Enroll Now. Search Search. The link between gum disease and heart disease Posted on February 6, in General oral health Heart disease is a leading cause of death in the United States, and studies show a relationship between heart disease and gum disease. Oral bacteria may be the link to heart disease The main cause of gum disease is harmful oral bacteria found in tooth plaque and tartar. Smoking is strongly associated with gum disease, it weakens the immune system which makes it harder to fight any infections.
Floss at least once daily. These molecules can be shed from the cell surface and soluble forms are markers of endothelial activation. In relation to the systemic inflammation model it is hypothesized that cytokines and inflammatory mediators produced in periodontal disease act systemically to promote systemic disease.
In addition, the release of bacteria and bacterial by-products such as LPS into the circulation may also trigger a systemic inflammatory response. Increased levels of circulating cytokines can activate vascular endothelial cells, ultimately leading to the development of atherosclerosis.
In addition to activating inflammatory cells, bacterial LPS may trigger and enhance atherosclerosis by increasing oxidative stress and modifying lipid metabolism A number of studies showed that patients with severe periodontitis have increased levels of systemic inflammatory markers IL-6, CRP, haptoglobin, and leukocytosis — In addition, periodontitis patients were also found to exhibit dyslipidemia and endothelial dysfunction as assessed by flow-mediated dilatation of the brachial artery Periodontal intervention studies have been implemented to further investigate the contribution of periodontal infection to systemic markers of inflammation and vascular health.
In the long-term, endothelial function improves and is evident up to 6 months post-therapy , The long-term effects of periodontal therapy in relation to systemic cytokine levels are inconsistent among studies, especially with regard to the cytokines affected and the time frame at which the effect was observed.
While Buhlin et al. In contrast, periodontitis patients receiving intensive periodontal therapy standard periodontal therapy plus local administration of minocycline had significant reductions in IL-6, CRP, lipid markers, and systolic blood pressure SBP 2 months post-therapy compared with patients who received standard therapy alone. In addition, patients receiving intensive periodontal therapy also displayed reductions in Framingham CV-risk scores 2 and 6 months following therapy In patients with hypertension followed for 3 months, non-surgical periodontal therapy resulted in reduced levels of CRP, IL-6, and fibrinogen Tonetti et al.
Periodontal therapy, including surgery, reduced levels of vascular health PAI-1, sE-selectin, sVCAM-1, MMP-9, and myeloidperoxidase in patients with periodontitis; however, only reduced levels of sE-selectin were maintained 1 month after the completion of the periodontal therapy regime A summary inflammation score used to assess the systemic inflammatory burden of each patient indicated that there was a high degree of patient variability in the systemic inflammatory response to therapy.
The apparent patient variability in systemic inflammation may be due to host genetic factors. Another marker of chronic inflammation is anemia. Anemia of chronic diseases ACD , as it is otherwise known, is a cytokine-mediated anemia that is characterized by impaired mobilization of iron from reticuloendothelial stores, reduced red blood cell survival, and impaired erythropoiesis.
Periodontal infections have been associated with anemia of chronic inflammation. Periodontitis patients have been shown to exhibit an anemic state as indicated by reduced hematocrit levels, decreased erythrocyte numbers, and reduced hemoglobin levels , Intervention studies have further supported this association demonstrating that non-surgical periodontal therapy can result in significant increases in hemoglobin and hematocrit levels within treatment groups as well as compared with control patients who received no periodontal therapy While there are inconsistencies among studies, the general trend is that periodontal therapy can improve systemic markers of inflammation and vascular health; however, the long-term effects of this with regards to CV events remain unknown.
It is difficult to interpret the results of the intervention studies due to differences in periodontal therapy including duration , time frame at which samples were assessed, and the exclusion of control, non-intervention, groups in some studies.
