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Biological foundation for periodontitis as a potential risk factor for atherosclerosis

dc.contributor.authorChun, Yong-Hee P.en_US
dc.contributor.authorChun, Kyoung-Ryul J.en_US
dc.contributor.authorOlguin, De'Avlinen_US
dc.contributor.authorWang, Hom-Layen_US
dc.date.accessioned2010-04-01T15:37:18Z
dc.date.available2010-04-01T15:37:18Z
dc.date.issued2005-02en_US
dc.identifier.citationChun, Yong-Hee P.; Chun, Kyoung-Ryul J.; Olguin, De'Avlin; Wang, Hom-Lay (2005). "Biological foundation for periodontitis as a potential risk factor for atherosclerosis." Journal of Periodontal Research 40(1): 87-95. <http://hdl.handle.net/2027.42/66109>en_US
dc.identifier.issn0022-3484en_US
dc.identifier.issn1600-0765en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/66109
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=15613084&dopt=citationen_US
dc.description.abstractLinks between periodontal diseases and systemic diseases have been well documented by epidemiological studies. Recently, research has shifted to elucidating the biologic mechanism for a causal relationship. One focus of interest is atherosclerosis, the underlying event of cardiovascular diseases due to its serious health impact. However, it is still not clear whether periodontopathic pathogens are truly etiologic agents or ubiquitous bystanders. This article reviews the current understanding about the molecular biological interactions between periodontal disease and atherosclerosis and the biological plausibility of periodontitis as a potential risk factor for cardiovascular disease. Materials and methods:  The current literature regarding periodontal diseases and atherosclerosis and coronary vascular disease was searched using the Medline and PubMed databases. Results:  In vitro experiments and animal models are appropriate tools to investigate the biological interactions between periodontal disease and atherosclerosis at the cell molecular level. The concepts linking both pathologies refer to inflammatory response, immune responses, and hemostasis. In particular, Porphyromonas gingivalis appears to have unique, versatile pathogenic properties. Whether or not these findings from isolated cells or animal models are applicable in humans with genetic and environmental variations is yet to be determined. Likewise, the benefit from periodontal therapy on the development of atherosclerosis is unclear. Approaches targeting inflammatory and immune responses of periodontitis and atherosclerosis simultaneously are very intriguing. Conclusion:  An emerging concept suggests that a pathogenic burden from different sources might overcome an individual threshold culminating in clinical sequela. P. gingivalis contributes directly and indirectly to atherosclerosis.en_US
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dc.publisherMunksgaard International Publishersen_US
dc.publisherBlackwell Publishing Ltden_US
dc.rights2004 Blackwell Munksgaard Ltden_US
dc.subject.otherAtherosclerosisen_US
dc.subject.otherBacteremiaen_US
dc.subject.otherCardiovascular Diseaseen_US
dc.subject.otherPeriodontal Diseaseen_US
dc.subject.otherPorphyromonas Gingivalisen_US
dc.titleBiological foundation for periodontitis as a potential risk factor for atherosclerosisen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelDentistryen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationum* Department of Periodontics/Prevention/Geriatrics, School of Dentistry, University of Michigan, Ann Arbor, Michigan, USAen_US
dc.contributor.affiliationother† AK St. Georg, Medical Clinic II, Department of Cardiology, Hamburg, Germanyen_US
dc.identifier.pmid15613084en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/66109/1/j.1600-0765.2004.00771.x.pdf
