跳到主要內容

臺灣博碩士論文加值系統

(44.192.22.242) 您好!臺灣時間:2021/08/03 18:29
字體大小: 字級放大   字級縮小   預設字形  
回查詢結果 :::

詳目顯示

我願授權國圖
: 
twitterline
研究生:李明儒
研究生(外文):Ming-Ru Lee
論文名稱:以脂多醣體和人工合成雙股核醣核酸類似物探討細菌伴隨病毒感染對於人類造骨細胞之影響
論文名稱(外文):The concomitant effects of bacterial and viral infection on human osteoblasts in a model of lipopolysaccharide and polyinosinic: polycytidylic acid
指導教授:洪善鈴李亞芸
指導教授(外文):Shan-Ling HungYa-Yun Lee
學位類別:碩士
校院名稱:國立陽明大學
系所名稱:口腔生物研究所
學門:醫藥衛生學門
學類:牙醫學類
論文種類:學術論文
論文出版年:2009
畢業學年度:97
語文別:中文
論文頁數:89
中文關鍵詞:Pg菌人工合成雙股核醣核酸類似物皰疹病毒牙周炎牙髓病環氧酵素
外文關鍵詞:porphyromonas gingivalispoly I:Cherpesvirusesperiodontitisendodontic diseasescyclooxygenase-2
相關次數:
  • 被引用被引用:0
  • 點閱點閱:115
  • 評分評分:
  • 下載下載:0
  • 收藏至我的研究室書目清單書目收藏:0
牙周病及牙髓病所引起的發炎反應常伴隨組織破壞與骨吸收,而發炎反應大都由於外來微生物入侵所致。文獻指出,細菌是引起牙周病及牙髓病的主要原因,此外,近來發現皰疹病毒家族中的HSV(herpes simplex virus)、EBV(Epstein-Barr Virus)及HCMV(Human Cytomegalovirus)與牙周、牙髓炎有密切關係,且在牙周炎和根尖周圍病變的組織檢體中,偵測出皰疹病毒家族和牙周致病菌的同時存在,這些微生物有機會由牙周組織、根尖孔或側枝根管開口與造骨細胞接觸,然而過去研究中,對於微生物的致炎性分子結構可能引起造骨細胞炎性反應與路徑調控,並未有深入瞭解。因此,本研究以來自Pg(porphyromonas gingivalis)菌之脂多醣體Pg-LPS和人工合成雙股核醣核酸類似物poly I:C為模型,探討細菌及病毒共同影響下,對於造骨細胞炎性分子IL-6(interleukin-6)、PGE2(prostaglandin E2)的影響及可能之調控路徑,另外也針對牙科常用之抗微生物劑chlorhexidine(CHX)及povidone-iodine(PVP-I)對於致炎分子分泌之影響進行研究。結果顯示,隨著Pg-LPS或poly I:C濃度提升,上清液中IL-6和PGE2的量有上升的趨勢,而Pg-LPS和poly I:C共同處理,對於IL-6和PGE2的分泌具有加成性的效果;針對炎性分子IL-6和PGE2可能調控之訊息傳導路徑之研究結果顯示,p38 MAPK、JNK磷酸化表現有隨Pg-LPS或poly I:C濃度上升而上升的趨勢,但ERK磷酸化卻下降,而Pg-LPS和poly I:C共同處理,p38 MAPK、JNK磷酸化具有加成性的效果;另外,探討調控PGE2上游環氧酵素cyclooxygenase-2 (COX-2)蛋白表現,亦有相同趨勢,具有加成性效果;以雷射共軛焦顯微鏡發現細胞內NF-κB(nuclear factor-kappa B)有隨著Pg-LPS或poly I:C濃度提升,其轉位作用明顯上升,而Pg-LPS和poly I:C共同處理,轉位作用更加明顯,具有加成性的效果。此外,針對牙科常用抗微生物劑CHX或PVP-I對於IL-6和PGE2分泌量影響進行探討,結果顯示,CHX和PVP-I皆可些微抑制Pg-LPS引起之IL-6分泌量上升,而PVP-I可抑制Pg-LPS和poly I:C引起之PGE2的分泌。本研究結果顯示,Pg-LPS和poly I:C促進骨吸收相關因子IL-6和PGE2的分泌以及活化COX-2表現,可能與MAPK(mitogen-activated protein kinase)和NF-κB路徑有關。若加入CHX或PVP-I,則部分抑制IL-6和PGE2的分泌量上升,顯示出CHX和PVP-I可能具有抗發炎作用及降低組織破壞與骨吸收,用於臨床上對於牙周病及牙髓病的治療可能具有輔助的效果。
Tissue destruction and bone resorption, the clinical features of periodontal and endodontic diseases, are resulted from the interactions between microbial infection and host immune response. It is generally accepted that bacteria are the causative factors in both periodontal and endodontic diseases. Recent evidence suggests an association between viral and bacterial infection in the development of periodontitis and apical periodontitis. These micro-organisms have the opportunity to contact with osteoblasts through periodontal tissue, apical foramen or accessory canal. However, little is known about the concomitant effects of the molecular structure of these micro-organisms on host immune responses and the related signaling pathways involved in