Kardiovaskuläre Krankheiten

Cardiovascular disease refers to the class of diseases that involve the heart and/or blood vessels (arteries and veins). While the term technically refers to any disease that affects the cardiovascular system, it is usually used to refer to those related to atherosclerosis (arterial disease). These conditions have similar causes, mechanisms, and treatments. In practice, cardiovascular disease is treated by cardiologists, thoracic surgeons, vascular surgeons, neurologists, and interventional radiologists, depending on the organ system that is being treated. There is considerable overlap in the specialties, and it is common for certain procedures to be performed by different types of specialists in the same hospital.

Most Western countries face high and increasing rates of cardiovascular disease. Each year, heart disease kills more Americans than cancer. Diseases of the heart alone caused 30% of all deaths, with other diseases of the cardiovascular system causing substantial further death and disability. It is the number 1 cause of death and disability in the United States and most European countries. A large histological study (PDAY) showed vascular injury accumulates from adolescence, making primary prevention efforts necessary from childhood. By the time that heart problems are detected, the underlying cause (atherosclerosis) is usually quite advanced, having progressed for decades. There is therefore increased emphasis on preventing atherosclerosis by modifying risk factors, such as healthy eating, exercise and avoidance of smoking.

SCIENTIFIC PAPERS

(1996). "Periodontal management of patients with cardiovascular diseases. American Academy of Periodontology." J Periodontol 67(6): 627-35.

ABSTRACT: Periodontists are often called upon to provide periodontal therapy for patients with a variety of cardiovascular diseases. Safe and effective periodontal treatment requires a general understanding of the underlying cardiovascular diseases, their medical management, and necessary modifications to dental/periodontal therapy that may be required. In this informational paper more common cardiovascular disorders will be discussed and dental management considerations briefly described. This paper is intended for the use of periodontists and members of the dental profession.

(2002). "Periodontal management of patients with cardiovascular diseases." J Periodontol 73(8): 954-68.

Andrews, P. A. (2005). "Inflammatory periodontal disease as a potential marker of cardiovascular risk." Transplantation 80(1): 1-2.

Armitage, G. C. (2000). "Periodontal infections and cardiovascular disease--how strong is the association?" Oral Dis 6(6): 335-50.

ABSTRACT: In the past decade there has been renewed interest in the old hypothesis that infections increase the risk of developing cardiovascular disease and stroke. There is now a convincing body of evidence that atherosclerosis has a major inflammatory component and is much more than the simple vascular accumulation of lipids. Infectious agents that have been linked to an increased risk of coronary heart disease (CHD) include Chlamydia pneumoniae, Helicobacter pylori, cytomegalovirus, and herpesviruses. The concept has emerged that each of these agents is an independent risk factor for CHD and that common chronic infections are important. In addition, periodontal infections have also been implicated as one of several factors contributing to the development of CHD. Evidence supporting a causative role of chronic infections in CHD is largely circumstantial. However, the evidence is sufficiently strong to warrant further examination of the possible link between chronic infections and CHD. In this review the lines of evidence for a causative role of C. pneumoniae in the development of CHD are summarized and contrasted with the lines of evidence suggesting a periodontal infection--CHD association. If common or widespread chronic infections are truly important risk factors for CHD, it is unlikely that a single infection will be shown to be causative. It is likely that the entire microbial burden of the patient from several simultaneous chronic infections is more important (e.g., H. pylori-caused gastric ulcers + C. pneumoniae-caused bronchitis + periodontitis). Increased cooperation between cardiologists and periodontists will be required to determine if, and what, combinations of common chronic infections are important in the pathogenesis of CHD and stroke.

Beck, J., R. Garcia, et al. (1996). "Periodontal disease and cardiovascular disease." J Periodontol 67(10 Suppl): 1123-37.

ABSTRACT: It is our central hypothesis that periodontal diseases, which are chronic Gram-negative infections, represent a previously unrecognized risk factor for atherosclerosis and thromboembolic events. Previous studies have demonstrated an association between periodontal disease severity and risk of coronary heart disease and stroke. We hypothesize that this association may be due to an underlying inflammatory response trait, which places an individual at high risk for developing both periodontal disease and atherosclerosis. We further suggest that periodontal disease, once established, provides a biological burden of endotoxin (lipopolysaccharide) and inflammatory cytokines (especially TxA2, IL-1 beta, PGE2, and TNF-alpha) which serve to initiate and exacerbate atherogenesis and thromboembolic events. A cohort study was conducted using combined data from the Normative Aging Study and the Dental Longitudinal Study sponsored by the United States Department of Veterans Affairs. Mean bone loss scores and worst probing pocket depth scores per tooth were measured on 1,147 men during 1968 to 1971. Information gathered during follow-up examinations showed that 207 men developed coronary heart disease (CHD), 59 died of CHD, and 40 had strokes. Incidence odds ratios adjusted for established cardiovascular risk factors were 1.5, 1.9, and 2.8 for bone loss and total CHD, fatal CHD, and stroke, respectively. Levels of bone loss and cumulative incidence of total CHD and fatal CHD indicated a biologic gradient between severity of exposure and occurrence of disease.

Beck, J. D. and S. Offenbacher (2001). "The association between periodontal diseases and cardiovascular diseases: a state-of-the-science review." Ann Periodontol 6(1): 9-15.

ABSTRACT: Early case-control and cross-sectional studies demonstrating associations between chronic periodontitis and cardiovascular disease (CVD) were quickly followed by secondary analyses of data available from existing longitudinal studies, which indicated that individuals with periodontitis, as determined by clinical measures, were at greater risk for CVD events. Many of these studies contained large numbers of subjects and were adjusted for traditional risk factors. Within the last 18 months, one case-control study and one longitudinal study have reported finding positive associations that were not statistically significant. The earlier studies stimulated a number of studies focused on identifying potential biological mechanisms that might underlie this association. While still early in that process, such studies have implicated a systemic role for oral microorganisms and for the quality and quantity of the host inflammatory response as key biologic processes that may underlie the association of CVD with the clinical manifestation of periodontitis. It is a positive development when changes in our knowledge regarding biologic mechanisms result in reevaluation of past studies, and this reevaluation leads to new studies that incorporate the design elements demanded by this new knowledge. In that spirit, we conclude that all longitudinal studies reported to date can be characterized as follows: none were initially designed to actually test the association of interest; almost all were restricted to clinical measures of periodontitis to index the exposure and lacked measures of infectious burden and host response; and they used a variety of cardiovascular clinical events to index the outcome and did not include subclinical measures of atherosclerosis. In addition, the longitudinal studies that failed to show a significant association between periodontitis and CVD used the least sensitive and crudest clinical measures of periodontal disease. Based upon the current state-of-the-science, all previous studies should be viewed as lacking sufficiently sensitive and comprehensive measures of periodontal disease as a systemic exposure. Since the potential health care impact of this relationship might be extensive, it is time to enter the next phase of research by conducting molecular epidemiology studies that are appropriately designed to test our current understanding of the molecular and cellular mechanisms involved.

