Caries: Why it occurs and how it is treated

Dental caries is a multifactorial disease of hard tissues in which, against the background of dental plaque (biofilm) and the consumption of free sugars, organic acids dissolve enamel and dentin, forming lesions ranging from chalky spots to cavities. The disease is asymptomatic for a long time and is often detected late, when fillings or root canal treatment are already required. Correct diagnosis in the early stages allows for the process to be stopped without drilling and preserves tooth tissue. [1]

According to the World Health Organization and global disease burden estimates, untreated dental caries in permanent teeth is the most common human disease; in 2021, billions of cases occurred worldwide. This is not only a medical problem but also a socioeconomic one: pain, missed work and school, and a reduced quality of life. Children, low-income individuals, and patients with chronic xerostomia are particularly vulnerable. [2]

Caries is now considered a manageable, dysbiosis-dependent disease: the balance between demineralization and remineralization can be shifted in favor of health through fluoride, reduced sugar intake, hygiene, and an individualized risk plan (CAMBRA/CariesCare). This allows, in some cases, to avoid invasive treatment and stop lesions at the spot stage. [3]

Modern dentistry relies on a "minimally invasive" strategy: the sooner we find the problem, the less we drill. Options include fissure sealants, resin infiltration, fluoride varnishes, 38% silver diamine fluoride (SDF), atraumatic restorative treatment (ART), and, if necessary, precision restorations and crowns. The choice depends on the ICDAS stage, location, age, and caries risk. [4]

Epidemiology

According to the Global Burden of Disease 2021-2024, permanent dental caries remains the most common condition affecting humans, affecting billions. One recent analysis reports an estimated 2.37 billion cases of permanent dental caries in 2021, highlighting the scale of the problem. [5]

Prevalence varies by region and social group: populations with high sugar consumption and insufficient access to fluoride and dental care are more likely to suffer. However, dental caries in primary teeth remains significant in preschool-aged children, affecting nutrition, sleep, and academic performance. [6]

The burden is also uneven by age: in adolescents, molar fissures are more often affected, in adults, the approximal surfaces are affected, and in the elderly, the incidence of root caries increases due to gum recession. Immunosuppression and decreased salivation further increase the risk. [7]

Another layer is economic: treatment of dental caries and its complications accounts for a significant share of dental costs. Public health strategies (water/salt fluoridation, school sealant programs, sugar restriction) demonstrate the best cost-benefit ratio at the population level. [8]

Table 1. Global caries burden benchmarks

Indicator	Score/Trend
The most common condition according to GBD	Untreated caries of permanent teeth
Cases (2021)	≈2.37 billion (estimate)
The most vulnerable	Children, low-income groups, people with xerostomia
Main drivers	Free sugars, fluoride deficiency, access to care

Reasons

The primary causative factor is the frequent consumption of free sugars, which are metabolized by plaque microorganisms into acids; the pH drops, and enamel minerals dissolve. WHO guidelines recommend limiting free sugars to <10% of daily energy, and preferably <5% (≈25 g/day) for additional benefit. [9]

Microbial communities play a key role: acid-producing and acid-tolerant species (e.g., mutans streptococci, lactobacilli) dominate in a "sweet" diet and low pH, replacing the healthy microbiome. This is not a "single-bacterium infection," but a shift in biofilm ecology toward dysbiosis. [10]

Demineralization occurs when the pH curve (Stefan's curve) frequently and for long periods falls below a critical level (~5.5 for enamel, ~6.2 for the root). Fluoride and mineral-rich saliva during "alkaline" periods return calcium and phosphate to the enamel—this is remineralization. Balance is the essence of the disease. [11]

Systemic factors exacerbate the process: hyposalivation (medication-induced, syndromic), gastroesophageal reflux (acid load), poor mechanical cleansing, and low awareness. At the population level, access to fluoride-containing products and drinking water is important. [12]

Risk factors

The most powerful modifiable factor is the frequency and stickiness of sugars (sweet drinks, snacks). The more frequent the acid attacks, the higher the risk; replacing frequent snacks with regular meals reduces demineralization. [13]

Hyposalivation (dry mouth) increases the risk due to the loss of saliva's buffering and remineralizing functions. Causes include medications, radiation therapy, and autoimmune diseases. In this group, standard prophylaxis is enhanced with high fluoride concentrations and salivary replacement therapy. [14]

