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Dental Caries

Caries dentium

For medical students2 min readUpdated 2026-10-10

Dental caries is a pathological process involving the demineralization and destruction of hard dental tissues, resulting in a cavity defect. It is driven by organic acids produced by dental plaque microorganisms during carbohydrate fermentation.

Main PathogenStreptococcus mutans, which synthesizes acids and polysaccharides.
Critical pHDemineralization of dental enamel begins at pH 4.5–5.
SubstrateDietary mono- and disaccharides.
ProtectionSaliva (lysozyme, IgA) and fluoride (forms fluorapatite).

Etiology and Pathogenesis

The development of caries begins with the formation of dental plaque and biofilm. The core of the plaque consists of microorganisms (predominantly Streptococcus mutans and lactobacilli) that anchor to the acquired pellicle of the tooth.

Bacteria ferment dietary carbohydrates, releasing organic acids (lactic, pyruvic, etc.). These acids locally decrease the pH, triggering demineralization—the leaching of minerals from hard tissues. Subsequently, microbial hydrolytic enzymes (proteinases, hyaluronidase) destroy the exposed organic matrix of the tooth.

Saliva plays a protective role (cleansing, containing antibacterial agents) alongside fluoride, which replaces hydroxyapatite in the enamel with fluorapatite, making it more resistant to acids.

Enamel Caries (Initial and Superficial)

In initial caries, the integrity of the dentino-enamel junction remains intact. Notably, demineralization is most active in the subsurface zone of the enamel, forming a cone-shaped defect.

Stages of initial caries:

In superficial caries, the enamel becomes rough due to the destruction of enamel prisms and interprismatic substance.

Dentin Caries (Moderate and Deep)

The process progresses faster in dentin due to the presence of dentinal tubules, which provide high permeability. Bacteria penetrate the tubules, destroying the odontoblast processes.

In moderate caries, the dentino-enamel junction is destroyed, and the floor of the cavity consists of dentin. In deep caries, a large cavity (caverna) is formed.

Morphologically, the floor of the carious cavity exhibits distinct zones (from the surface to the pulp):

  1. Zone of softened dentin (containing detritus and microbes).
  2. Zone of unchanged dentin.
  3. Zone of transparent (hypermineralized, sclerotic) dentin — tubules are obliterated, serving as a protective barrier.
  4. Zone of secondary (irregular) and tertiary (replacement) dentin — a compensatory reaction by the pulp.

During rapid progression of deep caries, the transparent dentin zone fails to form.

Clinical Forms and Features

Aside from typical presentations, specific forms exist:

In children, caries progresses more aggressively due to lower tissue resistance. Deciduous incisors and molars are frequently affected, and the process can encompass all surfaces of the tooth, leading to rapid tooth loss.

Frequently asked questions

What organic acids are produced by dental plaque bacteria and cause enamel demineralization?

Dental plaque bacteria produce a range of organic acids, with lactic acid playing the leading role. Demineralization of hard dental tissues occurs under the action of the following acids:

  • Lactic acid (lactate) — the main product of carbohydrate fermentation, dissolving inorganic components.
  • Pyruvic acid (pyruvate).
  • Acetic acid (acetate).
  • Malic acid (malate).

A drop in local pH to critical values (4.5–5.0) triggers the leaching of minerals from the enamel.

What microbial hydrolytic enzymes destroy the organic matrix of the tooth during caries?

The destruction of the exposed organic matrix of the tooth during caries is carried out by the hydrolytic enzymes of the microflora. Proteinases and hyaluronidase play the leading role. They break down the organic matrix after it is exposed due to tissue demineralization by acids.

What protective factors of saliva prevent the development of caries?

Saliva prevents the development of caries through mechanical cleansing of the oral cavity and the presence of protective components. These include:

  • lysozyme, which has bactericidal activity;
  • mucin, which neutralizes acids and alkalis;
  • immunoglobulins, protecting against pathogenic microflora;
  • salivary proteolytic enzymes.

Additionally, saliva is a source of calcium, phosphorus, and zinc for the enamel.

How does moderate caries morphologically differ from deep caries?

Moderate caries: the floor of the cavity defect consists of dentin, and the dentino-enamel junction is destroyed.

Deep caries: a large cavity defect (caverna) is formed; as it progresses, the layer of replacement dentin disappears, and hydropic degeneration of odontoblasts is observed in the pulp. Odontoblast necrosis, pulp sclerosis, and the formation of pseudocysts and denticles are also possible. Perforation of the cavity floor results in exposure of the pulp chamber.

Why does dental calculus form, and does it cause caries?

Dental calculus forms through the calcification of undisturbed dental plaque. While it does not directly cause caries, it serves as an ideal platform for the accumulation of new dental plaque.

What are "dead tracts" in dentin?

These are areas of intratubular dentin sclerosis (tubule petrification) arising in response to the necrosis of odontoblast processes caused by bacterial toxins. They isolate the pulp from toxins.

Is the carious process reversible?

The process is reversible only at its very earliest stage—the white (chalky) enamel spot stage—when remineralization is possible. Later changes become irreversible.

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