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Current Oral Health Reports

Erschienen in:

01.06.2014 | Immunology (G Nussbaum, Section Editor)

Neutrophil Dysfunction and Host Susceptibility to Periodontal Inflammation: Current State of Knowledge

verfasst von: Corneliu Sima, Michael Glogauer

Erschienen in: Current Oral Health Reports | Ausgabe 2/2014

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Abstract

Normal polymorphonuclear neutrophil (PMN) function is critical for the maintenance of host-biofilm equilibrium and periodontal tissue homeostasis. Mounting evidence suggests that PMNs play important roles in the control of commensal periodontal flora and initiation of resolution following inflammation caused by accumulating subgingival plaque. Quantitative and qualitative alterations of PMNs in bone marrow, blood, periodontal tissues, and gingival crevicular fluid contribute to host-microbial dysbiosis and onset of irreversible loss of clinical attachment around teeth. Recent findings of specific PMN phenotypes associated with different disease states bring us closer to understanding disease activity and addressing chronic, non-resolved, periodontal inflammation to better monitor and predict patient-specific treatment outcomes. The present review addresses the current state of knowledge in PMN biology in the pathogenesis of periodontal inflammation and the onset of periodontitis.

Summers C, Rankin SM, Condliffe AM, Singh N, Peters AM, Chilvers ER. Neutrophil kinetics in health and disease. Trends Immunol. 2010;31:318–24.PubMedCentralPubMedCrossRef

Pillay J, den Braber I, Vrisekoop N, Kwast LM, de Boer RJ, Borghans JAM, et al. In vivo labeling with 2H2O reveals a human neutrophil lifespan of 5.4 days. Blood. 2010;116:625–7.PubMedCrossRef

Bekkering S, Torensma R. Another look at the life of a neutrophil. World J Hematol. 2013;2:44–58.CrossRef

4.•

Hajishengallis G. Immunomicrobial pathogenesis of periodontitis: keystones, pathobionts, and host response. Trends Immunol. 2013;35:3–11. This review addresses the host biofilm interations in pathogenesis of periodontitis with focus on inflammation.PubMedCrossRef

Delima AJ, Van Dyke TE. Origin and function of the cellular components in gingival crevice fluid. Periodontol 2000. 2003;31:55–7.PubMedCrossRef

Tonetti MS, Imboden MA. Neutrophil migration into the gingival sulcus is associated with transepithelial gradients of interleukin-8 and ICAM-1. J Periodontol. 1998;69:1139–47.PubMedCrossRef

Zenobia C, Luo XL, Hashim A, Abe T, Jin L, Chang Y, et al. Commensal bacteria-dependent select expression of CXCL2 contributes to periodontal tissue homeostasis. Cell Microbiol. 2013;15:1419–26.PubMedCrossRef

8.•

Kolaczkowska E, Kubes P. Neutrophil recruitment and function in health and inflammation. Nat Rev Immunol. 2013;13:159–75. This review addresses the mechanisms of PMN recruitment and their bactericidal function, including the formation of NETs.PubMedCrossRef

Sima C, Rhourida K, Van Dyke TE, Gyurko R. Type 1 diabetes predisposes to enhanced gingival leukocyte margination and macromolecule extravasation in vivo. J Periodontol Res. 2010;45:748–56.CrossRef

10.

Hajishengallis E, Hajishengallis G. Neutrophil homeostasis and periodontal health in children and adults. J Dent Res. 2014;93(3):231–7.PubMedCrossRef

11.

Serhan C, Jain A, Marleau S, Clish C, Kantarci A, Behbehani B, et al. Reduced inflammation and tissue damage in transgenic rabbits overexpressing 15-lipoxygenase and endogenous anti-inflammatory lipid mediators. J Immunol. 2003;171(12):6856–65.PubMedCrossRef

12.

Eskan MA, Jotwani R, Abe T, Chmelar J, Lim JH, Liang S, et al. The leukocyte integrin antagonist Del-1 inhibits IL-17-mediated inflammatory bone loss. Nat Immunol. 2012;13(5):465–73.PubMedCentralPubMedCrossRef

13.

Martire B, Rondelli R, Soresina A, Pignata C, Broccoletti T, Finocchi A, et al. Clinical features, long-term follow-up and outcome of a large cohort of patients with chronic granulomatous disease: an Italian multicenter study. Clin Immunol. 2008;126:155–64.PubMedCrossRef

14.

Cohen MS, Leong PA, Simpson DM. Phagocytic cells in periodontal defense: periodontal status of patients with chronic granulomatous disease of childhood. J Periodontol. 1985;56(10):611–7.PubMedCrossRef

15.

Johnstone AM, Koh A, Goldberg MB, Glogauer M. A hyperactive neutrophil phenotype in patients with refractory periodontitis. J Periodontol. 2007;78:1788–94.PubMedCrossRef

16.

