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BRIEF COMMUNICATION Table of Contents   
Year : 2010  |  Volume : 13  |  Issue : 2  |  Page : 159-161
Periodontal diseases: A risk factor to cardiovascular disease


1 Department of Periodontology, Rural Dental College-Loni, Maharashtra, India
2 Department of Microbiology, Rural Medical College-Loni, Maharashtra, India
3 Department of Prosthodontics, Rural Dental College-Loni, Maharashtra, India

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Date of Web Publication3-May-2010
 

How to cite this article:
Saini R, Saini S, Saini SR. Periodontal diseases: A risk factor to cardiovascular disease. Ann Card Anaesth 2010;13:159-61

How to cite this URL:
Saini R, Saini S, Saini SR. Periodontal diseases: A risk factor to cardiovascular disease. Ann Card Anaesth [serial online] 2010 [cited 2019 Apr 19];13:159-61. Available from: http://www.annals.in/text.asp?2010/13/2/159/62936


Periodontitis is a destructive inflammatory disease of the supporting tissues of the teeth and is caused by specific microorganisms or group of specific microorganisms resulting in progressive destruction of periodontal ligament and alveolar bone with periodontal pocket formation, gingival recession or both. [1],[2] The host responds to the periodontal infections with an array of events involving both innate and adaptive immunity. Atherosclerosis and its consequent cardiovascular diseases represent one of the leading causes of death in the industrialized world and its etiological pathway is one of the chronic inflammatory diseases. [2] Periodontitis has been proposed as having an etiological or modulating role in cardiovascular and cerebrovascular disease, diabetes, respiratory disease and adverse pregnancy outcome and several mechanisms have been proposed to explain or support such theories and oral lesions are indicators of disease progression and oral cavity can be a window to overall health and body systems. One of these is based around the potential for the inflammatory phenomenon of periodontitis to have effects by the systemic dissemination of locally produced mediators such as C-reactive protein (CRP), interleukins -1 beta (IL-1b) and -6 (IL-6) and tumor necrosis factor alpha (TNF-a). This concept has been supported by work suggesting that elevated levels of a number of inflammatory molecules (together with sialic acid (SA) may be accurate indicators of cardiovascular risk. [3] Oral disease, periodontitis has, for many years, been considered a disease confined to the oral cavity. It is only in the past several years that substantial scientific data have emerged that indicate that the localized infections characteristic of periodontitis can have a significant effect on the systemic health of both humans and animals. [4] There is strong relationship between the periodontal and cardiovascular diseases and two directions have been the focus of delineating the relationship: (I) bacteria from the oral cavity directly exacerbating the cardiovascular disease or altering systemic risk factors for cardiovascular disease; and, (II) the chronic periodontal inflammation at the focus of infection increasing circulating levels of host inflammatory macromolecules, and/or bacteria translocated to the circulation eliciting elevations in systemic host inflammatory macromolecules that exacerbate cardiovascular disease directly or alter other systemic risk factors for cardiovascular disease. [4]


   Bacteremia and Oral Infections Top


Bacteria are the prime etiological agents in periodontal diseases, and it is estimated that more than 500 different bacterial species are capable of colonizing the adult mouth [1] and the lesions of the oral cavity have an immense impact on the quality of life of patient with complex advance diseases. [5] Poor dental hygiene and periodontal or periapical infections may produce bacteremia even in the absence of dental procedures. The incidence and magnitude of bacteremia of oral origin are directly proportional to the degree of oral inflammation and infection. [6] Transient bacteremia is common with manipulation of the teeth and periodontal tissues, and there is a wide variation in reported frequencies of bacteremia in patients resulting from dental procedures: tooth extraction (10 to 100%), periodontal surgery (36 to 88%), scaling and root planing (8 to 80%), teeth cleaning (up to 40%), rubber dam matrix/wedge placement (9 to 32%), and endodontic procedures (up to 20%), [7] an estimated 8% of all cases of infective endocarditic are associated with periodontal or dental diseases, without preceding dental procedure. [8]


   Oral Cavity and Pathogenesis of Cardiovascular Diseases Top


The mouth is a reflection of a patient's overall health, harmful habits and nutritional status. The oral cavity is a portal of entry as well as the site of disease for microbial infections that affect general health. Streptococcus viridian is the main infective agent that can enter the bloodstream from areas with considerable bleeding such as the oral cavity, urinary tract and gastrointestinal tract. These bacteria may lodge on the valves, inflame the myocardium and cause ulcerations on the inner walls of an artery. Patients with artificial joints, structural heart defects, prosthesis or previous severe infections are at a higher risk. These risks are from an implied association between dental treatments and endocarditis. Several theories exist to explain the link between periodontal disease and heart disease. One theory is that oral bacteria can affect the heart when they enter the blood stream, attaching to fatty plaques in the coronary arteries (heart blood vessels) and contributing to clot formation. Coronary artery disease is characterized by a thickening of the walls of the coronary arteries due to the buildup of fatty proteins. Blood clots can obstruct normal blood flow, restricting the amount of nutrients and oxygen required for the heart to function properly. This may lead to heart attacks. Another possibility is that the inflammation caused by periodontal disease increases plaque buildup, which may contribute to swelling of the arteries. Researchers have found that people with periodontal disease are almost twice as likely to suffer from coronary artery disease as those without periodontal disease. [9] Periodontal bacteria are known to invade the systemic circulation. Oral pathogens and inflammatory mediators (IL-1β, TNF-α) from periodontal lesions intermittently reach the bloodstream inducing chronic low-level bacteremia and systemic inflammatory reactants (C-reactive protein, systemic antibodies), all of which may represent a pathogenetic link between periodontal disease and heart disease. [10]