Beck, J. D. and S. Offenbacher (2005). "Systemic effects of periodontitis: epidemiology of periodontal disease and cardiovascular disease." J Periodontol 76(11 Suppl): 2089-100.

ABSTRACT: There have been 42 published studies describing associations between oral conditions and cardiovascular diseases. In the absence of randomized controlled trials, the 16 longitudinal studies represent the highest level of evidence available. However, two databases produced eight of the 16 studies. There also is extensive variability in definitions of the oral exposure that include salivary flow, reported periodontal disease, number of teeth, oral organisms, antibodies to oral organisms, Total Dental Index, Community Periodontal Index of Treatment Needs, plaque scores, probing depth, attachment loss, and bone level. Variability also exists in the cardiovascular outcomes that include atherosclerosis measures and events, such as hospitalization for coronary heart disease (CHD), chronic CHD, fatal CHD, total stroke, ischemic stroke, and revascularization procedures. One of the criticisms of this research is that the exposure has not been represented by measures of infection. To begin to address this concern, we present new data showing that patterns of high and low levels of eight periodontal pathogens and antibody levels against those organisms are related to clinical periodontal disease as well as other characteristics of the individuals, such as age, race, gender, diabetic status, atherosclerosis, and CHD. As others before us, we conclude that the cumulative evidence presented above supports, but does not prove, a causal association between periodontal infection and atherosclerotic cardiovascular disease or its sequelae. A number of legitimate concerns have arisen about the nature of the relationship and, indeed, the appropriate definitions for periodontal disease when it is thought to be an exposure for systemic diseases. There is still much work needed to identify which aspects of the exposure are related to which aspects of the outcome. Principal component analyses illustrate the complexity of the interactions among risk factors, exposures, and outcomes. These analyses provide an initial clustering that describes and suggests the presence of specific syndromes.

Bokhari, S. A. and A. A. Khan (2006). "The relationship of periodontal disease to cardiovascular diseases--review of literature." J Pak Med Assoc 56(4): 177-81.

ABSTRACT: Association of Oral and Systemic diseases has gained importance because the high occurrence of oral diseases is an extremely common source of infection. Epidemiological Studies have presented periodontal diseases as a risk factor for development of cardiovascular diseases. A chronic oral infection such as periodontitis is a constant potential source of infection and has now been considered as a separate risk factor for cardiovascular diseases, cerebrovascular diseases, peripheral arterial disease and respiratory diseases as well as delivery of low-birth-weight infants. The possible pathways linking oral infections to systemic diseases are metastatic infections, bacterial endotoxins, and systemic vascular injury. People with a history of periodontal disease and/or tooth loss were found at higher risk for Peripheral arterial disease (PAD) as compared to those without periodontal disease and/or tooth loss. All studies on the relationship of periodontal diseases to cardiovascular diseases are inconclusive and most of the data is based on epidemiological studies.

Chong, P. H. and B. Kezele (2000). "Periodontal disease and atherosclerotic cardiovascular disease: confounding effects or epiphenomenon?" Pharmacotherapy 20(7): 805-18.

ABSTRACT: Recent evidence suggests that periodontal disease may predispose to atherosclerotic cardiovascular disease. Data support mechanisms of host-derived local and systemic proinflammatory responses similar to atherosclerosis, consisting of monocytic-derived cytokines and other inflammatory mediators, which are induced by periodontal pathogens and its endotoxin, lipopolysaccharide. These mechanisms may contribute to the start of vascular endothelial dysfunction and further sequelae leading to atherosclerosis. Experimental evidence and biologic plausibility appear to support this proposal. However, clinical evidence from a MEDLINE search from January 1966-December 1999 proposed a weak or no correlation primarily due to confounding factors. The aim of care is to reduce vulnerable pathogens from the infected periodontium by standard treatment; however, new approaches appear promising. Increased awareness of a potential link among infective agents, immunoinflammatory processes, and atherosclerosis may clarify clinical implications.

Chow, J. P. (1998). "Periodontal and cardiovascular diseases." J Am Dent Assoc 129(4): 410.

Craig, R. G. (2004). "Inflammation, cardiovascular disease and destructive periodontal diseases. The evolving role of the dental profession." N Y State Dent J 70(5): 22-6.

ABSTRACT: Destructive periodontal diseases have been associated with increased risk of atherosclerotic complications, including myocardial infarction (MI) and stroke. This finding comes at a time when our understanding of atherosclerotic complications are changing from a focus on the occlusion of arteries, due to the buildup of plaque deposits, to an increased awareness of the role of inflammation in plaque rupture and thrombus formation. The role of inflammation can have great significance to the dental profession if inflammatory cells and factors derived from chronic infections, such as destructive periodontal diseases, are shown to contribute to plaque rupture. This "Perspectives" feature will review the role of inflammation in atherosclerotic complications, and the association between destructive periodontal diseases, systemic inflammation and atherosclerotic complications. It will also highlight ongoing research designed to determine whether destructive periodontal diseases contribute to atherosclerotic complications.

Cunha-Cruz, J. and P. Nadanovsky (2003). "[Does periodontal disease cause cardiovascular disease? Analysis of epidemiological evidences]." Cad Saude Publica 19(2): 357-68.

ABSTRACT: This article reports a critical analysis of epidemiologic studies that evaluated periodontal disease as a cause of cardiovascular disease. Thirty-five studies were identified through a manual search of the special abstracts volumes of the Journal of Dental Research, as well as an electronic search on MEDLINE, LILACS, and ISI and inspection of the articles' bibliographies. Inclusion criteria were: articles in any language published between 1989 and 2000 reporting the presence or absence of an association between periodontal and cardiovascular diseases. Available studies are scarce, and interpretations are limited by potential bias and confounding. The studies analyzed (whether separately or jointly) fail to provide convincing epidemiologic evidence for a causal association between periodontal and cardiovascular diseases. Although the possibility that oral diseases can cause cardiovascular diseases cannot be discarded, until better data are available, periodontal disease should not be incriminated as a cause of cardiovascular disease.

