exists between the calcium and phosphate ions in saliva and the crystalline mineral of the enamel. Below it, saliva and plaque fluid become undersaturated and hydroxyapatite begins to dissolve. The threshold is not a fixed constant. It depends on the acidic pH as well as on the calcium and phosphate ion concentrations in the acidic medium, and it is further shaped by the solubility of enamel, i.e. the thermodynamic solubility product. Dentin has a higher threshold: the critical pH for the initiation of demineralization in dentin is 6.2 to 6.4, which is higher than that of enamel, so dentin is much more susceptible to demineralization than enamel at similar pH levels.

Early and cavitated lesions

The earliest visible enamel lesion is the white spot. It represents dissolution of the surface structure, with increased porosity, and takes on a dull appearance when air-dried because of the differences in light scattering from the surrounding enamel. Its surface often remains largely intact: the loss of mineral occurs in the bulk of the enamel, whereas the surface of the lesion remains relatively intact, a so-called pseudo-intact surface layer. Such lesions may maintain their surface integrity, become stained and arrested, or progress to frank cavitation. Enamel contributes to this limitation because it is the only tissue of the tooth that does not have the ability to grow or repair itself after maturation.

Cavitation changes the outlook. A cavitated enamel lesion cannot be cleaned sufficiently by the patient and will progress. Once a cavity forms, remineralization seems very unlikely under clinical conditions. In cavitated dentin, the outermost zone loses its organic matrix and mineral, which cannot be repaired, while the deeper zone affected by plaque acids may still recover.

Repeated challenges versus a single prolonged exposure

Frequency matters more than the amount consumed. It is not how much sugar you consume but how often you consume it that matters most. A prolonged drink does not produce one acid episode: sipping on a soft drink over an hour creates multiple acid attacks rather than one. Prolonged sipping also gives the mouth less time to recover between exposures. Each exposure resets the cycle, so the mouth never returns to a neutral state long enough for net remineralization to occur (each sugar exposure restarts the acid attack cycle, keeping oral pH low, and the mouth needs time between exposures to allow saliva to neutralize acids and remineralize enamel.). The consequence is cumulative mineral loss: if acid exposure is frequent and prolonged, increasing amounts of mineral are lost, which reduces crystal size and enlarges enamel pores.

Caries should be distinguished from dental erosion, which is the deterioration of dental hard tissue via a non-bacterial chemical process. Erosion typically occurs when the pH of fluids around the tooth drops below 4.5, a much lower level than the caries threshold.

Tooth structure and why enamel and dentin are vulnerable

Enamel: a dense mineral shell with little organic matrix

Enamel covers the crown and is the hardest tissue in the tooth. Its inorganic fraction is about 96% by weight, and that fraction is mainly carbonated hydroxyapatite crystals. The residual organic matrix makes up only about 1–2% of mature enamel and mainly serves to bind the crystals together. Its crystals are very long and tightly packed, which suits enamel to cutting and grinding food but also means that there are few organic barriers to slow acid penetration. Once the pH at the surface falls, the mineral lattice dissolves with little resistance, which is why enamel is the first tissue that acid-producing plaque attacks.

Dentin: a more organic, tubule-bearing tissue

Beneath enamel lies dentin, which forms most of the tooth's bulk. Published figures for its composition differ with the basis of measurement: one source gives roughly 70% mineral by weight, while another reports about 45% mineral by volume with 33% organic material and 22% water. Its crystals are smaller and more irregular than those of enamel, and its collagen-rich matrix is less mineralized and less brittle, which is why dentin is softer than enamel. Dentin is also pierced by tubules roughly 1 µm in diameter, numbering on the order of 30,000 to 50,000 per square millimetre. The peritubular dentin lining each tubule is far more mineralized than the intertubular dentin between them. Because the tubules are open channels, a breach in enamel gives acids and bacterial products a route to the inner tissue, and the dentin's lower mineral content makes it more easily dissolved once that route opens.

The tubules house the cytoplasmic extensions of odontoblasts, and they carry fluid that can transmit stimuli to nerve endings, which is part of the basis for tooth sensitivity.

Cementum and exposed root surfaces

Cementum covers the root and has a lower mineral content than enamel. Its porosity allows acids, enzymes from saliva and gingival fluid, and bacterial products to diffuse into it, and dentin becomes more porous as acid and enzymes remove its mineral. Because cementum sits under the gum, it is normally protected. Gingival recession, which becomes more common with age, exposes the root surface to plaque and acid. Root caries most often develops at or near the cemento-enamel junction, and one review reports that caries progresses on root dentin roughly twice as fast as on coronal enamel. Root caries is a major cause of tooth loss in older adults, and over half of people older than 65 have experienced it. Recession is the anatomical precondition, but the age-related rise in risk also reflects factors such as dry mouth, medications and reduced manual dexterity, which are covered elsewhere in this article.

The pulp and its response to invasion

The dental pulp, a soft tissue of connective tissue, blood vessels and nerves in the pulp chamber and root canals, supplies nutrition, immune defence and sensation to the tooth. Odontoblasts at its edge continuously deposit dentin throughout life. When bacteria and acids advance through enamel and dentin, the odontoblast processes and the pulp are exposed to these products. The pulp responds with inflammation and local innate immune activity. Odontoblasts can lay down reparative dentin that narrows the tubules, but if the challenge is persistent or intense, the inflammation becomes pulpitis, and the tissue may eventually die, allowing infection to spread to the periapical region. These later consequences are discussed in the section on complications.

Dental biofilm formation and maturation

Acquired pellicle

Within seconds to minutes of a tooth surface being cleaned, a thin conditioning film called the acquired pellicle forms on the enamel. It is built from salivary proteins and glycoproteins that adsorb onto the hydroxyapatite surface, mainly through electrostatic attraction between calcium and phosphate groups on the mineral and charged groups on the macromolecules. Mucins, proline-rich proteins, statherin, histatins and cystatins are among the components with a strong affinity for hydroxyapatite. The pellicle does more than coat the tooth: some receptors on salivary molecules are exposed to bacteria only after the molecule has adsorbed, so the film actively sets the terms of colonization. Any later plaque is therefore built on a surface that saliva has already conditioned.

Early and late colonizers

Bacteria arrive at the pellicle quickly. Early colonizers, mostly facultatively anaerobic Gram-positive streptococci such as Streptococcus sanguinis, S. mitis and S. oralis, together with Actinomyces species, are often recovered from cleaned enamel within an hour. Their first attachment is reversible and relies on weak van der Waals forces. Attachment becomes stable as adhesins on the bacterial surface engage specific receptors in the pellicle. Plaque then grows in two ways: the attached cells divide, and new species adhere to cells already present. Secondary colonizers bind to early colonizers through co-aggregation. Fusobacterium nucleatum is important here because it co-aggregates with many partners and so links early and late species. Later colonizers include anaerobes that accumulate as the community thickens.

The classic six-stage model, which treats succession as an orderly sequence, has been qualified by more recent work. Observations of bacterial aggregates in saliva suggest that multispecies units, rather than single cells, can reach the surface together, and that organisms traditionally labelled "early" and "late" can be found adhering in the same clusters.

Extracellular matrix

As the community matures, it embeds itself in a matrix of polymers of bacterial and salivary origin. The most intensively studied component is glucan, made from sucrose by glucosyltransferases (Gtfs) secreted by S. mutans. GtfB, GtfC and GtfD convert sucrose into water-insoluble and soluble glucans; the insoluble products are especially important for adhesion. Gtfs bound to the pellicle or to bacterial surfaces can synthesize glucan in situ within minutes once sucrose is present. The resulting glucan supplies sticky binding sites for other organisms, binds cells to one another and to the enamel, and forms a physical scaffold that resists clearance by saliva and host defenses. In one study, polysaccharides made up as much as 40% of the dry weight of dental plaque, depending on diet and sampling time. Because glucan can also be broken down as an internal carbon reserve, it may contribute to acid production when external sugars run out.