Aboodi GM, Goldberg MB, Glogauer M. Refractory periodontitis population characterized by a hyperactive oral neutrophil phenotype. J Periodontol. 2011;82:726–33.PubMedCrossRef

17.

Feng Z, Weinberg A. Role of bacteria in health and disease of periodontal tissues. Periodontol 2000. 2006;40:50–76.PubMedCrossRef

18.

Bostanci N, Thurnheer T, Aduse-Opoku J, Curtis MA, Zinkernagel AS, Belibasakis GN. Porphyromonas gingivalis regulates TREM-1 in human polymorphonuclear neutrophils via its gingipains. PLoS ONE. 2013;8:e75784.PubMedCentralPubMedCrossRef

19.•

Hajishengallis G, Liang S, Payne MA, Hashim A, Jotwani R, Eskan MA, et al. Low-abundance biofilm species orchestrates inflammatory periodontal disease through the commensal microbiota and complement. Cell Host Microbe. 2011;10:497–506. This study demonstrated that an inflammtory disease such as periodontitis can be caused by dysregulation of host-polymicrobial interactions instigated by a single species (Porphyromonas gingivalis) that appears to act as keystone pathogen.PubMedCentralPubMedCrossRef

20.

Brinkmann V. Neutrophil extracellular traps kill bacteria. Science. 2004;303:1532–5.PubMedCrossRef

21.

Cooper PR, Palmer LJ, Chapple ILC. Neutrophil extracellular traps as a new paradigm in innate immunity: friend or foe? Periodontol 2000. 2013;63:165–97.PubMedCrossRef

22.

Brinkmann V, Zychlinsky A. Beneficial suicide: why neutrophils die to make NETs. Nat Rev Microbiol. 2007;5:577–82.PubMedCrossRef

23.

Menegazzi R, Decleva E, Pietro D. Killing by neutrophil extracellular traps: fact or folklore? Blood. 2012;119:1214–6.PubMedCrossRef

24.

Bianchi M, Hakkim A, Brinkmann V, Siler U, Seger RA, Zychlinsky A, et al. Restoration of NET formation by gene therapy in CGD controls aspergillosis. Blood. 2009;114:2619–22.PubMedCentralPubMedCrossRef

25.

Papayannopoulos V, Metzler KD, Hakkim A, Zychlinsky A. Neutrophil elastase and myeloperoxidase regulate the formation of neutrophil extracellular traps. J Cell Biol. 2010;191:677–91.PubMedCentralPubMedCrossRef

26.••

Bartold PM, Van Dyke TE. Periodontitis: a host-mediated disruption of microbial homeostasis: unlearning learned concepts. Periodontol 2000. 2013;62:203–17. This paper overviews new concepts in periodontal disease pathogenesis that challenge the existing paradigm of biofilm-initiated tissue destruction.PubMedCrossRef

27.••

Serhan CN, Chiang N, Van Dyke TE. Resolving inflammation: dual anti-inflammatory and pro-resolution lipid mediators. Nat Rev Immunol. 2008;8:349–61. This paper is a landmark synthesis of concepts used in analysis of inflammation resolution. It also overviews a new class of endogenously produced pro-resolution lipid mediators.PubMedCentralPubMedCrossRef

28.

Jesenberger V, Jentsch S. Deadly encounter: ubiquitin meets apoptosis. Nat Rev Mol Cell Biol. 2002;3:112–21.PubMedCrossRef

29.

Tait SWG, Green DR. Caspase-independent cell death: leaving the set without the final cut. Oncogene. 2008;27:6452–61.PubMedCentralPubMedCrossRef

30.

Roos A, Xu W, Castellano G, Nauta AJ, Garred P, Daha MR, et al. Mini-review: a pivotal role for innate immunity in the clearance of apoptotic cells. Eur J Immunol. 2004;34:921–9.PubMedCrossRef

31.

Nauta AJ, Daha MR, van Kooten C, Roos A. Recognition and clearance of apoptotic cells: a role for complement and pentraxins. Trends Immunol. 2003;24:148–54.PubMedCrossRef

32.

Hébert MJ, Takano T, Holthöfer H, Brady HR. Sequential morphologic events during apoptosis of human neutrophils: modulation by lipoxygenase-derived eicosanoids. J Immunol. 1996;157:3105–15.PubMed

33.

Bellingan GJ, Caldwell H, Howie SE, Dransfield I, Haslett C. In vivo fate of the inflammatory macrophage during the resolution of inflammation: inflammatory macrophages do not die locally, but emigrate to the draining lymph nodes. J Immunol. 1996;157:2577–85.PubMed

34.