Czerniuk, M., K. J. Filipiak, et al. (1999). "[Periodontal state and cardiovascular diseases]." Pol Arch Med Wewn 101(5): 433-6.

D'Aiuto, F., M. Parkar, et al. (2006). "Periodontal infections cause changes in traditional and novel cardiovascular risk factors: results from a randomized controlled clinical trial." Am Heart J 151(5): 977-84.

ABSTRACT: BACKGROUND: Chronic infections, such as periodontitis, are associated with increased risk of systemic diseases driven by a persistent low-grade systemic inflammation and metabolic changes. Severity of periodontitis has also been associated with increased systolic blood pressure (BP). However, the issue remains poorly investigated. We aimed to estimate the effect of periodontal therapy on traditional and novel cardiovascular risk factors in systemically healthy individuals who have periodontitis. METHODS: We enrolled 40 otherwise healthy patients with severe chronic generalized periodontitis in a 6-month pilot intervention trial. Individuals were randomized either to a standard course of periodontal therapy (subgingival scaling and root planing) or an intensive one (including the adjunctive use of a locally delivered antimicrobial, IPT). RESULTS: Compared to control, IPT produced significant reductions in a cluster of inflammatory markers at 1 (P = .0406) and 2 (P = .0060) months together with an improvement in lipid markers at 2 (P = .0320) and 6 (P = .0432) months after therapy. Intensive periodontal therapy produced greater reductions in IL-6 at 1 (0.4 +/- 0.2 ng/L difference, 95% CI 0.03-0.9, P = .0284) and 2 months (0.3 +/- 0.2 ng/L difference, 95% CI 0.1-0.8, P = .0284), together with decreases in C-reactive protein (0.4 +/- 0.2 mg/L difference, 95% CI 0.01-0.8, P = .0438) and total cholesterol (0.3 +/- 0.1 mmol/L difference, 95% CI 0.04-0.6, P = .0254). Moreover, a 7 +/- 3-mm Hg decrease in systolic BP was observed at 2 months in the IPT group (95% CI 1-12, P = .0211), and this difference was greater in current smokers (14 +/- 5 mm Hg 95% CI 3-25, P = 0.0124). Intensive periodontal therapy subjects exhibited a 1.53% +/- 1.20% (95% CI 1.05-2.24, P = .0290) and 2.00% +/- 1.42% (95% CI 0.98-4.09, P = .0568) decreases in cardiovascular risk scores (Framingham) at 2 and 6 months, respectively, when compared to those in the standard group. CONCLUSIONS: Our findings suggest that intensive periodontal treatment reduces systemic inflammatory markers and systolic BP, and improves lipid profiles with subsequent changes in cardiovascular risk when compared to standard therapy.

D'Aiuto, F., D. Ready, et al. (2004). "Periodontal disease and C-reactive protein-associated cardiovascular risk." J Periodontal Res 39(4): 236-41.

ABSTRACT: BACKGROUND: Periodontitis has been associated with a moderate systemic inflammatory response. Successful periodontal therapy could decrease serum inflammatory parameters. The aim of this report was to explore the outcomes of periodontal therapy in terms of changes in C-reactive protein (CRP)-associated cardiovascular disease (CVD) risk as defined in a recent American Heart Association (AHA) consensus conference. METHODS: Ninety-four systemically healthy subjects suffering from severe generalized periodontitis received standard non-surgical periodontal therapy. Periodontal parameters and serum inflammatory responses [interleukin-6 (IL-6) and CRP] were monitored 2 and 6 months after therapy. RESULTS: At baseline, subjects with more severe and widespread periodontitis had a higher chance of having high CRP-associated CVD risk (OR 5.6, 95% CI 1.2-27.4). Age and body mass index were also significant in the analysis. After therapy, a significant decrease in number of subjects associated with a medium and high CRP-associated risk was observed (p < 0.001 chi(2)), with 40 of 94 subjects displaying a decrease in their class of risk. Patients who had a better oral response to periodontal therapy were also more likely to have decreased their inflammatory risk category (OR 4.8, 95% CI 1.4-15.8) after correcting for age, gender, ethnicity and cigarette smoking. CONCLUSIONS: This study indicated that periodontitis may add to the inflammatory burden of the individual and may result in increased levels of cardiovascular risk based on serum CRP concentrations. These observations will need to be confirmed in a definitive trial. Given the high prevalence of periodontitis in the population, these data would caution physicians to be aware of the possible oral source of an increased inflammatory burden.

D'Aiuto, F. and M. S. Tonetti (2005). "Contribution of periodontal therapy on individual cardiovascular risk assessment." Arch Intern Med 165(16): 1920-1.

Dave, S., E. L. Batista, Jr., et al. (2004). "Cardiovascular disease and periodontal diseases: commonality and causation." Compend Contin Educ Dent 25(7 Suppl 1): 26-37.

ABSTRACT: Periodontal diseases have long been recognized as a public health problem. Awareness of the destructive nature of periodontal diseases and the importance of a tight control of bacterial plaque are basic concepts of periodontal treatment. In the past decade, there has been a conceptual shift from periodontal diseases as an oral problem to periodontitis having an impact on systemic health. Recent evidence suggests a strong relationship between periodontal inflammatory disease and systemic diseases, such as cardiovascular disease. It is now generally accepted that inflammation plays an important role in atherosclerosis, and factors that systemically amplify inflammation are under close investigation. This article reviews some of the emerging concepts for the inflammatory mechanisms of periodontal diseases and atherosclerosis and examines the potential role of local inflammation in systemic inflammatory disease.

Demmer, R. T. and M. Desvarieux (2006). "Periodontal infections and cardiovascular disease: the heart of the matter." J Am Dent Assoc 137 Suppl: 14S-20S; quiz 38S.

