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PATHOGENIC ROLE OF THE MICROBAL PERSISTENCE OF DENTAL PLAQUE IN PERIODONTITIS DEVELOPMENT

Authors: Demkovych A.

Pages: 174-180

Abstract


This article presents the role of microbial factors in the development of inflammation in periodontal. The leading role in the formation of inflammation in the mouth belongs resistant obligate anaerobic and microaerophilic organisms. During invasion of bacteria produce compounds that reduce or completely block the activity of protective systems. Factors that induce prolonged inflammation and periodontal tissue destruction usually are attributed exo- and endotoxins by pathogenic bacteria, in particular Porphyromonas gingivalis, the number of which increases substantially in periodontal diseases, especially in fresh lesions. Identification of P. gingivalis indicates the progression risk of chronic inflammation in parodontum.

The aim of the work is to analyze the scientific literature data of the microbial etiology of periodontitis, for the development of the disease, a combination of these conditions: pathogenic bacteria in an amount sufficient to start the inflammatory process; living conditions in the mouth should contribute to the growth and reproduction of pathogenic organisms; in periodontal tissues should be absent microorganisms – bacteria parodontopatogenic antagonists; microorganisms have spatially localized so that they (or) their metabolic products could act directly on target cells; the human body must be sensitive to bacteria and their toxins. Gums have of features associated with the structure of this component periodontal mucosa. Found that in most places periodontal destruction and often occur P. gingivalis, A. actinomycetemcomitans, P. intermedia, T. forsythensis, E. corrodens, F. nucleatum. P. melanogenica, V. parvula, Peptostreptococcus micros and others. Inflammation in periodontal tissues and is caused by microbial dental plaque. It with the development of periodontitis found to increase the number P. gingivalis, P. intermedia and T. forsythensis more than 100 times. Pathogenicity factors of is endotoxin, phospholipase A, that violates the integrity of the membrane epithelial cells and hemagglutinin protease and contributing active introduction of microorganisms in the periodontal tissues and their rapid destruction. Deep penetration of microorganisms in the gum tissue leads to a high probability relapse after therapy. P. gingivalis is one of the major pathogens involved in periodontitis. Predominance in tissues Porphyromonas gingivalis is a poor prognostic sign in typical forms of periodontitis. Porphyromonas gingivalis – gramnegative anaerobic fixed coli, which belong to the family Porphyromonadaceae. The surface is covered with P. gingivalis fibrils. They are the most frequent, followed Aggregatibacter Actinomycetemcomitans, pathogens of chronic generalized periodontitis. Especially a lot of them can be found in fresh area destruction. They are most closely associated with chronic periodontitis from all the pathogens . Intracellular Porphyromonas gingivalis able to subdue the metabolism of cells that are directly relevant to the development of the disease. So, after the invasion of Porphyromonas gingivalis in gingival epitheliocytes is inhibited the secretion of interleukin-8 weakens periodontal natural protection. In the situation that created microorganism, loses signal the presence of bacteria and not sent white blood cells to destroy them. P. gingivalis may prevent migration polymorphonuclear leukocytes and through the epithelial barrier.

Key words: Periodontal, periodontal disease, Porphyromonas gingivalis, microbe, inflammation.