Savill JS, Wyllie AH, Henson JE, Walport MJ, Henson PM, Haslett C. Macrophage phagocytosis of aging neutrophils in inflammation: programmed cell death in the neutrophil leads to its recognition by macrophages. J Clin Invest. 1989;83:865–75.PubMedCentralPubMedCrossRef

35.

Serhan CN, Savill J. Resolution of inflammation: the beginning programs the end. Nat Immunol. 2005;6:1191–7.PubMedCrossRef

36.

Hart TC, Atkinson JC. Mendelian forms of periodontitis. Periodontol 2000. 2007;45:95–112.PubMedCrossRef

37.•

Deas DE, Mackey SA, McDonnell HT. Systemic disease and periodontitis: manifestations of neutrophil dysfunction. Periodontol 2000. 2003;32:82–104.PubMedCrossRef

38.

Zaromb A, Chamberlain D, Schoor R, Almas K, Blei F. Periodontitis as a manifestation of chronic benign neutropenia. J Periodontol. 2006;77:1921–6.PubMedCrossRef

39.

Armitage GC, Cullinan MP. Comparison of the clinical features of chronic and aggressive periodontitis. Periodontol 2000. 2010;53:12–27.PubMedCrossRef

40.

Morley AA, Carew JP, Baikie AG. Familial cyclical neutropenia. Br J Haematol. 1967;13:719–38.PubMedCrossRef

41.

Ye Y, Carlsson G, Wondimu B, Fahlén A, Karlsson-Sjöberg J, Andersson M, et al. Mutations in the ELANE gene are associated with development of periodontitis in patients with severe congenital neutropenia. J Clin Immunol. 2011;31:936–45.PubMedCentralPubMedCrossRef

42.

Gaffen SL, Hajishengallis G. A new inflammatory cytokine on the block: re-thinking periodontal disease and the Th1/Th2 paradigm in the context of Th17 cells and IL-17. J Dent Res. 2008;87(9):817–28.PubMedCentralPubMedCrossRef

43.

Lagane B, Chow KYC, Balabanian K, Levoye A, Harriague J, Planchenault T, et al. CXCR4 dimerization and beta-arrestin-mediated signaling account for the enhanced chemotaxis to CXCL12 in WHIM syndrome. Blood. 2008;112:34–44.PubMedCrossRef

44.

Cancelas JA, Jansen M, Williams DA. The role of chemokine activation of Rac GTPases in hematopoietic stem cell marrow homing, retention, and peripheral mobilization. Exp Hematol. 2006;34:976–85.PubMedCrossRef

45.

Sima C, Gastfreund S, Sun C, Glogauer M. Rac-null leukocytes are associated with increased inflammation-mediated alveolar bone loss. Am J Pathol. 2013;184:472–82.PubMedCrossRef

46.

Pai S-Y, Kim C, Williams DA. Rac GTPases in human diseases. Dis Markers. 2010;29:177–87.PubMedCentralPubMedCrossRef

47.

Barros SP, Offenbacher S. Modifiable risk factors in periodontal disease. Periodontol 2000. 2013;64:95–110.CrossRef

48.

Ryder MI. Comparison of neutrophil functions in aggressive and chronic periodontitis. Periodontol 2000. 2010;53:124–37.PubMedCrossRef

49.

Eick S, Pfister W, Sigusch B, Straube E. Phagocytosis of periodontopathogenic bacteria by crevicular granulocytes is depressed in progressive periodontitis. Infection. 2000;28:301–4.PubMedCrossRef

50.••

Darveau RP. Periodontitis: a polymicrobial disruption of host homeostasis. Nat Rev Microbiol. 2010;8:481–90. This review integrates recent findings in periodontal microbiology and immunology into contemporary views of periodontitis pathogenesis.PubMedCrossRef

51.

Hajishengallis G, Lamont RJ. Beyond the red complex and into more complexity: the polymicrobial synergy and dysbiosis (PSD) model of periodontal disease etiology. Mol Oral Microbiol. 2012;27:409–19.PubMedCentralPubMedCrossRef

52.

Wang M, Krauss JL, Domon H, Hosur KB, Liang S, Magotti P, et al. Microbial hijacking of complement-toll-like receptor crosstalk. Sci Signal. 2010;3:ra11.PubMedCentralPubMed

53.

Hajishengallis G, Lamont RJ. Breaking bad: manipulation of the host response by Porphyromonas gingivalis. Eur J Immunol. 2014;44(2):328–38.PubMedCrossRef

54.

Lucas H, Bartold PM, Dharmapatni AASSK, Holding CA, Haynes DR. Inhibition of apoptosis in periodontitis. J Dent Res. 2009;89:29–33.CrossRef

55.••

Lang NP, Schätzle MA, Löe H. Gingivitis as a risk factor in periodontal disease. J Clin Periodontol. 2009;36:3–8. This work provides proof-of-concept evidence that gingival inflammation is a risk factor for periodontitis.PubMedCrossRef

56.

