Tooth decay is a global health problem and a major cause of tooth loss in the adult population. Currently, the most recognized theory of dental caries development is the chemical-parasitic theory of V.D. Miller that was suggested in 1884, and is relevant to date. According to this theory, oral microorganisms are capable of converting food carbohydrates to acids, which in turn dissolve the calcium phosphates present in the enamel, causing its demineralization.
Dental plaque is considered the key element in the development of dental caries, subsequently leading to the gradual formation of a dental plaque. Dental plaque (biofilm) is resulted from structurally and functionally ordered colonization of microorganisms on the tooth surface. This process is gradual and involves several links. Potential virulence factors are enzymes that are involved in the metabolism of sucrose and other carbohydrates that come with food. Continuous fermentation of carbohydrates results in a rapid local decrease in pH on the tooth enamel surface, reaching a critical level and dissolving of the apatite on the surface of the enamel in the most vulnerable areas. The prolonged existence of the foci of demineralization results in the dissolution of a more stable superficial enamel layer with the formation of a visible defect. In the projection of carious lesion of the enamel at the stages of the pigmented spot and superficial caries, pathological processes in the dentin are observed. Subsequently, the exposure to an acidic environment leads to destruction of the dentin-enamel border, contributing to spread of carious process onto the hard tooth tissues and forming a cavity in the dentin. Microscopically, the bottom of the carious cavity is represented by three layers of altered dentin. In dental caries, a physico-chemical type of occlusion of the dentinal tubules is observed, which is considered a protective mechanism, which significantly reduces the permeability of the affected dentin for microorganisms.
At the stage of medium caries, the odontoblast processes are affected by bacteria and their toxins, triggering a cascade of protective reactions in the pulp mediated by odontoblasts. After recognition of the pathogen, odontoblasts produce antibacterial substances, among which the most important are beta-defensins (BD) and nitric oxide (NO). The pro-inflammatory effect of BD-2 can be exacerbated by chemoattraction of immature antigen-presenting dendritic cells, macrophages, CD4 memory cells, and natural killers by binding to chemokine receptors. Activation of TLR4 increases BD-2 gene expression, indicating different odontoblasts’ response to gram-positive and gram-negative bacteria.
Exogenous factors, such as microorganisms and their toxins in dental caries, gradually destroy odontoblasts, and the stem cells of the dental pulp are differentiated into odontoblast-like cells, which provide the formation of reparative (replacement, irregular, secondary) dentine. However, the factors involved in the differentiation of odontoblast precursors and odontoblast-like cells are not known to date. In deep dental caries, a significant destruction of the hard tooth tissues is determined with the formation of a large cavity, the walls of which may lose a layer of transparent and intact dentin, while the zone of the replacement dentin is more pronounced. Moreover, deep dental caries causes the prominent inflammatory processes in the dental pulp. In the deep layers of the carious cavity Lactobacilli are found, which make up the vast majority of all microorganisms in deep dental caries. This fact should be taken into account during treatment and use inlays with antimicrobial activity to maintain the viability of the pulp.
Consequently, the development of dental caries and its course depends on the factors of virulence of the oral microorganisms and the severity of the compensatory protective mechanisms. Along with the processes of demineralization, the intensity of remineralization of the enamel and dentin is crucial. Superficial, medium and deep caries leads to changes in the dental pulp which should be considered in its treatment.
ETHIOPATHOGENETIC PARALLELS OF MORPHOLOGICAL CHANGES IN CHRONIC DENTAL CARIES AND ITS COMPLICATIONS