Spatial gradients in mature plaque

A mature plaque is not uniform. Early aerobic and facultative organisms consume oxygen, so the deeper layers of the biofilm become progressively oxygen-poor and dominated by anaerobes. Because diffusion through a dense matrix is slow, saliva buffers the acids produced at the surface only partly, and the pH near the enamel can fall far below the bulk fluid value; one review cites about 4.3 for a cariogenic biofilm, while the critical pH for enamel dissolution is generally put near 5.5. Microbial architecture also becomes organized into columnar structures in mature communities. Reduced oxygen and low pH reduce growth rates, which in turn makes cells near the tooth harder to kill with antimicrobials, a feature that links biofilm structure to the persistence of acid-producing communities discussed elsewhere in this entry.

Acidogenic and aciduric microbes, especially Streptococcus mutans

Streptococcus mutans

Among the organisms linked to caries, Streptococcus mutans has the most extensive experimental record. Its pathogenic profile rests on three traits: it produces acid from sugars, it tolerates low pH, and it builds sucrose-derived glucans that anchor it to the tooth. It is acidogenic and acid tolerant, uses sucrose to synthesize extracellular polysaccharides through glucosyltransferases, and can adhere to glucan-coated tooth surfaces. Acid is generated by fermentation of sugars through glycolysis, with lactic acid as the major product.

Glucosyltransferases (GtfB and GtfC, which generate water-insoluble glucans, and GtfD, which generates soluble glucans) convert sucrose into glucose-based polymers joined by glycosidic bonds. These polymers build a sticky matrix that holds the community together. Acid tolerance is equally important: S. mutans is more viable under acidic conditions than other Streptococcus species.

Experiments separating these traits show that they are not interchangeable. In a rat model, deleting glucan-binding protein genes reduced cariogenicity in only some mutants, and the attenuation was unlikely due to differences in acid-related properties since the mutants were at least as acidogenic and acid-tolerant as the parental strain. Adhesion to glucan, therefore, can be a limiting factor independent of acid output. The species is also not strictly necessary for disease: mutans was absent in more than 50% of the samples from adolescents with dental caries in one cited study.

Other aciduric and acidogenic organisms

Other members of the mutans group, notably S. sobrinus, share many of these properties, and lactobacilli and Actinomyces are commonly reported in lesions, particularly where root surfaces are exposed. Non-mutans streptococci also matter. When mutans streptococci are scarce, the so called non-mutans streptococci can increase in the plaque microbiota and make it more acidogenic. One example is S. gordonii: it is an acidogenic species that is able to tolerate low pH, and its abundance rose most strongly under sucrose exposure in an in vivo study.

Lactobacilli and bifidobacteria have also been detected in early childhood caries lesions. The detection of lactobacilli and Bifidobacterium in ECC lesions is in accord with the extended ecological hypothesis, which treats these organisms as part of a broader acid-producing and acid-tolerating community rather than as isolated pathogens. Kleinberg proposed that the proportions and numbers of acid-producing bacteria, rather than the presence of one species, determine caries activity.

Ecological plaque hypothesis

The ecological plaque hypothesis holds that frequent carbohydrate intake changes the plaque environment by lengthening acidic periods, which favors acid-tolerant species that keep metabolizing at low pH. The shift is usually caused by the frequent intake of fermentable carbohydrates, which leads to changes in the plaque environment, increased duration of acidic conditions. The environmental changes favor acid tolerant cariogenic bacteria that continue their catabolic activity even at low pH.

A later refinement emphasizes sugar-utilizing capacity as well as acid tolerance. Frequent intake of fermentable carbohydrates exposes the oral microbiota to carbohydrate concentrations that primarily favor bacteria with increased catabolic capacity or fermentation velocity. At sites where the acidic environment can last for a sufficient period, aciduric bacteria may be favored by the suppressed growth of non-aciduric species. Computational modelling supports the importance of timing: sugar frequency was found to be irrelevant for either very high or very low daily total amounts, and frequency was a determining factor for intermediate total amounts of sugar, including the estimated average human consumption. The extended version of the hypothesis links this microbial shift to the destabilization of the demineralization and remineralization balance towards a net mineral loss of the enamel.

Interspecies interactions

Interactions among species shape which organisms dominate. S. mutans acts as an early colonizer that utilizes interspecies coaggregation to promote the colonization of subsequent species and affect polymicrobial pathogenesis. Competition is also mediated by bacteriocins. One S. mutans strain of group I, UA140, produces both the lantibiotic mutacin I and the nonlantibiotic bacteriocin mutacin IV, which can suppress neighboring streptococci.

Cooperation with the fungus Candida albicans is among the best-described cross-kingdom interactions. GtfB, secreted by S. mutans, can bind to the C. albicans cell surface, promoting dual-species biofilm formation. The interaction of these organisms is often mediated via the binding of Glucosyltransferase (GtfB) enzyme secreted by S. mutans to C. albicans surface proteins Als1 and Hwp1. In a rat caries model, co-infection with both species resulted in increased biofilm biomass and tooth decay compared to the single species infection. The relationship is not purely synergistic, however: S. mutans can also restrain fungal filamentation through a secreted metabolite, mutanocyclin, which acts on the fungal PKA pathway.

Acid production and mineral loss

Acid generation inside the biofilm

Mineral loss begins with the metabolism of dietary <a>carbohydrates</a> by bacteria in the dental plaque. Plaque organisms ferment sugars and starches through fermentation, and lactic acid is the main product, with acetic and other organic acids formed in smaller amounts. Strains such as Streptococcus mutans, Lactobacillus and Actinomyces metabolize fermentable carbohydrates and produce organic acids that lower the local pH, where saliva's buffering is limited by the dense biofilm. Because the acid forms within the plaque in direct contact with the enamel, caries differs from erosion mainly in where the acid comes from: erosion involves acid delivered by food or beverages, whereas in caries the acid is generated inside the biofilm. Measured values in cariogenic plaque can drop to around pH 4.3.

Subsurface demineralization of enamel

Enamel is composed almost entirely of hydroxyapatite crystals, which are stable only while the surrounding fluid holds enough calcium and phosphate (ions) to remain saturated. The threshold at which dissolution begins is the so-called critical pH. It is generally estimated to be around pH 5.5, although a critical pH between 5 and 5.5, depending on the individual, has been proposed. The figure of 5.5 has a historical basis: it was derived from the theoretical solubility of enamel in saliva rather than in plaque fluid, and later studies noted that the pH inside plaque is not easily measured and is sometimes inhomogeneous.

Acid penetration is governed by diffusion through the biofilm. Acids become trapped between the tooth surface and the plaque biofilm, lowering enamel pH below about 5.6. The extracellular polysaccharide matrix affects how quickly hydronium ions move through the film. Because the acid-producing colonies tend to be anaerobic, the layer adjacent to the enamel is exposed to the most acidic conditions. Acid then enters the porous enamel and dissolves mineral beneath the surface, producing a subsurface lesion in which a comparatively intact outer layer overlies a demineralized body. This architecture explains why early lesions can look like white spots while the surface still appears sound.

Dentin: mineral loss followed by matrix breakdown

Dentin contains less mineral and more organic matrix than enamel, and its own critical pH is higher, around 6.0 for dentin compared with 5.5 for enamel. Dentin caries is often described as a two-stage process in which acid dissolution of the mineralized phase is followed by degradation of the collagen matrix by proteolytic enzymes. Once the mineral is removed, the exposed collagen becomes accessible to enzymes. Host matrix metalloproteinases such as MMP-2, -8, -9 and -20 are present in the dentin organic matrix, and acidic conditions can activate them. When the pH rises again during cyclical fluctuations, activated MMP-8 may degrade collagen, and the resulting gelatin fragments can be broken down further by gelatinases or other nonspecific proteases.