dc.identifier.doi10.1111/j.1600-0765.2004.00771.xen_US
dc.identifier.sourceJournal of Periodontal Researchen_US
dc.identifier.citedreferenceKannel WB, Castelli WP, McNamara PM. Serum lipid fractions and risk of coronary heart disease. The Framingham study. Minn Med 1969 ; 52 : 1225 – 1230.en_US
dc.identifier.citedreferenceKahn HA, Dawber TR. The development of coronary heart disease in relation to sequential biennial measures of cholesterol in the Framingham study. J Chronic Dis 1966 ; 19 : 611 – 620.en_US
dc.identifier.citedreferenceBrown MS, Goldstein JL. A receptor-mediated pathway for cholesterol homeostasis. Science 1986 ; 232 : 34 – 47.en_US
dc.identifier.citedreferenceYu H, Rifai N. High-sensitive C-reactive protein and atherosclerosis: from theory to therapy. Clin Biochem 2000 ; 33 : 601 – 610.en_US
dc.identifier.citedreferenceLopatin DE, Jaramillo E, Edwards CA, Van Poperin N, Combs A, Shelburne CE. Cellular localization of a Hsp90 homologue in Porphyromonas gingivalis. FEMS Microbiol Lett 1999 ; 181 : 9 – 16.en_US
dc.identifier.citedreferenceWald NJ, Watt HC, Law MR, Weir DG, McPartlin J, Scott JM. Homocysteine and ischemic heart disease. Results of a prospective study with implications regarding prevention. Arch Intern Med 1998 ; 158 : 862 – 867.en_US
dc.identifier.citedreferenceWilhelmsen L, Svardsudd K, Korsan-Bengtsen K, Larsson B, Welin L, Tibblin G. Fibrinogen as a risk factor for stroke and myocardial infarction. N Engl J Med 1984 ; 311 : 501 – 505.en_US
dc.identifier.citedreferenceMeade TW, Mellows S, Brozovic M et al. Haemostatic function and ischemic heart disease: Principle results of the Northwick Park Heart Study. Lancet 1986 ; 2 : 533 – 537.en_US
dc.identifier.citedreferenceKannel WB, Wolf PA, Castelli WP, D'Agostino RB. Fibrinogen and risk of cardiovascular disease: The Framingham study. JAMA 1987 ; 258 : 1183 – 1186.en_US
dc.identifier.citedreferenceRidker PM, Hennekens CH, Roitman-Johnson B, Stampfer MJ, Allen J. Plasma concentration of soluble intercellular adhesion molecule 1 and risks of future myocardial infarction in apparently healthy men. Lancet 1998 ; 351 : 88 – 92.en_US
dc.identifier.citedreferenceRidker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH. Plasma concentration of C-reactive protein and risk of developing peripheral vascular disease. Circulation 1998 ; 97 : 425 – 428.en_US
dc.identifier.citedreferenceRidker PM. Novel risk factors and markers for coronary disease. Adv Intern Med 2000 ; 45 : 391 – 418.en_US
dc.identifier.citedreferenceXu Q, Willeit J, Marosi M et al. Association of serum antibodies to heat shock protein 65 with carotid atherosclerosis. Lancet 1993 ; 341 : 255 – 259.en_US
dc.identifier.citedreferenceXu Q, Kiechl S, Mayr M et al. Association of serum antibodies to heat-shock protein 65 with carotid atherosclerosis: clinical significance determined in a follow-up study. Circulation 1999 ; 100 : 1169 – 1174.en_US
dc.identifier.citedreferenceDanesh J, Collins R, Appleby P, Peto R. Association of fibrinogen, C-reactive protein, albumin, or leukocyte count with coronary heart disease. Meta-analyses of prospective studies. JAMA 1998 ; 279 : 1477 – 1482.en_US
dc.identifier.citedreferenceChiu B. Multiple infections in carotid atherosclerotic plaques. Am Heart J 1999 ; 138 : S534 – S536.en_US
dc.identifier.citedreferenceForng RY, Champagne C, Simpson W, Genco CA. Environmental cues and gene expression in Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans. Oral Dis 2000 ; 6 : 351 – 365.en_US
dc.identifier.citedreferenceFolsom AR, Nieto FJ, Sorlie P, Chambless LE, Graham DY. Helicobacter pylori seropositivity and coronary heart disease incidence. Atherosclerosis risk in communities (ARIC) study investigators. Circulation 1998 ; 98 : 845 – 850.en_US
