ROLE OF INNATE IMMUNITY FACTORS IN PERIODONTITIS PATHOGENESIS

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Abstract

Chronic generalized periodontitis (CGP) is a disease of periodontium tissues supporting tooth induced by bacteria, that is characterized by the presence of processes of inflammation with destruction ofbone tissue. The knowledge of molecular mechanisms of CGP pathogenesis facilitates creation of the most effective methods of therapy of this disease. Bacterial infection is a primary factor in periodontitis etiology, however is not sufficient for its start and subsequent development. It is known, that bacterial factors induce a local inflammation reaction and activate the system of innate immunity through activation of Toll-like receptors (TLR), located on the surface of resident cells and leukocytes. Activation of these cells results in production of pro-inflammatory cytokines and recruitment of phagocytes and lymphocytes into the inflammation zone. In review we examined the known data regarding factors of immune protection of periodontium including cell populations and cytokines, as well as mechanisms of tissue destruction, that support the tooth. Perspectives of therapy are also discussed.

About the authors

L. V. Gankovskaya

Pirogov Russian National Research Medical University

Author for correspondence.
Email: noemail@neicon.ru
Russian Federation

N. M. Khelminskaya

Pirogov Russian National Research Medical University

Email: noemail@neicon.ru
Russian Federation

E. A. Molchanova

Pirogov Russian National Research Medical University

Email: noemail@neicon.ru
Russian Federation

O. A. Svitich

Mechnikov Research Institute of Vaccines and Sera

Email: noemail@neicon.ru
Russian Federation

References

  1. Боровский Е.В., Иванов В.С., Максимовский Ю.М. и др. Терапевтическая стоматология. М., Медицина, 1998.
  2. Иванюшко Т.П., Ганковская Л.В., Шаманаев С.В. и др. Изучение содержания дефенсинов у больных с гнойно-воспалительными заболеваниями челюстно-лицевой области. Стоматология. 2014, 93 (2): 23-26.
  3. Ковальчук Л.В., Ганковская Л.В., Мироншиченкова А.М. и др. Роль Toll-подобрых рецепторов в патогенезе инфекционных заболеваний человека. Человек и его здоровье. 2012, 2: 147-153.
  4. Курякина Н.В., Кутепова Т.Ф. Заболевания пародонта. М., Медицинская книга, 2003.
  5. Свитич О.А., Ковальчук Л.В., Ганковская Л.В. и др. Аналитический подход в изучении противовирусного и иммуномодулирующего действия препаратов на модели герпесвирусной инфекции in vitro. Российский иммунологический журнал. 2013, 4: 377-384.
  6. Adriana D. B., Gigante I., Colucci S. Periodontal disease: Linking the primary inflammation to bone loss. 2013, doi: 10.1155/2013/503754.
  7. Ara T., Kurata K., Hirai К. et al. Human gingival fibroblasts are critical in sustaining inflammation in periodontal disease. J. Periodontal Research. 2009, 1: 21-27.
  8. Bascones-Martinez A., Munoz-Corcuera M., Noronha S. et al. Host defence mechanisms against bacterial aggression in periodontal disease: Basic mechanisms. Med. Oral. Patol. Oral. Cir. Bucal. 2009, 14: 680-685.
  9. Benakanakere M., Kinane D.F Innate cellular responses to the periodontal biofilm. Frontiers of Oral. Biology. 2012, 1: 41-55.
  10. Brunetti G., Colucci S., Pignataro P et al. T cells support osteoclastogenesis in an in vitro model derived from human periodontitis patients. J. Periodontology. 2005, 10: 1675-1680.
  11. Crotti T., Smith M.D., Hirsch R. et al. Receptor activator NFкB ligand (RANKL) and osteopro-tegerin (OPG) protein expression in periodontitis. J. Periodontal Research. 2003, 4: 380-387.
  12. Dewhirst FE., Chen T., Izard J. et al. The human oral microbiome. J. Bacteriol. 2010, 192: 50025017.
