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

Epidemiological studies indicated that more than 15% of the population in western countries suffer because of severe forms of periodontitis, In this respect, the recognition of the relationship between oral and systemic health is growing, thus receiving remarkable interest in scientific literature. In fact, periodontitis may increase the risk for a group of life-threatening conditions such as atherosclerosis, stroke or low birth weight. The American Diabetes Association has reported that individuals with uncontrolled diabetes (defined as 200mg/dL of glucose on three consecutive readings) undergo an increased risk of infections, abnormal wound healing and consequent increased recovery time. Moreover, diabetics may be more likely to develop periodontal and cardiovascular disease than non diabetics, if note. History of poorly controlled chronic periodontal disease can alter diabetic/glycemic control. This may originate from a likely continuous passege of bacterial toxins and/or bacteria into the bloodstream, and/or from an exaggerated release of inflammatory mediators. This review is aimed at elucidating the connections between the status of oral health and glycemic control in diabetes.
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PMID:Does it make sense that diabetes is reciprocally associated with periodontal disease? 2000 97

The combination of obesity and its associated risk factors, such as insulin resistance and inflammation, results in the development of atherosclerosis. However, the effects of periodontitis on atherosclerosis in an obese body remain unclear. The aim of the study was to investigate the effects of ligature-induced periodontitis in Zucker fatty rats on initiation of atherosclerosis by evaluating aortic insulin resistance. Zucker fatty rats (n=24) were divided into two groups. In the periodontitis group, periodontitis was ligature-induced for 4 weeks, whereas the control group was left unligated. After the 4-week experimental period, descending aorta was used for measuring the levels of lipid deposits, immunohistochemical analysis, and evaluation of gene expression. Levels of serum C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-alpha), and insulin were also measured. Rats in the periodontitis group had significantly enhanced lipid deposits in the aorta, but not in the control group. Expression of suppressor of cytokine signaling 3, vascular cell adhesion molecule 1, reactive oxygen species, nitrotyrosine, and endothelin-1 in the periodontitis group was more intense than that in the control group. Significantly decreased levels of phosphatidylinositol 3-kinase (Pi3k) catalytic beta-polypeptide (Pi3kcb), Pi3kp85, and insulin receptor substrate 1 and 2 were observed in the periodontitis group. Levels of serum CRP and TNF-alpha were significantly increased in the periodontitis group. Under insulin-stimulated conditions, aorta in the periodontitis group altered the Akt phosphorylation. Periodontitis in obesity induced the initial stage of atherosclerosis and disturbed aortic insulin signaling.
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PMID:Effects of periodontitis on aortic insulin resistance in an obese rat model. 2006 45

Crosstalk between complement and Toll-like receptors (TLRs) coordinates innate immunity. We report a previously unknown immune subversion mechanism involving microbial exploitation of communication between complement and TLRs. Porphyromonas gingivalis, a major oral and systemic pathogen with complement C5 convertase-like activity, synergizes with C5a (fragment of complement protein C5) to increase cyclic adenosine monophosphate (cAMP) concentrations, resulting in suppression of macrophage immune function and enhanced pathogen survival in vitro and in vivo. This synergy required TLR2 signaling, a pertussis toxin- and thapsigargin-sensitive C5a receptor pathway, with protein kinase A and glycogen synthase kinase-3beta as downstream effectors. Antagonistic blockade of the C5a receptor abrogated this evasive strategy and may thus have important therapeutic implications for periodontitis and atherosclerosis, diseases in which P. gingivalis is implicated. This first demonstration of complement-TLR crosstalk for immunosuppressive cAMP signaling indicates that pathogens may not simply undermine complement or TLRs (or both) as separate entities, but may also exploit their crosstalk pathways.
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PMID:Microbial hijacking of complement-toll-like receptor crosstalk. 2015 52