dc.identifier.citedreferenceStrachan DP, Mendall MA, Carrington D et al. Relation of Helicobacter pylori infection to 13-year mortality and incident ischemic heart disease in the Caerphilly prospective heart disease study. Circulation 1998 ; 98 : 1286 – 1290.en_US
dc.identifier.citedreferenceRidker PM, Danesh J, Youngman L et al. A prospective study of Helicobacter pylori seropositivity and the risk for future myocardial infarction among socioeconomically similar U.S. men. Ann Intern Med 2001 ; 135 : 184 – 188.en_US
dc.identifier.citedreferenceWald NJ, Law MR, Morris JK, Bagnall AM. Helicobacter pylori infection and mortality from ischaemic heart disease: negative result from a large, prospective study. BMJ 1997 ; 315 : 1199 – 1201.en_US
dc.identifier.citedreferenceBlasi F, Ranzi ML, Erba M et al. No evidence for the presence of Helicobacter pylori in atherosclerotic plaques in abdominal aortic aneurysm specimens. Atherosclerosis 1996 ; 126 : 339 – 340.en_US
dc.identifier.citedreferenceDanesh J, Collins R, Peto R. Chronic infections and coronary heart disease: is there a link? Lancet 1997 ; 350 : 430 – 436.en_US
dc.identifier.citedreferenceMattila KJ, Nieminen MS, Valtonen V et al. Association between dental health and acute myocardial infarction. BMJ 1989 ; 298 : 779 – 782.en_US
dc.identifier.citedreferenceGenco R, Chadda S, Grossi S et al. Periodontal disease is a predictor of cardiovascular disease in native Americans. J Dent Res 1997 ; 76 : 408.en_US
dc.identifier.citedreferenceHujoel PP, Drangsholt M, Spiekerman C, DeRouen TA. Pre-existing cardiovascular disease and periodontitis: a follow-up study. J Dent Res 2002 ; 81 : 186 – 191.en_US
dc.identifier.citedreferenceJanket S-J, Baird AE, Chuang S-K, Jones JA. Meta-analysis of periodontal disease and risk of coronary heart disease and stroke. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2003 ; 95 : 559 – 569.en_US
dc.identifier.citedreferenceGrossi SG, Zambon JJ, Ho AW et al. Assessment of risk for periodontal disease. I. Risk indicators for attachment loss. J Periodontol 1994 ; 65 : 260 – 267.en_US
dc.identifier.citedreferenceDzink JL, Socransky SS, Haffajee AD. The predominant cultiviable microbiota of active and inactive lesions of destructive periodontal diseases. J Clin Periodontol 1988 ; 15 : 316 – 323.en_US
dc.identifier.citedreferenceLoesche WJ, Syed SA, Schmidt E, Morrison EC. Bacterial profiles of subgingival plaques in periodontitis. J Periodontol 1985 ; 56 : 447 – 456.en_US
dc.identifier.citedreferenceDuncan MJ, Nakao S, Skobe Z, Xie H. Interactions of Porphyromonas gingivalis with epithelial cells. Infect Immun 1993 ; 61 : 2260 – 2265.en_US
dc.identifier.citedreferenceLamont RJ, Oda D, Persson RE, Persson GR. Interaction of Porphyromonas gingivalis with gingival epithelial cells maintained in culture. Oral Microbiol Immunol 1992 ; 7 : 364 – 367.en_US
dc.identifier.citedreferenceSaglie FR, Marfany A, Camargo P. Intragingival occurrence of Actinobacillus actinomycetemconitans and Bacteroides gingivalis in active destructive periodontal lesions. J Periodontol 1988 ; 59 : 259 – 265.en_US
dc.identifier.citedreferenceDeshpande RG, Khan MB, Genco CA. Invasion of aortic and heart endothelial cells by Porphyromonas gingivalis. Infect Immun 1998 ; 66 : 5337 – 5343.en_US
dc.identifier.citedreferenceKhlgatian M, Nassar H, Chou H-H, Gibson FC, Genco CA. Fimbria-dependent activation of cell adhesion molecule expression in Porphyromonas gingivalis -infected endothelial cells. Infect Immun 2002 ; 70 : 257 – 267.en_US
dc.identifier.citedreferenceLopatin DE, Blackburn E. Avidity and titer of immunoglobulin G subclasses to Porphyromonas gingivalis in adult periodontitis patients. Oral Microbiol Immunol 1992 ; 7 : 332 – 337.en_US
