Caries develops when several factors combine: dental plaque microflora, easily fermentable dietary carbohydrates, a caries-susceptible tooth, and prolonged exposure time.

Microorganisms colonize tooth surfaces not subject to friction from the tongue, cheeks, and food fibers, forming a biofilm known as dental plaque. Carious lesions develop only in areas where plaque accumulates.

Frequent and prolonged consumption of easily fermentable carbohydrates increases the proportion of cariesogenic microflora in the biofilm, which can rapidly metabolize food carbohydrates to form organic acids and can also survive in low pH conditions. These are primarily Streptococcus mutans and Lactobacilli, but also Streptococcus sobrinus, Streptococcus oralis, Actinomyces israelii, Actinomyces gerencseriae, Bifidobacteria, and Prevotella. Streptococcus mutans also synthesize intra- and extracellular adhesive polysaccharides (glucans and fructans) that promote prolonged retention of bacteria on tooth surfaces.

Teeth are constantly bathed in saliva containing mineral substances. Saliva, due to its buffering capacity, helps maintain a neutral pH in the oral cavity. At neutral pH values (≈7), the processes of demineralization (dissolution of mineral component crystals) and remineralization (partial or complete restoration of mineral component crystals) of enamel and dentin are in equilibrium.

Bacterial metabolism of dietary carbohydrates (glucose, fructose, sucrose, maltose, and others) leads to acid accumulation and pH reduction.

If the pH drops low enough (5.2-5.5), minerals from the hard tissues of the tooth begin to dissolve. Gradual loss of minerals due to acid-induced dissolution (demineralization) is the main process in caries development.

The more frequently carbohydrates enter the oral cavity with food and the longer food debris remains on tooth surfaces, the more acid bacteria produce, lowering pH and progressing enamel demineralization. Upon reaching the dentin, in addition to continued acid production, bacteria also begin proteolytic activity. As a result, the organic component (collagen) of dentin is destroyed.

Caries progression can be slowed or stopped by reducing the frequency and duration of acid attacks, for example, by improving hygiene or limiting sugar consumption. Fluoride compounds promote remineralization processes and slow demineralization, reduce enamel solubility, and enhance its resistance to acid attacks.

Classification of Caries

By depth of lesion (radiographic classification):

E1 — outer half of enamel affected;
E2 — entire enamel layer affected;
D1 — outer third of dentin affected (superficial dentin caries);
D2 — outer and middle third of dentin affected (moderate caries);
D3 — outer, middle, and inner third of dentin affected without penetration into the pulp chamber (deep caries).

3D models of caries by depth of lesion:

Caries stages according to the radiological classification – stage E1

Caries stages according to the radiological classification – stage E2

Caries stages according to the radiological classification – stage D1

Caries stages according to the radiological classification – stage D2

Caries stages according to the radiological classification – stage D3

Black’s Classification (by lesion location):

Class I — in natural depressions (pits and fissures on the occlusal surface of posterior teeth, blind pits on incisors and canines);
Class II — on the proximal surfaces of posterior teeth;
Class III — on the proximal surfaces of anterior teeth without involving the incisal edge;
Class IV — on the proximal surfaces of anterior teeth involving the incisal edge;
Class V — in the cervical area of teeth.

Localization of carious cavities according to Black’s classification – class I

Localization of carious cavities according to Black’s classification – class II

Localization of carious cavities according to Black’s classification – class III

Localization of carious cavities according to Black’s classification – class IV

Localization of carious cavities according to Black’s classification – class V

Histological classification (by type of affected tooth tissue):

Enamel caries;
Dentin caries;
Cementum caries.

By method of occurrence:

Primary caries – develops in intact teeth without restorations;
Secondary caries – recurrence of the carious process after dental treatment.

Anatomy

Carious lesion always begins on the tooth surface that directly contacts the oral cavity: on the enamel surface, exposed root cementum, or exposed dentin. Caries more often develops in typical areas of plaque accumulation – in pits and fissures, on the lateral surfaces of teeth, in the cervical area. With high caries activity and insufficient hygiene, ‘immune zones’ can be affected by caries – smooth surfaces, the equator zone, and cusps.