   Prophylactic Antibiotic Regime Top


Dental procedures induce bacteremia with bacterial species that often cause endocarditis, and endocarditis carries high morbidity and mortality; therefore, antibiotics should be administered to susceptible patients before dental procedures to prevent endocarditis. [11] In general, prophylaxis is recommended for procedures associated with significant bleeding from hard or soft tissues, periodontal surgery, scaling and professional teeth cleaning. It is recognized that unanticipated bleeding may occur on some occasions. In such an event, data from experimental animal models suggest that antimicrobial prophylaxis administered within two hours following the procedure will provide effective prophylaxis. [6],[7] Viridans streptococci (a chemolytic streptococci) are the most common cause of endocarditis following dental or oral procedures, prophylaxis should be specifically directed against these organisms. The antibiotics amoxicillin, ampicillin and penicillin V are equally effective in vitro against ac-hemolytic streptococci; however, amoxicillin is recommended because it is better absorbed from the gastrointestinal tract and provides higher and more sustained serum levels. The newly recommended adult dose is 2.0-g of amoxicillin (pediatric dose is 50 mg/kg not to exceed the adult dose) to be administered one hour before the anticipated procedure. For individuals who are unable to take or unable to absorb oral medications, a parenteral agent may be necessary, ampicillin sodium is recommended. Individuals who are allergic to penicillins (such as amoxicillin, ampicillin, or penicillin) should be treated with the provided alternative oral regimens. Clindamycin hydrochloride is one recommended alternative. Individuals who can tolerate first-generation cephalosporins (cephalexin or cefadroxil) may receive these agents provided they have not had an immediate, local, or systemic IgE-mediated anaphylactic allergic reaction to penicillin. Azithromycin or clarithromycin are also acceptable alternative agents for the penicillin-allergic individual although they are more expensive than the other regimens, when parenteral administration is needed in an individual who is allergic to penicillin, clindamycin phosphate is recommended; cefazolin may be used if the individual does not have an immediate type local or systemic anaphylactic hypersensitivity to penicillin. [6],[7]

 
   References Top

1.Saini R. Periodontitis a true infection. Jrnl of Glo Infe dis 2009;1:149-51.  Back to cited text no. 1      
2.Aiuto FD. Periodontitis and atherogenesis: causal association or simple coincidence. J Clin Periodontol 2004;31:402-11.  Back to cited text no. 2      
3.Chambers JC, Eda S, Bassett P, Karim Y, Thompson SG, Gallimore JR, et al. C-reactive protein, insulin resistance, central obesity, and coronary heart disease risk in Indian Asians from the United Kingdom compared with European whites. Circulation 2001;104:145-50.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]  
4.Ebersole JL, Cappelli D. Acute-phase reactants in infections and inflammatory diseases. Periodontol 2000;23:19-49.  Back to cited text no. 4      
5.Saini R. Dental expression and role in palliative treatment. Ind J Pal Care 2009;15:26-9.  Back to cited text no. 5      
6.Dajani AS, Taubert KA, Wilson W, Bolger AF, Bayer A, Ferrieri P, et al. Prevention of bacterial endocarditis: recommendations by the American Heart Association. J Am Dent Assoc 1997;128:1142-51.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]  
7.Wilson W, Taubert KA, Gewitz M, Lockhart PB, Baddour LM, Levison M, et al. Prevention of infective endocarditis: Guidelines from the American Heart Association: A guideline 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;116:1736-54.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]  
8.Drangsholt MT. A new causal model of dental diseases associated with endocarditis. Ann Periodontol 1998;3:184.  Back to cited text no. 8  [PUBMED]    
9.Web source www.perio.org "as checked on February 21 st 2010"  Back to cited text no. 9      
10.Schluze A, Busse M. Periodontal disease and heart disease. Clinical Sports Medicine 2008;1:9-12.  Back to cited text no. 10      
11.Durack DT. Antibiotics for prevention of endocarditis during dentistry: Time to scale back? Ann Intern Med 1998;129:829-31.  Back to cited text no. 11  [PUBMED]  [FULLTEXT]  

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Correspondence Address:
Rajiv Saini
Department of Periodontology & Oral Implantology, Rural Dental College- Loni, Tehsil Rahata, Ahmednagar
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-9784.62936

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