dc.identifier.citedreferenceMahanonda R, Seymour GJ, Powell LW, Good MF, Halliday JW. Effect of initial treatment of chronic inflammatory periodontal disease on the frequency of peripheral blood T-lymphocytes specific to periodontopathic bacteria. Oral Microbiol Immunol 1991 ; 6 : 221 – 227.en_US
dc.identifier.citedreferenceMiller WD. The human mouth as a focus of infection. Dental Cosmos 1891 ; 33 : 689 – 713.en_US
dc.identifier.citedreferenceHunter W. Oral sepsis as a cause of disease. Br Med J 1900 ; 1 : 215 – 216.en_US
dc.identifier.citedreferenceSilver JG, Martin AW, McBride BC. Experimental transient bacteremias in human subjects with varying degrees of plaque accumulation and gingival inflammation. J Clin Periodontol 1977 ; 4 : 92 – 99.en_US
dc.identifier.citedreferenceHeimdahl A, Hall G, Hedberg M et al. Detection and quantification by lysis-filtration of bacteremia after different oral surgical procedures. J Clin Microbiol 1990 ; 28 : 2205 – 2209.en_US
dc.identifier.citedreferenceDaly CG, Mitchell DH, Highfield JE, Grossberg DE, Stewart DL. Bacteremia due to periodontal probing: a clinical and microbiological investigation. J Periodontol 2001 ; 72 : 210 – 214.en_US
dc.identifier.citedreferenceGeerts SO, Nys M, De MP et al. Systemic release of endotoxins induced by gentle mastication: association with periodontitis severity. J Periodontol 2002 ; 73 : 73 – 78.en_US
dc.identifier.citedreferenceHaraszthy VI, Zambon JJ, Trevisan M, Zeid M, Genco RJ. Identification of periodontal pathogens in atheromatous plaques. J Periodontol 2000 ; 71 : 1554 – 1560.en_US
dc.identifier.citedreferenceLibby P, Egan D, Skarlattos S. Roles of infectious agents in atherosclerosis and restenosis: an assessment of the evidence and need for future research. Circulation 1997 ; 96 : 4095 – 4103.en_US
dc.identifier.citedreferenceHirose K, Isogai E, Ueda I. Porphyromonas gingivalis fimbriae induce adhesion of monocytic cell line U937 to endothelial cells. Microbiol Immunol 2000 ; 44 : 17 – 22.en_US
dc.identifier.citedreferenceDorn BR, Dunn WAJ, Progulske-Fox A. Invasion of human coronary artery cells by periodontal pathogens. Infect Immun 1999 ; 67 : 5792 – 5798.en_US
dc.identifier.citedreferenceBhagat K, Moss R, Collier J, Vallence P. Endothelial ‘stunning’ following a brief exposure to endotoxin: a mechanism to link infection and infarction? Cardiovasc Res 1996 ; 32 : 822 – 829.en_US
dc.identifier.citedreferenceAmar S, Gokce N, Morgan S, Loukedeli M, Van Dyke TE, Vita JA. Periodontal disease is associated with brachial artery endothelial dysfunction and systemic inflammation. Arterioscler Thromb Vasc Biol 2003 ; 23 : 1245 – 1249.en_US
dc.identifier.citedreferenceBreslow JL. Mouse models of atherosclerosis. Science 1996 ; 272 : 685 – 688.en_US
dc.identifier.citedreferenceZhang SH, Reddick RL, Piedrahita JA, Maeda N. Spontaneous hypercholesterolemia and arterial lesions in mice lacking apolipoprotein E. Science 1992 ; 258 : 468 – 471.en_US
dc.identifier.citedreferencePlump AS, Smith JD, Hayek T et al. Severe hypercholesterolemia and atherosclerosis in apolipoprotein E-deficient mice created by homologous recombination in ES cells. Cell 1992 ; 71 : 343 – 353.en_US
dc.identifier.citedreferenceZhang SH, Reddick RL, Burkey B, Maeda N. Diet-induced atherosclerosis in mice heterozygous and homozygous for apolipoprotein E gene disruption. J Clin Invest 1994 ; 94 : 937 – 945.en_US
dc.identifier.citedreferenceLi L, Messas E, Batista EL, Levine RA, Amar S. Porphyromonas gingivalis infection accelerates the progression of atherosclerosis in a heterozygous apolipoprotein E-deficient murine model. Circulation 2002 ; 105 : 861 – 867.en_US