ABSTRACT: BACKGROUND: Oral infection models have emerged as useful tools to study the hypothesis that infection is a cardiovascular disease (CVD) risk factor. Periodontal infections are a leading culprit, with studies reporting associations between periodontal disease and CVD. The results, however, have varied, and it often is unclear what conclusions can be drawn from these data. SUMMARY: An association exists between periodontal disease and CVD. It is unknown, however, whether this relationship is causal or coincidental. Early studies predominantly used nonspecific clinical and radiographic definitions of periodontal disease as surrogates for infectious exposure. While most studies demonstrated positive associations between periodontal disease and CVD, not all studies were positive, and substantial variations in results were evident. More recent studies have enhanced the specificity of infectious exposure definitions by measuring systemic antibodies to selected periodontal pathogens or by directly measuring and quantifying oral microbiota from subgingival dental plaque. Results from these studies have shown positive associations between periodontal disease and CVD. CONCLUSIONS: Evidence continues to support an association among periodontal infections, atherosclerosis and vascular disease. Ongoing observational and focused pilot intervention studies may inform the design of large-scale clinical intervention studies. Recommending periodontal treatment for the prevention of atherosclerotic CVD is not warranted based on scientific evidence. Periodontal treatment must be recommended on the basis of the value of its benefits for the oral health of patients, recognizing that patients are not healthy without good oral health. However, the emergence of periodontal infections as a potential risk factor for CVD is leading to a convergence in oral and medical care that can only benefit the patients and public health.

Dennison, D. K. (1998). "Cardiovascular disease and periodontal disease." J Gt Houst Dent Soc 70(3): 12-7.

Dumitrescu, A. L. (2005). "Influence of periodontal disease on cardiovascular diseases." Rom J Intern Med 43(1-2): 9-21.

ABSTRACT: Periodontal medicine defines a rapidly emerging branch of periodontology focusing on the wealth of new data establishing a strong relationship between periodontal health or disease and systemic health or disease. The aim of this paper is to critically examine the evidence for an association between periodontal infections and cardiovascular disease. MATERIAL AND METHODS: Literature and data on periodontal diseases and their links to cardiovascular disease. Medline and Pub-Med search. Review of relevant information and data. RESULTS: There is increasing evidence that individuals with periodontal disease may be at higher risk for adverse medical outcomes, including cardiovascular disease. A number of studies to date indicate that this increased risk appears to be independent of other known behavioral and medical risk factors and also appears to be related to the severity of periodontal disease. This article evaluates the inflammatory mechanisms of periodontal disease and cardiovascular disease and examines the potential role of local inflammation in systemic inflammatory disease. CONCLUSIONS: Periodontal diseases may be risk factors for cardiovascular diseases.

Genco, R., S. Offenbacher, et al. (2002). "Periodontal disease and cardiovascular disease: epidemiology and possible mechanisms." J Am Dent Assoc 133 Suppl: 14S-22S.

ABSTRACT: BACKGROUND: Many early epidemiologic studies reported an association between periodontal disease and cardiovascular disease. However, other studies found no association or nonsignificant trends. This report summarizes the evidence from epidemiologic studies and studies that focused on potential contributing mechanisms to provide a more complete picture of the association between periodontal and heart disease. TYPES OF STUDIES REVIEWED: The authors summarize the longitudinal studies reported to date, because they represent the highest level of evidence available regarding the connection between periodontal disease and heart disease. The authors also review many of the case-control and cross-sectional studies published, as well as findings from clinical, animal and basic laboratory studies. RESULTS: The evidence suggests a moderate association--but not a causal relationship--between periodontal disease and heart disease. Results of some case-control studies indicate that subgingival periodontal pathogenic infection may be associated with myocardial infarction. Basic laboratory studies point to the biological plausibility of this association, since oral bacteria have been found in carotid atheromas and some oral bacteria may be associated with platelet aggregation, an event important for thrombosis. Animal studies have shown that atheroma formation can be enhanced by exposure to periodontal pathogens. CONCLUSIONS: The accumulation of epidemiologic, in vitro, clinical and animal evidence suggests that periodontal infection may be a contributing risk factor for heart disease. However, legitimate concerns have arisen about the nature of this relationship. These are early investigations. Since even a moderate risk contributed by periodontal disease to heart disease could contribute to significant morbidity and mortality, it is imperative that further studies be conducted to evaluate this relationship. One particularly important study to be carried out is the investigation of a possible clinically meaningful reduction in heart disease resulting from the prevention or treatment of periodontal disease.

Glurich, I., S. Grossi, et al. (2002). "Systemic inflammation in cardiovascular and periodontal disease: comparative study." Clin Diagn Lab Immunol 9(2): 425-32.

ABSTRACT: Epidemiological studies have implicated periodontal disease (PD) as a risk factor for the development of cardiovascular disease (CVD). These studies addressed the premise that local infection may perturb the levels of systemic inflammatory mediators, thereby promoting mechanisms of atherosclerosis. Levels of inflammatory mediators in the sera of subjects with only PD, only CVD, both diseases, or neither condition were compared. Subjects were assessed for levels of C-reactive protein (CRP), serum amyloid A (SAA), ceruloplasmin, alpha(1)-acid-glycoprotein (AAG), alpha(1)-antichymotrypsin (ACT), and the soluble cellular adhesion molecules sICAM-1 and sVCAM by enzyme-linked immunoabsorbent and/or radial immunodiffusion assays. CRP levels in subjects with either condition alone were elevated twofold above subjects with neither disease, whereas a threefold increase was noted in subjects with both diseases (P = 0.0389). Statistically significant increases in SAA and ACT were noted in subjects with both conditions compared to those with one or neither condition (P = 0.0162 and 0.0408, respectively). Ceruloplasmin levels were increased in subjects with only CVD (P = 0.0001). Increases in sVCAM levels were noted in all subjects with CVD (P = 0.0054). No differences in sICAM levels were noted among subject groups. A trend toward higher levels of AAG was noted in subjects with both conditions and for ACT in subjects with only PD. Immunohistochemical examination of endarterectomy specimens of carotid arteries from subjects with atherosclerosis documented SAA and CRP deposition in association with atheromatous lesions. The data support the hypothesis that localized persistent infection may influence systemic levels of inflammatory mediators. Changes in inflammatory mediator levels potentially impact inflammation-associated atherosclerotic processes.

Goldie, M. P. (2004). "C-reactive protein, cardiovascular disease, and periodontal disease." Int J Dent Hyg2(3): 139-41.

Golebiewska, M., K. Taraszkiewicz-Sulik, et al. (2006). "Periodontal condition in patients with cardiovascular diseases." Adv Med Sci 51 Suppl 1: 69-72.

