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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increasing evidence implicates periodontitis, a chronic inflammatory disease of the tooth-supporting structures, as a potential risk factor for increased morbidity or mortality for several systemic conditions including cardiovascular disease (atherosclerosis, heart attack, and stroke), pregnancy complications (spontaneous preterm birth [SPB]), and diabetes mellitus. Cross-sectional, case-control, and cohort studies indicate that periodontitis may confer two- and up to sevenfold increase in the risk for cardiovascular disease and premature birth, respectively. Given the recently acquired knowledge that systemic inflammation may contribute in the pathogenesis of atherosclerosis and may predispose to premature birth, research in the field of periodontics has focused on the potential of this chronic low-grade inflammatory condition to contribute to the generation of a systemic inflammatory phenotype. Consistent with this hypothesis clinical studies demonstrate that periodontitis patients have elevated markers of systemic inflammation, such as C-reactive protein (CRP), interleukin 6 (IL-6), haptoglobin, and fibrinogen. These are higher in periodontal patients with acute myocardial infarction (AMI) than in patients with AMI alone, supporting the notion that periodontal disease is an independent contributor to systemic inflammation. In the case of adverse pregnancy outcomes, studies on fetal cord blood from SBP babies indicate a strong in utero IgM antibody response specific to several oral periodontal pathogens, which induces an inflammatory response at the fetal-placental unit, leading to prematurity. The importance of periodontal infections to systemic health is further strengthened by pilot intervention trials indicating that periodontal therapy may improve surrogate cardiovascular outcomes, such as endothelial function, and may reduce four- to fivefold the incidence of premature birth. Nevertheless, further research is needed to fully discern the underlying mechanisms by which local chronic infections can have an impact on systemic health, and in this endeavor periodontal disease may serve as an ideal disease model.
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PMID:Low-grade inflammation in chronic infectious diseases: paradigm of periodontal infections. 1719 71

It is becoming increasingly clear that infections and chronic inflammatory conditions, such as periodontitis can be linked with atherosclerotic process. Periodontitis and atherosclerosis have many pathogenetic mechanisms in common. The objective of this based on current knowledge review is to present the putative mechanisms whereby periodontitis which is chronic and inflammatory in nature and initiated by microbial plaque can influence the atherosclerosis. Two main processes in particular are worthy of consideration and may provide the link between these two diseases. Induction of the chronic systemic inflammation has been proposed to be of pathogenetic relevance in the association of infection and atherosclerosis, and may rely in part on the endothelial toxicity of bacterial endotoxin and the action of proinflammatory cytokines (PGE-2, IL-1beta, TNF-alpha). Another well-founded proatherogenetic property of infectious illness may be the induction of autoimmunity and autoagression. It has been suggested that humoral immune cross-reaction of the same antibodies to heat shock proteins (HSP), both bacterial mHSP65 and human endothelial HSP60 may play an important role in the process of vascular endothelial injury. Both of these mechanisms are believed to be a key event in the pathogenesis of artheriosclerosis.
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PMID:[The impact of periodontal infection on systemic inflammatory process and atherosclerosis]. 1744 82

Treponema denticola, a major pathogen of periodontitis, has also been detected in the lesions of atherosclerosis. The aim of this study was to investigate induction of chemokine production in human umbilical vein endothelial cells (HUVECs) by T. denticola and determine whether those chemokines were degraded by a protease, dentilisin. T. denticola ATCC35405 or dentilisin-deficient mutant K1 were added to HUVECs and levels of interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) in the culture supernatants were determined by enzyme-linked immunosorbent assay. T. denticola ATCC35405 induced production of IL-8 in a time-dependent manner, with both production of IL-8 and expression of IL-8 mRNA showing higher levels than with exposure to dentilisin-deficient mutant K1. Although exposure to ATCC35405 induced expression of MCP-1 mRNA in the HUVECs, MCP-1 levels were remained similar to that in unstimulated cells. IL-8 and MCP-1 showed partial hydrolysis with exposure to T. denticola ATCC35405, but not with T. denticola K1. These results suggest that T. denticola can evade host defense mechanisms by modulating production of IL-8 and MCP-1, and that this play a role in the development of chronic infections such as periodontitis. The association of T. denticola infection to atherosclerosis was also discussed based on the present study.
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PMID:Treponema denticola induces interleukin-8 and macrophage chemoattractant protein 1 production in human umbilical vein epithelial cells. 1753 51