A recent meta-analysis of six studies investigating the effects of periodontal therapy on CRP has provided further insight into the strength of the relationship, and concluded a modest association between periodontal therapy and reduced levels of CRP The reduction in inflammatory markers after periodontal therapy provides evidence that the elevated levels of systemic inflammation were due to periodontal disease rather than other inflammatory conditions and supports the hypothesis that periodontal inflammation may add to the systemic inflammatory burden of affected individuals.
There is increasing evidence that immune responses may also be involved in the progression of atherosclerosis One mechanism in which infection may initiate and facilitate the progression of atherosclerotic lesions can be explained in terms of the immune response to bacterial HSPs, termed GroEL HSPs are expressed by prokaryotic and eukaryotic cells in response to various forms of stress temperature, mechanical stress, infection, and oxygen radicals During infection, bacterial HSPs are highly immunogenic Due to the homologous nature of HSPs across species, the immune system may not be able to differentiate between host and bacterial HSPs.
As a result of this molecular mimicry, there may be cross-reactivity of the immune response to bacterial HSPs with HSPs expressed by stressed endothelial cells leading to endothelial dysfunction and subsequent development of atherosclerosis The presence of CV-risk factors such as hypertension and hypercholesterolemia would enhance the expression of hHSP60 and adhesion molecules by endothelial cells and result in progression from early fatty streak lesions to more severe and irreversible atherosclerotic alterations.
Supporting this, Perschinka et al. Elevated levels of antibodies to hHSP60 have been associated with the presence and severity of coronary artery disease and atherosclerosis In particular, Metzler et al.
These antibodies were cross-reactive with other bacterial HSPs and were able to lyse stressed — but not unstressed — endothelial cells Elevated anti-hHSP60 levels have also been found in patients with carotid stiffness , borderline hypertension, and have been associated with early atherosclerosis The mechanism by which antibodies to self-antigens, such as hHSP60, are generated is unclear. It is currently proposed that anti-hHSP60 antibodies could represent a cross-reactive host immune response to bacterial HSPs in susceptible individuals or result from a primary immune response to altered self-HSP60 expression The GroEL proteins are major antigens in several pathogenic bacterial GroEL proteins and homologues have been identified in several oral bacteria including P.
GroEL from P. Patients with periodontal disease have been shown to have a higher antibody response to hHSP60 and P. In addition, these antibodies were cross-reactive with P. Previous studies have demonstrated the presence and cross-reactivity of hHSP60, P. Furthermore, antibodies to P. In an intervention study, Yamazaki et al. Similarly, Buhlin et al. Murine models of atherosclerosis have also provided evidence for the role of HSP immunity in atherosclerosis.
This is supported by an intervention study that demonstrated protection from atherosclerosis following oral tolerance to HSP60 In addition, Ford et al. There is clear evidence of an epidemiological association between oral infections and CVD and in vitro and in vivo mechanistic studies have established a plausible link between oral bacteria and atherosclerosis. The interactions between oral bacteria and CVD are extremely complex and it's highly likely that more than one mechanism is involved.
Recent studies provide strong support for the roles of systemic inflammation and immune cross-reactivity in atherogenesis. Furthermore, intervention studies have demonstrated that periodontal therapy can reduce systemic markers of inflammation and vascular health as well as antibody responses to heat shock proteins.
Future studies are now required to determine the long-term effects of periodontal therapy on CVD outcomes. Nevertheless, a recent consensus report on periodontitis and atherosclerotic CVD, published in the American Journal of Cardiology and the Journal of Periodontology , has recommended that patients with moderate to severe periodontitis should be informed of a possible increased risk of CVD and those with more than one CV-risk factor should undergo a medical evaluation of CV-risk.
There is no conflict of interest in the present study for any of the authors. National Center for Biotechnology Information , U. Journal List J Oral Microbiol v. J Oral Microbiol. Published online Dec Shaneen J. Ford 1. Pauline J. Author information Copyright and License information Disclaimer.