Low socioeconomic status and poor access to prevention and treatment are associated with higher caries rates in children and adults. Fissure sealant programs and school-based prevention are particularly effective in reducing these inequalities. [15]

Individual hygiene habits and skills also determine risk: irregular brushing with fluoride toothpaste, lack of interdental cleaning, smoking, bruxism (crumbled enamel) - all of which increase the need for a personalized risk plan (CAMBRA/CariesCare). [16]

Table 2. Risk factors and controllability

Factor	Controllability	Comment
Frequent free sugars	Yes	Limit <10%, better <5% energy
Low fluoride intake	Yes	Pastes 1000-1500 ppm F, varnishes according to risk
Hyposalivation	Partially	Correction of causes, saliva substitutes
Low SES/access	Partially	School sealants, fluoride programs
Poor hygiene	Yes	Education, plaque control

Pathogenesis

The dental biofilm is a complex ecosystem. With high-frequency sugar consumption, acid-producing bacteria predominate; matrix polysaccharides retain acids at the surface. "Acid attacks" trigger the release of calcium and phosphate ions from the enamel. In the early stages, this is reversible. [17]

Saliva is the primary protector: it neutralizes acids, delivers minerals, and contains proteins and fluoride. With xerostomia or nighttime snacking without a salivary "buffer," the process accelerates. Regular fluoride (paste/varnish) is incorporated into the crystals, increasing their acid resistance. [18]

Clinically, early demineralization manifests as a chalky spot (ICDAS 1-2), followed by subsurface cavitation and dentin loosening (ICDAS 3-5). The critical pH for the root is higher, so with gum recession, the picture progresses more rapidly. [19]

If risk factors are not corrected, lesions coalesce, cavities develop, and sensitivity to sweets and cold develops; this then leads to pulpitis, periodontitis, and the need for endodontics or extractions. This justifies early diagnosis and risk-based management. [20]

Symptoms

Early lesions are often asymptomatic. The patient may notice whitish, matte spots in the cervical area or between teeth that do not disappear after brushing. At this stage, the process is reversible—active fluoride and sugar reduction are essential. [21]

As the cavity progresses, sensitivity to sweets and cold, food sticking, and roughness develop. A visible cavity does not always indicate pain; rather, it is cavitation, requiring minimally invasive repair. [22]

In children, the molar fissures and cervical areas are most often affected; in adults, the contact surfaces between the teeth; in the elderly, the root surfaces with "worn down" enamel in the recession zone. Clinical presentations vary, which is important when choosing a method. [23]

Pain from sweets/cold is short-lived and resolves after the stimulus is removed—this is typical of superficial lesions. Prolonged spontaneous pain indicates pulpal complications and requires immediate intervention. [24]

Forms and stages

For standardization, the ICDAS scale (0-6) is used, which captures the entire spectrum—from an early stain to large cavitation with visible dentin. This helps select a gentle approach and avoid "overtreatment." [25]

A distinction is made between coronal, approximal, fissure, and root caries based on location, as well as active and inactive caries based on clinical signs (opacity, softness of the base, plaque). Active lesions require immediate behavioral and therapeutic measures. [26]

“Hidden” lesions under intact enamel in fissures and contact zones are a separate issue; they are identified using targeted bitewings at an individual interval, taking into account the risk. [27]

In children, staging by activity and depth is widely used to choose between sealing, infiltration, atraumatic restoration or crowns using the Hall technique - without preparation and anesthesia in some cases. [28]

Table 3. ICDAS stages (simplified)

Code	Clinic	Tactics in general
0	There is no defeat	Prevention, control
1-2	Chalk stain (enamel)	NIP: fluoride, infiltration/sealing
3	Initial enamel cavitation	Minimally invasive restoration
4-5	Cavitation with dentin	Restoration/onlay
6	Extensive cavitation	Comprehensive rehabilitation

Complications and consequences

Left untreated, caries progresses to pulpitis and periapical periodontitis, leading to pain, abscesses, and possibly tooth extraction. This puts additional stress on adjacent teeth and can trigger a chain reaction of problems. [29]

In children, multiple dental caries limits sleep and nutrition, and impairs growth and academic performance. Early treatment and parental education are key to breaking the vicious cycle of dental pain and fear. [30]

The economic consequences are significant: fillings, crowns, and endodontics are more expensive than preventative care. At the healthcare system level, funding preventative programs (fluoride, sealants) pays for itself by reducing the need for complex interventions. [31]