Charalampakis G, Dahlén G, Carlén A, Leonhardt Å. Bacterial markers vs. clinical markers to predict progression of chronic periodontitis: a 2-yr prospective observational study. Eur J Oral Sci. 2013;121:394–402.PubMedCrossRef

57.

Lalla E, Cheng B, Lal S, Kaplan S, Softness B, Greenberg E, et al. Diabetes mellitus promotes periodontal destruction in children. J Clin Periodontol. 2007;34:294–8.PubMedCrossRef

58.

Mattout C, Bourgeois D, Bouchard P. Type 2 diabetes and periodontal indicators: epidemiology in France 2002-2003. J Periodontol Res. 2006;41:253–8.CrossRef

59.

Novak KF, Taylor GW, Dawson DR, Ferguson JE, Novak MJ. Periodontitis and gestational diabetes mellitus: exploring the link in NHANES III. J Public Health Dent. 2006;66:163–8.PubMedCrossRef

60.

Sarelius IH. Macromolecule permeability of in situ and excised rodent skeletal muscle arterioles and venules. Am J Physiol Heart Circ Physiol. 2005;290:H474–80.PubMedCentralPubMedCrossRef

61.

Manouchehr-Pour M, Spagnuolo PJ, Rodman HM, Bissada NF. Impaired neutrophil chemotaxis in diabetic patients with severe periodontitis. J Dent Res. 1981;60:729–30.PubMedCrossRef

62.

McMullen JA, Van Dyke TE, Horoszewicz HU, Genco RJ. Neutrophil chemotaxis in individuals with advanced periodontal disease and a genetic predisposition to diabetes mellitus. J Periodontol. 1981;52:167–73.PubMedCrossRef

63.

Gkrania-Klotsas E, Ye Z, Cooper AJ, Sharp SJ, Luben R, Biggs ML, et al. Differential white blood cell count and type 2 diabetes: systematic review and meta-analysis of cross-sectional and prospective studies. PLoS ONE. 2010;5:e13405.PubMedCentralPubMedCrossRef

64.

Gyurko R, Siqueira CC, Caldon N, Gao L, Kantarci A, Van Dyke TE. Chronic hyperglycemia predisposes to exaggerated inflammatory response and leukocyte dysfunction in Akita mice. J Immunol. 2006;177:7250–6.PubMedCentralPubMedCrossRef

65.

Gamonal J, Sanz M, O'Connor A, Acevedo A, Suarez I, Sanz A, et al. Delayed neutrophil apoptosis in chronic periodontitis patients. J Clin Periodontol. 2003;30:616–23.PubMedCrossRef

66.

Vitkov L, Klappacher M, Hannig M, Krautgartner WD. Neutrophil fate in gingival crevicular fluid. Ultrastruct Pathol. 2010;34:25–30.PubMedCrossRef

67.

Lakschevitz FS, Aboodi GM, Glogauer M. Oral neutrophil transcriptome changes result in a pro-survival phenotype in periodontal diseases. PLoS ONE. 2013;8:e68983.PubMedCentralPubMedCrossRef

68.

Klinkhamer JM. Quantitative evaluation of gingivitis and periodontal disease: I. The orogranulocytic migratory rate. Periodontics. 1968;6:207–11.PubMed

69.

Bird L. Tumour immunology: neutrophil plasticity. Nat Rev Immunol. 2009;9:672–3.

70.

Fridlender ZG, Sun J, Kim S, Kapoor V, Cheng G, Ling L, et al. Polarization of tumor-associated neutrophil phenotype by TGF-β: “N1” versus ‘N2’ TAN. Cancer Cell. 2009;16:183–94.PubMedCentralPubMedCrossRef

71.

Lakschevitz FS, Aboodi GM, Glogauer M. Oral neutrophils display a site-specific phenotype characterized by expression of T-cell receptors. J Periodontol. 2013;84:1493–503.PubMedCrossRef

72.

Pelletier M, Maggi L, Micheletti A, Lazzeri E, Tamassia N, Costantini C, et al. Evidence for a cross-talk between human neutrophils and Th17 cells. Blood. 2010;115:335–43.PubMedCrossRef

Titel: Neutrophil Dysfunction and Host Susceptibility to Periodontal Inflammation: Current State of Knowledge
verfasst von: Corneliu Sima
Michael Glogauer
Publikationsdatum: 01.06.2014
Verlag: Springer International Publishing
Erschienen in: Current Oral Health Reports / Ausgabe 2/2014
Elektronische ISSN: 2196-3002
DOI: https://doi.org/10.1007/s40496-014-0015-x

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Springer Medizin

Neutrophil Dysfunction and Host Susceptibility to Periodontal Inflammation: Current State of Knowledge

Abstract

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Parodontalbehandlung verbessert Prognose bei Katheterablation

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