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References

1. Nahirnyi YaP, Stefaniv IV, Gorban YeM. [Basic trends in the development of new drugs for the treatment of periodontitis and gingivitis]. Ukr. Clinical Dentistry. 2011;4:22–26.
2. Zabolotnyi TD, Markov AV, Shylivskyi IV. Generalizovanyi parodontyt [Generalized perio-dontitis]. Lviv: GalDent Publ., 2011. 240 p.
3. Mudra VM. [Study of proinflammatory cyto-kines (TNF-α, IL-1β) in blood and their products in cultures mononuclear patients with chronic generalized periodontitis who need dental implants]. Ukr. Implantology. Paradontology. Osteology. 2011;4:10–16.
4. Kowalski M, Brocka E, Barylski M. [et al.]. Assessment of the periodontal state in subjects with metabolic syndrome. Pol. Merkur. Lekarski. 2009;26(156):620–625.
5. Neporada KS, Mykytenko AO, Yankovskyi DS. [et al.]. [Chronic generalized periodontitis as a result of violation of biofilm of oral cavity]. Bel. Modern Dentistry. 2013;3:22–25.
6. Hajishengallis G, Abe T, Maekawa T. [et al.] Role of complement in host-microbe homeosta-sis of the periodontium. Semin. Immunol. 2013;25(1):65–72.
7. Pashchenkov MV, Alzahova BI, Lvov VL. [et al.]. [Features of the induction of pro-inflammatory genes in dendritic cells and mac-rophages under the influence glucoseminilmu-ramiltripeptide Gram-negative bacteria]. Rus. Immunology. 2013;1:10–15.
8. Grudyanov AI, Ovchinnikova VV. [The detec-tion rate of various representatives parodontopatogen microflora in periodontitis of varying severity]. Rus. Stomatology. 2009;3:34–37.
9. Zoryanova NV, Grygoryan AS, Grudyanov AI. [Species composition of anaerobic microflora of periodontal pockets depending on the stage of periodontitis]. Rus. Stomatology. 2009;4:43–47.
10. Kavushevska NS, Tyupka TI, Masliy YuS. [In-vestigation of antimicrobial activity of dental gels based on lysozyme]. Ukrainian biophar-maceutical Journale. 2012;5-6(22-23):94–97.
11. Kupchak OI. [Analysis of the microbial compo-sition of the root canal in patients with chronic apical periodontitis and periodontal inflammatory diseases]. Ukr. The world of medicine and biology. 2014;2:47–50.
12. Verkaik MJ, Busscher HJ, Rustema-Abbing M. [et al.]. Oral biofilm models for mechanical plaque removal. Clin. Oral Invest. 2010;14:403–409.
13. Zorina OA, Kulakov AA, Grudyanov AI. [Mi-crobiocenosis the mouth in normal and inflam-matory periodontal diseases]. Rus. Stomatology. 2011;1:73–78.
14. Volkova MN. [Analysis of the microbial com-position of subgingival plaque patients with chronic periodontitis]. Rus. Bulletin of the Vi-tebsk State Medical University. 2012;(1):138–145.
15. Dmitrieva LA, Atrushkeych VG, Galieva DT. [Comparative analysis of the microbial content of root canals and periodontal pockets in pa-tients with chronic generalized periodontitis and with intact periodontium]. Rus. Endodontics Тоday. 2010;2:2–13.
16. Skochko OV, Bobrova NA, Izmailova OV. [et al.]. [The role of some microorganisms and parodontopatogennyh Asp299Gly polymor-phism of TLR4 in the pathogenesis of athero-sclerosis]. Rus. Journal Microbiology Epidemi-ology and Immunobiology. 2011;5:83–86.
17. Shymanskyi ShL, Chilikin VN, Malyshev IY. [et al.]. [Phagocytic periodontal protection and ways to activate]. Rus. Stomatology. 2013;92(5):64–69.
18. Ramamoorthy RD, Nallasamy V, Reddy R. A review of C-reactive protein: A diagnostic indi-cator in periodontal medicine. Journal Pharm. Bioallied. Sci. 2012;4:422–426.