  13. Dunsche A., Agil Y, Dommisch H. et al. The novel human beta-defensin-3 is widely expressed in oral tissues. Eur. J. Oral. Sci. 2002, 110: 121-124.
  14. Elson G., Dunn-Slegrist I., Daubeuf B. et al. Contribution of Toll- like receptors to the innate immune response to Gram-positive and Gram-negative bacteria. Blood. 2007, 109: 1574-1583.
  15. Ekhlassi S., Scruggs L.Y., Garza T. et al. Porphyromonas gingivalis lipopolysaccharide induces tumor necrosis factor- and interleukin-6 secretion, and CCL25 gene expression, in mouse primary gingival cell lines: interleukin-6-driven activation of CCL2. J. Periodontal Research. 2008, 4: 431439.
  16. Garlet G.P., Martins Jr. W, Fonseca B.A. et al. Matrix metalloproteinases, their physiological inhibitors and osteoclast factors are differentially regulated by the cytokine profile in human periodontal disease. J. Clinical Periodontology. 2004, 8: 671-679.
  17. Gemmell E., Seymour G.J. Immunoregulatory control of Th1/Th2 cytokine profiles in periodontal disease. Periodontol. 2000. 2004, 35: 21-41.
  18. Graves D.T., Cochran D. The contribution of interleukin-1 and tumor necrosis factor to periodontal tissue destruction. J. Periodontology. 2003, 3: 391-401.
  19. Graves D. Cytokines that promote periodontal tissue destruction. J. Periodontology. 2008, 8: 15851591.
  20. Hans M., Hans YM. Toll-like receptors and their dual role in periodontitis: a review. J. Oral Science. 2011, 53 (3): 263-271.
  21. Hansson G.K., Edfeldt K. Toll to be paid at the gateway to the vessel wall. Arteriosclerosis, Thrombosis, Vascular Biology. 2005, 6: 1085-1087.
  22. Hauber H.P., Tulic M.K., Tsicopoulos A. Toll-like receptors 4 and 2 expression in the bronchial mucosa of patients with cystic fibrosis. Can. Respir. J. 2005, 12: 13-18.
  23. Hayashi F., Means T.K., Luster A.D. Toll-like receptors stimulate human neutrophil function. Blood. 2003, 7: 2660-2669.
  24. Hemmi H., Takeuchi O., Kawai T. et al. Toll-like receptor recognizes bacterial DNA. Nature. 2000, 408 (6813): 740-745.
  25. Honda T., Domon H., Okui T. et al. Balance of inflammatory response instable gingivitis and progressive periodontitislesions. Clin. Exp. Immunol. 2006, 144 (1): 35-40.
  26. Junemann S., Prior K., Szczepanowski R. et al. Bacterial community shift in treated periodontitis patients revealed by ion torrent 16S rRNA gene avplicon sequencing. PLoS One. 2012, 7 (8): е41606.
  27. Jung I.H., Lee D.E., Yun J.H. et al. Anti-inflammatory effect of (-)epigallocatechin-3-gallate on Porphyromonas gingivalis lipopolysaccharide-stimulated fibroblasts and stem cells derived from human periodontal ligament. J. Periodontal Implant Science. 2012, 6: 185-195.
  28. Kim M., Jun H.K., Choi B.K. et al. Td92, an outer membrane protein of Treponema denticola, induces osteoclastogenesis via prostaglandin-E2-mediated RANKL/osteoprotegerin regulation. J.Periodontal Research. 2010, 6: 772-779.
  29. Lerner U.H. Inflammation-induced bone remodeling in periodontal disease and the influence of post-menopausal osteoporosis. J. Dental Research. 2006, 7: 596-607.
  30. Liang S., Domon H., Hosur K.B. et al. Age-related alterations in innate immune receptor expression and ability ofmacrophages to respond to pathogen challenge in vitro. Mech. Ageing. Dev. 2009, 130: 538-546.
  31. Lu H.K., Chen YL., Chang H.C. et al. Identification of the osteoprotegerin/receptor activator of nuclear factor-kappa B ligand system in gingival crevicular fluid and tissue of patients with chronic periodontitis. J. Periodontal Research. 2006, 41: 354-360.
  32. Marcopoulou C.E., Vavouraki H.N., Dereka X.E. et al. Proliferative effect of growth factors TGF-beta1, PDGF-BB and rhBMP-2 on human gingival fibroblasts and periodontal ligament cells. J. Int. Acad. Periodontol. 2003, 5 (3): 63-70.