dc.identifier.citedreferenceLalla E, Lamster IB, Hofmann MA et al. Oral infection with a periodontal pathogen accelerates early atherosclerosis in apolipoprotein E-null mice. Arterioscler Thromb Vasc Biol 2003 ; 23 : 1405 – 1411.en_US
dc.identifier.citedreferenceRoss R. Atherosclerosis – an inflammatory disease. N Engl J Med 1999 ; 340 : 115 – 126.en_US
dc.identifier.citedreferenceDe Nardin E. The role of inflammatory and immunological mediators in periodontitis and cardiovascular disease. Ann Periodontol 2001 ; 6 : 30 – 40.en_US
dc.identifier.citedreferenceGlass CK, Witzum JL. Atherosclerosis: the road ahead. Cell 2001 ; 104 : 503 – 516.en_US
dc.identifier.citedreferenceRoss R. The pathogenesis of atherosclerosis: a perspective for the 1990s. Nature 1993 ; 362 : 801 – 809.en_US
dc.identifier.citedreferenceFunk JL, Feingold KR, Moser AH, Grunfeld C. Lipopolysaccharide stimulation of RAW 264.7 macrophages induce lipid accumulation and foam cell formation. Atherosclerosis 1993 ; 98 : 67 – 82.en_US
dc.identifier.citedreferenceShapira L, Warbington M, Van Dyke TE. TNF alpha and IL-1 beta in serum of LJP patients with normal and defective neutrophil chemotaxis. J Periodont Res 1994 ; 29 : 371 – 373.en_US
dc.identifier.citedreferenceBeck J, Garcia R, Heiss G, Voskonas PS, Offenbacher S. Periodontal disease and cardiovascular disease. J Periodontol 1996 ; 67 : 1123 – 1137.en_US
dc.identifier.citedreferenceGosling J, Slaymaker S, Gu L et al. MCP-1 deficiency reduces susceptibility to atherosclerosis in mice that overexpress human apolipoprotein B. J Clin Invest 1999 ; 103 : 773 – 778.en_US
dc.identifier.citedreferenceKang I-C, Kuramitsu HK. Induction of monocyte chemoattractant protein-1 by Porphyromonas gingivalis in human endothelial cells. FEMS Immunol Med Microbiol 2002 ; 34 : 311 – 317.en_US
dc.identifier.citedreferenceQi M, Miyakawa H, Kuramitsu HK. Porphyromonas gingivalis induces murine macrophage foam cell formation. Microb Pathog 2003 ; 35 : 259 – 267.en_US
dc.identifier.citedreferenceKuramitsu HK, Kang IC, Qi M. Interactions of Porphyromonas gingivalis with host cells: implications for cardiovascular disease. J Periodontol 2003 ; 74 : 85 – 89.en_US
dc.identifier.citedreferenceOffenbacher S, Madianos PN, Champagne C et al. Periodontitis–atherosclerosis syndrome: an expanded model of pathogenesis. J Periodont Res 1999 ; 34 : 346 – 352.en_US
dc.identifier.citedreferenceJain A, Batista EL, Serhan C, Stahl GL, Van Dyke TE. Role for periodontitis in the progression of lipid deposition in an animal model. Infect Immun 2003 ; 71 : 6012 – 6018.en_US
dc.identifier.citedreferenceXu Q, Kleindienst R, Schett G et al. Regression of arteriosclerotic lesions induced by immunization with heat shock protein 65-containing material in normocholesterolemic, but not hypercholesterolemic rabbits. Atherosclerosis 1996 ; 123 : 145 – 155.en_US
dc.identifier.citedreferenceWick G, Kleindienst R, Schett G, Amberger A, Xu Q. Role of heat shock protein 65/60 in the pathogenesis of atherosclerosis. Int Arch Allergy Immunol 1995 ; 107 : 130 – 131.en_US
dc.identifier.citedreferenceMaeda H, Miyamoto M, Hongyo H, Nagai A, Kurihara H, Muryama Y. Heat shock protein 60 (GroEL) from Porphyromonas gingivalis : molecular cloning and sequence analysis of its gene and purification of the recombinant protein. FEMS Microbiol Lett 1994 ; 124 : 121 – 122.en_US
dc.identifier.citedreferenceLopatin DE, Shelburne CE, Van Poperin N, Kowalski CJ, Bagramian RA. Humoral immunity to stress proteins and periodontal disease. J Periodontol 1999 ; 70 : 1185 – 1193.en_US
dc.identifier.citedreferenceXu Q, Dietrich H, Steiner HJ et al. Induction of artherosclerosis in normocholesterolemic rabbits by immunization with heat-shock protein 65. Arterioscler Thromb 1992 ; 12 : 789 – 799.en_US
