open access

Vol 25, No 3 (2018)
Original articles - Clinical cardiology
Published online: 2017-02-01
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Relationship between past myocardial infarction, periodontal disease and Porphyromonas gingivalis serum antibodies: A case-control study

Radosław P. Łysek, Krystyna Szafraniec, Maciej Polak, Piotr Jankowski, Agnieszka Micek, Renata Wolfshaut-Wolak, Danuta Czarnecka, Jan Potempa, Andrzej Pająk
DOI: 10.5603/CJ.a2017.0015
·
Cardiol J 2018;25(3):386-392.

open access

Vol 25, No 3 (2018)
Original articles - Clinical cardiology
Published online: 2017-02-01

Abstract

Background: The relationship between chronic periodontitis (CP) and increased risk for cardiovas­cular disease (CVD) is known but quantitative assessments and mechanisms are not fully understood. The aim of this study was to assess the relationship between past myocardial infarction (MI) and the severity of CP, and the level of serum antibody titer against Porphyromonas gingivalis gingipains.

Methods: The study sample consisted of 97 patients after MI and 113 high risk controls with no history of coronary heart disease (CHD) matched with age, sex and place of residence (urban vs. rural). Data on the history of CHD and presence of risk factors were collected. Periodontal status was assessed using the Community Periodontal Index (CPI), clinical attachment loss (CAL), bleeding on probing (BOP) and pocket depth.

Results: After adjustment for potential confounders patients with BOP = 20–50% and BOP > 50% had more than four times higher odds of past MI (OR = 4.56; 95% CI 2.03–10.27). Patients with CPI code = 4 had a three times higher odds of past MI (OR = 3.18, 95% CI 1.01–10.06). CAL ≥ 6 was related to higher odds of past MI (OR = 1.28, 95% CI 1.11–1.49). Patients with moderate antibody titer levels had an almost 3 times higher odds of past MI (OR = 2.82, 95% CI 1.02–7.84).

Conclusions: There was an association between CP and past MI, which was independent of classical CVD risk factors and confirmed by an association between past MI and immunological reaction against P. gingivalis gingipains.

Abstract

Background: The relationship between chronic periodontitis (CP) and increased risk for cardiovas­cular disease (CVD) is known but quantitative assessments and mechanisms are not fully understood. The aim of this study was to assess the relationship between past myocardial infarction (MI) and the severity of CP, and the level of serum antibody titer against Porphyromonas gingivalis gingipains.

Methods: The study sample consisted of 97 patients after MI and 113 high risk controls with no history of coronary heart disease (CHD) matched with age, sex and place of residence (urban vs. rural). Data on the history of CHD and presence of risk factors were collected. Periodontal status was assessed using the Community Periodontal Index (CPI), clinical attachment loss (CAL), bleeding on probing (BOP) and pocket depth.

Results: After adjustment for potential confounders patients with BOP = 20–50% and BOP > 50% had more than four times higher odds of past MI (OR = 4.56; 95% CI 2.03–10.27). Patients with CPI code = 4 had a three times higher odds of past MI (OR = 3.18, 95% CI 1.01–10.06). CAL ≥ 6 was related to higher odds of past MI (OR = 1.28, 95% CI 1.11–1.49). Patients with moderate antibody titer levels had an almost 3 times higher odds of past MI (OR = 2.82, 95% CI 1.02–7.84).

Conclusions: There was an association between CP and past MI, which was independent of classical CVD risk factors and confirmed by an association between past MI and immunological reaction against P. gingivalis gingipains.

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Keywords

periodontal disease, myocardial infarction, Porphyromonas gingivalis gingipains, cardiovascular disease risk factors

About this article
Title

Relationship between past myocardial infarction, periodontal disease and Porphyromonas gingivalis serum antibodies: A case-control study

Journal

Cardiology Journal

Issue

Vol 25, No 3 (2018)

Pages

386-392

Published online

2017-02-01

DOI

10.5603/CJ.a2017.0015

Bibliographic record

Cardiol J 2018;25(3):386-392.

Keywords

periodontal disease
myocardial infarction
Porphyromonas gingivalis gingipains
cardiovascular disease risk factors

Authors

Radosław P. Łysek
Krystyna Szafraniec
Maciej Polak
Piotr Jankowski
Agnieszka Micek
Renata Wolfshaut-Wolak
Danuta Czarnecka
Jan Potempa
Andrzej Pająk

