Inter J Stomatol ›› 2017, Vol. 44 ›› Issue (5): 528-532.doi: 10.7518/gjkq.2017.05.007
• Periodontitis • Previous Articles Next Articles
Huang Yuehua1, 2, Tang Xiaolin1
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[1] Chow A, Brown BD, Merad M. Studying the mon-onuclear phagocyte system in the molecular age[J]. Nat Rev Immunol, 2011, 11(11):788-798. [2] Stansfield BK, Ingram DA. Clinical significance of monocyte heterogeneity[J]. Clin Transl Med, 2015, 4:5. [3] Ziegler-Heitbrock L. The CD14 + CD16 + blood mo-nocytes: their role in infection and inflammation[J]. J Leukoc Biol, 2007, 81(3):584-592. [4] Yang J, Zhang L, Yu C, et al. Monocyte and macro-phage differentiation: circulation inflammatory monocyte as biomarker for inflammatory diseases[J]. Biomark Res, 2014, 2(1):1. [5] Geissmann F, Jung S, Littman DR. Blood monocytes consist of two principal subsets with distinct migra-tory properties[J]. Immunity, 2003, 19(1):71-82. [6] Kundu D, Bandyopadhyay P, Nair V, et al. Aggres-sive periodontitis: a clinico-hematological appraisal [J]. J Indian Soc Periodontol, 2014, 18(2):166-171. [7] Nagasawa T, Kobayashi H, Aramaki M, et al. Expre-ssion of CD14, CD16 and CD45RA on monocytes from periodontitis patients[J]. J Periodontal Res, 2004, 39(1):72-78. [8] Jagannathan R, Lavu V, Rao SR. Comparison of the proportion of non-classic (CD14 + CD16 + ) monocytes/macrophages in peripheral blood and gingiva of healthy individuals and patients with chronic perio-dontitis[J]. J Periodontol, 2014, 85(6):852-858. [9] Papapanou PN, Sedaghatfar MH, Demmer RT, et al. Periodontal therapy alters gene expression of peri-pheral blood monocytes[J]. J Clin Periodontol, 2007, 34(9):736-747. [10] Idzkowska E, Eljaszewicz A, Miklasz P, et al. The role of different monocyte subsets in the pathogene-sis of atherosclerosis and acute coronary syndromes [J]. Scand J Immunol, 2015, 82(3):163-173. [11] Klimek E, Mikołajczyk T, Sulicka J, et al. Blood monocyte subsets and selected cardiovascular risk markers in rheumatoid arthritis of short duration in relation to disease activity[J]. Biomed Res Int, 2014, 2014:736853. [12] Zhou X, Liu XL, Ji WJ, et al. The kinetics of circula-ting monocyte subsets and monocyte-platelet aggre-gates in the acute phase of ST-elevation myocardial infarction: associations with 2-year cardiovascular events[J]. Medicine(Baltimore), 2016, 95(18):e3466. [13] 曹雪涛. 医学免疫学[M]. 6版. 北京: 人民卫生出版社, 2013:110. Cao XT. Medical immunology[M]. 6th ed. Beijing: People’ Medical Publishing House, 2013:110. [14] 史秀娣, 马红梅. 口腔生物材料对机体巨噬细胞生物学行为影响研究进展[J]. 中国实用口腔科杂志, 2016, 9(12):756-760. Shi XD, Ma HM. Effects of oral biomaterials on biological behavior of macrophages[J]. Chin J Pract Stomatol, 2016, 9(12):756-760. [15] Murray PJ, Allen JE, Biswas SK, et al. Macrophage activation and polarization: nomenclature and expe-rimental guidelines[J]. Immunity, 2014, 41(1):14-20. [16] Mantovani A, Sica A, Sozzani S, et al. The chemo-kine system in diverse forms of macrophage activa-tion and polarization[J]. Trends Immunol, 2004, 25 (12):677-686. [17] Mosser DM, Edwards JP. Exploring the full spec-trum of macrophage activation[J]. Nat Rev Immunol, 2008, 8(12):958-969. [18] Xu J, Zhang H, Chen L, et al. Schistosoma japonicum infection induces macrophage polarization[J]. J Bio-med Res, 2014, 28(4):299-308. [19] Edin S, Wikberg ML, Dahlin AM, et al. The distri-bution of macrophages with a M1 or M2 phenotype in relation to prognosis and the molecular charac-teristics of colorectal cancer[J]. PLoS One, 2012, 7 (10):e47045. [20] Gemmell E, McHugh GB, Grieco DA, et al. Cos-timulatory molecules in human periodontal disease tissues[J]. J Periodontal Res, 2001, 36(2):92-100. [21] 冯利, 冯洁, 王春华, 等. 牙周炎龈组织中巨噬细胞超微结构的观察[J]. 四川大学学报(自然科学版), 2002, 39(S1):90-92. Feng L, Feng J, Wang CH, et al. Ultrastructural ob-servation of macrophages in gingival tissue of perio-dontitis[J]. J Sichuan Univ(Natur Sci Ed), 2002, 39 (S1):90-92. [22] Lam RS, O'Brien-Simpson NM, Lenzo JC, et al. Macrophage depletion abates Porphyromonas gin-givalis -induced alveolar bone resorption in mice[J]. J Immunol, 2014, 193(5):2349-2362. [23] Holden JA, Attard TJ, Laughton KM, et al. Por - phyromonas gingivalis lipopolysaccharide weakly activates M1 and M2 polarized mouse macrophages but induces inflammatory cytokines[J]. Infect Immun, 2014, 82(10):4190-4203. [24] Navarrete M, García J, Dutzan N, et al. Interferon-γ, interleukins-6 and -4, and factor ⅩⅢ-A as indirect markers of the classical and alternative macrophage activation pathways in chronic periodontitis[J]. J Periodontol, 2014, 85(5):751-760. [25] Gonzalez OA, Novak MJ, Kirakodu S, et al. Diffe-rential gene expression profiles reflecting macro-phage polarization in aging and periodontitis gingival tissues[J]. Immunol Invest, 2015, 44(7):643-664. [26] Xuan D, Han Q, Tu Q, et al. Epigenetic modulation in periodontitis: interaction of adiponectin and JMJD3-IRF4 Axis in macrophages[J]. J Cell Physiol, 2015, 231(5):1090-1096. |