[1] Cutler CW, Kalmar JR, Genco CA. Pathogenic strategies of the oral anaerobe, Porphyromonas gingivalis [J]. Trends Microbiol, 1995, 3(2)∶45-51 [2] Kolenbrander PE. Multispecies communities:Interspecies interactions influence growth on saliva as sole nutritional source [J]. Int J Oral Sci, 2011, 3(2)∶49-54 [3] Petti S, Scully C. Oral cancer knowledge and awareness: primary and secondary effects of an information leaflet [J]. Oral Oncol, 2007, 43(4)∶408-415 [4] Nagy KN,Sonkodi I,Szoke I,et al.The microflora associated with human oral carcinomas [J]. Oral oncology, 1998, 34(4)∶304-308 [5] Sayehmiri F, Sayehmiri K, Asadollahi K, et al. The prevalence rate of Porphyromonas gingivalis and its association with cancer: A systematic review and meta-analysis [J]. Int J Immunopathol Pharmacol, 2015, 28(2)∶160-167 [6] Ha NH, Woo BH, Kim DJ, et al. Prolonged and repetitive exposure to Porphyromonas gingivalis increases aggressiveness of oral cancer cells by promoting acquisition of cancer stem cell properties [J]. Tumour Biol, 2015,36(12)∶9947-9960 [7] Binder Gallimidi A, Fischman S, Revach B, et al. Periodontal pathogens porphyromonas gingivalis and Fusobacterium nucleatum promote tumor progression in an oral-specific chemical carcinogenesis model [J]. Oncotarget, 2015, 6(26)∶22613-22623 [8] Metzger Z, Blasbalg J, Dotan M, et al. Enhanced attachment of Porphyromonas gingivalis to human firbroblasts mediated by Fusobacterium nucleatum [J]. J Endo, 2009, 35(1)∶82-85 [9] Saito A, Inagaki S, Kimizuka R, et al. Fusobacterium nucleatum enhances invasion of human gingival epithelial and aortic endothelial cells by Porphyromonas gingivalis [J]. FEMS Immunol Med Microbiol, 2008, 54(3)∶349-355 [10] Pan C, Xu X, Tan L, et al. The effects of Porphyromonas gingivalison the cell cycle progression of human gingival epithelial cells [J]. Oral Diseases, 2014, 20(1)∶100-108 [11] 潘春玲,赵海礁,谭丽思,等.牙龈卟啉单胞菌感染MG63细胞对细胞周期的影响[J].口腔医学研究,2015,31(9)∶863-866 [12] Bhattacharya R, Xu F, Dong G, et al. Effect of bacteria on the wound healing behavior of oral epithelial cells [J]. PLoS One, 2014, 9(2)∶e89475 [13] Shenker BJ, Datar S. Fusobacterium nucleatum inhibits human T-cell activation by arresting cells in the mid-G1 phase of the cell cycle [J]. Infect Immun, 1995, 63(12)∶4830-4836 [14] Binder Gallimidi A, Fischman S, Revach B, et al. Periodontal pathogens Porphyromonas gingivalis and Fusobacterium nucleatum promote tumor progression in an oral-specific chemical carcinogenesis model [J]. Oncotarget, 2015, 6(26)∶22613-22623 [15] Jian SL, Hsieh HY, Liao CT, et al. Gα12 Drives Invasion of Oral Squamous Cell Carcinoma through up-regulation of proinflammatory Cytokines [J]. PLoS One, 2013, 8(6)∶e66133 [16] 郭永华,吴亚菲, 刘天佳, 等. 不同fimA基因型牙龈卟啉单胞菌刺激口腔上皮细胞白细胞介素-8的表达[J].华西口腔医学杂志,2008,32(06)∶652-655 [17] Guentsch A, Ronnebeck M, Puklo M, et al. Influence of serum on interaction of Porphyromonas gingivalis ATCC 33277 and Aggregatibacter actinomycetemcomitans Y4 with an epithelial cell line [J]. J Periodontal Res, 2010, 45(2)∶229-238 [18] Yee M, Kim S, Sethi P, et al. Porphyromonas gingivalis stimulates IL-6 and IL-8 secretion in GMSM-K, HSC-3 and H413 oral epithelial cells [J]. Anaerobe., 2014, 28(1)∶62-67 [19] Watanabe K, Yilmaz O, Nakhjiri SF, et al. Association of mitogen-activated protein kinase pathways with gingival epithelial cell responses to Porphyromonas gingivalis infection [J]. Infect Immun, 2001, 69(11)∶6731-6737 |