dc.identifier.citedreferenceMori Y, Kitamura H, Song QH, Kobayashi T, Uemura S, Oyong JC. A new murine model for atherosclerosis with inflammation in the periodontal tissue induced by immunization with heat shock protein. Hypertens Res 2000 ; 23 : 475 – 481.en_US
dc.identifier.citedreferenceChoi J, Chung S-W, Kim S-J, Kim S-J. Establishment of Porphyromonas gingivalis -specific T cell lines from atherosclerosis patients. Oral Microbiol Immunol 2001 ; 16 : 316 – 318.en_US
dc.identifier.citedreferenceChoi J-I, Chung S-W, Kang H-S, Rhim BY, Kim S-J, Kim S-J. Establishment of Porphyromonas gingivalis heat-shock-protein-specific T-cell lines from atherosclerosis patients. J Dent Res 2002 ; 81 : 344 – 348.en_US
dc.identifier.citedreferenceChung S-W, Kang H-S, Park H-R, Kim S-J, Kim S-J, Choi J-I. Immune responses to heat shock protein in Porphyromonas gingivalis infected periodontitis and atherosclerosis patients. J Periodont Res 2003 ; 38 : 388 – 393.en_US
dc.identifier.citedreferenceRidker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med 1997 ; 336 : 973 – 979.en_US
dc.identifier.citedreferenceKoenig W, Sund M, Frohlich M et al. C-reactive protein, a marker of inflammation, predicts future risk of coronary heart disease in initially healthy middle-aged men: results from the MONICA (Monitoring Trend and Determinants in Cardiovascular Disease) Augsburg cohort study, 1984–92. Circulation 1999 ; 99 : 237 – 242.en_US
dc.identifier.citedreferenceKuller LH, Tracy RP, Shaten J, Meilahn EN. Relation of C-reactive protein and coronary heart disease in the MRFIT nested case-control study. Multiple risk factor intervention trial. Am J Epidemiol 1996 ; 144 : 537 – 547.en_US
dc.identifier.citedreferenceRidker PM, Hennekens CH, Buring JE, Rifai N. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med 2000 ; 342 : 836 – 843.en_US
dc.identifier.citedreferenceZhang YX, Cliff WJ, Schoefl GI, Higgins G. Coronary C-reactive protein distribution: its relation to development of atherosclerosis. Atherosclerosis 1999 ; 145 : 375.en_US
dc.identifier.citedreferencePepys MB, Rowe IF, Baltz ML. C-reactive protein: binding to lipids and lipoproteins. Int Rev Exp Pathol 1985 ; 27 : 83 – 111.en_US
dc.identifier.citedreferenceFolsom AR, Pankow JS, Tracy RP et al. The investigator of the NHBLI family heart study. Association of C-reactive protein with markers of prevalent atherosclerotic disease. Am J Cardiol 2001 ; 15 : 112 – 117.en_US
dc.identifier.citedreferenceZwaka TP, Hombach V, Torzewski J. C-reactive protein-mediated low density lipoprotein uptake by macrophages: implications for atherosclerosis. Circulation 2001 ; 103 : 1194 – 1197.en_US
dc.identifier.citedreferenceSeifert PS, Hugo F, Hansson GK, Bhakdi S. Prelesional complement activation in experimental atherosclerosis. Terminal C5b-9 complement deposition coincides with cholesterol accumulation in the aortic intima of hypercholesterolemic rabbits. Lab Invest 1989 ; 60 : 747 – 754.en_US
dc.identifier.citedreferenceLagrand WK, Niessen HWM, Wolbink G-J et al. C-reactive protein colocalizes with complement in human hearts during myocardial infarction. Circulation 1997 ; 95 : 97 – 103.en_US
dc.identifier.citedreferenceTorzewski J, Torzewski M, Bowyer DE et al. C-reactive protein frequently colocalizes with the terminal complement complex in the intima of early atherosclerotic lesions of human coronary arteries. Arterioscler Thromb Vasc Biol 1998 ; 18 : 1386 – 1392.en_US
dc.identifier.citedreferenceReynolds GD, Vance RP. C-reactive protein immunohistochemical localization in normal and atherosclerotic human aortas. Arch Pathol Lab Med 1987 ; 111 : 265 – 269.en_US