osteoblasts. Therefore, the purpose of this study was to investigate the concomitant effects of virus and bacteria on human osteoblasts. Specially, Pg-LPS (porphyromonas gingivalis lipopolysaccharide) and poly I:C (polyinosinic: polycytidylic acid) were used as a model to detect the expression of inflammatory molecules IL-6 (interleukin-6) and PGE2 (prostaglandin E2) and the possible signaling pathways in osteoblasts. The results showed that, the expression of IL-6 and PGE2 was increased by Pg-LPS or poly I:C in a dose-dependent manner. When cells were co-treated with Pg-LPS and poly I:C, synergistic effects on IL-6 and PGE2 secretion was observed. In addition, the possible signaling pathways of IL-6 and PGE2 production were investigated. Pg-LPS or poly I:C treatment increased, phosphorylation of p38 MAPK and JNK expression were increased in a dose-dependent manner, while decreased phosphorylation of ERK. When cells were co-treated with Pg-LPS and poly I:C. Pg-LPS and poly I:C synergized on the phosphorylation of p38 MAPK and JNK. In addition, cyclooxygenase-2 (COX-2) expression followed the same trend. When cells co-treated with Pg-LPS and poly I:C, synergistic effects on COX-2 expression were also observed. Laser confocal microscopic examination found that Pg-LPS and poly I:C activated nuclear factor-kappa B (NF-κB) and a marked increase in translocation was detected in the co-treatment experiment. Moreover, the effects of commonly used dental anti-microbial agents, chlorhexidine (CHX) and povidone-iodine (PVP-I) on the secretion of IL-6 and PGE2 were investigated. CHX and PVP-I inhibited Pg-LPS-induced IL-6 secretion, while PVP-I inhibited Pg-LPS- or poly I:C-induced PGE2 secretion. The results of this study showed that Pg-LPS and poly I:C induced the secretion of bone resorption factors, IL-6 and PGE2 and activated COX-2 expression in osteoblasts, which might be related to MAPK and NF-κB signaling pathway. Addition of CHX or PVP-I partially inhibited IL-6 and PGE2 secretion, showing that CHX and PVP-I might have anti-inflammatory effects, and could reduce tissue destruction and bone resorption during clinical periodontal and endodontic treatment.
頁次
目錄……………………………………………………………………...I
圖次目錄………………………………………………………………..II
中文摘要………………………………………………………………IV
英文摘要……………………………………………………………....VI
導論……………………………………………………………............1
材料與方法……………………………………………………………14
結果……………………………………………………………………24
討論……………………………………………………………………32
圖列……………………………………………………………………38
附錄……………………………………………………………………68
參考文獻………………………………………………………………71
1. Paster BJ, Olsen I, Aas JA, Dewhirst FE. The breadth of bacterial diversity in the human periodontal pocket and other oral sites. Periodontol 2000 2006; 42: 80-7.
