Are Dentists Really Causing Infective Endocarditis?

August 29, 2012

By Jeffrey Krutoy, DDS

Faculty Peer Reviewed

Bacterial infective endocarditis is a potentially devastating disease, and while it may be an easy tradition to blame the dentist, recent research and new guidelines from the American Heart Association (AHA) indicate that it may not be so simple.

Infective endocarditis (IE), while relatively uncommon (with yearly incidence rates ranging from 2 to 6 cases per 100,000 people), results in high rates of morbidity and mortality even when treated.[1] For this reason, physicians have emphasized the importance of identifying the offending pathogens and sources of infection, with the goal of preventing new cases.  Many bacterial species, especially streptococci, staphylococci, and enterococci, are well known causes of endocarditis.  Prior to recent studies indicating increasing incidence of multidrug resistant staphylococcal IE, viridans streptococci have long been the most frequently noted microbes affecting heart valves in subacute infections. [2,3]

The knowledge that viridans streptococci are normal residents of the oral cavity led to the assumption that dental procedures are responsible for many cases of infective endocarditis.   For this reason, the first set of guidelines written in the 1950s  recommended antibiotic prophylaxis prior to dental procedures in an attempt to prevent cases of IE in susceptible individuals.  A recent overhaul of these guidelines has caused confusion among patients and medical practitioners alike.

The American Heart Association’s guidelines on antibiotic prophylaxis for IE have been updated many times since they first appeared in 1955.  By 1997, antibiotic premedication was recommended in all high- and moderate-risk cardiac patients.  These included people with congenital malformations, prosthetic valves, acquired valve disorders (eg, rheumatic heart disease), hypertrophic cardiomyopathy, and mitral valve prolapse with regurgitation (see Table 1).   It was suggested that patients stratified into these high and moderate risk categories should be prescribed prophylactic antibiotics prior to undergoing certain dental procedures known to cause bleeding.  The listed treatments included extractions, periodontal surgery and scaling, dental implant placement, and complicated endodontic (root canal) treatments.  Excluded were less invasive procedures such as standard restorative dentistry (crowns, bridges, fillings), local anesthesia injections, and most orthodontic work.[4] These guidelines were complicated for both patients and practitioners, and it was therefore not uncommon to note over-prescription of antibiotic prophylaxis to low-risk patients for even non-invasive procedures “just in case.”[5] As time passed, the quality of the evidence behind the recommendations came under increasing scrutiny.

Table 1 (From 1997 Guidelines) [4]
High Risk: Low Risk (no prophylaxis necessary):
Prosthetic Cardiac Valves Isolated secundum atrial septal defect
Cyanotic Congenital Heart Disease Surgical repair of atrial septal defect, ventricular septaldefect, or patent ductus arteriosus (without residua >6 mo)
History of Bacterial Endocarditis Previous coronary artery bypass graft surgery
Pulmonary Shunts (surgically created) MVP without valvular regurgitation
Moderate Risk: Physiological, functional, or innocent heart murmurs
Any other congenital cardiac abnormality Previous Kawasaki disease without valvular dysfunction
Hypertrophic Cardiomyopathy Cardiac pacemakers and implanted defibrillators
Mitral Valve Prolapse with regurgitation (or with thickened leaflets)
Acquired valve injuries (rheumatic heart disease)

The 2007 guidelines took a less aggressive, more evidence-based approach to endocarditis prophylaxis.  The AHA recognized that many of the previous guidelines were based on “expert opinion, clinical experience, and descriptive studies” rather than solid scientific evidence.  They acknowledged that even with perfect compliance using the most efficacious antibiotic, dental prophylaxis would be unlikely to prevent most cases of infectious endocarditis.  They recognized that unnecessary prophylaxis is potentially problematic for several other reasons: adverse medication reactions, antibiotic resistance, and cost.  For these reasons, the AHA narrowed the prophylaxis recommendations to include only those patients at highest risk for endocarditis (Table 2) when undergoing procedures during which bleeding is expected. [6]

Table 2 (From 2007 Guidelines) [6]
Highest Risk (only category recommended to continue receiving prophylaxis as per AHA)
Prosthetic cardiac valve or prosthetic material used for cardiac valve repair
Previous IE
Congenital heart disease (CHD)- Unrepaired cyanotic CHD, including palliative shunts and conduits- Completely repaired congenital heart defect with prosthetic material or device, whether placed by surgery or by catheter intervention, during the first 6 months after the procedure - Repaired CHD with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device (which inhibit endothelialization)
Cardiac transplantation recipients who develop cardiac valvulopathy

Other organizations, such as the National Institute for Health and Clinical Excellence (NICE) in England went even further by publishing recommendations in 2008 that no antibiotics at all were recommended prior to any dental procedures.[7]  The same year, the Cochrane Collaboration found not only a lack of data to support dental prophylaxis, but also expressed uncertainty that dental procedures actually cause many cases of IE.[8]