dc.identifier.citedreferenceYudkin JS, Stehouwer CD, Emeis JJ, Coppack SW. C-reactive protein in healthy subjects: association with obesity, insulin resistance, and endothelial dysfunction: a potential role for cytokines originating from adipose tissue? Arterioscler Thromb Vasc Biol 1999 ; 19 : 972 – 978.en_US
dc.identifier.citedreferenceFichtlscherer S, Rosenberger G, Walter DH, Breuer S, Dimmler S, Zeiher AM. Elevated C-reactive protein levels and impaired endothelial vasoreactive patients with coronary artery disease. Circulation 2000 ; 102 : 1000 – 1006.en_US
dc.identifier.citedreferenceSitzer M, Markus HS, Mendall MA, Liehr R, Knorr U, Steinmetz H. C-reactive protein and carotid intimal medial thickness in a community population. J Cardiovasc Risk 2002 ; 9 : 97 – 103.en_US
dc.identifier.citedreferenceDanesh J, Wheeler JG, Hirschfield GM et al. C-reactive protein and other circulating markers of inflammation in the prediction of coronary heart disease. N Engl J Med 2004 ; 350 : 1387 – 1397.en_US
dc.identifier.citedreferenceEbersole JL, Machen RL, Steffen ML, Willmann DE. Systemic acute-phase reactants, C-reactive protein and haptoglobin, in adult periodontitis. Clin Exp Immunol 1997 ; 107 : 347 – 352.en_US
dc.identifier.citedreferenceFredriksson MI, Figueredo CMS, Gustafsson A, BergstrÖm KG, Asman BE. Effect of periodontitis and smoking on blood leukocytes and acute-phase proteins. J Periodontol 1999 ; 70 : 1355 – 1360.en_US
dc.identifier.citedreferenceLoos BG, Craandijk J, Hoek FJ, Wertheim-van-Dillen PM, van der Velden U. Elevation of systemic markers related to cardiovascular diseases in the peripheral blood of periodontitis patients. J Periodontol 2000 ; 71 : 1528 – 1534.en_US
dc.identifier.citedreferenceWu T, Trevisan M, Genco RJ, Falkner KL, Dorn JP, Sempos CT. Examination of the relation between periodontal health status and cardiovascular risk factors: serum total high density lipoprotein cholesterol, C-reactive protein and plasma fibrinogen. Am J Epidemidol 2000 ; 151 : 273 – 282.en_US
dc.identifier.citedreferenceSlade GD, Offenbacher S, Beck JD, Heiss G, Pankow JS. Acute-phase inflammatory response to periodontal disease in the US population. J Dent Res 2000 ; 79 : 49 – 57.en_US
dc.identifier.citedreferenceNoack B, Genco RJ, Trevisan M, Grossi S, Zambon JJ, De Nardin E. Periodontal infections contribute to elevated systemic C-reactive protein level. J Periodontol 2001 ; 72 : 1221 – 1227.en_US
dc.identifier.citedreferenceGlurich I, Grossi S, Albini B et al. Systemic inflammation in cardiovascular and periodontal disease: Comparative study. Clin Diagn Lab Immunol 2002 ; 9 : 425 – 432.en_US
dc.identifier.citedreferenceGhezzi E, Ship JA. Systemic diseases and their treatments in the elderly: impact on oral health. J Public Health Dent 2000 ; 60 : 289 – 296.en_US
dc.identifier.citedreferenceJoshipura K, Pitiphat W, Douglass CW. Validation of self-reported periodontal measures among health professionals. J Public Health Dent 2002 ; 62 : 115 – 121.en_US
dc.identifier.citedreferenceWakai K, Kawamura T, Umemura O et al. Association of medical status and physical with periodontal disease. J Clin Periodontol 1999 ; 26 : 664 – 672.en_US
dc.identifier.citedreferenceCraig RG, Yip JK, So MK, Boylan RJ, Socranscy SS, Haffajee AD. Relationship of destructive periodontal disease to the acute-phase response. J Periodontol 2003 ; 74 : 1007 – 1016.en_US
dc.identifier.citedreferenceMattila K, Vesanen M, Valtonen V et al. Effect of treating periodontitis on C-reactive protein levels: a pilot study. BMC Infect Dis 2002 ; 2 : 30 – 33.en_US
dc.identifier.citedreferenceMcGill HCJ. Fatty streaks in the aorta and coronary arteries and aorta. Lab Invest 1968 ; 18 : 560 – 564.en_US