The contribution of bacterial collagenases remains disputed. Some studies suggest that bacterial collagenases may not withstand the acidic drop to pH 4.3 during the demineralization phase of a pH-cycling model, and robust evidence for the presence of endogenous and salivary proteases in dentin and root caries remains elusive. The ecological model of dentin and root caries nonetheless proposes that proteolysis follows demineralization as a distinct stage.

Laboratory measurement of lesion depth and mineral loss

Much of the quantitative knowledge about lesion development comes from in vitro models, in which enamel or dentin specimens are exposed to controlled acid challenges. Time-lapse methods using digital microradiography and polarised light microscopy have been used to follow the kinetics of demineralization advance, and the two techniques have been compared for sensitivity. Micro-CT three-dimensional reconstructions have been used to relate mineral density change to the pH of lactic acid and to characterize the shape of the resulting lesions. Mechanical properties provide a complementary readout: the process substantially degrades the mechanical properties of the affected tissue. Such laboratory data are informative, but their limits are recognized, since much of the existing evidence relies on in vitro models, which may only partially mimic the natural development of caries lesions.

Host, diet and saliva as modifying factors

Dietary sugar: frequency and quantity

Dietary sugar is the substrate on which cariogenic plaque depends, but whether frequency or total amount matters more is still debated. Sheiham and James reanalysed population data and described the link between sugar intake and caries as log-linear from 0% to 10% of energy from sugar, which implies that risk keeps rising even at low intakes. Their analysis supported public-health goals below 5% of energy, which the WHO also suggests, roughly 25 g daily for an adult diet. Because the two variables move together, separating them is hard: an increase in one factor results in an increase in the other. Bowen and colleagues argued instead that the time that sugars are available to microorganisms in the mouth matters more than the number of ingestion events themselves. In a Brazilian nursery study, 3-year-old children from low-income families who snacked most often at the nursery were 4.7 times more likely to show a high caries increment over one year. Mechanistically, sugar-rich diets promote increased proportions of acid-producing and acid-tolerating bacterial species within dental biofilms, which lowers the pH of the plaque fluid and pushes the balance toward demineralization.

Saliva as a buffer and mineral source

Saliva limits caries through several channels at once. Stimulation by taste and chewing leads to an increase in the pH and buffering capacity, due primarily to elevated levels of bicarbonate, as well as supersaturation of saliva with calcium and phosphate. Bicarbonate is the main buffer in this system, and it neutralizes organic acids such as lactic and acetic acid produced by plaque bacteria, thereby reducing demineralization. Flow itself also matters, since salivary flow allows dilution of the acids, and this clearance function is often regarded as the most important caries-preventive function of saliva. The calcium and phosphate supplied by saliva (ions that help maintain the balance between enamel mineral and the surrounding fluid) are also tied to flow: calcium increases in parallel with the salivary flow rate. Clinical studies are not uniform on salivary calcium, however; one review notes that no association between salivary calcium and dental caries has been demonstrated. Consistent with the protective role of flow and buffering, one comparison found that in caries active children, mean levels of salivary flow rate, pH and buffering capacity were significantly decreased relative to caries-free controls.

Oral hygiene and plaque mass

Plaque removal by brushing with fluoride toothpaste and by interdental cleaning limits the amount of biofilm in which acid-forming bacteria can accumulate. Hygiene matters most in the period after eating: each exposure to fermentable carbohydrates starts a fall in plaque pH that typically lasts tens of minutes before the pH returns toward neutral. Frequent snacking therefore keeps the surface acidic for longer, which is one reason why hygiene and diet timing interact. The cleaning effect is limited when plaque is dense or when eating occurs very often, so hygiene reduces but does not remove the effect of diet.

Medications, radiotherapy and systemic conditions

Several factors reduce saliva or increase plaque retention. Dry mouth is a central pathway: xerostomia strongly increases the risk for dental caries, difficulties with chewing, swallowing and sleep disorders. In one retrospective study of more than 12,000 dental patients, predictors for patient-reported xerostomia were intake of more medications, recreational drug use, rheumatic diseases, psychiatric diseases, eating disorders and radiotherapy. Polypharmacy is therefore a major contributor, and it increases with age, partly due to the frequent use of multiple medications by the elderly. Head and neck radiotherapy damages the salivary glands directly. Salivary gland hypofunction is a major risk factor for post-radiotherapy dental caries, and dose matters: higher radiotherapy dose and fraction were negatively associated with unstimulated salivary flow. Gland-sparing techniques reduce this risk; the shift to IMRT has lowered salivary gland dose and reduced xerostomia, translating into a lower baseline risk of radiation caries. Systemic diseases that reduce salivary secretion, such as diabetes and autoimmune conditions like Sjögren syndrome, act through the same route. Fixed orthodontic appliances, meanwhile, create brackets and wire surfaces that trap plaque and make enamel around them more prone to early white-spot lesions, even when the patient's saliva is otherwise normal.

Genetic and developmental susceptibility

Caries risk is partly heritable, but the size of the genetic contribution is still debated. Interest dates to animal experiments more than seventy years ago, and the classic twin model has since been applied to caries in many populations. Reported heritability varies widely. One often-cited twin study in a low-income, non-fluoridated community estimated about 70% heritability for surface-based caries prevalence in children aged 1 to 8, while a later analysis of early childhood caries found only about 9%, and a study of young Indian twins about 15%. Heritability also changes with age: an analysis of child twins found estimates highest at 1.5 years, lowest at 4 years and higher again at 6. A systematic review and meta-analysis of twin studies found that monozygotic twins agree more closely on caries experience than dizygotic twins do, which supports a genetic component, although the magnitude remains uncertain.

The limits of these estimates are substantial. Small samples, age-specific patterns and the assumption that identical and fraternal twins share equal environments all complicate interpretation. Shared family environment, including feeding practices, diet and parental education, often explains more variation than genes do. For that reason, researchers caution against using a single heritability figure to infer a strong genetic etiology. Genetic influence may also act through behavior: heritable differences in sucrose sweetness preference have been associated with caries experience in twin samples.

Because enamel quality and quantity directly affect how readily a tooth resists acid, enamel-formation genes have been the main candidates in association studies. Amelogenin, encoded by AMELX, is the principal protein of the enamel matrix during its secretory stage; enamelin, encoded by ENAM, is the largest enamel matrix protein and contributes to mineralization and structural organization. Other candidates include AMBN (ameloblastin), MMP20 (a matrix metalloproteinase that processes enamel proteins) and KLK4, a protease involved in enamel maturation. Results have been inconsistent. A 2020 meta-analysis reported that several variants across these genes jointly contributed to caries risk, with individual ENAM and AMELX variants showing associations in some subgroups. A more recent meta-analysis of LTF, ENAM and AMELX variants found no consistent association with susceptibility across the pooled studies, and its authors called for larger, ethnically diverse samples. In vitro work using a biofilm model of Streptococcus mutans has reported that ENAM genotype influenced how deeply enamel demineralized, which offers a mechanistic link that epidemiological data have not yet confirmed.

Developmental enamel defects provide another route to susceptibility. In hypoplasia, the enamel is quantitatively reduced because ameloblasts were disturbed during a particular stage of formation, whereas in hypomineralization the enamel reaches normal volume but is insufficiently mineralized. Molar incisor hypomineralization (MIH) is a qualitative defect that affects one or more permanent first molars and sometimes incisors. Its pooled prevalence in a 2021 systematic review was about 13.5%, although the estimates were highly heterogeneous. Affected enamel appears as opacities ranging from white to yellow or brown, and it is fragile and prone to fracture under masticatory forces. Porous, hypomineralized enamel is more readily penetrated by acids, which is why these teeth are regarded as more vulnerable to caries.