2. Hargreaves KM, Goodis HE. Interrelationship of dental pulp and apical periodontitis. In: P S, editor. Seltzer and Bender's Dental Pulp. Chicago: Quintessence; 2002. p. 389-409.
3. Nair PN. Apical periodontitis: a dynamic encounter between root canal infection and host response. Periodontol 2000 1997; 13: 121-48.
4. Sabeti M, Valles Y, Nowzari H, Simon JH, Kermani-Arab V, Slots J. Cytomegalovirus and Epstein-Barr virus DNA transcription in endodontic symptomatic lesions. Oral Microbiol Immunol 2003; 18: 104-8.
5. Li H, Chen V, Chen Y, Baumgartner JC, Machida CA. Herpesviruses in endodontic pathoses: association of Epstein-Barr virus with irreversible pulpitis and apical periodontitis. J Endod 2009; 35: 23-9.
6. Slots J, Nowzari H, Sabeti M. Cytomegalovirus infection in symptomatic periapical pathosis. Int Endod J 2004; 37: 519-24.
7. Chen V, Chen Y, Li H, Kent K, Baumgartner JC, Machida CA. Herpesviruses in abscesses and cellulitis of endodontic origin. J Endod 2009; 35: 182-8.
8. Saygun I, Yapar M, Ozdemir A, Kubar A, Slots J. Human cytomegalovirus and Epstein-Barr virus type 1 in periodontal abscesses. Oral Microbiol Immunol 2004; 19: 83-7.
9. Slots J. Herpesviruses in periodontal diseases. Periodontol 2000 2005; 38: 33-62.
10. Sunde PT, Olsen I, Enersen M, Beiske K, Grinde B. Human cytomegalovirus and Epstein-Barr virus in apical and marginal periodontitis: a role in pathology? J Med Virol 2008; 80: 1007-11.
11. Slots J. Update on human cytomegalovirus in destructive periodontal disease. Oral Microbiol Immunol 2004; 19: 217-23.
12. Saboia-Dantas CJ, Coutrin de Toledo LF, Sampaio-Filho HR, Siqueira JF, Jr. Herpesviruses in asymptomatic apical periodontitis lesions: an immunohistochemical approach. Oral Microbiol Immunol 2007; 22: 320-5.
13. Yildirim S, Yapar M, Kubar A, Slots J. Human cytomegalovirus, Epstein-Barr virus and bone resorption-inducing cytokines in periapical lesions of deciduous teeth. Oral Microbiol Immunol 2006; 21: 107-11.
14. Sabeti M, Slots J. Herpesviral-bacterial coinfection in periapical pathosis. J Endod 2004; 30: 69-72.
15. Slots J, Sabeti M, Simon JH. Herpesviruses in periapical pathosis: an etiopathogenic relationship? Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2003; 96: 327-31.
16. Sabeti M, Simon JH, Slots J. Cytomegalovirus and Epstein-Barr virus are associated with symptomatic periapical pathosis. Oral Microbiol Immunol 2003; 18: 327-8.
17. Parra B, Slots J. Detection of human viruses in periodontal pockets using polymerase chain reaction. Oral Microbiol Immunol 1996; 11: 289-93.
18. Slots J. Herpesviral-bacterial synergy in the pathogenesis of human periodontitis. Curr Opin Infect Dis 2007; 20: 278-83.
19. Muller HP. Periodontal Microbiology. Periodontology: The Essentials New York Thieme; 2004. p. 12-23.
20. Jung IY, Choi BK, Kum KY, et al. Molecular epidemiology and association of putative pathogens in root canal infection. J Endod 2000; 26: 599-604.
21. Sandros J, Karlsson C, Lappin DF, Madianos PN, Kinane DF, Papapanou PN. Cytokine responses of oral epithelial cells to Porphyromonas gingivalis infection. J Dent Res 2000; 79: 1808-14.
22. Okahashi N, Inaba H, Nakagawa I, et al. Porphyromonas gingivalis induces receptor activator of NF-kappaB ligand expression in osteoblasts through the activator protein 1 pathway. Infect Immun 2004; 72: 1706-14.
