MOLECULAR-BIOLOGICAL ASSOCIATIONS BETWEEN PERIODONTITIS AND ATHEROSCLEROSIS

Ostrovska S. S., Shatorna V. F., Gerasimchuk P. G., Leonova G. O.

LITERATURE REVIEWS

Scentific article

The fact that oral sepsis and the extraction of teeth are the cause of infective endocarditis has long been known, numerous data on the connection between periodontitis and atherosclerosis were obtained. The causes of periodontitis and atherosclerosis are diverse and include a complex interaction between lifestyle, genetic, environmental and other factors. Age, smoking, alcohol abuse, race/ethnicity, education and socioeconomic status, diabetes and overweight are all factors associated with both atherosclerosis and periodontitis. The role of smoking in the observed association between periodontitis and atherosclerosis is critical, and smoking cessation becomes an essential component of maintaining health and preventing many diseases, including periodontitis and atherosclerosis, while periodontitis can be an important factor in determining recurrent cardiovascular diseases in patients with myocardial infarction, and not just a marker of the effects of cigarette smoking. It has been shown that periodontitis and atherosclerosis interact with each other through the systemic release of specific pro-and antiinflammatory cytokines, small signaling molecules and enzymes that modulate the initiation and progression of the chronic inflammatory response associated with both diseases. Periodontal pathogens were identified within atherosclerotic lesions and blood clots, isolated from patients with myocardial infarction. LDL cholesterol, a persistent risk factor for atherosclerosis, is also associated with periodontitis and the statins used to treat atherosclerosis effectively prevent or reduce the development of periodontitis. Data on common factors of genetic susceptibility which is characteristic of both diseases are being accumulated. These data confirm the presence of common features in the pathogenic mechanisms involved in both inflammatory diseases. Systemic inflammation is tested by several inflammatory markers, including C-reactive protein, which is a predictor of future cardiovascular diseases, including myocardial infarction, stroke, peripheral arterial disease and sudden cardiac death. Paradontitis is similarly associated with the increase in systemic inflammatory markers except for C-reactive protein, – tumor necrosis factors α, IL-1, IL-6 and IL-8. This is accompanied by cell activation with the inclusion of cell adhesion molecules and activation of nuclear factor-κB. As a result, the interaction between endothelium, monocytes and platelets can become proatherogenic, indirectly contributing to atherosclerosis with an unfavourable outcome due to rupture of atheromatous plaque, which is observed in patients with periodontitis. Risk factors for cardiovascular diseases, especially atherosclerosis, can be reduced with the help of proper treatment of periodontitis and its effective prevention. Today, the most important is regular dental follow-up from early adolescence.

