ETHIOPATHOGENETIC PARALLELS OF MORPHOLOGICAL CHANGES IN CHRONIC DENTAL CARIES AND ITS COMPLICATIONS
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.
2. Petersen PE, Bourgeois D, Ogwa H, Estupinan-Day S, and Ndiaye C. The global burden of disease and risks to oral health. Bull world health organ. 2005; 83: 661-9.
3. Faustova MO, Ananieva MM, Basarab YO, Dobrobolska OV, Vovk IM, Loban' GA. Bacterial factors of cariogenicity (literature review). Wiad Lek. 2018;71(2 pt 2): 378-82.
4. Aas JA, Paster BJ, Stokes LN, Olsen I, Dewhirst FE. Defining the normal bacterial flora of the oral cavity. Journal of Clinical Microbiology. 2005; 43 (11): 5721-32.
5. Sommer F, Backhed F. The gut microbiota - masters of host development and physiology. Nature Reviews Microbiology. 2013; 4: 227-38.
6. Stepanova TYu, Tymofeeva AV. Mykrobyom rotovoi polosty cheloveka. Sovremennie problemi nauky y obrazovanyia. 2016; 5: URL: http://www.science-education.ru/ru/article/view?id=25212. ( Russian)
7. Dewhirst FE, Chen T, Izard J, Paster BJ, Tanner AC, Yu WH, et al. Wade The human oral microbiome. Journal of Bacteriology. 2010; 192: 5002-17.
8. Valm AM. The Structure of Dental Plaque Microbial Communities in the Transition from Health to Dental Caries and Periodontal Disease. 2019, 431(16): 2957-69.
9. Schoilew K, Ueffing H, Dalpke A, Wolff B, Frese C, Wolff D et al. Bacterial biofilm composition in healthy subjects with and without caries experience. Journal of Oral Microbiology. 2019; 11: 1633194.
10. Marsh PD. Dental plaque as a microbial biofilm. Caries Res. 2004; 38:204-11.
11. Marsh PD. Dental plaque as a biofilm and a microbial community - implications for health and disease. BMC Oral Health. 2006; 6 (l): 14.
12. Nyvad B, Takahashi N. Integrated hypothesis of dental caries and periodontal diseases. Journal of Oral Microbiology. 2020; 12:1.
13. Yadav K, Prakash S. Dental Caries: A Microbiological Approach. J Clin Infect Dis. 2017; 2:118.
14. Banas JA, Takanami E, Hemsley RM, Villhauer A, Zhu M, Qian F, et al. Evaluating the relationship between acidogenicity and acid tolerance for oral streptococci from children with or without a history of caries. Journal of Oral Microbiology. 2020; 12:1.
15. Takahashi N, Nyvad B. The role of bacteria in the caries process: ecological perspectives. J Dent Res. 2011;90:294–303.
16. Yu OY, Zhao IS, Mei ML, Lo EC-M, Chu C-H. A Review of the Common Models Used in Mechanistic Studies on Demineralization-Remineralization for Cariology. Research Dent. J. 2017; 5: 20.
17. Featherstone J. Dental caries: a dynamic disease process. Australian Dental Journal. 2008; 53: 286-291.
18. Kokoceva-Ivanovska O, Carcev M. Ultra-Structural Changes of the Early Childhood Caries Starting Phases of Development. Balk J Dent Med, 2014; 18:38-40.
19. Tkachenko IM, Braylko NN, Kovalenko VV, Nazarenko ZYu, Sheshukova OV. Morfolohycheskoe yssledovanye emaly y dentyna zubov s karyoznim protsessom y nekaryoznimy porazhenyiamy. Wiadomosci Lekarskie. 2018; LXXI (5): 1001-5.(Russian)
20. Paltsev MA, Kakturskyi LV, Zairatiants OV, hl.red. Patolohycheskaia anatomyia : natsyonalnoe rukovodstvo. Moskva: HEOTAR-Medya 2011. 1264 s. ( Russian)
21. Shahmoradi M, Swain MV. Micro-CT analysis of naturally arrested brown spot enamel lesions. Journal of Dentistry. 2017; 56: 105-11.
22. Hrynyshyn OB, Fylenko BM. Morfolohichni zminy pulpy pry eksperymentalnomu poverkhnevomu kariiesi. Visnyk problem biolohii i medytsyny. 2013; 3(103): 278-80.(Ukrainian)
23. Rajaram N, Ramani P, Premkumar P, Natesan A, Sherlin HJ Dentinal tubule morphology in carious lesions: A confocal microscopic study. International Journal of Orofacial Biology. 2018; 2(1): 16-9.
24. Lager AH. Dentine caries: acid-tolerant microorganisms and aspects on collagen degradation. Swed Dent J Suppl. 2014;(233):89-94.
25. Yoshihara K, Nagaoka N, Nakamura A, Hara T, Hayakawa S, Yoshida Y et al. Three-dimensional observation and analysis of remineralization in dentinal caries lesions. Scientific Reports. 2020;10:4387.
26. Lee J-K, Chang SW, Perinpanayagam H. Antibacterial efficacy of a human β-defensin-3 peptide on multispecies biofilms. Journal of Endodontics. 2013; 39 (12): 1625–29.
27. Farges J-C, Alliot-Licht B, Renard E, Ducret M, Gaudin A, Smith AJ, et al. Dental Pulp Defence and Repair Mechanisms in Dental Caries. Mediators of Inflammation. 2015; 230251. http://dx.doi.org/10.1155/2015/230251.
28. Bedoya SK, Lam B, Lau K, Larkin J. Th17 cells in immunity and autoimmunity. Clinical and Developmental Immunology. 2013; 986789. https://doi.org/10.1155/2013/986789.
29. Korkmaz Y, Lang H, Beikler T. Irreversible inflammation is associated with decreased levels of the alpha1-, beta1-, and alpha2-subunits of sGC in human odontoblasts. Journal of Dental Research. 2011; 90 (4): 517–22.
30. Kawashima N, Okiji T. Odontoblasts: Specialized hard tissue forming cells in the dentin pulp complex. Congenital anomalies. 2016; 56 (4): 144-53.
31. Hrynyshyn OB, Fylenko BM. Morfolohichni zminy riznykh dilianok zuba pry eksperymentalnomu serednomu kariiesi u shchuriv. Aktualni problemy suchasnoi medytsyny: Visnyk Ukrainskoi medychnoi stomatolohichnoi akademii. 2013; 44(13): 85-7.
32. Charadram N, Austin C, Trimby P, Simonian M, Swain MV, Hunter N. Structural analysis of reactionary dentin formed in response to polymicrobial invasion. J Struct Biol. 2013; 181(3): 207–22.
33. Hrynyshyn OB, Fylenko BM. Morfolohichni zminy tkanyn zuba pry eksperymentalnomu hlybokomu kariiesi u shchuriv. Visnyk problem biolohii i medytsyny. 2014; 2 (107): 119–22.(Ukrainian)
34. Neelakantan P, Rao CVS, Indramohan J. Bacteriology of deep carious lesions underneath amalgam restorations with different pulp-capping materials – an in vivo analysis. J Appl Oral Sci. 2012; 20(2): 139–45.
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