ABSTRACT: The cardiovascular system diseases constitute a serious problem for modern medicine. THE AIM: To investigate the potential risk and the connection of periodontal diseases and cardiovascular disorders. MATERIAL: The examination was performed in the group of 104 patients of both sexes, aged 50-90 years. The patients were divided into two groups: group I--patients with hypertension (47 subjects), group II--patients with fresh myocardial infarction, treated with primary coronary angioplasty (57 subjects). METHODS: The OHI index, according to Greene and Vermillion, was used to assess the oral hygiene and periodontal clinical conditions were evaluated according to Russell's PI index, modified by Davies. CPI index was used to estimate the state of periodontium. Teeth loss was classified according to the Eichner's classification. RESULTS: The value of OHI index differs in both groups. Highest value was registered at 5 patients in the I group vs 2 in the II group. Lowest value was recorded in 11 patients in the I group and 4 in the II group. The value 0.0-0.2 PI was recorded at 14 persons in the I group and 11 in the II group. The value 1.6-3.8 of PI index was registered at 2 in the I group and 6 in the II group. Healthy periodontium was stated in 10 patients with hypertension and only 2 with myocardial infarction. The CPI = 2 was shown in 12 patients with hypertension and 11 with myocardial infarction, CPI = 3 was shown in 23 patients with myocardial infarction. CONCLUSION: The studies revealed bad condition of the oral cavities of patients with hypertension, and specifically with fresh myocardial infarction.

Howell, T. H., P. M. Ridker, et al. (2001). "Periodontal disease and risk of subsequent cardiovascular disease in U.S. male physicians." J Am Coll Cardiol 37(2): 445-50.

ABSTRACT: OBJECTIVES: We sought to prospectively assess whether self-reported periodontal disease is associated with subsequent risk of cardiovascular disease in a large population of male physicians. BACKGROUND: Periodontal disease, the result of a complex interplay of bacterial infection and chronic inflammation, has been suggested to be a predictor of cardiovascular disease. METHODS: Physicians' Health Study I was a randomized, double-blind, placebo-controlled trial of aspirin and beta-carotene in 22,071 U.S. male physicians. A total of 22,037 physicians provided self-reports of presence or absence of periodontal disease at study entry and were included in this analysis. RESULTS: A total of 2,653 physicians reported a personal history of periodontal disease at baseline. During an average of 12.3 years of follow-up, there were 797 nonfatal myocardial infarctions, 631 nonfatal strokes and 614 cardiovascular deaths. Thus, for each end point, the study had >90% power to detect a clinically important increased risk of 50%. In Cox proportional hazards regression analysis adjusted for age and treatment assignment, physicians who reported periodontal disease at baseline had slightly elevated, but statistically nonsignificant, relative risks (RR) of nonfatal myocardial infarction, (RR, 1.12; 95% confidence interval [CI], 0.92 to 1.36), nonfatal stroke (RR, 1.10; CI, 0.88 to 1.37) and cardiovascular death (RR, 1.20; CI, 0.97 to 1.49). Relative risk for a combined end point of all important cardiovascular events (first occurrence of nonfatal myocardial infarction, nonfatal stroke or cardiovascular death) was 1.13 (CI, 0.99 to 1.28). After adjustment for other cardiovascular risk factors, RRs were all attenuated and nonsignificant. CONCLUSIONS: These prospective data suggest that self-reported periodontal disease is not an independent predictor of subsequent cardiovascular disease in middle-aged to elderly men.

Joshipura, K. J., H. C. Wand, et al. (2004). "Periodontal disease and biomarkers related to cardiovascular disease." J Dent Res 83(2): 151-5.

ABSTRACT: Periodontal disease is a chronic infection of the gums characterized by a loss of attachment between the tooth and bone, and by bone loss. We evaluated cross-sectionally the association between periodontal disease and C-reactive protein (CRP), fibrinogen, factor VII, tissue plasminogen activator (t-PA), LDL-C, von Willebrand factor, and soluble tumor necrosis factor receptors 1 and 2. The final sample consisted of 468 men (ages 47-80 yrs), participating in the Health Professional Follow-up Study, who provided blood and were free of CVD, diabetes, and cancer. In multivariate regression models controlling for age, cigarette smoking, alcohol intake, physical activity, and aspirin intake, self-reported periodontal disease was associated with significantly higher levels of CRP (30% higher among periodontal cases compared with non-cases), t-PA (11% higher), and LDL-C (11% higher). Based on our data, periodontal disease showed significant associations with biomarkers of endothelial dysfunction and dyslipidemia, which may potentially mediate the association between periodontal and cardiovascular disease.

Katz, J., G. Chaushu, et al. (2001). "On the association between hypercholesterolemia, cardiovascular disease and severe periodontal disease." J Clin Periodontol 28(9): 865-8.

ABSTRACT: BACKGROUND: Premature death in men is known to be significantly associated with coronary heart disease (CHD). More and more studies are pointing toward a possible association between periodontal disease and increased risk of cardiovascular disease. The association of poor oral hygiene and atherosclerosis can be explained by the effect of chronic inflammatory disease on blood rheology. The purpose of the present study was to assess the relationship between CHD and periodontal disease. PATIENTS AND METHODS: The study population included 1094 Israeli army service men aged 26-53 years (mean: 39+/-5 years). The study group comprised 151 subjects classified as having coronary heart disease CHD, i.e., myocardial infarction, and or anginal syndrome with angiographic evidence of significant coronary disease, or suffer from atherosclerotic risk factors, i.e., diabetes (fasting glucose) and HTN according to strict, well-established criteria. Blood levels of cholesterol and triglycerides were also determined. The severity of periodontal disease was assessed by the aid of CPITN. The control group comprised 943 healthy subjects. Statistical analysis was performed with chi2 test. RESULTS: Statistical analysis showed a significant association of CPITN score 4 with hypercholesterolemia and a possible association with CHD. CONCLUSIONS: The generation of higher cholesterol blood levels is proposed as a possible link between chronic periodontal inflammation and atherosclerosis.

Kinane, D. F. (1998). "Periodontal diseases' contributions to cardiovascular disease: an overview of potential mechanisms." Ann Periodontol 3(1): 142-50.