23. Kang IC, Kuramitsu HK. Induction of monocyte chemoattractant protein-1 by Porphyromonas gingivalis in human endothelial cells. FEMS Immunol Med Microbiol 2002; 34: 311-7.
24. Ohno T, Okahashi N, Morisaki I, Amano A. Signaling pathways in osteoblast proinflammatory responses to infection by Porphyromonas gingivalis. Oral Microbiol Immunol 2008; 23: 96-104.
25. McCuskey RS, Urbaschek R, Urbaschek B. The microcirculation during endotoxemia. Cardiovasc Res 1996; 32: 752-63.
26. Rietschel ET, Brade H, Holst O, et al. Bacterial endotoxin: Chemical constitution, biological recognition, host response, and immunological detoxification. Curr Top Microbiol Immunol 1996; 216: 39-81.
27. Chen LL, Yan J. Porphyromonas gingivalis lipopolysaccharide activated bone resorption of osteoclasts by inducing IL-1, TNF, and PGE. Acta Pharmacol Sin 2001; 22: 614-8.
28. Zou W, Bar-Shavit Z. Dual modulation of osteoclast differentiation by lipopolysaccharide. J Bone Miner Res 2002; 17: 1211-8.
29. Shoji M, Tanabe N, Mitsui N, et al. Lipopolysaccharide enhances the production of nicotine-induced prostaglandin E2 by an increase in cyclooxygenase-2 expression in osteoblasts. Acta Biochim Biophys Sin (Shanghai) 2007; 39: 163-72.
30. Yoshimura K, Hanazawa S. Production of IL-1 like cytokine by cultured bone cells: inducing effect of Haemophilus actinomycetemcomitans lipopolysaccharide on the cytokine production. Meikai Daigaku Shigaku Zasshi 1989; 18: 420-9.
31. Darveau RP, Pham TT, Lemley K, et al. Porphyromonas gingivalis lipopolysaccharide contains multiple lipid A species that functionally interact with both toll-like receptors 2 and 4. Infect Immun 2004; 72: 5041-51.
32. Knipe DM, Howley PM, Griffin DE, et al. The Family Herpesviridae: A Brief Introduction. In: Pellett PE, Roizman B, editors. Field's Virology. Philadelphia: Lippincott Williams & Wilkins 2007. p. 2479-99.
33. Jacobs BL, Langland JO. When two strands are better than one: the mediators and modulators of the cellular responses to double-stranded RNA. Virology 1996; 219: 339-49.
34. Clemens MJ, Elia A. The double-stranded RNA-dependent protein kinase PKR: structure and function. J Interferon Cytokine Res 1997; 17: 503-24.
35. Nakamura K, Deyama Y, Yoshimura Y, Suzuki K, Morita M. Toll-like receptor 3 ligand-induced antiviral response in mouse osteoblastic cells. Int J Mol Med 2007; 19: 771-5.
36. Cooper KE, Blahser S, Malkinson TJ, Merker G, Roth J, Zeisberger E. Changes in body temperature and vasopressin content of brain neurons, in pregnant and non-pregnant guinea pigs, during fevers produced by Poly I:Poly C. Pflugers Arch 1988; 412: 292-6.
37. Kimura M, Toth LA, Agostini H, Cady AB, Majde JA, Krueger JM. Comparison of acute phase responses induced in rabbits by lipopolysaccharide and double-stranded RNA. Am J Physiol 1994; 267: R1596-605.
38. Fortier ME, Kent S, Ashdown H, Poole S, Boksa P, Luheshi GN. The viral mimic, polyinosinic:polycytidylic acid, induces fever in rats via an interleukin-1-dependent mechanism. Am J Physiol Regul Integr Comp Physiol 2004; 287: R759-66.
39. Lemaitre B, Nicolas E, Michaut L, Reichhart JM, Hoffmann JA. The dorsoventral regulatory gene cassette spatzle/Toll/cactus controls the potent antifungal response in Drosophila adults. Cell 1996; 86: 973-83.