Periodontal diseases are highly prevalent in the population. Several studies implicated that chronic periodontitis may affect the arterial wall inducing subclinical atherosclerosis by triggering a systemic inflammatory response. Three theories have been put forward to explain potential mechanisms involved: the theory of bacterial invasion, the cytokine theory and the autoimmunization theory. Periodontal inflammation could have a role in the initiation and progression of arterial diseases such as coronary artery disease and carotid atherosclerosis. Further clinical studies are required to investigate if there is a causal relationship of chronic periodontitis with echolucent unstable carotid plaques.
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PMID:Periodontitis and carotid atheroma: is there a causal relationship? 2022 28

Evidence from epidemiologic studies suggests that periodontal infections are independently associated with subclinical and clinical atherosclerotic vascular disease. Although the strength of the reported associations is modest, the consistency of the data across diverse populations and a variety of exposure and outcome variables suggests that the findings are not spurious or attributable only to the effects of confounders. Analysis of limited data from interventional studies suggests that periodontal treatment generally results in favorable effects on subclinical markers of atherosclerosis, although such analysis also indicates considerable heterogeneity in responses. Experimental mechanistic in vitro and in vivo studies have established the plausibility of a link between periodontal infections and atherogenesis, and have identified biological pathways by which these effects may be mediated. However, the utilized models are mostly mono-infections of host cells by a limited number of 'model' periodontal pathogens, and therefore may not adequately portray human periodontitis as a polymicrobial, biofilm-mediated disease. Future research must identify in vivo pathways in humans that may (i) lead to periodontitis-induced atherogenesis, or (ii) result in treatment-induced reduction of atherosclerosis risk. Data from these studies will be essential for determining whether periodontal interventions have a role in the primary or secondary prevention of atherosclerosis.
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PMID:"Gum bug, leave my heart alone!"--epidemiologic and mechanistic evidence linking periodontal infections and atherosclerosis. 2063 10

Periodontitis may be a risk factor for atherosclerosis and coronary heart disease. The influence of periodontal pathogens in cardiovascular diseases needs further investigation. Therefore, the aims of this clinical study are: to test the presence of periodontal bacteria DNA in aortic valves and to assess the concomitant presence of the same periodontal bacteria DNA in whole blood samples in patients affected by aortic valve stenosis and chronic periodontitis. Nineteen consecutive patients (12 males and 7 females, age: 49-85 years) were enrolled in this study after having been subjected to a complete periodontal evaluation to confirm the diagnosis of chronic periodontitis. All patients were scheduled for aortic valve replacement surgery. After clinical and microbial periodontal examination, the aortic valve tissue specimens were obtained by excision during valve replacement surgery and the patients were subjected to the whole blood sampling before the surgery. The polymerase chain reaction technology was used to detect the putative periodontal pathogens Tannerella forshytia, Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Prevotella intermedia, Fusobacterium nucleatum, Campylobacter rectus, Eikenella corrodens and Treponema denticola. Neither the 19 aortic valve specimens nor the blood samples were positive for the genoma of the selected periodontal pathogens. The selected periodontal pathogens did not colonize the aortic valve of patients affected by stenosis and bacterial genoma was not present in whole blood samples. A high blood pressure at the aortic valve may prevent the adhesion and proliferation of bacterial colonies.
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PMID:Examination of periodontal pathogens in stenotic valve specimens and in whole blood samples in patients affected by aortic valve stenosis and chronic periodontitis. 2064 51

Clinical observations and a few research reports seem to suggest that intraoral infection as well as periodontal teeth could potentially lead to systemic infections including atherosclerosis. The aim of our investigations was to determine whether periodontal disease might aggravate atherosclerosis and whether interferon-gamma (IFNG), widely recognized as a potent multifunctional cytokine, might serve as a marker of the process. This is the first research based on tissue material such as atheromata and periodontal pocket granulation tissue. The study population consisted of 15 patients with periodontitis and atherosclerosis. Control group comprised 15 non-atherosclerotic patients with periodontitis. IFNG, IFNGR1 and IFNGR2 expression was analysed using qRT-PCR profiling in the inflammatory granulation tissue and atheroma. Granulation tissue samples obtained from non-atherosclerotic group showed a significant increase in IFNG and a decrease of IFNGR1, IFNGR2 expression whereas granulation tissue and atheromata of patients with systemic disease demonstrated lower IFNG and higher IFNGR1 and IFNGR2 expression.
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PMID:Interferon gamma in the etiology of atherosclerosis and periodontitis. 2065 98