  33. Matsumoto C., Oda T., Yokoyama S. et al. Toll-like receptor 2 heterodimers, TLR2/6 and TLR2/1 induce prostaglandin E production by osteoblasts, osteoclast formation and inflammatory periodontitis. Biochem. Biophys. Res. Communications. 2012, 1: 110-115.
  34. Morandini A.C., Sipert C.R., Gasparoto T.H. et al. Differential production of macrophage inflammatory protein-1, stromal-derived factor-1, and IL-6 by human cultured periodontal ligament and gingival fibroblasts challenged with lipopolysaccharide from P. gingivalis. J. Periodontology. 2010, 2: 310-317.
  35. Nanbara H., Wara-Aswapati N., Nagasawa T. et al. Modulation of Wnt5a expression by periodon-topathic bacteria. PLoS One. 2012, 4: ID e34434.
  36. Nifulescu E.A., Craifoiu M^., Banina M.I. et al. The involvement of TGF-P1 and CTGF in regional gingival overgrowth. Rom. J. Morphol. Embryol. 2012, 53 (1): 143-150.
  37. Page R.C., Offenbacher S., Schroeder H.E. et al. Advances in the pathogenesis of periodontitis: summary of developments, clinical implications and future directions. Periodontol. 2000. 1997, 14: 216-248.
  38. Park Y.D., Kim YS., Jung Y.M. et al. Porphyromonas gingivalis lipopolysaccharide regulates interleukin (IL)-17 and IL-23 expression via SIRT1 modulation in human periodontal ligament cells. Cytokine. 2012, 1: 284-293.
  39. Rakoff-Nahoum S., Paglino J., Eslami-Varzaneh F. et al. Recognition of commensal microflora by Toll-like receptors is required for intestinal homeostasis. Cell. 2004, 118: 229-241.
  40. Ren L., Jiang Z.Q., Fu Y. et al. The interplay of lipo-polysaccharide-binding protein and cytokines in periodontal health and disease. J. Clin. Periodontol. 2009, 36: 619-626.
  41. Ritchlin C.T., Haas-Smith S.A., Li P et al. Mechanisms of TNF- and RANKL-mediated osteo-clastogenesis and bone resorption in psoriatic arthritis. J. Clinical Investigation. 2003, 6: 821-831.
  42. Scheres N., Laine M.L., de Vries T.J. et al. Gingival and periodontal ligament fibroblasts differ in their inflammatory response to viable Porphyromonas gingivalis. J. Periodontal Research. 2010, 2: 262-270.
  43. Tang Y., Sun F., Li X. et al. Porphyromonas endodontalis lipopolysaccharides induce RANKL by mouse osteoblast in a way different from that of Escherichia coli lipopolysaccharide. J. Endodontics. 2011, 12: 1653-1658.
  44. Tew J.G., El Shikh M.E., El Sayed R.M. et al. Dendritic cells, antibodies reactive with oxLDL, and inflammation. J. Dental Research. 2012, 1: 8-16.
  45. Trevani A.S., Chorny A., Salamone G. et al. Bacterial DNA activates human neutrophils by a CpG-independent pathway. Eur. J. Immunology. 2003, 11: 3164-3174.
  46. Yarilina A., Xu K., Chen J. et al. TNF activates calcium-nuclear factor of activated T cells (NFAT) c1 signaling pathways in human macrophages. Proc. Nat. Acad. Sci. USA. 2011, 4: 1573-1578.
  47. Yoshihiro A., Masto S., Michiko N. et al. Role of b-defensins in oral epithelial health and disease. Med. Mol. Morphol. 2007, 40: 179-184.
  48. Zadeh H.H., Kreutzer D.L. Evidence for involvement of superantigens in human periodontal diseases: skewed expression of T cell receptor variable regions by gingival T cells. Oral Microbiological Immunology. 1996, 11 (2): 88-95.
  49. Zhang W, Swearingen E.B., Rigney J. et al. Porphyromonas gingivalis invades osteoblasts and inhibits bone formation. Microb. Infection. 2010, 11: 838-845.
  50. Zhang W, Rigney T., Tribble G. Integrin alpha5 beta1- fimbriae binding and actin rearrangement are essential for Porphyromonas gingivalis invasion of osteoblasts and subsequent activation of the JNK pathway. BMC Microbiology. 2013, 1: 13-15.

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Copyright (c) 2016 Gankovskaya L.V., Khelminskaya N.M., Molchanova E.A., Svitich O.A.

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