Cosmetic problems (darkening, chipping) impact psychosocial well-being. Minimally invasive approaches in the early stages allow for maintaining aesthetics without extensive preparation. [32]

Table 4. Frequent complications

Complication	How does it manifest itself?	What prevents
Pulpitis/periodontitis	Pain, swelling	Early detection and NIP/restoration
Tooth loss	Deficit of chewing	Filling/onlay/canals on time
Multiple restorations	"Escalation" of interventions	Reducing sugars, fluoride
Aesthetic defects	Stains, chips	Infiltration, composites

Diagnostics

The basic procedure is a dry examination, assessment of the activity of the lesions, and gentle probing without forcibly puncturing the enamel. The ICDAS scale and photographic recording are helpful for monitoring. Excessive pressure with the probe can damage the surface and accelerate progression. [33]

Bitewing X-rays are essential for detecting interdental caries and hidden lesions. The interval is determined by risk: 6-12 months for high-risk teeth, 2-3 years for low-risk teeth, in accordance with recommendations of the FDA/ADA and specialized societies. In children, the frequency is also determined by the stage of eruption. [34]

Risk assessment is the basis of the plan (CAMBRA/CariesCare): nutrition, saliva, fluoride, plaque, social factors, and clinical findings are considered, and then prevention and treatment are prescribed in a stepwise manner. This increases predictability and reduces interventions. [35]

Specialized tests (fluorescent/laser devices) can complement, but do not replace, examination and X-rays. Decisions are made based on the combined clinical data and risk. [36]

Table 5. Diagnostics and its tasks

Method	What does it give?	When needed
Inspection + ICDAS	Stage and activity	To all patients
Bitewings	Interdental/hidden caries	By risk (6-36 months)
CAMBRA/CariesCare	Individual plan	To everyone, especially high-risk ones
Photographic documentation	Monitoring	NPCs and dynamics

Differential diagnosis

White spots on enamel are not limited to caries: fluorosis, hypoplasia, erosion (acid-induced non-carious wear), and post-orthodontic white spots require differentiation. An active carious spot is matte, rough, and localized in plaque "risk zones." [37]

Dentin hypersensitivity due to gingival recession can mimic "caries pain" but without cavitation. Vitality testing, staining, and imaging are helpful. [38]

Wedge-shaped defects at the neck of the tooth - abfraction and erosion - do not have a soft bottom and plaque, but require correction of factors (occlusion, acidic drinks) and protective restorations when indicated. [39]

In children, early childhood caries (ECC) is sometimes confused with primary fluorosis; history, location, and rate of progression help differentiate the conditions and guide treatment.[40]

Table 6. "Stain on enamel": what could it be?

State	Key Features	Tactics
Early caries	Matteness, roughness, plaque zone	Fluoride, NIP, control
Mild fluorosis	Symmetrical, shiny surface	Observation, aesthetics as desired
Erosion	Smooth, "fused" enamel	Diet, neutralization of acids
Hypoplasia	Developmental defect, marginal lines	Individually, often restoration

Treatment

Non-drug and drug-based prevention in the early stages. Daily brushing with fluoride toothpaste (≥1000 ppm for children, 1350-1500 ppm for adults), professional fluoride varnishes for high-risk patients, dietary modification (reducing sugar intake), and plaque control. Fluoride varnishes and fluorides have been proven to reduce caries incidence in children and adolescents. [41]

Fissure sealants. Resin sealants prevent caries on chewing surfaces and can "seal" non-cavitated lesions (arrests). The effectiveness of sealants has been confirmed by systematic reviews and guidelines. Glass ionomers are an alternative in difficult-to-seal environments. [42]

Resin infiltration (Icon) for contact spots. This method "impregnates" porous enamel and blocks acid diffusion, slowing/stopping the progression of early interdental lesions; there is evidence of high 3-7-year efficacy compared to observation. It is suitable as a gentle alternative to drilling in ICDAS stages 1-3. [43]

Silver diamine fluoride 38% (SDF) allows for the arrest of active carious lesions (especially in children and the elderly) without drilling; it forms a dark pigmentation as an arrest marker. Systematic reviews show a high arrest rate, comparable to or superior to alternatives in primary teeth. [44]

Atraumatic restorative treatment (ART) and glass ionomer. Manual removal of softened dentin and cavity closure with high-viscosity glass ionomer is the method of choice when access to equipment is limited and in children; it provides fluoride release and chemical adhesion. [45]