Evidence of immune stimulation has been noted in opiate dependent patients for many decades. Documented changes have included lymphadenopathy, round cell infiltration of the hepatic portal triads, diffuse peri-bronchitis, hyperglobulinaemia, lymphocytosis, monocytosis, systemic cytokine stimulation, and cytokine and chemokine activation within the neuraxis. A parallel literature describes an elevated list of chronic degenerative disease as common in such patients including neurodegenerative conditions, atherosclerosis, nephrosclerosis, hepatic fibrosis and cirrhosis, chronic obstructive and fibrotic lung disease, osteoporosis, chronic periodontitis, various cancers, hair greying, and stem cell suppression. All of these disorders are now known to have an important immunological role in their pathogenic pathways. The multisystem nature of these myriad changes strongly suggest that the ageing process itself is stimulated in these patients. The link between the immunostimulation on the one hand and the elevated and temporally advanced nature of the chronic degenerative diseases on the other appears not to have been made in the literature. Moreover as immunostimulation is also believed to be an important, potent and principal contributor to the ageing process it appears that experimental and studies of this putative link are warranted. Verification of such an hypothesis would also carry management implications for dose and duration of chronic pain and addiction treatment, pharmacotherapeutic selection, and novel treatments such as long term naltrexone implant therapy and heroin trials.
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PMID:Chronic immune stimulation as a contributing cause of chronic disease in opiate addiction including multi-system ageing. 2080 Mar 62

Extracellular membrane vesicles (MVs) 30-1000 nm in diameter and of varying cellular origins are increasingly recognized for their participation in a range of processes, including the pathogenesis of various diseases, such as: (1) atherosclerosis, (2) thromboembolism, (3) osteoarthritis (OA), (4) chronic renal disease and pulmonary hypertension, (5) tissue invasion and metastasis by cancer cells, (6) gastric ulcers and bacterial infections, and (7) periodontitis. MVs are derived from many different cell types and intracellular mechanisms, and perform different metabolic functions or roles, depending on the cell of origin.The presence of a metabolically active, outer membrane is a distinguishing feature of all MVs, regardless of their cell type of origin and irrespective of terminologies applied to them such as exosomes, microparticles, or matrix vesicles. The MV membrane provides one of the few protected and controlled internal microenvironments outside cells in which specific metabolic objectives of the host cell may be pursued vigorously at a distance from the host cell. MVs are also involved in various forms of normal and abnormal intercellular communication. Evidence is emerging that circulating MVs are good predictors of the severity of several diseases. In addition, recently, the role of MVs in inducing immunity against cancer cells and bacterial infections has become a topic of interest to researchers in the area of therapeutics. The main objective of this review is to list and briefly describe the increasingly well-defined roles of MVs in selected diseases in which they seem to have a significant role in pathogenesis.
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PMID:Role of extracellular membrane vesicles in the pathogenesis of various diseases, including cancer, renal diseases, atherosclerosis, and arthritis. 2080 91

A growing body of evidence indicates that the incidence of atherosclerosis is increased in subjects with periodontitis - a chronic infection of the oral cavity. This article summarizes the evidence that suggests periodontitis shifts the lipoprotein profile to be more proatherogenic. LDL-C is elevated in periodontitis and most studies indicate that triglyceride levels are also increased. By contrast, antiatherogenic HDL tends to be low in periodontitis. Periodontal therapy tends to shift lipoprotein levels to a healthier profile and also reduces subclinical indices of atherosclerosis. In summary, periodontal disease alters lipoprotein metabolism in ways that could promote atherosclerosis and cardiovascular disease.
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PMID:Lipoproteins and lipoprotein metabolism in periodontal disease. 2083


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