The etiology of MIH is considered multifactorial. A 2023 meta-analysis associated illness during pregnancy, low birth weight, childhood illness, antibiotic use and high fever in early childhood with the defect, and up to 20% of affected children have no identifiable risk factor. Several genetic associations have also been reported, including variants in MMP20, ENAM and AMBN, and some studies describe a stronger effect in homozygous carriers. These findings are generally based on small case-control or family designs and have not yet been consistently replicated.

Gene–environment interaction is conceptually central to this area, because a genetic variant may matter only under particular exposures, such as a specific fluoride regime, a dietary pattern or a systemic illness. The explicit testing of such interactions remains limited. Recent reviews have identified this as a priority, arguing that studies must examine genetic and environmental factors together rather than in isolation before individual susceptibility can be meaningfully assessed.

Lesion types and classification

Pit-and-fissure, smooth-surface and root lesions

Carious lesions are usually grouped by the tooth surface where they begin, because anatomy and plaque retention differ between surfaces. Pit-and-fissure lesions start in the occlusal pits and grooves. These narrow, deep recesses are hard to clean with a toothbrush, so biofilm accumulates there, and the enamel at their base is often thinner and less mature than on the smooth surface. Smooth-surface lesions develop on the buccal, lingual and proximal faces. Proximal (interdental) lesions are the most difficult to reach with a brush and are often detected only radiographically.

Root caries is a separate category with its own risk profile. It forms on cementum and exposed root dentin after gingival recession, and it tends to occur near the gingival margin, where plaque collects. Its prevalence rises with age. A systematic review of community-dwelling older adults reported a range of 8% to 74% across countries, while caries overall in the same groups ranged from 25% to 99%. A 2015/16 national survey in China found root caries in 62% of adults aged 65 to 74. Risk is higher where roots are exposed and where xerostomia is present, and in one Hong Kong study of older adults in long-term care, lingual root surfaces and mandibular anterior roots showed the lowest rates. Researchers have noted that recession and root caries are not simply age changes; longitudinal modelling suggests they are cumulative outcomes that are more common in older cohorts because teeth are retained for longer.

Primary versus permanent dentition

Primary (deciduous) teeth have thinner enamel and a relatively large pulp chamber, and in general their lesions reach dentin sooner than in permanent teeth. Progression data reflect this. A review of approximal lesions reported that rates ranging from 70% to 90% of approximal caries progression have been shown for primary teeth after 1 or 2-year follow-up, figures that exceed those reported for permanent teeth. A retrospective study of bitewing radiographs estimated that a lesion needed roughly 0.8 years to pass from the outer enamel to the dentino-enamel junction in primary teeth. In permanent teeth, earlier longitudinal work has suggested that a lesion typically needs at least four years to traverse the enamel.

Population-level data point the same way. A systematic review of 43 studies found that the annual decline in caries-free children ranged from 3.8% to 12.2% in the primary dentition and from 0.8% to 10.2% in the permanent dentition. The same review noted that progression tended to follow predictable rates that depended largely on baseline caries severity. Longer follow-up of initial lesions in primary teeth has shown that enamel-confined lesions progress slowly, whereas cavitated lesions carry a higher risk.

Early versus cavitated lesions

The key distinction is whether the surface has broken down. A non-cavitated (early) lesion keeps an intact surface, usually appearing as a white or chalky opaque area of enamel. Because water in the porous lesion masks its appearance, the tooth is normally dried before examination, and early white-spot lesions are easily missed when the tooth is wet. A cavitated lesion has a physical defect and, once it reaches dentin, cannot be restored to health by remineralization alone. Non-cavitated approximal lesions are generally easier to control, since the absence of a cavity leaves no niche for biofilm to accumulate.

Clinical criteria also address activity. Active lesions tend to look whitish or yellowish, opaque and rough, with a loss of surface luster, whereas inactive (arrested) lesions appear brownish or black, and are smooth and hard. The ICDAS working definition states that active lesions have a greater likelihood of progressing, arresting or regressing than inactive ones.

International detection and assessment systems

Because earlier systems produced data that could not easily be compared, an international group of caries researchers developed the International Caries Detection and Assessment System (ICDAS). Its core criteria, first published in 2004, cover coronal and root surfaces as well as caries adjacent to restorations and sealants, and a 2009 addition addressed coronal caries in primary teeth. The detection codes run from 0 (sound) to 6 (extensive cavity with visible dentin). Codes 1 and 2 describe visual change in enamel, code 3 localized enamel breakdown without visible dentin, code 4 a dark shadow from underlying dentin, and codes 5 and 6 cavities with visible dentin. Restoration and sealant status and examination exclusions are recorded with separate codes, and root surfaces that cannot be visualized directly are excluded from scoring. The assessment component classifies each lesion by stage (non-cavitated or cavitated) and activity (active or inactive). ICDAS is applied to clean, dry teeth, and the examination is normally performed with a ball-ended probe, since a sharp probe may damage the surface of an early lesion. Other systems, including the Nyvad criteria, remain in use, and the diversity of criteria is a recognized obstacle to comparing results between studies.

Diagnosis and caries risk assessment

Clinical diagnosis still relies on visual-tactile examination, usually supplemented by radiographs. This combination is commonly regarded as broadly effective at detecting caries that has progressed into dentine and reached a threshold where restoration is necessary. Visual assessment is the weak point for early lesions. Even when standardized systems such as ICDAS-II are used, visual inspection remains inherently subjective and depends on examiner experience, surface conditions and lesion activity. Staging systems such as Nyvad's criteria describe an active lesion as an opaque, whitish or yellowish surface that has lost its luster and feels rough under a probe, with no clinically detectable loss of substance (Surface of enamel is whitish/yellowish opaque with loss of luster; feels rough when the tip of the probe is moved gently across the surface). The tactile step itself is contested. The use of a sharp explorer has been criticized for more than a decade, because its tip can cause irreversible damage to demineralized enamel and create cavities. A ball-ended explorer is generally recommended as the safer alternative.

Radiography is the standard method for interproximal surfaces, which are hidden by adjacent teeth. In bitewing imaging, a beam of X-ray passes from the cheek side of the tooth through the interproximal contacts, and mineral loss appears as areas of reduced radiodensity (radiodense areas have higher mineral content, and radiolucent areas have lower mineral content). Its accuracy is uneven. For interproximal caries, bitewings show sensitivity of roughly 0.69–0.84 and specificity of 0.94–0.99, but they are ineffective for occlusal lesions, and X-ray images usually significantly underestimate the actual size or depth of a carious lesion. Because a lesion becomes visible only after substantial demineralization, by the time a lesion is visible on an X-ray bitewing, the only effective therapy is invasive surgical restoration, which is the principal reason radiographic detection is poorly suited to early lesions. The radiation cost is modest per image, with an effective dose of roughly 1–10 µSv per exposure, but children are more radiosensitive, and guidance therefore asks clinicians to limit their recommendation of bitewing radiography in children, and to plan the time intervals for obtaining bitewing radiographs according to the caries risk.

Adjunct optical and electronic methods were developed to detect early demineralization without ionizing radiation. These include fluorescence, transillumination, optical coherence tomography and quantitative light-induced fluorescence. The best-known laser device, the DIAGNOdent, measures changes in back-scattered fluorescence to detect caries lesions, and its fluorophores have been identified as bacterial porphyrins. Reported accuracy varies with lesion site and threshold. In a case series of adults aged 55 and over, the overall sensitivity was 90.8% and the specificity was 74.0% for separating active from arrested lesions, and the optimal cut-off differed by surface, with higher values for furcation and crown-margin sites. In an in vitro study of dentine lesions, laser fluorescence was reported to outperform bitewing radiography in specificity. Systematic reviews consistently note that differences in lesion location, dentition type and diagnostic thresholds across studies make it difficult to draw definitive clinical conclusions. For this reason, these devices are usually recommended as a complementary tool to visual-tactile inspection in cases where precise lesion detection is critical, rather than as replacements. No single method is regarded as ideal. None of the digital diagnostic aids has shown ideal performance in detecting dental caries, especially at an early stage.