A question arose: if it is not clear that dental procedures cause IE, why are oral bacteria often found in infected heart valves?  Numerous studies have been conducted in recent years to investigate the idea that transient bacteremia from daily hygiene activities such as tooth brushing and flossing causes endocarditis. In a randomized controlled trial published in Circulation by Lockhart and colleagues, researchers drew blood cultures from participants at 6 time points before, during, and after either tooth extraction or tooth brushing.[9]  They demonstrated bacteremia after extraction and, to a lesser extent, after tooth brushing.  This finding has an important implication: the average person brushes his or her teeth twice per day (and, realistically, flosses much less) but only visits the dentist twice per year, making the cumulative daily transient bacteremia riskier than almost any procedure performed during a single dental visit. [9-12]

Patients may be concerned about engaging in a daily hygiene ritual that may expose them to harm.  Good news comes in the form of other studies that reveal that dental plaque accumulation and gingival inflammation (bleeding gingiva while brushing) are related to an increased degree of bacteremia following daily oral health care.[13, 14] If a patient takes care of his or her dental and periodontal health, fewer bacteria are seeded into the bloodstream every day.

A few closing observations can be made.  First, solid evidence linking dental procedures to endocarditis is scarce and will likely remain so, as the low incidence of IE makes definitive research difficult to perform. Next, in light of current evidence and guidelines, the routine prescription of antibiotic prophylaxis to low-risk patients should be highly discouraged.  There is no such thing as a totally safe drug, and antibiotic resistance is a major concern.  Finally, and perhaps most important, emphasis should be placed on educating patients and improving oral health.

Jeffrey Krutoy, DDS is a 3rd year medical student at NYU School of Medicine

Peer reviewed by Robert Donnino, MD, Division of Cardiology, NYU Langone Medical Center

Image courtesy of Wikimedia Commons

References:

[1] Tleyjeh IM, Abdel-Latif A, Rahbi H, et al. A systematic review of population-based studies of infective endocarditis. Chest. 2007;132(3):1025-1035. http://journal.publications.chestnet.org/article.aspx?articleid=1085332

[2] Baddour LM, Wilson WR, Bayer AS, et al. AHA Scientific Statement: Infective Endocarditis. Diagnosis, antimicrobial therapy, and management of complications:

a statement for healthcare professionals from the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, and the Councils on Clinical Cardiology, Stroke, and Cardiovascular Surgery and Anesthesia, American Heart Association. Circulation. 2005; 111(23):e394-e434. http://www.ncbi.nlm.nih.gov/pubmed/15956145

[3] Karchmer AW. Infective endocarditis. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012:

[4] Dajani AS, Taubert KA, Wilson W, et al. Prevention of bacterial endocarditis: Recommendations by the American Heart Association. Circulation. 1997;96(1):358–366.

[5] Shaw D, Conway DI. Pascal’s Wager, infective endocarditis and the ‘‘no-lose’’ philosophy in medicine. Heart. 2010;96(1):15–18.

[6] Wilson W, Taubert KA, Gewitz M, et al. Prevention of infective endocarditis. Guidelines from the American Heart Association Rheumatic Fever, Endocarditis and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation. 2007; 116(15):1736–1754.

[7]  National Institute for Health and Clinical Excellence. Prophylaxis against infective endocarditis: antimicrobial prophylaxis against infective endocarditis in adults and children undergoing interventional procedures. NICE Clinical Guideline No 64. London: National Institute for Health and Clinical Excellence. Published March 2008. Updated January 23, 2011.  http://guideline.gov/content.aspx?id=14323

[8]  Oliver R, Roberts G, Hooper L, Worthington HV. Antibiotics for the prophylaxis of bacterial endocarditis in dentistry. Cochrane Database Syst Rev. 2008; 4:CD003813.

[9] Lockhart PB, Brennan MT, Sasser HC, Fox PC, Paster BJ, Bahrani-Mougeot FK.  Bacteremia associated with toothbrushing and dental extraction. Circulation. 2008; 117(24):3118–3125. http://www.ncbi.nlm.nih.gov/pubmed/18541739

[10]  Lucas VS, Gafan G, Dewhurst S, Roberts GJ. Prevalence, intensity and nature of bacteraemia after toothbrushing. J Dent. 2008;36(7):481–487.

[11]  Crasta K, Daly CG, Mitchell D, Curtis B, Stewart D, Heitz-Mayfield LJ. Bacteraemia due to dental flossing. J Clin Periodontol. 2009;36(4)323–332.

[12]  Sakamoto H, Karakida K, Otsuru M, Aoki T, Hata Y, Aki A.  Antibiotic prevention of infective endocarditis due to oral procedures: myth, magic, or science? J Infect Chemother. 2007;13(4):189–195. http://www.ncbi.nlm.nih.gov/pubmed/17721679

[13]  Tomás I, Diz P, Tobías A, Scully C, Donos N. Periodontal health status and bacteraemia from daily oral activities: systematic review/meta-analysis. J Clin Periodontol. 2012;39(3):213–228. http://www.ncbi.nlm.nih.gov/pubmed/22092606

[14] Lockhart PB, Brennan MT, Thornhill M, et al. Poor oral hygiene as a risk factor for infective endocarditis-related bacteremia  J Am Dent Assoc. 2009;140(10):1238-1244.

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