Pediatric therapy: Hall technique and preformed crowns. For molars with caries and no pulpal symptoms, the crown is placed without preparation or anesthesia; according to meta-analyses, this tactic demonstrates a higher survival rate compared to direct fillings. [46]

Restorations and onlays. For cavitation within the enamel/superficial dentin, gentle preparation and composite with adhesive protocols are used; for larger defects, onlays/inlays (ceramics/composite) are used to preserve the tooth walls. The choice of material depends on the load, moisture control, and occlusion. [47]

Adjunctive therapies. Sugar-free gum (xylitol) may reduce caries incidence, but the quality of evidence is mixed; it is used as a supplement to, not a replacement for, fluoride. CPP-ACP (casein phosphopeptide/amorphous calcium phosphate) shows potential for white spot remineralization; data are evolving, and the effect is often considered adjunctive. [48]

The role of antibacterial and mouthwashes. Chlorhexidine varnishes/rinses may temporarily reduce the number of S. mutans, but are not a routine substitute for fluoride and mechanical plaque control; they are prescribed as indicated and in courses due to side effects. [49]

Table 7. Gentle methods vs. drilling

Situation	First choice method	Alternative
Fissures without cavitation	Sealant	Observation + fluoride
Interdental stain (ICDAS 1-3)	Infiltration	Fluorlax, controlled observation
Active foci in children/elderly	38% SDF	ART, sealing
Average cavitation	Minimal preparation + composite	Overlay for large defects

Table 8. Prevention by risk level (CAMBR example)

Risk	Home measures	Prevention in the clinic
Short	Paste 1350-1500 ppm F, 2×/day	Inspection every 12-24 months
Average	+ Interdental cleaning, limiting sugars	Fluoride varnish 2-4 times/year
High	+ Additional fluoride (gels/rinses), xylitol if tolerated	Fluorovarnish 4 times a year, sealants, NIP/infiltration

Prevention

The best "cure" is fewer sugar cravings and regular fluoride. Limit free sugars to <10% of energy, and preferably <5%; replace sweet drinks with water/unsweetened milk; brush your teeth twice a day with fluoride toothpaste (for children, adjust the amount according to their age). Interdental cleaning should be done daily. [50]

Discuss a personalized risk management plan with your dentist: fissure sealants for children and adolescents, fluoride varnishes for high-risk teeth, infiltration of "questionable" contact areas, scheduled preventive X-rays, monitoring for dry mouth and medications. This approach allows for minimal or complete avoidance of drilling. [51]

Forecast

With early detection and proper prevention, the prognosis is excellent: lesions at the spot stage can be stabilized, and the risk of new lesions can be significantly reduced. Regular fluoride, sealants, and sugar control have been proven to reduce the incidence of caries in children and adults. [52]

If risk factors persist (frequent sugar intake, xerostomia, lack of fluoride and hygiene), the likelihood of progression is high, including pulp complications and tooth loss. Even with high-quality restorations, without control of these factors, "secondary caries" often develops at the margins of fillings. Therefore, the prognosis is determined not only by the filling material but also by lifestyle. [53]

FAQ

• Can caries be treated without drilling?

Yes, if it's an early stage (ICDAS 1-2): fluoride varnishes, resin infiltration, fissure sealants, and sugar control can stop the process and restore minerals. If a cavity is present, minimally invasive restoration will be required. [54]

• What is more important: not eating sweets or brushing your teeth?

Both: the frequency of sugar "attacks" determines the outcome, while fluoride and mechanical brushing shift the balance toward remineralization. Optimally, reduce the frequency of sugar "attacks" and brush twice a day with fluoride toothpaste. [55]

• Are bitewing x-rays necessary every year?

The interval depends on the risk: for high risk – 6-12 months; for low risk – 2-3 years. The decision is made by the dentist based on the recommendations of the FDA/ADA and specialized societies. [56]

• Should I specifically look for toothpastes with xylitol or CPP-ACP?

These are supplements. For most people, fluoride remains the baseline. Xylitol and CPP-ACP may be useful in certain situations (high risk, white spots), but the quality of the evidence is mixed; use under the advice of a physician. [57]

• What is SDF and why does tooth darken?

38% silver diamine fluoride is a solution for stopping active caries without drilling, especially in children and the elderly. It "preserves" the lesion but darkens its pigmentation—a normal sign of arrest. Aesthetics are discussed in advance. [58]