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Endodontic Infections: Risk for Cardiovascular Diseases??

Vishal Sahayata

Correspondence Address :

Vishal Sahayata, B.D.S, M.D.S
Periodontist, Senior lecturer at Department of Periodontology and Oral Implantology
Faculty of Dental Science
Dharmsinh Desai University
Gujarat
India
Email: drvishalsahayata@yahoo.co.in

Received on: August 29, 2016, Accepted on: September 22, 2016, Published on: September 30, 2016

Citation: Vishal Sahayata (2016). Endodontic Infections: Risk for Cardiovascular Diseases??

Copyright: 2016 Vishal Sahayata. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Cardiovascular diseases (CVD) have a complex etiology which includes genetic component and environmental factors. For the development of CVD, low-grade chronic inflammation plays a determining role in development of atherosclerosis [1,2]. Experimental studies have shown that upregulation of IL-1 activity favours the progression of atherosclerosis [3].

Both periodontal infections and endodontic infections have a similar and a complex microbiology and are associated with elevated cytokine levels [4]. Absence of epithelial barrier between the necrotic pulp and periapical tissues makes the spread of bacteria and inflammatory mediators more pronounced in contrast to periodontal infections [5].

Apical periodontitis occurs as a consequence to endodontic infection when the host defences give way to microbial factors [6]. Patients with apical periodontitis have three to tenfold greater amounts of IL-1 [4]. IL-1β is the predominant form of interleukin found in human periapical lesions and their exudates [7]. Periapical pathology leads to liberation of inflammatory mediators like IL-1, 6, 8 and 17 [4,8].

Endodontic surgical and non-surgical instrumentation of root canals can produce a transient bacteremia. However, it may also occur due to direct spread of endodontic bacteria into the bloodstream [9].

Even a small contribution to CHD development by endodontic disease might be important from a public health perspective. One review reported the presence of Lesion of Endodontic Origin in 14-70% of all participants and 0.6-8.5% of all teeth, with root-filled teeth evident in 22-78% of participants and 1.3-21.5% of teeth [10]. Lesion of Endodontic Origin are more common in root-filled than non-root filled teeth, and poorer-quality treatment has been associated with LEO (Lesion of Endodontic Origin) [10-12].

A more precise understanding of the connection between endodontic infection and inflammation and cardiovascular disease risk would be of great interest from a public health perspective. Only a more focused and rigorous scientific research can determine a definitive opinion on the relationship between endodontic disease and CVD.

References

1. Stollberger C, Finsterer J. Role of infectious and immune factors in coronary and cerebrovascular arteriosclerosis. Clin Diagn Lab Immunol. 2002;9(2):207-215.

2. Naoum JJ, Chai H, Lin PH, Lumsden AB, Yao Q, Chen C. Lymphotoxin-α and cardiovascular disease: clinical association and pathogenic mechanisms. Med Sci Monit. 2006;12(7):121-124.

3. Bhaskar V, Yin J, Mirza AM, et al. Monoclonal antibodies targeting IL-1 beta reduce biomarkers of atherosclerosis in vitro and inhibit atherosclerotic plaque formation in Apolipoprotein E-deficient mice. Atherosclerosis. 2011;216(2):313-320.

4. Beck J, Garcia R, Heiss G, Vokonas PS, Offenbacher S. Periodontal disease and cardiovascular disease. J Periodontol. 1996;67(10):1123-1137.

5. Silva TA, Garlet GP, Fukada SY, Silva JS, Cunha FQ. Chemokines in oral inflammatory diseases apical periodontitis and periodontal disease. J Dent Res. 2007;86(4):306-319.

6. Nair PN. Pathogenesis of apical periodontitis and the causes of endodontic failures. Crit Rev Oral Biol Med. 2004;15(6):348-381.

7. Lim GC, Torabinejad M, Kettering J, Linkhardt TA, Finkelman RD. Interleukin 1-beta in symptomatic and asymptomatic human periradicularlesions. J Endod. 1994;20(5):225-227.

8. Stashenko P, Yu SM, Wang CY. Kinetics of immune cell and bone resorptive responses to endodontic infections. J Endod. 1992;18(9):422-426.

9. Cotti E, Dessi C, Piras A, Mercuro G. Can a chronic dental infection be considered a cause of cardiovascular disease? A review of the literature. Int J Cardiol. 2010;148(1):4-10.

10. Caplan DJ. Epidemiologic issues in studies of association between apical periodontitis and systemic health. Endod Top. 2004;8(1):15-35.

11. Buckley M, Spangberg LS. The prevalence and technical quality of endodontic treatment in an American subpopulation. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1995;79(1):92-100.

12. Ray HA, Trope M. Periapical status of endodontically treated teeth in relation to the technical quality of the root filling and the coronal restoration. Int Endod J. 1995;28(1):12-18.

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Endodontic Infections: Risk for Cardiovascular Diseases??

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