40. Rock FL, Hardiman G, Timans JC, Kastelein RA, Bazan JF. A family of human receptors structurally related to Drosophila Toll. Proc Natl Acad Sci U S A 1998; 95: 588-93.
41. Hoshino K, Takeuchi O, Kawai T, et al. Cutting edge: Toll-like receptor 4 (TLR4)-deficient mice are hyporesponsive to lipopolysaccharide: evidence for TLR4 as the Lps gene product. J Immunol 1999; 162: 3749-52.
42. Poltorak A, He X, Smirnova I, et al. Defective LPS signaling in C3H/HeJ and C57BL/10ScCr mice: mutations in Tlr4 gene. Science 1998; 282: 2085-8.
43. Hayashi F, Smith KD, Ozinsky A, et al. The innate immune response to bacterial flagellin is mediated by Toll-like receptor 5. Nature 2001; 410: 1099-103.
44. Takeuchi O, Hoshino K, Kawai T, et al. Differential roles of TLR2 and TLR4 in recognition of gram-negative and gram-positive bacterial cell wall components. Immunity 1999; 11: 443-51.
45. Yang RB, Mark MR, Gray A, et al. Toll-like receptor-2 mediates lipopolysaccharide-induced cellular signalling. Nature 1998; 395: 284-8.
46. Chaouche-Drider N, Kaparakis M, Karrar A, et al. A commensal Helicobacter sp. of the rodent intestinal flora activates TLR2 and NOD1 responses in epithelial cells. PLoS One 2009; 4: e5396.
47. Que-Gewirth NL, Ribeiro AA, Kalb SR, et al. A methylated phosphate group and four amide-linked acyl chains in leptospira interrogans lipid A. The membrane anchor of an unusual lipopolysaccharide that activates TLR2. J Biol Chem 2004; 279: 25420-9.
48. Hemmi H, Takeuchi O, Kawai T, et al. A Toll-like receptor recognizes bacterial DNA. Nature 2000; 408: 740-5.
49. Kawai T, Adachi O, Ogawa T, Takeda K, Akira S. Unresponsiveness of MyD88-deficient mice to endotoxin. Immunity 1999; 11: 115-22.
50. Adachi O, Kawai T, Takeda K, et al. Targeted disruption of the MyD88 gene results in loss of IL-1- and IL-18-mediated function. Immunity 1998; 9: 143-50.
51. Burns K, Martinon F, Esslinger C, et al. MyD88, an adapter protein involved in interleukin-1 signaling. J Biol Chem 1998; 273: 12203-9.
52. Cao Z, Xiong J, Takeuchi M, Kurama T, Goeddel DV. TRAF6 is a signal transducer for interleukin-1. Nature 1996; 383: 443-6.
53. Kopp E, Medzhitov R, Carothers J, et al. ECSIT is an evolutionarily conserved intermediate in the Toll/IL-1 signal transduction pathway. Genes Dev 1999; 13: 2059-71.
54. Dong C, Davis RJ, Flavell RA. MAP kinases in the immune response. Annu Rev Immunol 2002; 20: 55-72.
55. Johnson GL, Lapadat R. Mitogen-activated protein kinase pathways mediated by ERK, JNK, and p38 protein kinases. Science 2002; 298: 1911-2.
56. Lee JC, Laydon JT, McDonnell PC, et al. A protein kinase involved in the regulation of inflammatory cytokine biosynthesis. Nature 1994; 372: 739-46.
57. Westra J, Doornbos-van der Meer B, de Boer P, van Leeuwen MA, van Rijswijk MH, Limburg PC. Strong inhibition of TNF-alpha production and inhibition of IL-8 and COX-2 mRNA expression in monocyte-derived macrophages by RWJ 67657, a p38 mitogen-activated protein kinase (MAPK) inhibitor. Arthritis Res Ther 2004; 6: R384-92.