Caries risk assessment is distinct from lesion detection. It estimates the likelihood of future disease and uses that estimate to set monitoring intervals and preventive intensity. Such tools combine clinical findings, such as existing lesions, restorations and plaque, with diet, salivary status and social history. Their predictive value has been judged modest in several evaluations, and evidence for individual tools varies in strength; most have not been validated through randomized controlled trials comparing risk-guided and standard care. Their use is therefore generally framed as a structured clinical judgment informed by the evidence-based medicine literature rather than as a precise forecast of an individual's outcome.

Global burden and epidemiology

Global estimates

Untreated caries ranks among the most widespread conditions in global health statistics. In the Global Burden of Disease (GBD) 2021 round, the Lancet analysis counted 2,240 million prevalent cases of untreated permanent-tooth caries in 2021, against 525 million for deciduous teeth. Expressed as rates, about 7.55% of children had untreated caries in deciduous teeth, and 27.54% of adults had caries in permanent teeth. The age-standardised prevalence for permanent teeth was 27,500 per 100,000 population, which makes it the leading oral condition in the GBD framework. Earlier GBD rounds gave different totals; for 2017 they reported 2.4 billion people with untreated caries in permanent teeth, so the figures should be compared across rounds with care. The GBD team also projected forward, expecting deciduous-tooth prevalence to fall while permanent-tooth prevalence rises: by 2050 the prevalence of deciduous caries is projected to decrease by −15.80%, while permanent caries is predicted to rise by +23.77%.

Trends over time and between regions

Case counts and rates have moved in different directions. Between 1990 and 2021, the percentage change in cases of permanent-tooth caries was 53.0%, while the change in age-standardised prevalence was −2.78%, so population growth and ageing drove most of the rise in counts. Regional patterns also diverge. The African and Eastern Mediterranean regions showed the largest increases in prevalent cases and DALYs for most oral conditions, while the European region showed the smallest increases or no change. The European region was the only region with decreasing age-standardised prevalence of untreated caries in both deciduous and permanent teeth.

In high-income countries, long-term declines in childhood caries are well documented. In Germany, a caries decline (DMFT value) from 4.1 to 0.4 was achieved in 12-year-old children between 1989 and 2014. The fall began earlier in the United States and in Western and Nordic European countries, where the decline started in the mid-1970s of the previous century after effective fluoride toothpaste became widely used. In Eastern Europe, by contrast, the decline only started after the fall of the iron curtain, and caries remains higher there than in the west. Across 36 European countries, one meta-analysis found a strong negative correlation between income and caries experience.

Age, dentition and measurement

Caries burden varies with age. The GBD analysis found that the incidence of untreated dental caries peaked at the ages of 5–9 and 20–24 years, and the prevalence and years lived with disability at 1–4, 20–24, and 60–64 years. Surveys for children and for adults use different reference groups and indices. The DMFT index counts decayed, missing and filled permanent teeth, and in adulthood, caries experience is commonly quantified by the DMFT index (decayed, missing, filled teeth), which captures cumulative lifetime burden. For primary teeth, the lowercase dmft is used. The WHO's reference group for cross-country comparison is 12-year-olds, and these values classify Germany as a low-caries-prevalence country according to WHO criteria.

Inequality and the growing burden in lower-income settings

Burden is unevenly distributed between countries. A GBD analysis of structural determinants found that countries that had better structural indicators had lower mean prevalence of untreated caries in primary teeth. By contrast, in the permanent dentition, between-countries inequalities were not identified. Within countries, the gap is often sharper: in the Middle East and North Africa, the prevalence of childhood caries in low-income communities is 3–4 times higher than in urban centers, according to one regional analysis. Taken together, these patterns suggest that while high-income settings have largely reduced caries in children, the absolute burden in adults and in low- and middle-income regions remains high.

Social inequality and social determinants

Dental caries follows a steep social gradient. Within countries, people with lower income, less education, and more precarious employment tend to have higher rates of caries, tooth loss, and impaired oral function. The WHO describes this as a life-course pattern: people of low socioeconomic status carry a higher burden of oral diseases throughout the life course. At the global level, the WHO's 2019 figures put untreated dental caries at about 2.5 billion people, and about three-quarters of the people affected by oral diseases lived in middle-income countries.

Income, education and employment

In a 2011–2020 analysis of US adults using the National Health and Nutrition Examination Survey (NHANES), lower socioeconomic status measured by five indicators was consistently linked to higher caries experience. For employment, education and income, the study found clear dose–response relationships, where lower SES categories were associated with a progressively higher caries experience. The education gap was the one that widened: disparities by education showed evidence of widening, while the gaps by employment, income, insurance and food security persisted. A systematic review of adults found that educational level, income, occupation and the Gini coefficient are associated with dental caries.

Several mechanisms have been proposed. Low socioeconomic status, low monthly household income and low educational level are associated with less access to dental services and oral hygiene products, poorer knowledge regarding oral health and oral hygiene. Some studies suggest education can matter independently of income: a Thai study found education remained a strong predictor of untreated caries even after controlling for income, suggesting that mechanisms such as health literacy may be paramount. Evidence from life-course designs points the same way, with a gradient shaped by life-long socioeconomic trajectories. Ecological comparisons also link national wealth to caries: one analysis of 170 countries found a significant association between a country's income level and the mean DMFT of its population. Such country-level correlations cannot establish causation on their own.

Ethnicity, race and rural–urban residence

In US nonelderly adults, the rate of untreated caries among Hispanics (36%) and non-Hispanic Blacks (42%) is much higher than the rate for non-Hispanic Whites (22%), according to figures cited in one study. Income shows a similar split: untreated caries rates among low-income adults (below 200% FPL) are more than twice as high compared to higher income adults. Race and ethnicity are not simply independent markers, however. In a study of older Americans, age and ethnicity were rendered statistically insignificant once affordability was included, which suggests that cost accounts for much of the apparent ethnic difference.

Rural residence is associated with a heavier burden as well. In one US state review, people living in rural areas have a higher disease burden due primarily to difficulties in accessing preventive and treatment services. Disparities also appear in children: a comparison of public and private schools in one setting found that children from public schools exhibited a significantly higher burden of disease, with higher caries prevalence, greater mean dmft/DMFT scores and substantially more untreated decay. Because school type often serves as a proxy for family standing, this pattern reflects social rather than purely geographic factors.

Insurance, affordability and access to preventive care

Coverage is one of the clearest levers. Nationally representative US data for 2011–2014 showed 12.4 million children and 57.6 million adults with untreated caries. The odds of untreated caries associated with financial barriers were 2.06 for children and 2.84 for adults while the odds of untreated caries associated with non-financial barriers were 2.86 for children and 1.67 for adults. Coverage rules have also been uneven by age: there are no coverage requirements for working-age adults or seniors, which is reflected in downward trends in dental benefits coverage. Among older adults, untreated root caries occurred in 42.5% of those who could not afford dental care, and 14% of those who could afford dental care. Adults with Medicaid dental coverage have more dental visits and reduced prevalence of untreated dental caries, although the causal evidence on such links remains scant.

Universal health coverage and primary care

Globally, access is shaped by the health system itself. High income countries generally have more dentists, greater use of preventive care, and lower levels of untreated disease, whereas many low and middle income countries face high disease burdens, scarce oral health workforce, and large gaps in access to basic dental treatment. In China, for example, coverage of restorative and prosthodontic services through basic health insurance remains limited and uneven, and oral health services are only partially included in universal health coverage arrangements in many middle- and high-income countries.