Enamel caries: at the initial stage, after removing plaque and drying the tooth, the enamel macroscopically appears intact, with a focus of demineralization visible as a matte white spot (E1). At a later stage (E2), the white spot is noticeable even on the moist enamel surface. The spot can be stained in various shades of brown by food dyes. In the enamel, the lesion has the shape of a cone with its apex directed towards the enamel-dentin junction (EDJ). When the process reaches the EDJ and penetrates the dentin, the further direction of the lesion spread corresponds to the course of dentinal tubules.

Dentin caries: demineralized enamel in the defect area may remain intact (pseudo-intact enamel), preventing bacteria from penetrating the demineralization focus. Macroscopically, such a defect looks like a pigmented fissure or spot on the enamel surface, under which darker contours of the affected dentin may be discerned.

When about 30-40% of minerals in the enamel lesion focus are lost, it becomes so porous and fragile that it can easily break and form a cavity-like defect. Bacteria rush deep into the defect, under the influence of their proteases, the demineralized dentin becomes necrotic (bacterial penetration zone), and the demineralization zone spreads deeper towards the pulp. Around the demineralization focus, reactive dentin sclerosis occurs. The outer (D1), middle (D2), and inner (D3) thirds of dentin are sequentially affected. Macroscopically, an active lesion looks like a cavity filled with soft, sticky, yellowish-brown necrotic dentin that is easily removed by scraping. In a stalled lesion, the affected dentin is denser and darker.

Cementum caries in the form of a cavity filled with softened dentin develops on the tooth root surface in the presence of gingival recession and exposed root cementum. Its development follows the same mechanisms as crown caries.

Gingival recession and cementum caries in the canine region of the maxilla – 3D model

Secondary caries develops as linear staining, a spot, or cavity at the border between tooth tissues and restoration with compromised marginal integrity. This type of lesion consists of a surface area of demineralization at the enamel-restoration interface, and a ‘wall’ lesion between the restoration and the cavity. The surface focus spreads along the enamel prisms towards the EDJ and then along the dentinal tubules. The ‘wall’ lesion is a narrow slit-like cavity, later spreading along the dentinal tubules and in the lateral direction.

Secondary caries of a mandibular molar – 3D model

Diagnosis

Main methods:

Visual inspection – the presence of a visible stain or cavity on surfaces accessible to inspection. In the case of aproximal caries, the lesion may be visible from the occlusal surface as a gray shadow translucent through the intact enamel. For a better visual diagnosis, it is recommended to clean plaque and dry the teeth;
Percussion of the affected tooth is painless;
Probing – determining the depth and relief of the lesion, painless in enamel caries, painful when probing the EDJ in moderate caries and the floor of the carious cavity in deep caries.

Additional methods:

Radiography – lucency on radiograph in the enamel (E1,E2), outer, middle or inner third of dentin (D1-D3). Intraoral contact radiography, radiovisiography, bite-wing radiography (to diagnose occlusal and aproximal caries), orthopantomography (OPTG), and cone beam computed tomography (CBCT) are used;
Temperature test – air jet, cold spray, heated gutta-percha sticks are used. The response to a temperature stimulus disappears immediately, or a few seconds after the stimulus ceases;
Fiberoptic transillumination (FOTI) – shining through the teeth through the contact point, the carious lesion appears as a dark spot;
Quantitative laser fluorescence – healthy and decayed tooth tissues fluoresce with light waves of different wavelengths when exposed to laser light;
Electrical impedanceometry – demineralized tissues have a lower electrical impedance than healthy tissues (the method is of limited use for occlusal surfaces);
Temporary separation of teeth with rubber rings (for visualization of aproximal lesions);
Staining — demineralized enamel and denatured dentin collagen absorb dye unlike healthy tissues.

Clinical manifestations

Enamel caries (E1, E2) do not cause complaints; the patient may be concerned about the aesthetic defect. Clinically, a white or pigmented spot on the enamel is detected.