58. Matsumoto M, Sudo T, Saito T, Osada H, Tsujimoto M. Involvement of p38 mitogen-activated protein kinase signaling pathway in osteoclastogenesis mediated by receptor activator of NF-kappa B ligand (RANKL). J Biol Chem 2000; 275: 31155-61.
59. Ishimi Y, Miyaura C, Jin CH, et al. IL-6 is produced by osteoblasts and induces bone resorption. J Immunol 1990; 145: 3297-303.
60. Ghosh S, Karin M. Missing pieces in the NF-kappaB puzzle. Cell 2002; 109 Suppl: S81-96.
61. Lin L, DeMartino GN, Greene WC. Cotranslational biogenesis of NF-kappaB p50 by the 26S proteasome. Cell 1998; 92: 819-28.
62. Pahl HL. Activators and target genes of Rel/NF-kappaB transcription factors. Oncogene 1999; 18: 6853-66.
63. Exton JH. Phosphatidylcholine breakdown and signal transduction. Biochim Biophys Acta 1994; 1212: 26-42.
64. Kargman S, Charleson S, Cartwright M, et al. Characterization of Prostaglandin G/H Synthase 1 and 2 in rat, dog, monkey, and human gastrointestinal tracts. Gastroenterology 1996; 111: 445-54.
65. Appleby SB, Ristimaki A, Neilson K, Narko K, Hla T. Structure of the human cyclo-oxygenase-2 gene. Biochem J 1994; 302 ( Pt 3): 723-7.
66. Hinz B, Brune K. Cyclooxygenase-2--10 years later. J Pharmacol Exp Ther 2002; 300: 367-75.
67. Takahashi N, Akatsu T, Udagawa N, et al. Osteoblastic cells are involved in osteoclast formation. Endocrinology 1988; 123: 2600-2.
68. Harada SI, Balena R, Rodan GA, Rodan SB. The role of prostaglandins in bone formation. Connect Tissue Res 1995; 31: 279-82.
69. Sanchez C, Gabay O, Salvat C, Henrotin YE, Berenbaum F. Mechanical loading highly increases IL-6 production and decreases OPG expression by osteoblasts. Osteoarthritis Cartilage 2009; 17: 473-81.
70. Zhang X, Schwarz EM, Young DA, Puzas JE, Rosier RN, O'Keefe RJ. Cyclooxygenase-2 regulates mesenchymal cell differentiation into the osteoblast lineage and is critically involved in bone repair. J Clin Invest 2002; 109: 1405-15.
71. Katori M, Majima M. Cyclooxygenase-2: its rich diversity of roles and possible application of its selective inhibitors. Inflamm Res 2000; 49: 367-92.
72. Rolla G, Melsen B. On the mechanism of the plaque inhibition by chlorhexidine. J Dent Res 1975; 54 Spec No B: B57-62.
73. Hennessey TS. Some antibacterial properties of chlorhexidine. J Periodontal Res Suppl 1973; 12: 61-7.
74. Schiott CR, Loe H, Jensen SB, Kilian M, Davies RM, Glavind K. The effect of chlorhexidine mouthrinses on the human oral flora. J Periodontal Res 1970; 5: 84-9.
75. Vinholis AH, Figueiredo LC, Marcantonio Junior E, Marcantonio RA, Salvador SL, Goissis G. Subgingival utilization of a 1% chlorhexidine collagen gel for the treatment of periodontal pockets. A clinical and microbiological study. Braz Dent J 2001; 12: 209-13.
76. Oppermann RV. Effect of chlorhexidine on acidogenicity of dental plaque in vivo. Scand J Dent Res 1979; 87: 302-8.
77. Bonesvoll P, Lokken P, Rolla G. Influence of concentration, time, temperature and pH on the retention of chlorhexidine in the human oral cavity after mouth rinses. Arch Oral Biol 1974; 19: 1025-9.
78. Gennaro AR. Povidone iodine. Remington's Pharmaceutical Sciences Philadelphia Mack; 1990. p. 1169.
79. Higashitsutsumi M, Kamoi K, Miyata H, et al. Bactericidal effects of povidone-iodine solution to oral pathogenic bacteria in vitro. Postgrad Med J 1993; 69 Suppl 3: S10-4.