19. Bielecka E, Scavenius C, Kantyka T. [et al.]. Peptidyl arginine deiminase from Porphyromo-nas gingivalis abolishes anaphylatoxin C5a ac-tivity. J. Biol. Chem. 2014;289(47):32481–32487.
20. Komiyama Y, Kafkova LR, Barasch A. [et al.] Origin of galactose-deficient immunoglobuling in gingival crevicular fluid in periodontitis. J. Periodontol. 2014;85(2):1779–1785.
21. Naiff PF, Ferraz R, Cunha CF. [et al.]. Im-munophenotyping in saliva as an alternative approach for evaluation of immunopathogenesis in chronic periodontitis. J. Periodontol. 2014;85(5):111–120.
22. Nespryadko VP, Zhdavovych IO. [Features immunologic adaptation in generalized periodontitis]. Bel. Modern Dentistry. 2011;3:60–62.
23. Duragina LH, Sedyh VP, Dorofeeva OV. [State of systemic and local immunity of patients with simultaneous lesions of periodontal and oral mucosa in combination with depressive disor-ders]. Ukr. Bulletin of the problems of biology and medicine. 2014;2(1):140–145.
24. Shcherba VV, Korda MM. [Effect of inhibitors of NO-synthase expression of cytokines and condition of connective tissue in periodontitis on a background of concomitant chronic hepatitis]. Ukr. Medicines Ukraine. 2013;5:55–58.
25. Nemec A, Pavlica Z, Petelin M. [et al.]. Systemic use of selective iNOS inhibitor 1400W or non-selective NOS inhibitor L-NAME differently affects systemic nitric oxide formation after oral Porphyromonas gingivalis inoculation in mice. Arch. Oral. Biol. 2010;55(7):509–514.
26. Stathopoulou PG, Benakanakere MR, Galicia JC. [et al.]. The host cytokine response to Por-phyromonas gingivalis is modified by gingi-pains. Oral Microbiol. Immunol. 2009;24(1):11–17.
27. Zhu C, Yang J, Sun J. [et al.]. Induction of im-mune response and prevention of alveolar bone loss with recombinant Porphyromonas gingi-valis peptidylarginine deiminase. Arch. Oral Biol. 2013;58(12):1777–1783.
28. Jeong E, Lee JY, Kim SJ. [et al.]. Predominant immunoreactivity of Porphyromonas gingivalis heat shock protein in autoimmune diseases. J. Periodontal Res. 2012;47(6):811–816.
29. Darveau RP. Porphyromonas gingivalis neutro-phil manipulation: risk factor for periodontitis? Trends Microbiol. 2014;22(8):428–429.
30. Bartold PM, Marino V, Cantley M. [et al.]. Ef-fect of Porphyromonas gingivalis-induced in-flammation on the development of rheumatoid arthritis. J. Clin. Periodontol. 2010;37(5):405–411.
31. Duran-Pinedo AE, Baker VD, Frias-Lopez J. The periodontal pathogen Porphyromonas gingivalis induces expression of transposases and cell death of Streptococcus mitis in a biofilm model. Infect. Immun. 2014;82(8):3374–3382.
32. Shcherba VV, Korda MM. [Pathogenetic pecu-liarities of periodontitis on a background of chronic hepatitis]. Ukr. Medical Chemistry. 2012;14(2):64–68.
33. Mariano FS, Campanelli AP, Nociti Jr FH. [et al.]. Antimicrobial peptides and nitric oxide production by neutrophils from periodontitis subjects Braz. J. Med. Biol. Res. 2012;45(11):1017–1024.
34. Nemec A, Pavlica Z, Crossley DA. [et al.]. Chronic ingestion of Porphyromonas gingivalis induces systemic nitric oxide response in mice. Oral Microbiol. Immunol. 2009;24:204–210.
35. Pleskanovskaya NV, Ippotilov EV, Tsyarov VN. [et al.]. [Rationale and assessment of the effectiveness of combination of local (anti-inflammatory, antibacterial and immunotropic) therapy in treatment of inflammatory periodon-tal diseases]. Rus. Stomatology. 2013;1:26–30.
36. Sharma A, Pradeep R. Clinical efficacy of 1% alendronate gel in adjunct to mechanotherapy in the treatment of aggressive periodontitis: a randomized controlled clinical trial J. Periodon-tol. 2012;83(1):19–26.