periodontitis, atherosclerosis, their interrelation

1. Aarabi G, Eberhard J, Reissmann DR, Heydecke G, Seedorf U. Interaction between periodontal disease and atherosclerotic vascular disease – fact or fiction? Aterosclerosis. 2015;241(2):555-60.
2. Mattila KJ. Dental infections as a risk factor for acute myocardial infarction. Eur Heart Journal. 1993;14(suppl K):51-3.
3. Chun YH, Chun KR, Olguin D, Wang HL. Biological foundation for periodontitis as a potential risk factor for atherosclerosis. Journal of Periodontal Res. 2005;40(1):87-95.
4. Cho I, Blaser MJ. The human microbiome: at the interface of health and disease. Nat Rev Genet. 2012;13(4):260-70.
5. Round JL, Mazmanian SK. The gut microbiota shapes intestinal immune responses during health and disease. Nat Rev Immunol. 2009;9(5): 313-23.
6. Mark Welch JL, Rossetti BJ, Rieken CW, Dewhirst FE, Borisy GG. Biogeography of a human oral microbiome at the micron scale. Proc Natl Acad Sci USA. 2016;113(6):791-800.
7. Utter DR, Mark JL, Welch GG. Borisy Individuality, stability and variability of the plaque microbiome. Front Microbiol. 2016;7:564-70.
8. Mager DL, Ximenez-Fyvie LA, Haffajee AD, Socransky SS. Distribution of selected bacterial species on intraoral surfaces. Journal of Clin Periodontol. 2003;30(7):644-54.
9. Hujoel PP, Drangsholt M, Spiekerman C, DeRouen TA. Periodontal disease and coronary heart disease risk. JAMA. 2000;284:1406-10.
10. Dorn JM, Genco RJ, Grossi SG, Falkner KL, Hovey KM, Iacoviello L, et al. Periodontal disease and recurrent cardiovascular events in survivors of myocardial infarction (MI): the Western New York Acute MI Study. Journal of Periodontol. 2010;81(4):502-11.
11. Pietiäinen M, Liljestrand JM, Kopra E, Pussinen PJ. Mediators between oral dysbiosis and cardiovascular diseases. Eur Journal Oral Sci. 2018;126(l):26-36.
12. Kaptoge S, Di Angelantonio E, Lowe G, Pepys MB, Thompson SG, Collins R, et al. Emerging Risk Factors Collaboration. C-reactive protein concentration and risk of coronary heart disease, stroke, and mortality: an individual participant meta-analysis. Lancet. 2010;375(9709):132-40.
13. Lerman A, McConnell JP. Lipoprotein-associated phospholipase A2: a risk marker or a risk factor? Am Journal of Cardiol. 2008;101(12A):11F22F.
14. Heslop CL, Frohlich JJ, Hill JS. Myeloperoxidase and C-reactive protein have combined utility for long-term prediction of cardiovascular mortality after coronary angiography. Journal of Am Coll Cardiol. 2010;55(11):1102-9.
15. Green D, Foiles N, Chan C, Schreiner PJ, Liu K. Elevated fibrinogen levels and subsequent subclinical atherosclerosis: the CARDIA Study. Atherosclerosis. 2009;202:623-31.
16. Loos BG. Systemic markers of inflammation in periodontitis. Journal of Periodontol. 2005;76(l):2106-15.
17. Chun YH, Chun KR, Olguin D, Wang HL. Biological foundation for periodontitis as a potential risk factor for atherosclerosis. Journal of Periodontal Res. 2005;40(1):87-95.
18. Offenbacher S, Elter JR, Lin D, Beck JD. Evidence for periodontitis as a tertiary vascular infection. Journal of Int Acad Periodontol. 2005;7:39-48.
19. Maekawa T, Tabeta K, Kajita-Okui K, Nakajima T, Yamazaki K. Increased expression of C-reactive protein gene in inflamed gingival tissues could be derived from endothelial cells stimulated with interleukin-6. Arch Oral Biol. 2011;56(11):1312-8.
20. Beck J, Garcia R, Heiss G, Vokonas PS, Offenbacher S. Periodontal disease and cardiovascular disease. Journal of Periodontol. 1996;67(10): 1123-37.
21. Wu T, Trevisan M, Genco RJ, Dorn JP, Falkner KL, Sempos CT. Periodontal disease and risk of cerebrovascular disease: the first national health and nutrition examination survey and its follow-up study. Arch. Intern. Med. 2000;160(18):2749-55.
22. Teeuw WJ, Slot DE, Susanto H, Gerdes VE, Abbas F, D’Aiuto F, et al. Treatment of periodontitis improves the atherosclerotic profile: a systematic review and meta-analysis. Journal of Clin Periodontol. 2014;41(1):70-9.
23. D’Aiuto F, Orlandi M, Gunsolley JC. Evidence that periodontal treatment improves biomarkers and CVD outcomes. Journal of Clin Periodontol. 2013;40(14):85-105.
24. Beck JD, Couper DJ, Falkner KL, Graham SP, Grossi SG, Gunsolley JC, et al. The Periodontitis and Vascular Events (PAVE) pilot study: adverse events. Journal of Periodontol. 2008;79(1):90-6.
25. Sen S, Giamberardino LD, Moss K, Morelli T, Rosamond WD, Gottesman RF, et al. Periodontal disease, regular dental care use, and incident ischemic stroke. Stroke. 2018;49(2):355-62.

«Bulletin of problems biology and medicine» Issue 1 Part 1 (148), 2019 year, 53-56 pages, index UDK 61.314.17-002:616.13-004.6]-02-036.3:576.32/.36

10.29254/2077-4214-2019-1-1-148-53-56