Inter J Stomatol ›› 2017, Vol. 44 ›› Issue (4): 484-487.doi: 10.7518/gjkq.2017.04.022
• Reviews • Previous Articles Next Articles
Wang Nana, Chen Lili, Ding Peihui
CLC Number:
| [1] Kebschull M, Demmer RT, Papapanou PN. “Gum bug, leave my heart alone!”—epidemiologic and mechanistic evidence linking periodontal infections and atherosclerosis[J]. J Dent Res, 2010, 89(9):879- 902. [2] Madianos PN, Bobetsis YA, Offenbacher S. Adverse pregnancy outcomes(APOs) and periodontal disease: pathogenic mechanisms[J]. J Periodontol, 2013, 84(4 Suppl):S170-S180. [3] Janssen KM, Vissink A, de Smit MJ, et al. Lessons to be learned from periodontitis[J]. Curr Opin Rheu-matol, 2013, 25(2):241-247. [4] Franchi L, Eigenbrod T, Muñoz-Planillo R, et al. The inflammasome: a caspase-1-activation platform that regulates immune responses and disease patho-genesis[J]. Nat Immunol, 2009, 10(3):241-247. [5] Schroder K, Tschopp J. The inflammasomes[J]. Cell, 2010, 140(6):821-832. [6] Mariathasan S, Weiss DS, Newton K, et al. Cryop-yrin activates the inflammasome in response to to-xins and ATP[J]. Nature, 2006, 440(7081):228-232. [7] Dinarello CA. Immunological and inflammatory functions of the interleukin-1 family[J]. Annu Rev Immunol, 2009, 27:519-550. [8] Hoffman HM, Wanderer AA. Inflammasome and IL-1beta-mediated disorders[J]. Curr Allergy Asthma Rep, 2010, 10(4):229-235. [9] Kanneganti TD, Özören N, Body-Malapel M, et al. Bacterial RNA and small antiviral compounds ac-tivate caspase-1 through cryopyrin/Nalp3[J]. Nature, 2006(7081):233-236. [10] Song-Zhao GX, Srinivasan N, Pott J, et al. Nlrp3 activation in the intestinal epithelium protects against a mucosal pathogen[J]. Mucosal Immunol, 2014, 7 (4):763-774. [11] Rehaume LM, Jouault T, Chamaillard M. Lessons from the inflammasome: a molecular sentry linking Candida and Crohn’s disease[J]. Trends Immunol, 2010, 31(5):171-175. [12] Zaki MH, Boyd KL, Vogel P, et al. The NLRP3 in-flammasome protects against loss of epithelial in-tegrity and mortality during experimental colitis[J]. Immunity, 2010, 32(3):379-391. [13] Kummer JA, Broekhuizen R, Everett H, et al. In-flammasome components NALP 1 and 3 show dis-tinct but separate expression profiles in human tissues suggesting a site-specific role in the inflammatory response[J]. J Histochem Cytochem, 2007, 55(5): 443-452. [14] Belibasakis GN, Meier A, Guggenheim B, et al. Oral biofilm challenge regulates the RANKL-OPG system in periodontal ligament and dental pulp cells[J]. Mic-rob Pathog, 2011, 50(1):6-11. [15] Brandtzaeg P. Inflammatory bowel disease: clinics and pathology. Do inflammatory bowel disease and periodontal disease have similar immunopathogeneses [J]. Acta Odontol Scand, 2001, 59(4):235-243. [16] Darveau RP, Hajishengallis G, Curtis MA. Porphy-romonas gingivalis as a potential community activist for disease[J]. J Dent Res, 2012, 91(9):816-820. [17] Bostanci N, Emingil G, Saygan B, et al. Expression and regulation of the NALP3 inflammasome com-plex in periodontal diseases[J]. Clin Exp Immunol, 2009, 157(3):415-422. [18] Park E, Na HS, Song YR, et al. Activation of NLRP3 and AIM2 inflammasomes by Porphyromonas gin-givalis infection[J]. Infect Immun, 2014, 82(1):112- 123. [19] Gamonal J, Acevedo A, Bascones A, et al. Levels of interleukin-1β, -8, and -10 and RANTES in gingival crevicular fluid and cell populations in adult perio-dontitis patients and the effect of periodontal treat-ment[J]. J Periodontol, 2000, 71(10):1535-1545. [20] Yilmaz O, Sater AA, Yao L, et al. ATP-dependent activation of an inflammasome in primary gingival epithelial cells infected by Porphyromonas gingivalis [J]. Cell Microbiol, 2010, 12(2):188-198. [21] Bostanci N, Meier A, Guggenheim B, et al. Regula-tion of NLRP3 and AIM2 inflammasome gene ex-pression levels in gingival fibroblasts by oral bio-films[J]. Cell Immunol, 2011, 270(1):88-93. [22] Safavi KE, Nichols FC. Effects of a bacterial cell wall fragment on monocyte inflammatory function [J]. J Endod, 2000, 26(3):153-155. |