by Deborah M. Lyle, RDH, MS, and Carol A. Jahn, RDH, MS
Cardiovascular diseases (CVD) claim more lives annually than any other disease. It is the number one killer of women. Every year, CVD kills more than 2.4 million people, representing 39 percent of reported deaths. It is estimated that 64.4 million people in the United States have one or more forms of cardiovascular disease. This includes hypertension, stroke, and coronary heart disease such as congestive heart failure, congenital cardiovascular defects, and other diseases of the circulatory system.1,2
Atherosclerosis contributes to heart disease. Atherosclerosis is the narrowing of the coronary arteries due to plaque buildup and is likely to produce angina pectoris (chest pain), heart attack, or both. Ethnicity plays a role in the prevalence of CVD. It is estimated that 30 percent of non-Hispanic white men and 24 percent of non-Hispanic white women have CVD. This is compared to 41 percent of African American men and 40 percent of African American women. Additionally, CVD is also the number one killer of Latino/Hispanic Americans, responsible for 30 percent of the deaths each year.1,2
Fact versus myth
Remember the saying, "There's a heart attack waiting to happen?" Most of us believe that a diet high in saturated fats, being overweight, having a family history, a sedentary lifestyle, smoking, diabetes, hypertension, and high cholesterol predispose us to a heart attack. And it's true; the majority of people who develop a fatal cardiovascular disease exhibit at least one of the traditional risk factors.
New research is indicating that certain conditions such as smoking, hypertension, or diabetes produce chronic, low levels of inflammation.3 This inflammation has the potential to destabilize cholesterol deposits in the coronary arteries, which may lead to heart attack or stroke.4 Additionally, a diet high in saturated fats and/or sugar coupled with no exercise allow the body to become inflamed more easily.5
Inflammation produces increased levels of homo-cysteine, fibrinogen, lipoprotein(a), or C-reactive protein.6 C-reactive protein has been given significant attention in the medical and dental literature as a new, potential way to identify inflammation and is an increased risk for CVD.
The perio-cardiovascular link
Various forms of periodontal disease affect about 75 percent of adults in the United States. In many instances, inflammation is a hallmark of early disease such as gingivitis, but is often present chronically for years in people with periodontal disease, culminating in pocket formation, bone resorption, and subsequent tooth loss. Moreover, in periodontal disease, the inflammatory host response has been identified as a critical factor in disease progression. Markers of inflammation such as the pro-inflammatory mediators IL-1
The elevation in C-reactive protein is important because C-reactive protein has been shown to be a moderate predictor of coronary heart disease7 and a stronger predictor of cardiovascular events than LDL cholesterol level.8 Other studies show a positive association with acute myocardial infarction and sudden cardiac-related death.9,10 In a recent study, CRP was the strongest and most significant predictor of the risk of future cardiovascular disease compared to other markers of inflammation in women.11
While this may all point to a direct link between periodontal disease and CVD, what complicates matters is that both diseases have several risk factors in common. Most notable are smoking and diabetes, two very strong predisposing factors for CVD.
The question remains: Is there a cause and effect between periodontal infections and CVD, and if so, what is the true link? Is the inflammation from periodontal disease or gingivitis enough to cause heart disease or is it an exacerbating factor which, when coupled with smoking, high blood pressure, obesity, or diabetes becomes an additional trigger?5 Presently, evidence is limited; however, there are several major studies currently underway. Systematic reviews conclude a moderate association but there is no evidence that shows a causal relationship.12,13
Intervention studies are important in establishing a causal relationship. Recent studies have measured the systemic effects of periodontal therapy. The studies had similar nonsurgical treatment including scaling and root planing with ultrasonics, using local anesthesia. Both had significant reductions in plaque index, bleeding index, and probing depths. However, only one study demonstrated a significant reduction in serum CRP levels.14,15
Chronic bacterial infections that lead to inflammation, including periodontitis, are one of the risk factors for elevated CRP levels.16 Studies also show a positive correlation between severity of periodontal disease and elevated levels of CRP.16,17 Noack et al. also demonstrated a strong relationship between increased CRP levels and the presence of subgingival pathogenic bacteria.17 Eliminating periodontal infections is the desired outcome from nonsurgical therapy regardless of the impact on the incidence or severity of cardiovascular disease. Review of the American Heart Association guidelines for conditions requiring antibiotic prophylaxis for dental treatment is advised.
