Dental Caries: Etiology, Anatomy, Classification, Clinical Presentation, Treatment

Tooth decay, also known as dental caries, is an infection that leads to the mineral breakdown and destruction of the hard tissues of the teeth.

Etiology

The condition tends to develop when a combination of factors is in play. These may include a pathological bacterial plaque, high consumption of readily fermentable carbohydrates, susceptible teeth, prolonged exposure to unfavorable conditions, etc.

Microorganisms colonize tooth surfaces not subject to friction from the tongue, cheeks, and food fibers, forming a biofilm known as dental plaque. Typical sites of decay are found where the 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. The most commonly founf strains are Streptococcus mutans and Lactobacilli, as well as Streptococcus sobrinus, Streptococcus oralis, Actinomyces israelii, Actinomyces gerencseriae, Bifidobacteria, and Prevotella. Streptococcus mutans also synthesizes 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 levels (≈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 balance.

As bacteria process food carbohydrates (glucose, fructose, sucrose, maltose, etc.), acids build up, thus reducing pH.

Minerals in the hard tissues of the teeth start to dissolve, as soon as the pH drops to 5.2–5.5. This gradual process of mineral loss caused by dissolution under acidic conditions is called demineralization, the driver of tooth decay.

The amount of acid bacteria produce increases when carbohydrates are consumed more often and food debris containing them remains longer on the tooth surface. Consequently, the pH decreases and the enamel loses more minerals. Upon reaching the dentin, in addition to continued acid production, bacteria also begin proteolytic activity. The process causes the organic component of the dentin, collagen, to degrade.

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. To this end, fluorine compounds (also known as fluoride) are especially useful. They promote remineralization, slow down the reverse process of demineralization, decrease enamel solubility, and reinforce its resistance to acids.

Classification of Caries

By depth of lesion (radiographic classification):

• E1 — the outer half of the enamel is affected;
• E2 — the entire enamel coat is affected;
• D1 — the outer one— third of the dentin is affected (superficial dentin caries);
• D2 — the outer and middle one— thirds of the dentin are affected (dentin caries);
• D3 — the outer, middle, and inner one— thirds of the dentin are affected (deep caries).

3D Models of Tooth Decay Stages according to Radiographic Classification:

Stage E1

Stage E2

Stage D1

Stage D2

Stage D3

By localization (Black classification):

• Class I — in natural deepenings (pits and fissures in the occlusal surfaces of molars and premolars, pits on incisor and canine teeth);
• Class II — in lateral (approximal) surfaces of molars and premolars;
• Class III — in lateral (approximal) surfaces of anterior teeth with the incisal edge unaffected;
• Class IV — in lateral (approximal) surfaces of anterior teeth with the incisal edge affected;
• Class V — in the neck area of teeth.

3D Models of Tooth Decay Localiztion according to Black Classification:

Class I Cavity

Class II Cavity

Class III Cavity

Class IV Cavity

Class V Cavity

By type of tooth tissue affected (histological classification):

• Enamel caries;
• Dentin caries;
• Cementum caries.

By method of occurrence:

• Primary caries — decay in intact teeth that have not undergone restoration;
• Secondary caries — relapsed decay post-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. The most typical locations for tooth decay are pits and fissures, lateral tooth surfaces, and neck areas. Intensive decay process, in combination with poor hygiene, may impact “immune areas”, including smooth surfaces, tooth contour, and cusps.

Enamel caries

This is an initial stage of decay (E1). After plaque has been removed and the tooth is dry, the enamel is visually integral with a dull white spot of demineralization. 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

In this case, the demineralized enamel in the lesion area may show no evidence of decay (a so-called pseudo-intact enamel), thus preventing bacteria from reaching the demineralization focus. Macroscopically, this defect looks like a pigmented fissure or spot on the enamel surface that covers darker edges of the affected dentin.
When the damaged enamel loses around 30–40 % of its minerals, it becomes highly porous and fragile. At this point, it can break easily and create a cavity. 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. An arrested lesion, on the other hand, presents with a denser and darker-colored dentin.

Cementum caries

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.

Secondary caries

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 is characterized by a superficial demineralized area at the interface between the enamel and the restored tooth, in combination with wall decay. 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.

Diagnosis

Main methods:

• Visual examination helps identify any visible spots or cavities on surfaces available for 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 better visibility, any plaque should be removed and teeth should be dried.
• An affected tooth should be painless to percussion.
• Probing is used to estimate the lesion’s depth and line. It is painless in enamel caries but may be tender in cases of dentin caries when the DEJ is being probed or in cases of deep caries when the decay cavity bottom is examined.

Additional methods:

• Radiographic detection is based on radiolucency in the enamel area (E1, E2), outer, middle, and inner one-thirds of the dentin (D1–D3). This method comprises intraoral contact radiography, radiovisiography, bite-wing radiography (employed to diagnose occlusal and approximal lesions), dental panoramic radiography (DPR), and cone-beam computed tomography (CBCT).
• A thermal sensibility test utilizes an air stream, a cold spray, or heated gutta-percha rods. A thermal sensibility test utilizes an air stream, a cold spray, or heated gutta-percha rods.
• Fiber optic transillumination (FOTI) involves transillumination of teeth via a contact point, which makes decay appear as a dark spot.
• The basic principle of quantitative light-induced fluorescence is the disparity in fluorescence radiance between affected and healthy tooth tissues.
• Electrical impedance spectroscopy is based on the fact that demineralized tissues demonstrate decreased electrical resistance compared to healthy ones. It should be noted that the method is limited to occlusal surfaces only.
• In order to get access to approximal lesions, temporary separation with rubber rings may be employed.
• Last but not least is the tinting technique. It is assumed that, in contrast to healthy tissues, demineralized enamel and denaturated dentin collagen tend to absorb a dye.

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, and secondary caries: there may be no specific complaints, but a patient may be concerned about a cavity in their tooth, a cosmetic imperfection, short-term localized tenderness after chemical, thermal, mechanical irritation, food impaction, or difficulties when trying to use dental floss. Upon clinical examination, a range of signs may be identified. These may include a pigmented pit or fissure, edges of previous restorations, a probe stuck in them (class I according to Black classification, secondary caries), a gray shadow under the marginal ridge, inflammation of interdental papilla adjacent to the affected tooth, food impaction in the interdental space (class II), dark spots upon transillumination (class II, III), and visible decay cavities made of softened dentin (class I–V, cementum caries).

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Treatment

In cases of enamel caries without cavities, the defects are treated using remineralization or infiltration methods. The treatment is only effective when combined with proper personal hygiene, nutrition, and follow-up.

Dentin caries, cementum caries, or secondary caries require more invasive techniques, including the preparation of tooth tissues and dental filling using various dental restorative materials.