Email: ua. Leishman et al. This article has been cited by other articles in PMC. Abstract In terms of the pathogenesis of cardiovascular disease CVD the focus has traditionally been on dyslipidemia. Keywords: oral bacteria, cardiovascular disease, systemic inflammation, cross-reactivity, heat shock proteins.
Host—bacterial interactions in periodontal disease P. Proteases Proteases cleave peptide bonds and are characterized according to their catalytic activity. Fimbriae Fimbriae are hair-like protein structures protruding from the cell surface of bacteria, particularly Gram-negative bacteria. Leukotoxins Leukotoxins are a group of exotoxins that have primary toxic effects against leukocytes, particularly polymorphonuclear cells PMNs.
Capsule Capsules protect bacteria from phagocytosis, aid in cell attachment, and subsequent biofilm formation. Current evidence for the role of oral bacteria in cardiovascular disease CVD While many studies have shown an association between oral infection and CVD, the relationship remains to be established as a causal one. Direct arterial infection It is hypothesized that transient bacteremia during periodontal infection may lead to direct bacterial invasion of endothelial cells.
Platelet aggregation There is increasing evidence that oral bacteria interact with platelets. Systemic inflammation Currently there is strong evidence to support the role of systemic inflammation in the development and progression of atherosclerosis. Cross-reactivity There is increasing evidence that immune responses may also be involved in the progression of atherosclerosis Conclusion There is clear evidence of an epidemiological association between oral infections and CVD and in vitro and in vivo mechanistic studies have established a plausible link between oral bacteria and atherosclerosis.
Conflict of interest and funding There is no conflict of interest in the present study for any of the authors. References 1. Ross R. Atherosclerosis is an inflammatory disease. Am Heart J. Queensland burden of disease and injury circular series 1, no 1. Brisbane: Queensland health; Overview of the burden of disease and injury in Queensland, Crouse JR.
Progress in coronary artery disease risk factor research: what remains to be done? Clin Chem. Consensus report for periodontal diseases: pathogenesis and microbial factors. Ann Periodontol. Papapanou PN. Periodontal diseases: epidemiology. Dental infections and coronary atherosclerosis. Dental disease and risk of coronary heart disease and mortality. Valtonen VV. Role of infections in atherosclerosis.
Relationship of periodontal disease to carotid artery intima-media wall thickness: the atherosclerosis risk in communities ARIC study. Arterioscler Thromb Vasc Biol. Periodontal destruction is associated with coronary artery disease and periodontal infection with acute coronary syndrome.
J Periodontol. Poor oral health and coronary heart disease. J Dent Res. Periodontal disease and cardiovascular disease. Pre-existing cardiovascular disease and periodontitis: a follow up study. The prevalence and incidence of coronary heart disease is significantly increased in periodontitis: a meta-analysis. Markers of systemic bacterial exposure in periodontal disease and cardiovascular disease risk: a systematic review and meta-analysis. Periodontal disease and coronary heart disease incidence: a systematic review and meta-analysis.
J Gen Intern Med. Porphyromonas gingivalis infection accelerates the progression of atherosclerosis in a heterozygous apolipoprotein E-deficient murine model. Oral infection with a periodontal pathogen accelerates early atherosclerosis in apolipoprotein E-null mice. Anti- P. J Clin Periodontol. Rosan B, Lamont RJ. Dental plaque formation.
This content does not have an English version. This content does not have an Arabic version. See more conditions. Request Appointment. Healthy Lifestyle Adult health. Products and services. Free E-newsletter Subscribe to Housecall Our general interest e-newsletter keeps you up to date on a wide variety of health topics.
Sign up now. Will taking care of my teeth help prevent heart disease? Answer From Thomas J. Salinas, D. Show references Mathews MJ, et al. Oral health and coronary artery disease. Stand by for more studies on the link between oral health and overall health. Until then, keep brushing, flossing and seeing your dentist. Robert H. He is also the program director of the Rheumatology Fellowship.
0コメント