The evidence supports reduction of subgingival periodontal pathogens and inflammatory mediators. Scaling and root planing with ultrasonic and hand instruments continues to be the gold standard as evidenced by the reduction of the bacterial load and inflammation. The challenge is motivating patients to maintain the effects at home. There are several products on the market that enhance compliance such as powered toothbrushes and flossers, various interdental cleaners, and mouthrinses. Home irrigation should be considered as studies have repeatedly shown reduction of subgingival pathogenic bacteria even in 6 mm pockets.18,19 Additionally, daily irrigation with water has demonstrated reductions in both serum and GCF levels of inflammatory mediators.20,21
It is hypothesized that inflammatory and immunological reactions induced by periodontal infections contribute to atherogenesis and subsequent CVD.
Future studies are needed to conclusively show a causal relationship. Preliminary evidence that non-surgical periodontal therapy may have a positive impact on systemic markers will elevate the role of dental hygiene in the management and prevention of cardiovascular diseases.
Deborah M. Lyle, RDH, MS, is currently employed by Waterpik Technologies as the manager of professional marketing and education. Her tenure in dental hygiene includes private practice, faculty appointments, and research. Lyle is also chair of the ADHA Council on Education. She may be reached at [email protected].
Carol Jahn, RDH, MS is the educational programs manager for Waterpik Technologies where she designs multimedia educational programs for dental professionals. She provides continuing education programs in the areas of periodontics, patient compliance, and diabetes. Carol may be reached by phone at (800) 525-2020 or by e-mail at [email protected].References1. American Heart Association. Cardiovascular disease statistics. www.americanheart.org. Accessed August 17, 2004.
2. American Heart Association. Heart Facts 2004. www.americanheart.org. Accessed August 17, 2004.
3. Willerson JT, Ridker PM, Inflammation as a cardiovascular risk factor. Circulation. 2004; 109: II2-10.
4. Shen CX, Chen HZ, Ge, JB. The role of inflammation in inflammatory stress in acute coronary syndrome. Chin Med J. 2004; 117:133-9.
5. Gorman G, Park A. The fires within. Time Magazine, 2004, February 23; 39-46.
6. Mayo Clinic. Novel risk factors: Identifying new culprits in heart disease. www.mayoclinic.com. Accessed August 17, 2004.
7. Danesh J, et al. C-reactive protein and other circulating markers of inflammation in the prediction of coronary heart disease. N Engl J Med 2004; 350:1387-1397.
8. Ridker PM, et al. Comparison of C-reactive protein and low-density lipoprotein cholesterol levels in the prediction of first cardiovascular events. N Engl J Med 2002; 347:1557-1565.
9. Luzzo G, et al. The prognostic value of C-reactive protein and serum amyloid A protein in severe unstable angina. N Engl J Med 1994; 331:417-424.
10. Thompson SG, et al. for the European Concerted Action on Thrombosis and Disabilities Angina Pectoris Study Group. Hemostatic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris. N Engl J Med 1995; 332:635-641.
11. Ridker PM, et al. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med 2000; 342:836-843.
12. Khader YS, et al. Periodontal diseases and the risk of coronary heart and cerebrovascular diseases: A meta-analysis. J Periodontol 2004; 75:1046-1053.
13. Scannapieco FA, Bush RB, Paju S. Associations between periodontal disease and risk for atherosclerosis, cardiovascular disease, and stroke. A systematic review. Ann Periodontol 2003; 8:38-53.
14. Ide M, et al. Effect of treatment of chronic periodontitis on levels of serum markers of acute-phase inflammatory and vascular responses. J Clin Periodontol 2003; 30:334-340.
15. D'Aiuto F, et al. Periodontitis and atherogenesis: causal association or simple coincidence? J Clin Periodontol 2004; 31:402-411.
16. Slade DG, et al. Acute-phase response to periodontal disease and atherosclerosis: A possible link. J Dent Res 2000; 79:49-57.
17. Noack B, et al. Periodontal infections contribute to elevated systemic C-reactive protein level. J Periodontol 2001; 72:1221-1227.
18. Cobb CM, et al. Ultrastructural examination of human periodontal pockets following the use of an oral irrigation device in vivo. J Periodontol 1988; 59: 155-163.
19. Chaves ES, et al. Mechanism of irrigation effects on gingivitis. J Periodontol 1994; 65: 1016-1021.
20. Cutler C, et al. Clinical benefits of oral irrigation for periodontitis are related to reduction of pro-inflammatory cytokine levels and plaque. J Clin Periodontol 2000; 27: 134-143.
21. Al-Mubarak S, et al. Comparative evaluation of adjunctive oral irrigation in diabetics. J Clin Periodontol 2002; 29: 295-300.