Researchers working in this area argue that dental coverage alone is insufficient. One US–China analysis concludes that policies that seek to improve oral health equity must therefore combine improvements in dental coverage and service delivery with broader social policies that address poverty, educational disadvantage and the social patterning of health-related behaviours. The WHO's broader framework places the same weight on structure: its Global Oral Health Status Report emphasized that vulnerable and marginalized communities are disproportionately affected by oral diseases and that contextual and structural disadvantages – rather than personal choices alone – are the main causes of these disparities. Oral health is therefore usually discussed alongside social determinants of health, primary-health-care and universal-health-coverage.

Prevention: fluoride, sealants, diet and hygiene

Fluoride: mechanisms and delivery

Fluoride is usually understood to act through three overlapping routes: it lowers enamel solubility, speeds the repair of early lesions, and suppresses the metabolism of plaque bacteria. Fluoride is credited with its main caries-preventive effect through reducing enamel solubility, promoting enamel remineralization, and inhibiting bacterial metabolism. Its chemistry explains the first route. Fluoride substitutes into the hydroxyapatite of enamel to form fluorapatite and fluorhydroxyapatite, and one review places the critical pH for demineralization at about 4.5 in such enamel, compared with about 5.5 in unmodified enamel. During recovery, fluoride adsorbed onto partly dissolved crystals draws in calcium, and the supersaturated saliva then drives mineral back into the lesion. Fluoride's action on bacteria is more specific. Its undissociated form, hydrogen fluoride, can cross bacterial membranes and release fluoride inside the cell, where it binds the glycolytic enzyme enolase and inhibits the membrane proton pump F-ATPase. The result is less acid from glycolysis and reduced acid tolerance in organisms such as Streptococcus mutans.

Delivery is designed around exposure time in the mouth. Fluoride toothpaste maintains a low, sustained level in plaque fluid during and after brushing. Professionally applied varnishes and gels provide a concentrated dose that adheres to the tooth, and varnish is among the most widely used topical anti-caries measures. Mouthrinses and supplements (historically tablets or drops in areas without fluoridated water) extend coverage to people who cannot easily use other methods. The effect is limited when the plaque layer is very thick, because fluoride diffuses less readily into subsurface enamel, and when salivary flow or buffering is reduced.

Pit-and-fissure sealants

Sealants are thin resin or glass-ionomer layers placed over the deep pits and fissures of occlusal surfaces, where plaque accumulates and the enamel is often thin. A systematic review by the American Dental Association and the American Academy of Pediatric Dentistry identified 23 RCTs published between 1976 and 2016 with a minimum of 2 years' follow-up, and a guideline panel from those bodies recommended sealants for children and adolescents with caries risk. Application is technique-sensitive: it requires optimum isolation, cleaning of the tooth surface, etching, and the application of a thin bonding layer, and retention depends on recall and repair. In a meta-analysis of four trials involving 1,249 children, comparing sealants with fluoride varnish on first permanent molars over 24 months, the difference was not statistically significant. The evidence base is weaker for primary molars, where a review concluded that there are currently insufficient well-controlled randomized controlled clinical trials to establish benefit in preventing or arresting occlusal caries.

Diet and hygiene

Dietary advice focuses on how often fermentable carbohydrates are eaten, because each exposure lowers plaque pH and starts a demineralization episode; frequent snacking therefore matters more than the total amount consumed in one sitting. Limiting between-meal intake of sugary foods and drinks is the principal dietary measure, and fluoride toothpaste is usually recommended alongside it.

Xylitol, a sugar alcohol that most cariogenic bacteria cannot ferment, is used mainly in sugar-free chewing gum. Laboratory and clinical work suggests that it reduces the attachment of S. mutans to tooth surfaces. Clinical evidence is mixed. One review found that in the ten evaluated xylitol chewing gum studies xylitol consumption significantly reduced caries occurrence when compared with no treatment or a placebo polyol gum, with the benefit most evident in children with moderate or high baseline caries, whereas a separate analysis of xylitol-only gum in children rated the evidence as very low. Xylitol candies showed no consistent effect in the same review. Authors of these reviews generally treat xylitol as an adjunct to dietary change and fluoride, not a replacement for them.

Mechanical plaque control completes the picture. Brushing with fluoride toothpaste, and cleaning between the teeth, disrupts the biofilm and reduces the plaque mass in which acid is generated; its effect depends on regularity and technique more than on the instrument used.

Fluoride policy and safety debates

Community water fluoridation and caries outcomes

Community water fluoridation adjusts the fluoride content of a public supply, usually to about 0.5–1.0 mg/L, so that a population receives a steady low-level exposure. The US Community Preventive Services Task Force reported in the early 2000s that starting fluoridation reduced caries in children aged 4–17 by roughly 30–50%, and that stopping it increased caries by about 18%. A later update that combined new studies with the earlier review found a median reduction of about 15 percentage points in caries after fluoridation began. National reviews have produced similar estimates: an Australian review put the reduction at 26–44% across children, adolescents and adults. A 2024 Cochrane update found that fluoridation at current Australian levels was associated with lower caries prevalence in both primary and permanent teeth. Reviewers have noted that the included studies were of low to moderate quality, and that the benefit is greatest where access to preventive care is limited. Some recent analyses argue that the incremental benefit is smaller where fluoride toothpaste is already widely used.

Salt and milk programs

Salt fluoridation is more common than water fluoridation in parts of Europe and Latin America. Switzerland introduced fluoridated domestic salt in 1955, and sources differ on the date of formal authorization for human consumption, which is given as 1980–82. Shares of domestic salt that are fluoridated reached about 85% in Switzerland and 67% in Germany. In Latin America, the first effectiveness studies were conducted in Colombia, Hungary and Switzerland between about 1965 and 1985. Mexico adopted salt fluoridation in 1991, adding potassium fluoride at about 250 mg per kilogram of salt. Costa Rica and Jamaica began in 1996–97. Program-reported caries reductions among 12-year-olds were about 84% in Jamaica, 73% in Costa Rica and 40% in Uruguay, at an average cost of about US$0.06 per person per year. These figures come from program evaluations rather than randomized trials. Implementation depends on purchasing habits and on whether fluoridated salt reaches school meals or commercial bread. Milk fluoridation has been used on a smaller scale in countries including Bulgaria, Thailand and Chile.

Dental fluorosis and drinking-water limits

Dental fluorosis is the most consistently documented adverse effect of excess fluoride intake. It occurs when enamel is forming in childhood and appears as a change in enamel structure and appearance. The WHO guideline value for fluoride in drinking water is 1.5 mg/L, a figure based on epidemiological evidence that fluorosis risk rises above this concentration and that skeletal fluorosis risk increases at higher levels. The WHO also advises that national standards consider total intake from all sources and be set lower where intake reaches 6 mg per day. The guideline sits above the 0.5–1.0 mg/L range used for artificial fluoridation. In hot climates, where water consumption is higher, fluorosis can appear below 1.5 mg/L. An earlier WHO background document cited mild fluorosis prevalence of 12–33% at 0.9–1.2 mg/L. A systematic review of water fluoridation estimated that at 1 ppm about 12.5% of exposed people would find fluorosis aesthetically concerning. The United States sets an enforceable limit of 4 mg/L and a non-enforceable secondary standard of 2 mg/L. Most severe fluorosis arises from naturally high groundwater fluoride rather than from fluoridation programs, and it is documented in parts of Africa, Asia and Latin America.