ABSTRACT: Periodontitis and atherosclerosis have complex etiologies, genetic and gender predispositions, and potentially share many risk factors-the most significant of which may be smoking status. These diseases also have many pathogenic mechanisms in common. It is becoming increasingly clear that infections and chronic inflammatory conditions such as periodontitis may influence the atherosclerotic process. The severity and chronicity of periodontal disease provides a rich source of subgingival microbial and host response products and effects over a long time period. The objective of this review is to consider the mechanisms whereby diseases such as periodontitis, which is chronic and Inflammatory In nature and initiated by microbial plaque, can predispose to atherosclerosis. In common with periodontal disease. the pathogenesis of atherosclerosis is not completely understood and both diseases are currently under Intensive investigation. Two main processes in particular are worthy of consideration and may provide the link between these 2 diseases, namely the lipopolysaccharide-related responses and the hyperresponsive monocyte phenomenon. Insufficient experimental evidence exists, however, to further support these hypotheses at present and clearly more research is needed on both of these processes and the interrelationships between both diseases.

Kinane, D. F. and G. D. Lowe (2000). "How periodontal disease may contribute to cardiovascular disease." Periodontol 2000 23: 121-6.

Klinger, A., M. Goldstein, et al. (2002). "[Periodontal disease--an additional risk factor for cardiovascular diseases?]." Refuat Hapeh Vehashinayim 19(2): 67-74, 79.

ABSTRACT: In 1989, a case-control study was published, linking between coronary heart disease and periodontal disease in the studied population. Since then, a number of additional studies, focused the attention to the possible role of dental infections in the pathogenesis of atherosclerosis. Some of these newer cohort studies, are prospective in nature, measuring incidence of the two diseases in large patient populations. The present article reviews these studies, and the proposed mechanisms which might explain the relationships between these two systemically distinct diseases.

Kornman, K. S. and G. W. Duff (2001). "Candidate genes as potential links between periodontal and cardiovascular diseases." Ann Periodontol 6(1): 48-57.

ABSTRACT: Recent epidemiological associations between periodontal disease and cardiovascular disease have led to a search for biological mechanisms that explain the associations. Genetic factors that influence biological processes involved in both diseases represent one of the potential mechanisms that may link periodontitis and cardiovascular disease. At present, several candidate genes have been investigated in one of the diseases but not the other. Although there are limited data to support a specific candidate gene as the explanation for observed associations between the 2 diseases, a few candidates look promising. One candidate that influences inflammation, interleukin-1 gene polymorphisms, has been associated with periodontal disease and cardiovascular disease. This review will consider biological mechanisms and genes that may be reasonable candidates for an etiological mechanism that influences the clinical characteristics of both periodontal disease and cardiovascular disease.

Kuramitsu, H. K., M. Qi, et al. (2001). "Role for periodontal bacteria in cardiovascular diseases." Ann Periodontol 6(1): 41-7.

ABSTRACT: BACKGROUND: Several epidemiological studies as well as a recent animal model approach have suggested a role for periodontal diseases in the development of cardiovascular disease (CVD). This relationship could be mediated by inflammatory responses induced by periodontal pathogens as well as direct interaction of these organisms with cardiac tissue. METHODS: In order to explore these possibilities, the effects of the periodontal pathogen Porphyromonas gingivalis on cellular events proposed to play a role in CVD were investigated. RESULTS: P. gingivalis, as well as its outer membrane vesicles (OMV), was able to induce foam cell formation (an important characteristic of CVD) in the murine macrophage cell line J774 A.1. This property appears to be mediated by the lipopolysaccharide (LPS) fraction of the cells. Several other oral bacteria were also able to induce foam cell formation. Furthermore, since the rupture of the fibrous cap of plaque appears to be an important factor in acute coronary syndrome, it was demonstrated that P. gingivalis 381 degraded fibrous caps isolated from autopsy samples. In addition, it was observed that strain 381 strongly induced matrix metalloproteinase (MMP)-9 protease activity, implicated in plaque rupture, from the J774 A.1 macrophages. Finally, strain 381 was able to enhance monocyte chemoattractant protein-1 (MCP-1) and NADH oxidase expression from endothelial cells. CONCLUSIONS: Therefore, P. gingivalis exhibits several properties which could play a role in CVD as mediators of LDL oxidation, foam cell formation, and rupture of atherosclerotic plaque.

Loesche, W. J. (2000). "Periodontal disease: link to cardiovascular disease." Compend Contin Educ Dent21(6): 463-6, 468, 470 passim; quiz 484.

ABSTRACT: Poor oral hygiene that leads to dental infections could contribute to adverse medical outcomes such as cardiovascular disease. Twelve studies of varying degrees of design rigor have associated dental conditions, such as periodontal disease, missing teeth, and edentulousness, with either coronary heart disease or a cerebral vascular accident. Six of the studies were longitudinal so that the demonstration of the oral health parameters as significant predictors of the cardiovascular event would elevate the dental parameter to the status of a risk factor. Because dental diseases (especially periodontal disease) are treatable, the dental component is a modifiable risk factor; therefore, maintaining good oral health should receive the highest priority for a healthy life.

Loesche, W. J. (2000). "Periodontal infection a risk factor for cardiovascular disease?" Postgrad Med107(5): 17, 20.

Losche, W. (2007). "Periodontitis and cardiovascular disease: periodontal treatment lowers plasma cholesterol." South Med J 100(7): 663-4.

Nesse, W., F. K. Spijkervet, et al. (2006). "[Links between periodontal disease and general health. 1. Pneumonia and cardiovascular disease]." Ned Tijdschr Tandheelkd 113(5): 186-90.

ABSTRACT: The possible link between oral and general health is based on an old concept. This paper summarizes current ideas on the role of translocation of oral pathogens to other parts of the body in the development of systemic disease. It appears that colonisation of the oral cavity by respiratory pathogens is a risk factor in the development of pneumonia in institutionalised elderly and intensive care patients. Using a chloorhexidine oral rinse may reduce the risk of pneumonia. Furthermore, periodontal disease is associated with an increased risk of cardiovascular disease. Translocation of oral microorganisms and an increase in serum concentrations of inflammatory mediators are considered to play a role in the development of cardiovascular disease. Potentially, preventive oral health care and periodontal intervention could play a part in preventing cardiovascular disease.

Paquette, D. W. (2004). "The periodontal-cardiovascular link." Compend Contin Educ Dent 25(9): 681-2, 685-92; quiz 694.