Several reports have demonstrated a possible association of periodontal infections with coronary heart disease (CHD) by elevated antibody titre to periodontopathic bacteria in CHD patients compared with non-diseased controls. Although each periodontopathic bacterium may vary in virulence for periodontitis and atherosclerosis, antibody response to multiple bacteria in CHD patients has not been understood fully. Therefore, serum levels of antibody to 12 periodontopathic bacteria together with other atherosclerotic risk markers were compared among 51 patients with CHD, 55 patients with moderate to severe chronic periodontitis and 37 healthy individuals. The antibody response was the most prevalent for Porphyromonas gingivalis, a major causative organism, in CHD as well as periodontitis patients. However, antibody positivity was different between CHD and periodontitis if the response was analysed for two different strains of P. gingivalis, namely FDC381 and Su63. While periodontitis patients were positive for both P. gingivalis FDC381 and Su63, a high frequency of antibody positivity for P. gingivalis Su63 but not for FDC381 was observed in CHD patients. The results indicate that the presence of particular periodontopathic bacteria with high virulence may affect atherogenesis. Identifying the virulence factors of P. gingivalis Su63 may gain insight into the new therapeutic modality for infection-induced deterioration of atherosclerosis.
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PMID:Relationship of periodontal infection to serum antibody levels to periodontopathic bacteria and inflammatory markers in periodontitis patients with coronary heart disease. 1764 69

Gender differences and variations in inflammatory disease (e. g. atherosclerosis, neurological disorders, periodontitis and rheumatoid arthritis) severity with female sex hormone level have been reported, suggesting that female sex hormones modulate the inflammatory response. Estrogens act on gene transcription via estrogen receptors alpha and beta. Identification of estrogen-regulated genes is a matter of great interest since it will contribute significantly to the understanding of the physiological importance of estrogens. Anti-inflammatory as well as pro-inflammatory responses to estrogens have been reported. Data have been presented showing that estrogens down-regulate the expression of adhesion and chemokine molecules in response to inflammation promoters in various experimental systems. Functional data show that estrogen treatment attenuates recruitment and adhesion of leukocytes to the endothelium induced by inflammation promoters offering a possible mechanism by which estrogens exert an anti-inflammatory effect. These effects of estrogens, with focus on the interactions of monocytes with the vascular endothelium, are highlighted in this review.
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PMID:Modulation of the inflammatory response by estrogens with focus on the endothelium and its interactions with leukocytes. 1765 31

The accumulation of epidemiologic, pathologic, and animal model studies suggests that periodontal infection may be a contributing risk factor for atherosclerosis. The Toll-like receptor-4 (TLR4) signaling pathway plays an important role in the initiation and progression of periodontitis-associated atherosclerotic disease. We postulate that suppression of TLR4 signaling pathway can be an effective treatment for atherosclerosis. These strategies include prevention of ligand binding to TLR4, blocking the interactions of TLR4s and adaptors in signaling pathways, blocking the enzymes in signaling pathways, and immunostimulation with vaccine adjuvants. However, we should be aware that there may be unknown risks about the new technologies and these drugs, which may cause some unknown side effects in long-term administration.
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PMID:Inhibition of TLR4 signaling pathway: molecular treatment strategy of periodontitis-associated atherosclerosis. 1768 3

Oral conditions such as gingivitis and chronic periodontitis are found worldwide and are among the most prevalent microbial diseases of mankind. The cause of these common inflammatory conditions is the complex microbiota found as dental plaque, a complex microbial biofilm. Despite 3000 years of history demonstrating the influence of oral status on general health, it is only in recent decades that the association between periodontal diseases and systemic conditions such as coronary heart disease and stroke, and a higher risk of preterm low birth-weight babies, has been realised. Similarly, recognition of the threats posed by periodontal diseases to individuals with chronic diseases such as diabetes, respiratory diseases and osteoporosis is relatively recent. Despite these epidemiological associations, the mechanisms for the various relationships remain unknown. Nevertheless, a number of hypotheses have been postulated, including common susceptibility, systemic inflammation with increased circulating cytokines and mediators, direct infection and cross-reactivity or molecular mimicry between bacterial antigens and self-antigens. With respect to the latter, cross-reactive antibodies and T-cells between self heat-shock proteins (HSPs) and Porphyromonas gingivalis GroEL have been demonstrated in the peripheral blood of patients with atherosclerosis as well as in the atherosclerotic plaques themselves. In addition, P. gingivalis infection has been shown to enhance the development and progression of atherosclerosis in apoE-deficient mice. From these data, it is clear that oral infection may represent a significant risk-factor for systemic diseases, and hence the control of oral disease is essential in the prevention and management of these systemic conditions.
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PMID:Relationship between periodontal infections and systemic disease. 1771 90

