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.
The perfect knowledge of the microscopic structure of the appropriate organ is crucial in the solution of many urgent problems of clinical medicine. Better preservation of tissue structures is achieved when the tissues are embedded into epoxy resins followed up with the semi-thin section making. In contrast to the thick sections that are used for light microscopy, due to the greater awareness and relative cost effectiveness without the need of complicated expensive equipment, the method of semithin sections today is currently used in morphological studies. The paper was aimed at the study of the prospects of using the semi-thin section method to evaluate the immobilization stress-induced structural changes in the lungs. The resulting study showed the appropriateness of the use of semi-thin sections to study structural changes in lungs, induced by the experimental stress. The study of the semi-thin sections is the beneficial technique of the morphological analysis that permits to evaluate the structure of the studied material at the tissue and cellular level.
Stress-related studies remain relevant notwithstanding its long-lasting history of research. Experimental studies are crucial in the study the impact of stress on a living organism. Currently, there is a great variety of simulation animal acute stress reaction models, in particular, cervical fold suspension of mice, which is cost effective and easy-to-use. However, there are insufficient data on using this technique to reproduce the acute stress response in rats, particularly, in studying the impact of immobilization stress on the liver. The purpose of the work was to study the impact of 6-hour-long cervical fold suspension simulation model of acute immobilization stress on the albino rats’ liver. Material and methods. Based on the international bioethical regulations, 20 male albino rats were involved into the study. The intact animals were assigned into group I (n=10) (control); the animals, exposed to 6-hour-long cervical fold suspension simulation model of acute immobilization stress were assigned to experimental group (n=10) (group II). After euthanasia, macro- and microscopic examination of the liver was performed. Micro-specimens were stained with hematoxylin and eosin. Results and discussion. The macroscopic examination of the liver did not reveal any visual differences in the rats of the experimental group compared to the control ones. Histological study of the liver specimens of group II rats showed that the experimental model of simulated acute immobilization stress in rats by atraumatic cervical fold suspension for 6 hours caused significant changes. They were especially pronounced in the bloodstream of the liver, manifested by the plethora and the phenomena of interlobular vein thrombosis. The central veins were also plethoric and a significant dilatation of the perisinusoidal spaces was noted. Changes in the hemomicrocirculation were characterized by manifestations of blood stasis and sludge in most sinusoidal capillaries. We detected the phenomena of tissue infiltration by the segmented neutrophils, as well as macrophages and lymphocytes perivascularly and in the portal tracts. Changes were also found in the liver cells, namely, the phenomena of karyopyknosis; subcapsular focal colliquational necrosis in the individual hepatocytes; hydropic dystrophy in hepatocytes located on the periphery of the liver lobuli. Conclusion. The implementation of experimental model of acute immobilization stress in rats by atraumatic cervical fold suspension caused significant histological changes in rat liver
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