ABSTRACT: Cardiovascular disease (CVD) and periodontitis are common chronic conditions, and the former remains a major contributor to human mortality. Recent attention has focused on a potential link between periodontal disease and CVD. Observational studies consistently indicate that people with destructive periodontitis may be 1.3 to 2 times more likely to have CVD. This association appears to be biologically plausible, and investigations in atherosclerosis animal models demonstrate larger atheroma sizes in animals infected with the periodontal pathogen, Porphyromonas gingivalis, compared with control animals. Although direct intervention data on the effects of periodontal therapy on CVD risk in patients are not currently available, indirect data suggest that mechanical periodontal therapy can decrease surrogate cardiovascular markers such as serum C-reactive protein. After a recent systematic review on the periodontal-cardiovascular link, a consensus panel concluded that patients and clinicians should be informed that periodontal therapy may prevent the onset or progression of CVD.

Paquette, D. W., N. Brodala, et al. (2007). "Cardiovascular disease, inflammation, and periodontal infection." Periodontol 2000 44: 113-26.

Persson, R. E., L. G. Hollender, et al. (2002). "Assessment of periodontal conditions and systemic disease in older subjects. II. Focus on cardiovascular diseases." J Clin Periodontol 29(9): 803-10.

ABSTRACT: BACKGROUND: Panoramic radiographs (PMX)s may provide information about systemic health conditions. AIMS: i). To study clinical periodontal conditions and collect self-reported health status in a cohort of 1084 older subjects; ii). to study signs of alveolar bone loss and carotid calcification from panoramic radiographs obtained from these subjects; and iii). to study associations between study parameters. MATERIAL AND METHODS: PMXs from 1064 adults aged 60-75 (mean age 67.6, SD +/- 4.7) were studied. Signs of alveolar bone loss, vertical defects, and molar furcation radiolucencies defined periodontal status. Medical health histories were obtained via self-reports. Signs of carotid calcification were identified from panoramic radiographs. RESULTS: The PMX allowed assessment of 53% of the films (Seattle 64.5% and Vancouver 48.4%). A self-reported history of a stroke was reported by 8.1% of men in Seattle and 2.9% of men in Vancouver (P < 0.01). Heart attacks were reported by 12% of men in Seattle and 7.2% in Vancouver (N.S.). PMX evidence of periodontitis was found in 48.5% of the subjects, with carotid calcification in 18.6%. The intraclass correlation score for PMX findings of carotid calcification and stroke was 0.24 (95% CI: 0.10-0.35, P < 0.001). The odds ratio for PMX carotid calcification and periodontitis was 2.1 (95% CI: 1.3-3.2, P < 0.001), and for PMX carotid calcification and stroke 4.2 (95% CI: 1.9-9.1, P < 0.001). The associations disappeared when smoking was accounted for. A history of a heart attack was associated with stroke, gender, age, and PMX scores of alveolar bone loss. CONCLUSIONS: PMXs may provide valuable information about both oral conditions and signs of carotid calcification, data that are consistent with self-reported health conditions. Alveolar bone loss as assessed from PMXs is associated with cardiovascular diseases.

Pinero, J. (1998). "Nd:YAG-assisted periodontal curettage to prevent bacteria before cardiovascular surgery." Dent Today 17(3): 84-7.

Pussinen, P. J., K. Tuomisto, et al. (2007). "Endotoxemia, immune response to periodontal pathogens, and systemic inflammation associate with incident cardiovascular disease events." Arterioscler Thromb Vasc Biol 27(6): 1433-9.

ABSTRACT: OBJECTIVE: In periodontitis, overgrowth of gram-negative bacteria may cause endotoxemia and systemic inflammation leading to cardiovascular diseases (CVD). We investigated in a prospective study the associations of serum endotoxin, antibodies to periodontal pathogens, and inflammation markers with the risk of incident CVD. METHODS AND RESULTS: The FINRISK 1992 cohort of 6051 individuals was followed up for 10 years. We examined 185 incident CVD events and a control cohort of 320 individuals using a prospective case-cohort design. High antibody response to periodontal pathogens independently predicted incident CVD events with hazard ratios (HR, quartile 4 versus quartiles 1 to 3, 95% CI) of 1.87 (1.13 to 3.08). The subjects with a high antibody response and high CRP or interleukin (IL)-6 had multivariate-adjusted HRs of 3.01 (1.27 to 7.09) and 3.11 (1.42 to 6.83) compared with low-responders, respectively. The corresponding HRs for high endotoxin concentration were 1.82 (1.22 to 2.73, alone), 3.92 (1.99 to 7.74, with CRP), 3.54 (1.78 to 7.03, with IL-6), and 2.26 (1.13 to 4.52, with tumor necrosis factor (TNF)-alpha) after adjusting for age and gender. These associations were abolished after adjusting for serum lipids. High endotoxin/HDL ratio, however, had a multivariate-adjusted HR of 1.92 (1.19 to 3.08) for CVD events. CONCLUSIONS: Our results suggest that the exposure to periodontal pathogens or endotoxin induces systemic inflammation leading to increased risk for CVD.

Renvert, S. (2003). "Destructive periodontal disease in relation to diabetes mellitus, cardiovascular diseases, osteoporosis and respiratory diseases." Oral Health Prev Dent 1 Suppl 1: 341-57; discussison 358-9.

Scannapieco, F. A., R. B. Bush, et al. (2003). "Associations between periodontal disease and risk for atherosclerosis, cardiovascular disease, and stroke. A systematic review." Ann Periodontol 8(1): 38-53.

ABSTRACT: BACKGROUND: Recent studies implicate exposure to systemic conditions involving chronic inflammation, including chronic periodontitis, in the etiology of atherosclerosis. RATIONALE: A systematic review of the literature was conducted to assess the association between chronic inflammatory periodontal disease and atherosclerosis. FOCUSED QUESTION: Does periodontal disease influence the initiation/progression of atherosclerosis and, therefore, cardiovascular disease (CVD), stroke, and peripheral vascular disease (PVD)? SEARCH PROTOCOL: MEDLINE, pre-MEDLINE, MEDLINE Daily Update, and the Cochrane Controlled Trials Register were searched to identify human studies that related variables associated with atherosclerosis to periodontal disease. Searches were made for papers published from 1966 through March 2002. INCLUSION CRITERIA: Published randomized controlled clinical trials (RCTs), longitudinal, cohort, and case-control studies were included. Study participants included those with atherosclerosis, myocardial infarction (MI), stroke, or PVD. Oral conditions included periodontal disease. EXCLUSION CRITERIA: Only studies on humans were included. DATA COLLECTION AND ANALYSIS: Because the studies used different oral assessment measures, it was not possible to perform a meta-analysis of the data reported. Weighted mean differences, relative risks, or odds ratios were compared for cohort studies. MAIN RESULTS: 1. Of the initial 1,526 studies identified, 31 (including 8 case-control and 18 cross-sectional reports) were included in the analysis. Taken together, most of the literature supports a modest association between periodontal disease and atherosclerosis. However, data reported in several studies do not show this association. 2. The absence of a standard definition and measures for periodontal disease complicates interpretation of results, as do potential confounding risk factors common to both conditions. REVIEWERS' CONCLUSIONS: 1. Periodontal disease may be modestly associated with atherosclerosis, MI, and CVD. 2. Additional large-scale longitudinal epidemiologic and intervention studies are necessary to validate this association and to determine causality.

