Etiology and pathogenesis
The development of caries begins with the formation of dental plaque and dental biofilm. The basis of the plaque consists of microorganisms (primarily Streptococcus mutans and lactobacilli), which attach to the dental pellicle.
Bacteria ferment dietary carbohydrates, releasing organic acids (lactic, pyruvic, etc.). These acids locally lower the pH, initiating demineralization—the leaching of minerals from hard tissues. Following this, microbial hydrolytic enzymes (proteinases, hyaluronidase) destroy the exposed organic matrix of the tooth.
A protective role is played by saliva (cleanses, contains antibacterial agents) and fluoride, which replaces hydroxyapatite in the enamel with fluorapatite, which is more resistant to acids.
Enamel caries (initial and superficial)
In initial caries, the integrity of the dentino-enamel junction is preserved. Importantly, demineralization is most active in the subsurface zone of the enamel, forming a cone-shaped defect.
Stages of initial caries:
- White (chalky) spot stage: the surface is smooth, the process is reversible (remineralization is possible).
- Pigmented spot stage: the spot turns yellow or dark due to bacterial pigments (genus Bacteroides). It is not subject to remineralization.
In superficial caries, the enamel becomes rough due to the destruction of enamel prisms and interprismatic substance.
Dentin caries (moderate and deep)
The process in dentin is faster due to the presence of dentinal tubules, which provide high permeability. Bacteria penetrate into the tubules, destroying the processes of odontoblasts.
In moderate caries, the dentino-enamel junction is destroyed, and the floor of the cavity consists of dentin. In deep caries, a large cavity is formed.
Morphologically, the following zones are distinguished at the bottom of the carious cavity (from the surface to the pulp):
- Zone of softened dentin (with detritus and microbes).
- Zone of unchanged dentin.
- Zone of transparent (hypermineralized, sclerrosed) dentin — the tubules are obliterated; this is a protective barrier.
- Zone of secondary (irregular) and tertiary (replacement) dentin — a compensatory reaction from the pulp.
With rapid progression of deep caries, the transparent dentin zone does not have time to form.
Clinical forms and features
In addition to the typical course, specific forms are distinguished:
- Cementum caries: occurs in elderly people when the root is exposed against the background of periodontitis. The leading microbes are Streptococcus salivaris. Breakdown of cementum (cementolysis) is characteristic.
- Circular caries: ring-like surrounds the neck of the tooth, proceeds acutely, without the formation of a protective zone of sclerosed dentin.
- Retrograde caries: develops from the inside (from the pulp) outwards. Found in purulent pulpitis or trauma.
In children, caries is more aggressive due to lower tissue resistance. Deciduous incisors and molars are often affected, and the process can cover all surfaces of the tooth, leading to its rapid loss.
Briefly: answers to topical questions
Which organic acids are produced by dental plaque bacteria and cause enamel demineralization?
Dental plaque bacteria produce a number of organic acids, among which lactic acid plays the leading role. Demineralization of hard dental tissues occurs under the influence of the following acids:
- Lactic acid (lactate) is the main product of carbohydrate fermentation, dissolving inorganic components.
- Pyruvic acid (pyruvate).
- Acetic acid (acetate).
- Malic acid (malate).
A drop in the local pH level to critical values (4.5–5.0) triggers the process of mineral leaching from the enamel.
Which hydrolytic enzymes of microorganisms destroy the organic matrix of the tooth during caries?
The destruction of the exposed organic matrix of the tooth in caries is carried out by hydrolytic enzymes of the microflora. Proteinases and hyaluronidase play a leading role. They destroy the organic matrix after it is exposed due to tissue demineralization by acids.
Which protective factors of saliva prevent the development of caries?
Saliva prevents the development of caries due to the mechanical cleansing of the oral cavity and the presence of protective components. These include:
- lysozyme, which has a bactericidal effect;
- mucin, which neutralizes acids and alkalis;
- immunoglobulins protecting against pathogenic microflora;
- proteolytic enzymes of saliva.
In addition, 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 is represented by dentin, the dentino-enamel junction is destroyed.
Deep caries: a large defect is formed — a cavity; as it progresses, the layer of replacement dentin disappears, and hydropic dystrophy of odontoblasts is observed in the pulp. Necrosis of odontoblasts, pulp sclerosis, formation of pseudocysts, and denticles are also possible. With perforation of the cavity floor, the dental pulp cavity is opened.
Class and exam questions
Why does dental calculus form and does it cause caries?
Dental calculus is formed by the calcification of undisturbed dental plaque. By itself, it does not cause caries, but 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 under the influence of bacterial toxins. They isolate the pulp from toxins.
Is the carious process reversible?
The process is reversible only at the very first stage — the white (chalky) spot stage of enamel, when remineralization is possible. Later, the changes become irreversible.
What else to study on this topic
- Pathomorphological changes in the pulp in deep caries (denticles, hydropic dystrophy)
- Degrees of caries activity in children
- Complications of caries (transition to pulpitis)
- Fluorosis as the most common non-carious lesion
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