dc.identifier.citedreferenceLowe GDO. Etiopathogenesis of cardiovascular disease: hemostasis, thrombosis, and vascular medicine. Ann Periodontol 1998 ; 3 : 121 – 126.en_US
dc.identifier.citedreferenceHerzberg MC, Brintzenhofe KL, Clawson CC. Aggregation of human platelets and adhesion of Streptococcus sanguis. Infect Immun 1983 ; 39 : 1457 – 1469.en_US
dc.identifier.citedreferenceHerzberg MC, Meyer MW. Effects of oral flora on platelets: Possible consequences in cardiovascular disease. J Periodontol 1996 ; 67 : 1138 – 1142.en_US
dc.identifier.citedreferenceSharma A, Novak EK, Sojar HT, Swank RT, Kuramitsu HK, Genco RJ. Porphyromonas gingivalis platelet aggregation activity: outer membrane vesicles are potent activators of murine platelets. Oral Microbiol Immunol 2000 ; 15 : 393 – 396.en_US
dc.identifier.citedreferenceKuramitsu HK, Qi M, Kang I-C, Chen W. Role for bacteria in cardiovascular disease. Ann Periodontol 2001 ; 6 : 41 – 47.en_US
dc.identifier.citedreferenceO'Leary DH, Polak JF, Kronmal RA, Manolio TA, Burke GL, Wolfson SKJ. Carotid-artery intima and media thickness as a risk factor for myocardial infarction and stroke in older adults. Cardiovascular Health Study Collaborative Research Group. N Engl J Med 1999 ; 340 : 14 – 22.en_US
dc.identifier.citedreferenceChambless LE, Heiss G, Folsom AR et al. Association of coronary heart disease incidence with carotid arterial wall thickness and major risk factors: the Atherosclerosis Risk in Communities (ARIC) Study, 1987–93. Am J Epidemiol 1997 ; 146 : 483 – 494.en_US
dc.identifier.citedreferenceBeck JD, Elter JR, Heiss G, Couper D, Mauriello SM, Offenbacher S. Relationship of periodontal disease to carotid artery intima-media wall thickness. The Atherosclerosis Risk in Communities (ARIC) Study. Arterioscler Thromb Vasc Biol 2001 ; 21 : 1816 – 1822.en_US
dc.identifier.citedreferenceDesvarieux M, Demmer RT, Rundek T et al. Relationship between periodontal disease, tooth loss, and carotid artery plaque. The oral infections and vascular disease epidemiology study (INVEST). Stroke 2003 ; 34 : 2120 – 2125.en_US
dc.identifier.citedreferenceKiechl S, Egger G, Mayr M et al. Chronic infections and the risk of carotid atherosclerosis: prospective results from a large population study. Circulation 2001 ; 103 : 1064 – 1070.en_US
dc.identifier.citedreferenceEspinola-Klein C, Rupprecht HJ, Blankenberg S et al. Impact of infectious burden on extend and long-term prognosis of atherosclerosis. Circulation 2002 ; 105 : 15 – 21.en_US
dc.identifier.citedreferenceZhu J, Quyyumi AA, Norman JE et al. Effects of total pathogen burden on coronary artery disease risk and c-reactive protein level. Am J Cardiol 2000 ; 85 : 140 – 146.en_US
dc.identifier.citedreferenceEpstein SE, Zhu J, Burnett MS, Zhou YF, Vercellotti G, Hajjar D. Infection and atherosclerosis: potential roles of pathogen burden and molecular mimicry. Arterioscler Thromb Vasc Biol 2000 ; 20 : 1417 – 1420.en_US
dc.identifier.citedreferenceFrisk F, Hakeberg M, Ahlqwist M, Bengtsson C. Endodontic variables and coronary heart disease. Acta Odontol Scand 2003 ; 61 : 257 – 262.en_US
dc.identifier.citedreferenceJoshipura KJ, Douglass CW, Willett WC. Possible explanations for the tooth loss and cardiovascular disease relationship. Ann Periodontol 1998 ; 3 : 175 – 183.en_US
dc.identifier.citedreferenceHujoel PP, Drangsholt M, Spiekerman C, DeRouen TA. Examining the link between coronary heart disease and the elimination of chronic dental infections. J Am Dent Assoc 2001 ; 132 : 883 – 889.en_US
dc.identifier.citedreferenceCutler CW, Iacopino AM. Periodontal disease: links with serum lipid/ triglyceride levels? Review and new data. J Int Acad Periodontol 2003 ; 5 : 47 – 51.en_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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