Stanford, T. W., Jr. (2005). "Periodontal disease and cardiovascular disease: is there an association?" Tex Dent J 122(12): 1198-201.

Stein, H. (1999). "Periodontal disease as a risk factor for cardiovascular disease and myocardial infarction." Ont Dent 76(1): 16-20.

Taylor, B. A. and G. H. Tofler (2002). "Evidence for an association between periodontal disease and cardiovascular disease." Ann R Australas Coll Dent Surg 16: 82-3.

Vettore, M. V. (2004). "Periodontal disease and cardiovascular disease." Evid Based Dent 5(3): 69.

Vilkuna-Rautiainen, T., P. J. Pussinen, et al. (2006). "Serum antibody response to periodontal pathogens and herpes simplex virus in relation to classic risk factors of cardiovascular disease." Int J Epidemiol35(6): 1486-94.

ABSTRACT: BACKGROUND: Increasing evidence links chronic infections, especially burden of several infections, with increased risk for cardiovascular diseases (CVD). We studied joint immune response against two major periodontal pathogens and herpes simplex virus (HSV) in relation to established risk factors of CVD. METHODS: Serum antibody levels to HSV, Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis were determined by ELISA. The study included 1107 subjects, 734 from Finland and 373 from Russia. RESULTS: Combined antibody response to periodontal pathogens was associated inversely (OR, 95% CI) with high-density lipoprotein (HDL) cholesterol concentration (beta = 0.35; 0.20, 0.60; P < 0.001) and directly with HSV antibody quartiles: compared with the first quartile, ORs (95% CI) for quartiles 2-4 were 1.43 (0.88-2.32), 1.74 (1.07-2.82), and 1.89 (1.18-3.02), respectively (P for trend <0.001), after adjusting for age, gender, area, education, smoking, BMI, alcohol, triglycerides, and number of teeth. In linear regression analysis, the 3-pathogen antibody score (comprising antibody levels against periodontal pathogens and HSV) was inversely associated with HDL cholesterol concentration (beta = -0.067/1 mmol/l; -0.235, -0.018; P < 0.05). CONCLUSIONS: HSV infection may promote infection by periodontal pathogens. Furthermore, the infectious burden comprising HSV and periodontitis may increase the risk for CVD by clearly decreasing HDL cholesterol concentrations.

Willershausen, B., T. Krahwinkel, et al. (2003). "Correlation between inflammatory periodontal diseases and cardiovascular diseases." Eur J Med Res 8(11): 499-504.

ABSTRACT: AIMS: Since cardiovascular diseases can exhibit a possible connection with chronic periodontal diseases, the aim of the present study was to examine the presence of periodontal impairment in patients with coronary heart diseases (CHD). METHODS: For this purpose periodontal charts were raised for 101 patients (78 male, 23 female, mean age 61.8 +/- 10.5 years) with cardiovascular diseases; comparison was drawn between theses charts and those for a control group of 101 healthy patients (59 male, 42 female, mean age 56.6 +/- 9.9 years). Over and above the dental diagnosis (probing depth [mm], vitality, tooth mobility, plaque index (PI), inclination towards sulcus bleeding) each related to 6 characteristic teeth, various habitual aspects (diet, smoke and drink patterns, stress, body weight) were recorded. RESULTS: Within the CHD-group the periodontal chart revealed for all teeth examined a mean probing depth of 3.4 +/- 1.1mm, with the corresponding reading for the control group being 2.8 +/- 0.9 mm. The mean bleeding index (Van-der-Weiden) read 1.1 +/- 0.7 for the CHD-group and 0.7 +/- 0.6 for the control group. The mean plaque index reading was 1.4 +/- 0.9 for the group suffering from heart diseases and 0.7 +/- 0.8 for the control group. Comparison of these periodontal charts showed statistically significant differences (p<= 0.01), whereas mean degrees of tooth mobility did not differ in a statistically significant way. In summary, the results described hint at a correlation between an existent coronary heart disease and the presence of a periodontitis. CONCLUSION: However, also for consideration below are further influential factors, such as diet, individual life conduct, smoking habits, Body-Mass-Index or microbiological aspects.

Wu, T., M. Trevisan, et al. (2000). "Examination of the relation between periodontal health status and cardiovascular risk factors: serum total and high density lipoprotein cholesterol, C-reactive protein, and plasma fibrinogen." Am J Epidemiol 151(3): 273-82.

ABSTRACT: Using data from the Third National Health and Nutrition Examination Survey (1988-1994), the authors examined the relation between periodontal health and cardiovascular risk factors: serum total and high density lipoprotein cholesterol, C-reactive protein, and plasma fibrinogen. A total of 10,146 participants were included in the analyses of cholesterol and C-reactive protein and 4,461 in the analyses of fibrinogen. Periodontal health indicators included the gingival bleeding index, calculus index, and periodontal disease status (defined by pocket depth and attachment loss). While cholesterol and fibrinogen were analyzed as continuous variables, C-reactive protein was dichotomized into two levels. The results show a significant relation between indicators of poor periodontal status and increased C-reactive protein and fibrinogen. The association between periodontal status and total cholesterol level is much weaker. No consistent association between periodontal status and high density lipoprotein cholesterol was detectable. Similar patterns of association were observed for participants aged 17-54 years and those 55 years and older. In conclusion, this study suggests that total cholesterol, C-reactive protein, and fibrinogen are possible intermediate factors that may link periodontal disease to elevated cardiovascular risk.