References (30)
  1. Mattila KJ, Nieminen MS, Valtonen VV, et al. Association between dental health and acute myocardial infarction. BMJ. 1989; 298(6676): 779–781.
  2. Humphrey LL, Fu R, Buckley DI, et al. Periodontal disease and coronary heart disease incidence: a systematic review and meta-analysis. J Gen Intern Med. 2008; 23(12): 2079–2086.
  3. Teeuw WJ, Slot DE, Susanto H, et al. Treatment of periodontitis improves the atherosclerotic profile: a systematic review and meta-analysis. J. Clin. Periodontol. 2014; 41(1): 70–79.
  4. Cotti E, Dessì C, Piras A, et al. Can a chronic dental infection be considered a cause of cardiovascular disease? A review of the literature. Int. J. Cardiol. 2011; 148(1): 4–10.
  5. König J, Holtfreter B, Kocher T. Periodontal health in Europe: future trends based on treatment needs and the provision of periodontal services--position paper 1. Eur J Dent Educ. 2010; 14 Suppl 1: 4–24.
  6. http://www.mz.gov. pl/zdrowie-i-profilaktyka/programy-zdrowotne/wykaz-programow/monitorowanie-stanu-zdrowia-jamy-ustnej-populacji-polskiej-w-latach-2013-2015, entered: 10. ; 08: 2015.
  7. Holt SC, Ebersole JL. Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia: the "red complex", a prototype polybacterial pathogenic consortium in periodontitis. Periodontol. 2000. 2005; 38: 72–122.
  8. Yang HW, Huang YF, Chou MY. Occurrence of Porphyromonas gingivalis and Tannerella forsythensis in periodontally diseased and healthy subjects. J. Periodontol. 2004; 75(8): 1077–1083.
  9. Lamont RJ, Jenkinson HF. Life below the gum line: pathogenic mechanisms of Porphyromonas gingivalis. Microbiol. Mol. Biol. Rev. 1998; 62(4): 1244–1263.
  10. Potempa J, Pike R, Travis J. Titration and mapping of the active site of cysteine proteinases from Porphyromonas gingivalis (gingipains) using peptidyl chloromethanes. Biol. Chem. 1997; 378(3-4): 223–230.
  11. Friedewald VE, Kornman KS, Beck JD, et al. American Journal of Cardiology, Journal of Periodontology. The American Journal of Cardiology and Journal of Periodontology Editors' Consensus: periodontitis and atherosclerotic cardiovascular disease. Am. J. Cardiol. 2009; 104(1): 59–68.
  12. Tam V, O'Brien-Simpson NM, Chen YY, et al. The RgpA-Kgp proteinase-adhesin complexes of Porphyromonas gingivalis Inactivate the Th2 cytokines interleukin-4 and interleukin-5. Infect. Immun. 2009; 77(4): 1451–1458.
  13. Fagundes JA, Monoo LD, Euzébio Alves VT, et al. Porphyromonas gingivalis is associated with protease-activated receptor-2 upregulation in chronic periodontitis. J. Periodontol. 2011; 82(11): 1596–1601.
  14. Higashi Y, Goto C, Jitsuiki D, et al. Periodontal infection is associated with endothelial dysfunction in healthy subjects and hypertensive patients. Hypertension. 2008; 51(2): 446–453.
  15. Haraszthy VI, Zambon JJ, Trevisan M, et al. Identification of periodontal pathogens in atheromatous plaques. J. Periodontol. 2000; 71(10): 1554–1560.
  16. Brodala N, Merricks EP, Bellinger DA, et al. Porphyromonas gingivalis bacteremia induces coronary and aortic atherosclerosis in normocholesterolemic and hypercholesterolemic pigs. Arterioscler. Thromb. Vasc. Biol. 2005; 25(7): 1446–1451.
  17. Craig RG, Boylan R, Yip J, et al. Serum IgG antibody response to periodontal pathogens in minority populations: relationship to periodontal disease status and progression. J. Periodont. Res. 2002; 37(2): 132–146.
  18. Lwanga S.K., Lemeshow S. Sample size determination in health studies. World Health Organization, Geneva, 1991.
  19. Organization W. Oral Health Surveys: Basic Methods. Biometrics. 1971; 27(4): 1111.
  20. Ainamo J, Bay I. Problems and proposals for recording gingivitis and plaque. Int Dent J. 1975; 25(4): 229–235.
  21. Ainamo J, Barmes D, Beagrie G, et al. Development of the World Health Organization (WHO) community periodontal index of treatment needs (CPITN). Int Dent J. 1982; 32(3): 281–291.
  22. Zdzalik M, Karim AY, Wolski K, et al. Prevalence of genes encoding extracellular proteases in Staphylococcus aureus - important targets triggering immune response in vivo. FEMS Immunol. Med. Microbiol. 2012; 66(2): 220–229.
  23. Briggs JE, McKeown PP, Crawford VLS, et al. Angiographically confirmed coronary heart disease and periodontal disease in middle-aged males. J. Periodontol. 2006; 77(1): 95–102.
  24. Oe Y, Soejima H, Nakayama H, et al. Significant association between score of periodontal disease and coronary artery disease. Heart Vessels. 2009; 24(2): 103–107.
  25. Hujoel PP, Drangsholt M, Spiekerman C, et al. Periodontal disease and coronary heart disease risk. JAMA. 2000; 284(11): 1406–1410.
  26. Tuominen R, Reunanen A, Paunio M, et al. Oral health indicators poorly predict coronary heart disease deaths. J. Dent. Res. 2003; 82(9): 713–718.
  27. Pussinen PJ, Jousilahti P, Alfthan G, et al. Antibodies to periodontal pathogens are associated with coronary heart disease. Arterioscler. Thromb. Vasc. Biol. 2003; 23(7): 1250–1254.
  28. Beck JD, Eke P, Heiss G, et al. Periodontal disease and coronary heart disease: a reappraisal of the exposure. Circulation. 2005; 112(1): 19–24.
  29. Holmlund A, Hedin M, Pussinen PJ, et al. Porphyromonas gingivalis (Pg) a possible link between impaired oral health and acute myocardial infarction. Int. J. Cardiol. 2011; 148(2): 148–153.
  30. Schrodi J, Recio L, Fiorellini J, et al. The effect of aspirin on the periodontal parameter bleeding on probing. J. Periodontol. 2002; 73(8): 871–876.

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