Continuing controversies

Disagreement persists over whether systemic fluoride exposure affects neurodevelopment. In 2024 the United States National Toxicology Program published a monograph concluding, with moderate confidence, that exposure above 1.5 mg/L is associated with lower IQ in children. Other researchers and regulators have judged the evidence at fluoridation concentrations to be insufficient or inconclusive. Ethical debate centers on whether mass fluoridation of a shared supply is compatible with individual consent and choice, and on how to weigh that against its benefits for groups with limited access to dental care. In 2025, Utah and Florida enacted laws ending community water fluoridation, while many other jurisdictions have maintained their programs. These positions are presented here as ongoing disputes without evaluation.

Restorative and non-surgical treatment

Remineralization of early lesions

Non-cavitated lesions, which appear as chalky white spots on enamel, are usually managed without drilling. Fluoride-based products primarily enhance enamel remineralization and slow demineralization, which raises resistance to acid attack from cariogenic bacteria. Laboratory work on bovine enamel models found that a high-concentration fluoride varnish did not clearly restore mineral in the subsurface layer, but it did improve acid resistance in the deepest part of the lesion, which suggests that varnish mainly protects rather than rebuilds the tissue. Resin infiltration is a micro-invasive alternative. It fills the microporous enamel of non-cavitated lesions with low-viscosity, light-cured resins. Capillary forces draw the resin into pores that otherwise serve as routes for acids, bacteria and dissolved minerals. In a randomized trial of 180 initial proximal lesions, caries progression at one year occurred in 3% of lesions treated by infiltration, 18% of those treated with a remineralizing varnish, and 28.3% of untreated controls. Resin infiltration has also been studied in orthodontic white spot lesions, where a meta-analysis found a statistically significant reduction in colour difference favouring resin infiltration.

Silver diamine fluoride for cavitated lesions

Silver diamine fluoride (SDF) is used to arrest cavitated lesions without removing tissue. The formulation most often studied is a 38% solution, which contains about 44,800 parts per million fluoride. The evidence is strongest for specific groups. An umbrella review reported that systematic reviews consistently supported SDF's effectiveness for arresting coronal caries in the primary dentition and for arresting and preventing root caries in older adults. By contrast, there is insufficient evidence to draw conclusions on SDF for prevention in primary teeth and prevention and arrest in permanent teeth in children. One meta-analysis of primary teeth reported a pooled arrest rate at 12 months that was substantially higher than with other active materials or placebo, but a high variability regarding SDF application protocol was found, and caries arrest in these trials was generally judged by visual and tactile methods. The lack of a defined application frequency is a recognized limitation, so the value of SDF in a given setting depends on how it is applied and monitored.

Restorations and selective caries removal

Where a cavity must be restored, the modern approach aims to remove only the tissue that cannot be saved. Infected dentin is highly contaminated, necrotic or irreversibly denatured, and poorly suitable for remineralization, so it must be removed. Affected dentin, which can remineralize, may be preserved. Clinical studies have shown that this selective approach reduces the risk of pulp exposure and increases the probability of treatment success fourfold relative to conventional excavation. Chemomechanical agents such as sodium hypochlorite combined with amino acids have been used to soften and remove carious dentin while leaving harder tissue intact, and papain-based systems have been proposed as atraumatic alternatives, particularly in paediatric dentistry.

Atraumatic restorative treatment (ART) was designed for settings with few resources. It is defined as removing soft, demineralized dentin with hand instruments alone, then filling the cavity and sealing adjacent pits and fissures. ART commonly uses high-viscosity glass ionomer cement, which releases fluoride and bonds chemically to tooth tissue, and it avoids local anaesthesia and rotary instruments in many cases. Resin composites are chosen when aesthetics, adhesion and conservative preparation are priorities, and they require a dry, isolated field. Glass ionomer is preferred for low-load or paediatric restorations and for sites where moisture control is difficult. Amalgam, long the default for posterior teeth, has declined in use; the Minamata Treaty has advised the phasing-down of amalgam restorations due to environmental concerns over mercury levels.

Decisions about the pulp

The main aim of minimally invasive management is to keep the pulp vital. Selective caries removal, with or without indirect pulp capping, has become the norm for treating extensive lesions. When the pulp is already inflamed or infected, or when a tooth cannot be restored with a reasonable prognosis, the choice shifts to root canal treatment or extraction. These decisions depend on symptoms, the depth of the lesion relative to the pulp, the remaining tooth structure and the patient's circumstances.

Complications and consequences

Pulpal and periapical progression

Caries becomes a pulp problem when the lesion breaches the dentin and bacteria reach the pulp chamber. The pulp then becomes infiltrated and inflamed, and pulp necrosis ultimately results. Pulpitis is graded by how it behaves. Pulpitis is reversible when the pain is mild to moderate and lasts for a short time after a stimulus, such as cold; it is irreversible when the pain is severe, spontaneous, and lasts a long time after a stimulus.

Once the pulp dies, infection moves toward the root apex. Left untreated, pulpitis may progress to pulp necrosis and apical periodontitis. Periapical periodontitis is a likely outcome of untreated dental caries, and in such cases it can be considered a sequela in the natural history of tooth decay, irreversible pulpitis and pulpal necrosis. Pus may accumulate at the root tip as a periapical abscess. Such an abscess can point intraorally and eventually drain or may become a cellulitis. Spread into adjacent spaces can cause osteomyelitis, sinus involvement, or airway obstruction in severe cases such as Ludwig's angina. Rarely, the infection can spread to the bloodstream, resulting in systemic sepsis. Definitive management is usually endodontic or extractive: root canal therapy or extraction of the involved tooth, with antibiotics and drainage for spreading infection.

Tooth loss is a further outcome. Caries and periodontal disease are major causes of tooth loss. A tooth weakened by a large lesion or a non-vital pulp may therefore be lost even when the infection is controlled, and the loss itself changes chewing function.

Pain, eating, growth and speech

Pain is the most common presenting symptom. Dental caries is often the underlying cause of dental pain. In young children, the functional effects are more pronounced. Among preschool children, the most affected domains were pain, eating and drinking difficulties, sleep disturbance, irritability, and family distress. Pain and infection are the primary effects of early childhood caries, which can alter eating and sleeping habits and interfere with growth, with adverse effects on body weight and height and, ultimately, failure to thrive. Untreated early childhood caries has also been linked to speech disorders, malnutrition, premature tooth loss, and missed school. In adults, multiple untreated carious lesions have been associated with chewing deficiency, reduced food comminution, and food selection problems.

Quality of life and daily functioning

Oral health-related quality of life (OHRQoL) instruments quantify these effects from the perspective of the patient or caregiver. For preschool children, the Early Childhood Oral Health Impact Scale (ECOHIS) is the most widely used instrument, and studies using it have consistently found that caries is associated with lower scores. In one comparison, children with early childhood caries had poorer oral health-related quality of life than caries-free subjects. Improvement after treatment has also been recorded: at one-month follow-up after complete treatment, oral health-related quality of life improved significantly in children with caries. The effect extends to families. Dental pain and eating difficulties were the most frequent child impacts, while parental guilt and work disruption were commonly reported by caregivers. A systematic review found that greater caries severity, untreated lesions, and advanced disease consequences were generally linked to higher ECOHIS scores.

Burden measurement and global estimates

Because death from oral disease is uncommon, burden is measured mainly through morbidity. The Global Burden of Disease (GBD) approach uses years lived with disability, which are estimated only on those persons with unmet need for dental care. A DALY reflects a year of healthy life lost due to diseases or injuries, and years lived with disability are calculated from prevalence, disability weight and duration. This framework allows oral diseases to be compared with other conditions, but it also means that people who receive adequate care contribute little to the estimate.

On this basis, untreated caries is among the most substantial oral conditions. According to GBD 2021, untreated dental caries in permanent teeth is the most common health condition. The WHO reports that oral diseases affect nearly 3.7 billion people. Burden is rising in absolute terms because of population growth and ageing: the number of people with untreated oral conditions rose from 2.5 billion in 1990 to 3.5 billion in 2015, with a 64% increase in DALYs due to oral conditions. Estimates differ between study periods and models, so year-specific figures should be compared with care.

