Dental Disease, Coronary Heart Disease and Stroke, and Inflammatory Markers

Lowe, G. D. O.

doi:10.1161/01.cir.0000118643.41559.e2

Cited by 21 publications

(9 citation statements)

References 19 publications

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“…If this ultimately turns out to be the case, such a finding could open new prospects for prevention. Meanwhile, we agree with Lowe (2004) who, in his recent comment paper in the American Heart Association journal Circulation, states that the answer to the question, "Should dental health scores be used in addition to classical risk factors to predict an individual's risk of CHD and stroke?" simply is, "We do not know."…”

Section: (Ix) Conclusionmentioning

confidence: 54%

Oral Health, Atherosclerosis, and Cardiovascular Disease

Meurman

Sanz

Janket

2004

Critical Reviews in Oral Biology & Medicine

315

233

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During the last two decades, there has been an increasing interest in the impact of oral health on atherosclerosis and subsequent cardiovascular disease (CVD). The advent of the inflammation paradigm in coronary pathogenesis stimulated research in chronic infections caused by a variety of micro-organisms-such as Chlamydia pneumoniae, Helicobacter pylori, and cytomegalovirus-as well as dental pathogens, since these chronic infections are thought to be involved in the etiopathogenesis of CVD by releasing cytokines and other pro-inflammatory mediators (e.g., C-reactive protein [CRP], tumor necrosis factor [TNF-␣]) that may initiate a cascade of biochemical reactions and cause endothelial damage and facilitate cholesterol plaque attachment. Yet, due to the multi-factorial nature of dental infection and CVD, confirming a causal association is difficult, and the published results are conflicting. The main deficit in the majority of these studies has been the inadequate control of numerous confounding factors, leading to an overestimation and the imprecise measurement of the predictor or overadjustment of the confounding variables, resulting in underestimation of the risks. A meta-analysis of prospective and retrospective followup studies has shown that periodontal disease may increase the risk of CVD by approximately 20% (95% confidence interval [CI], 1.08-1.32). Similarly, the reported risk ratio between periodontal disease and stroke is even stronger, varying from 2.85 (CI 1.78-4.56) to 1.74 (CI 1.08-2.81). The association between peripheral vascular disease and oral health parameters has been explored in only two studies, and the resultant relative risks among individuals with periodontitis were 1.41 (CI 1.12-1.77) and 2.27 (CI 1.32-3.90), respectively. Overall, it appears that periodontal disease may indeed contribute to the pathogenesis of cardiovascular disease, although the statistical effect size is small.

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Section: (Ix) Conclusionmentioning

confidence: 54%

Oral Health, Atherosclerosis, and Cardiovascular Disease

Meurman

Sanz

Janket

2004

Critical Reviews in Oral Biology & Medicine

315

233

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“…There is a link established between periodontal disease and atherosclerosis (34–36). Periodontopathic bacteria have been isolated from atherosclerotic plaques (37).…”

Section: Discussionmentioning

confidence: 99%

Coordinate Stimulation of Macrophages by Microparticles and TLR Ligands Induces Foam Cell Formation

Keyel

Tkacheva

Larregina

et al. 2012

The Journal of Immunology

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Aberrant activation of macrophages in arterial walls by oxidized lipoproteins can lead to atherosclerosis. Oxidized lipoproteins convert macrophages to foam cells through lipid uptake and TLR signaling. To investigate the relative contributions of lipid uptake and TLR signaling in foam cell formation, we established an in vitro assay utilizing liposomes of defined lipid compositions. We found that TLRs signaling through Trif promoted foam cell formation by inducing both NF-KB signaling and Type I IFN production, whereas TLRs that do not induce IFN, like TLR2, did not enhance foam cell formation. Addition of IFNα to TLR2 activator promoted robust foam cell formation. TLR signaling further required PPARα, as inhibition of PPARα blocked foam cell formation. We then investigated the ability of endogenous microparticles (MP) to contribute to foam cell formation. We found that lipid containing MP promoted foam cell formation, which was enhanced by TLR stimulation or IFNα. These MP also stimulated foam cell formation in a human skin model. However, these MP suppressed TNFα production and T cell activation, showing that foam cell formation can occur by immunosuppressive microparticles. Taken together, the data reveal novel signaling requirements for foam cell formation and suggest that uptake of distinct types of MP in the context of activation of multiple distinct TLR can induce foam cell formation.

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“…Recent large trials of azithromycin in prevention of recurrent CV events after myocardial infarction were negative [74], which argues against a role for such infections in pathogenesis. Chronic dental infections (and their consequences such as tooth loss) have also been associated with increased circulating inflammatory markers and with risk of CVD; while a causal role is unproven, these common infections may also confound the relationships of inflammatory markers to CVD risk [75].…”

Section: Associations Of Circulating Inflammatory Markers With Cvd Rimentioning

confidence: 99%

Circulating inflammatory markers and risks of cardiovascular and non‐cardiovascular disease

Lowe

2005

Journal of Thrombosis and Haemostasis

179

148

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To cite this article: Lowe GDO. Circulating inflammatory markers and risks of cardiovascular and non-cardiovascular disease. J Thromb Haemost 2005; 3: 1618-27.Summary. There is current interest in the associations of circulating inflammatory markers (C-reactive protein, fibrinogen, white cell count, albumin, erythrocyte sedimentation rate, the factor VIII:von Willebrand factor complex, the tissue plasminogen activator:plasminogen activator inhibitor type 1 complex, fibrin D-dimer) not only with prognosis in acute coronary syndromes and acute stroke, but also in prediction of cardiovascular events in the general population. Recent meta-analyses of long-term prospective studies have established their associations with coronary heart disease (CHD) events, which may be cause, consequence or coincidence. These markers are also associated in epidemiologic studies of general populations with many cardiovascular risk factors (which may confound their associations with CHD risk), and also with asymptomatic arterial disease (of which they be consequences: Ôreverse causalityÕ). The causality of their associations with cardiovascular events is questioned by their lack of specificity for risk of cardiovascular events; and by the lack of association of their functional genotypes with CHD in ÔMendelian randomized trialsÕ. Hence, proof of causality awaits testing in randomized-controlled trials of long-term selective reduction by future agents. Markers are of little additional predictive value to current cardiovascular risk scores, and it is premature to advocate their use in screening for cardiovascular risk prior to careful evaluation of costs, risks, and benefits.

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Dental Disease, Coronary Heart Disease and Stroke, and Inflammatory Markers

Cited by 21 publications

References 19 publications

Oral Health, Atherosclerosis, and Cardiovascular Disease

Oral Health, Atherosclerosis, and Cardiovascular Disease

Coordinate Stimulation of Macrophages by Microparticles and TLR Ligands Induces Foam Cell Formation

Circulating inflammatory markers and risks of cardiovascular and non‐cardiovascular disease

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