80. Kawana R, Kitamura T, Nakagomi O, et al. Inactivation of human viruses by povidone-iodine in comparison with other antiseptics. Dermatology 1997; 195 Suppl 2: 29-35.
81. Amin MS, Harrison RL, Benton TS, Roberts M, Weinstein P. Effect of povidone-iodine on Streptococcus mutans in children with extensive dental caries. Pediatr Dent 2004; 26: 5-10.
82. Lopez L, Berkowitz R, Spiekerman C, Weinstein P. Topical antimicrobial therapy in the prevention of early childhood caries: a follow-up report. Pediatr Dent 2002; 24: 204-6.
83. Dajani AS, Taubert KA, Wilson W, et al. Prevention of bacterial endocarditis. Recommendations by the American Heart Association. Circulation 1997; 96: 358-66.
84. Nobukuni K, Hayakawa N, Namba R, et al. The influence of long-term treatment with povidone-iodine on thyroid function. Dermatology 1997; 195 Suppl 2: 69-72.
85. Cabral CT, Fernandes MH. In vitro comparison of chlorhexidine and povidone-iodine on the long-term proliferation and functional activity of human alveolar bone cells. Clin Oral Investig 2007; 11: 155-64.
86. Giannelli M, Chellini F, Margheri M, Tonelli P, Tani A. Effect of chlorhexidine digluconate on different cell types: a molecular and ultrastructural investigation. Toxicol In Vitro 2008; 22: 308-17.
87. Chen YT, Hung SL, Lin LW, Chi LY, Ling LJ. Attachment of periodontal ligament cells to chlorhexidine-loaded guided tissue regeneration membranes. J Periodontol 2003; 74: 1652-9.
88. Girish V, Vijayalakshmi A. Affordable image analysis using NIH Image/ImageJ. Indian J Cancer 2004; 41: 47.
89. Barton GM, Medzhitov R. Toll-like receptor signaling pathways. Science 2003; 300: 1524-5.
90. Wara-Aswapati N, Boch JA, Auron PE. Activation of interleukin 1beta gene transcription by human cytomegalovirus: molecular mechanisms and relevance to periodontitis. Oral Microbiol Immunol 2003; 18: 67-71.
91. Turkoglu O, Becerik S, Emingil G, Kutukculer N, Baylas H, Atilla G. The effect of adjunctive chlorhexidine mouthrinse on clinical parameters and gingival crevicular fluid cytokine levels in untreated plaque-associated gingivitis. Inflamm Res 2009; 58: 277-83.
92. Sharma S, Saimbi CS, Koirala B, Shukla R. Effect of various mouthwashes on the levels of interleukin-2 and interferon-gamma in chronic gingivitis. J Clin Pediatr Dent 2008; 32: 111-4.
93. Arancibia SA, Beltran CJ, Aguirre IM, et al. Toll-like receptors are key participants in innate immune responses. Biol Res 2007; 40: 97-112.
94. Meusel TR, Imani F. Viral induction of inflammatory cytokines in human epithelial cells follows a p38 mitogen-activated protein kinase-dependent but NF-kappa B-independent pathway. J Immunol 2003; 171: 3768-74.
95. Patil C, Zhu X, Rossa C, Jr., Kim YJ, Kirkwood KL. p38 MAPK regulates IL-1beta induced IL-6 expression through mRNA stability in osteoblasts. Immunol Invest 2004; 33: 213-33.
96. Webb SJ, McPherson JR, Pahan K, Koka S. Regulation of TNF-alpha-induced IL-6 production in MG-63 human osteoblast-like cells. J Dent Res 2002; 81: 17-22.
97. Vane JR. Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs. Nat New Biol 1971; 231: 232-5.
98. Miyauchi M, Ijuhin N, Nikai H, Takata T, Ito H, Ogawa I. Effect of exogenously applied prostaglandin E2 on alveolar bone loss--histometric analysis. J Periodontol 1992; 63: 405-11.