History of understanding and treatment

Caries is one of the oldest documented human diseases, and its prevalence has tracked changes in diet. Pleistocene hunter-gatherers in Morocco show a high rate of caries that linked a high prevalence of caries to a reliance on highly cariogenic wild plant foods, and this predates the first signs of food production by several thousand years. Comparative archaeological data show a clear rise with farming: carious lesions affected 2.2–48.1% of teeth in agricultural populations, but only 0–14.3% in hunter-gatherers. Among early farmers in central Germany, carious lesions were found in 68.3% of the adults. Written records appear later: the earliest known reference to caries in China comes from oracle bone inscriptions at the Yin Xu site.

Through the nineteenth century, the dominant explanation was the "worm theory," which held that a worm gnawed the tooth. In 1890–1891, W. D. Miller set out the chemoparasitic theory, which held that caries is caused by acids produced by oral bacteria following fermentation of sugars. Miller's experiments indicated that acid produced by microorganisms in the mouth caused caries of the enamel, with dentin affected by acidic decalcification. He also argued that no single bacterial species could be responsible, an idea later overturned when the role of Streptococcus mutans as a primary pathogen in caries was established in the 1950s. Plaque itself was described on tooth surfaces by G. V. Black and J. L. Williams in 1898, which supported the idea that a microbial biomass holds acid against the tooth. The broader context was the germ theory of disease, whose roots include the microscopic observations of Antonie van Leeuwenhoek and the bacteriology of Louis Pasteur.

Testing the theory was difficult until the 1950s, when germ-free mice were developed. In 1954, Orland and colleagues reported that mice raised under germ-free conditions did not develop caries. By the 1970s, the microbial basis of the disease seemed well enough established that dental researchers made a serious attempt to develop a vaccine against the cariogenic bacteria.

Fluoride's role emerged from an observation in Colorado in the early twentieth century, when dentists noted large, permanent brown stains on their teeth among residents who had few cavities. The stain was later identified as dental fluorosis, and the cause was traced to naturally high fluoride in the drinking water. H. Trendley Dean's research in the late 1930s and early 1940s determined that fluoride levels up to about 1.0 ppm in drinking water would not cause dental fluorosis in most people. The first controlled field trial began in 1945 in Grand Rapids, Michigan, with Muskegon as the control city. A wider study, starting in the same year in four pairs of cities in the United States and Canada, found that caries was reduced 50%-70% among children in the communities with fluoridated water after 13–15 years. The Grand Rapids study alone reported a 60-65% reduction in dental caries among children who consumed fluoridated water from birth over 11 years. The Centers for Disease Control and Prevention later cited community water fluoridation as one of the 20th century's greatest public health interventions.

Twentieth-century dentistry also standardized the description and treatment of cavities. G. V. Black's classification of cavities, developed in the late nineteenth and early twentieth centuries, provided a common vocabulary for operative procedures. Restorative materials changed over the same period, with amalgam long remaining the standard direct filling, followed by resin composites from the 1960s and glass ionomer cements in the early 1970s. These developments set the groundwork for the classification and restorative systems discussed in later sections.

Research frontiers and open questions

Much current work on caries aims to change the disease process without relying only on fluoride or broad-spectrum antimicrobials. Because the cariogenic biofilm depends on a few specific virulence traits, one approach is to block those traits rather than kill the whole community. The most studied target is the glucosyltransferase (Gtf) family in Streptococcus mutans. A 2025 screen of more than 1,000 compounds identified tannic acid as a Gtf inhibitor that reduced extracellular polysaccharide synthesis and biofilm formation, and the authors reported that it worked by blocking the enzyme rather than by killing the bacteria directly (The screen covered over 1,000 compounds from a natural product library, and tannic acid was identified as a potential Gtf inhibitor. In vitro work suggested it inhibits extracellular polysaccharide synthesis and biofilm formation by selectively antagonizing the enzyme rather than directly killing the bacteria.). An earlier compound of this type reduced the incidence and severity of smooth-surface and sulcal caries in a rat model, with a parallel fall in the share of S. mutans in plaque (It significantly reduced the incidence and severity of smooth and sulcal-surface caries in vivo with a concomitant reduction in the percentage of S. mutans in the animals' dental plaque.). Reviewers argue that this selectivity is the main advantage, since inhibiting Gtfs leaves the existence of other oral species largely intact (Targeting Gtfs selectively impairs S. mutans virulence without affecting the existence of S. mutans or other species in the oral cavity.). Whether such compounds can be formulated safely and sustain effect in human mouths remains untested at scale.

Probiotics and mineral-based alternatives

Probiotics are being investigated as a way to shift plaque toward a less cariogenic community. A 2025 systematic review of 12 randomized trials in children found that Lactobacillus rhamnosus SP1 and L. paracasei SD1, given via milk or tablets for 6–10 months, significantly reduced caries incidence and S. mutans counts compared with control groups. The same review judged the overall certainty of evidence to be moderate to low, and results varied by strain, delivery vehicle and outcome (The conclusions describe modest, strain-specific adjunctive benefits, with certainty of evidence moderate to low and findings inconsistent across strains, delivery vehicles and outcomes.). Evidence for preventing recurrence or reversing white spot lesions around orthodontic brackets is weaker (Evidence on secondary prevention and regression of white spot lesions in orthodontic patients was limited and inconsistent.).

Calcium-phosphate materials are a second line of work. Hydroxyapatite (HA) resembles the apatite crystals of enamel, and nano-sized forms have been proposed as more effective remineralizing agents because of their larger surface area. A meta-analysis, however, notes that this advantage has not been shown in clinical studies, while both nano- and micro-crystalline forms have been found clinically effective (Theoretical considerations suggest nano-HAP could outperform micro-HAP in enamel remineralization, but this has not been proven in any clinical studies so far. Both types of HAP have been demonstrated to be clinically effective.). Laboratory comparisons of bioactive glass and nano-HA varnishes have also reported remineralization after pH cycling in artificial lesions in primary teeth (n-BAG varnish and n-HAP varnish demonstrated superior remineralization efficacy after 7-day pH cycling compared to Enamel Pro varnish.). Such in vitro results do not establish comparable clinical performance, and bioactive glasses and nano-hydroxyapatite are not yet established replacements for fluoride.

Vaccine concepts

Immunization against caries has been explored in animal studies, mainly using antigens from S. mutans, including surface proteins and the Gtf enzymes that build its glucan matrix. The main difficulty is that the disease is a diet-dependent biofilm process rather than a single invading pathogen, so an antibody response would have to act in saliva and on the tooth surface without disrupting the wider oral biofilm. Questions about durable protection, the risk of cross-reactivity with commensal streptococci and the regulatory path for a preventive product for a non-life-threatening condition have limited translation to human trials.

Individual susceptibility and the oral microbiome

Caries is a multifactorial, sugar-dependent disease arising from interactions among cariogenic and commensal microbes within plaque (Dental caries is a multifactorial, sugar-dependent disease driven by the dynamic interactions of cariogenic and commensal microbes within dental plaque (biofilms) formed on tooth surfaces.). Yet people with similar diets, fluoride exposure and hygiene habits differ widely in lesion experience. Explanations under investigation include differences in salivary flow and buffering, immune responses, the composition of the microbiome as a whole rather than the abundance of a single species, and host genetics. Sequencing studies have shown that the balance among community members, not just the presence of S. mutans, can shape acid production. Whether a stable, low-cariogenic community can be engineered and maintained is an open question, and it drives much of the current interest in approaches that protect commensal diversity rather than eradicating bacteria.

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