Periodontitis increases the atherosclerosis risk, but information on the role of periodontal pathogens in atherogenesis is limited. In the present study we have investigated, whether the major periodontal pathogen, Aggregatibacter (Actinobacillus) actinomycetemcomitans, induces development of atherosclerosis in apolipoprotein E-deficient mice. The mice received 4, 6, or 8 weekly i.v. injections of live pathogen (10(7)CFU/50 microl/mouse) or saline as control, and were killed 1 week after the last injection. The atherosclerotic lesion formation was examined from whole aortas and aortic sinus cryosections after lipid staining. Neither the lesion area in the aortas or en face analyses, nor their immunoreactivity to the macrophage-marker CD68 differed significantly between the infected and the control mice. However, the pathogen administration increased serum C-reactive protein (CRP) concentrations, and induced proatherogenic lipoprotein profiles with smaller particle sizes in very-low density (VLDL), low density (LDL), and high density (HDL) lipoprotein fractions. It also caused elevated matrix metalloproteinase-9 expression in the aortas and increased serum gelatinase level. Lipopolysaccharide deriving from the pathogen was associated with proatherogenic lipoprotein fractions: VLDL and especially LDL. The results indicate that A. actinomycetemcomitans contributes to disturbed lipoprotein profiles, inflammatory reaction, and matrix remodelling which are known to promote the development of atherosclerosis.
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PMID:Aggregatibacter actinomycetemcomitans induces MMP-9 expression and proatherogenic lipoprotein profile in apoE-deficient mice. 1788 99

Although research has demonstrated that odontogenic foci of infection can be dangerous to the function of other organs, a direct relationship between orofacial infections and systemic health has not been proved. Recently, bacterial and viral organisms involved in chronic inflammatory processes have also been regarded as risk factors for atherosclerosis. Periodontitis is one of the most common chronic bacterial infections. One of the first researchers to indicate a relationship between orofacial infections and atherosclerosis were Mattila et al. In 1989 they published a paper which identified periodontal disease as an independent predictor of the risk of myocardial infarction. For over ten years several authors have discussed the correlation between oral infections, and periodontal disease in particular, and the occurrence of coronary heart disease, myocardial infarction, and ischemic stroke. A review of the knowledge of the effects of periodontal disease on the development of atheromatous plaque is presented here. No scientific evidence was found to prove a direct association between odontogenic infections and atherosclerosis. However, such a relationship is probable in the light of the reviewed articles. Reliable markers should be sought which could accurately indicate the effect of periodontal disease on the condition of the arteries.
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PMID:The effect of chronic periodontitis on the development of atherosclerosis: review of the literature. 1859 28

There is an epidemiological association between periodontitis and cardiovascular disease (CVD). In periodontitis, low grade systemic inflammation and bacteremia occur regularly. Such events may contribute to platelet activation and subsequent pro-coagulant state. This study aimed to investigate platelet activation in periodontitis patients. The study is composed of two parts. In the first part, plasma levels of soluble(s) P-selectin and sCD40 ligand were measured as general markers of platelet activation in periodontitis patients (n=85) and in healthy controls (n=35). In the second part, surface-exposed P-selectin and the ligand-binding conformation of the glycoprotein IIb-IIIa complex (binding of PAC-1 antibody) were determined on individual platelets in whole blood of periodontitis patients (n=18) and controls (n=16). Patients had significantly elevated plasma levels of sP-selectin (P<0.001) and increased binding of PAC-1 on isolated platelets (P=0.033). Platelet activation was more pronounced in the patients with more severe periodontal disease, showing a severity-dependence. The levels of sCD40 ligand and of platelet-bound P-selectin were not increased. Periodontitis is associated with increased platelet activation. Since platelet activation contributes to a pro-coagulant state and constitutes a risk for atherothrombosis, platelet activation in periodontitis may partly explain the epidemiological association between periodontitis and CVD.
Atherosclerosis 2009 Feb
PMID:Periodontitis is associated with platelet activation. 1861 75


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