99. Offenbacher S, Odle BM, Van Dyke TE. The use of crevicular fluid prostaglandin E2 levels as a predictor of periodontal attachment loss. J Periodontal Res 1986; 21: 101-12.
100. Oguntebi BR, Barker BF, Anderson DM, Sakumura J. The effect of indomethacin on experimental dental periapical lesions in rats. J Endod 1989; 15: 117-21.
101. Konig J, Storcks V, Kocher T, Bossmann K, Plagmann HC. Anti-plaque effect of tempered 0.2% chlorhexidine rinse: an in vivo study. J Clin Periodontol 2002; 29: 207-10.
102. Stanley A, Wilson M, Newman HN. The in vitro effects of chlorhexidine on subgingival plaque bacteria. J Clin Periodontol 1989; 16: 259-64.
103. Park JB, Park NH. Effect of chlorhexidine on the in vitro and in vivo herpes simplex virus infection. Oral Surg Oral Med Oral Pathol 1989; 67: 149-53.
104. Montefiori DC, Robinson WE, Jr., Modliszewski A, Mitchell WM. Effective inactivation of human immunodeficiency virus with chlorhexidine antiseptics containing detergents and alcohol. J Hosp Infect 1990; 15: 279-82.
105. Harbison MA, Hammer SM. Inactivation of human immunodeficiency virus by Betadine products and chlorhexidine. J Acquir Immune Defic Syndr 1989; 2: 16-20.
106. Russell AD, Furr JR. Inactivation of human immunodeficiency virus by chlorhexidine: the possible role of neutralizers. J Hosp Infect 1991; 18: 249-51.
107. Sabracos L, Romanou S, Dontas I, Coulocheri S, Ploumidou K, Perrea D. The in vitro effective antiviral action of povidone-iodine (PVP-I) may also have therapeutic potential by its intravenous administration diluted with Ringer's solution. Med Hypotheses 2007; 68: 272-4.
QRCODE
 
 
 
 
 
                                                                                                                                                                                                                                                                                                                                                                                                               
第一頁 上一頁 下一頁 最後一頁 top
無相關期刊
 
1. 第一型單純皰疹病毒對於人類口腔上皮細胞基因表現的影響及與磷脂醯肌醇3激酶訊息傳遞路徑的相關性
2. 檳榔萃取物對免疫細胞功能之調節作用
3. 現代漢語「穿」、「戴」動詞的功能及其賓語之研究
4. Porphyromonas gingivalis的GroEL蛋白在牙周病致病機轉之角色
5. 表沒食子兒茶素沒食子酸脂透過抑制第六型介白素 減少 Porphyromonas gingivalis 之脂多醣體引起之牙齦纖維細胞產生第一型基質金屬蛋白酶
6. 大蒜精減少受Porphyromonas gingivalis菌之酯多醣體刺激人類牙齦纖維母細胞表現的發炎激素以及NF-κB活化作用
7. 利用人類牙齦纖維細胞與U937巨噬細胞共同培養技術,探討環胞靈在P.g酯多醣體刺激環境下對於第二型及第九型基質金屬蛋白酶活性之抑制
8. 因聚集導致光動力治療效果增強之二元光感系統
9. 漢語量詞「一個」的臺灣當代口頭用法分析
10. 脫鎂葉綠素 a 在 4T1 腫瘤小鼠之光動力治療及藥物動力學研究
11. 光敏劑結合佐劑藥物於倉鼠口腔癌前病變動物模式之光動力診斷及治療研究
12. 米諾四環素加入亞甲基藍作為局部緩釋性藥物之牙周病原菌感受性及細胞毒性之研究
13. 基質金屬蛋白酶及其上游類鐸受體3在口腔癌腫瘤侵犯過程中扮演關鍵角色
14. 利用定量蛋白質體學技術平台系統性分析人類A431細胞在不同光動力療法條件下之氧化還原蛋白質體
15. 高濃度葡萄糖對U937巨噬細胞的影響