Dentin caries (D1–D3), cementum caries, secondary caries: complaints may be absent, the patient may be concerned about the presence of a cavity in the tooth or an aesthetic defect, short-term localized pain in the tooth from chemical, thermal, mechanical irritants, food getting stuck and difficulties when using dental floss. Clinically, pigmentation of the pit or fissure, borders of the old restoration, probe getting stuck in them (Black’s Class I, secondary caries), gray shadow under the marginal ridge, inflammation of the interdental papilla adjacent to the affected tooth, food debris in the interdental space (Class II), dark spots when illuminating teeth (Class II, III), visible carious cavities filled with softened dentin (Classes I–V, cementum caries) are detected.

Treatment

Enamel caries — for non-cavitated defects, remineralizing therapy, infiltration method, correction of home hygiene care, recommendations for rational nutrition, and dynamic observation are applied.

Dentin caries, cementum caries, secondary caries — tooth tissue preparation and filling of the carious cavity using dental restorative materials.

FAQ

1. What microorganisms cause caries development?

The main cariogenic microorganisms: Streptococcus mutans, Lactobacilli, Actinomyces. They form a biofilm (dental plaque) and can survive in low pH conditions.

2. How does enamel caries differ from dentin caries?

– Enamel caries is the initial stage, manifested by a white or pigmented spot.
– Dentin caries – accompanied by the destruction of dentin and the formation of a cavity.

3. What are the main methods of caries treatment?

• At the white spot stage — remineralization.
• When dentin is affected — preparation and filling.
• For complicated caries (pulp involvement) — endodontic treatment.

4. Caries and pulpitis: what are the differences?

Caries is a lesion of the hard tissues of the tooth (enamel and dentin) caused by the action of acids produced by microorganisms in dental plaque. In early stages, caries can be asymptomatic, and in later stages, it can cause short-term pain from irritants (cold, hot, sweet).

Pulpitis is a complication of caries, in which inflammation of the tooth pulp (neurovascular bundle) develops. Pulpitis is accompanied by severe, often radiating pain that can occur spontaneously, without external stimuli.

Main differences:

1. localization:
– Caries affects the enamel and dentin.
– Pulpitis affects the pulp of the tooth.

2. Symptoms:
– Caries: short-term pain occurs only when exposed to stimuli (cold, hot, sweet).
– Pulpitis: prolonged (more than 5 seconds) pain occurs when exposed to temperature stimuli, spontaneous pain is possible, pain irradiation.

3. Treatment:
– Caries: preparation and filling, remineralizing therapy.
– Pulpitis: treatment of root canals (endodontic treatment).

List of Sources

Toumba, K. J., Twetman, S., Splieth, C., Parnell, C., Van Loveren, C., Lygidakis, N. Α. (2019). Guidelines on the use of fluoride for caries prevention in children: an updated EAPD policy document. European Archives of Paediatric Dentistry, 20(6), 507–516.

https://doi.org/10.1007/s40368-019-00464-2

Meyer-Lueckel, H. (2013). Caries management: Science and Clinical Practice. Thieme Medical Pub.

Li, M. (2012b). Contemporary approach to dental caries. IntechOpen.

Xuedong, Z. (2016). Dental caries: Principles and Management. Springer.

Kidd, E. a. M., Fejerskov, O. (2016). Essentials of dental caries. Oxford University Press.

Eden, E. (2018). Evidence-Based caries prevention. Springer.

De Olivera Carrilho, M. R. (2017). Root caries: From Prevalence to Therapy. Karger Medical Scientific.

Askar, H., Krois, J., Göstemeyer, G. et al. Secondary caries: what is it, and how it can be controlled, detected, and managed?. Clin Oral Invest 24, 1869–1876 (2020).

https://doi.org/10.1007/s00784-020-03268-7

Askar H, Tu YK, Paris S, Yeh YC, Schwendicke F. Risk of caries adjacent to different restoration materials: Systematic review of in situ studies. J Dent. 2017 Jan;56:1-10. doi: 10.1016/j.jdent.2016.09.011.