Endotoxemia, Immune Response to Periodontal Pathogens, and Systemic Inflammation Associate With Incident Cardiovascular Disease Events

Pussinen, Pirkko J.; Tuomisto, Karolina; Jousilahti, Pekka; Havulinna, Aki S.; Sundvall, Jouko; Salomaa, Veikko

doi:10.1161/atvbaha.106.138743

Cited by 224 publications

(189 citation statements)

References 35 publications

Supporting

Mentioning

179

Contrasting

Unclassified

Order By: Relevance

“…IL-6 is estimated to increase from about 1 pg ml À1 at BMI of 22 mg kg À2 to about 2.5 pg ml À1 at BMI of 37 mg kg À2 (a state of severe obesity) (Figure 4b). This increase was very limited in amount compared with the IL-6 level of post-cardiac disease, 91 post-coronary artery bypass surgery patients 92 or experimental low-dose entotoxemia in healthy human subjects. 81 It is not convincing that the slight IL-6 elevation can contribute to the development of obesity-related metabolic diseases.…”

Section: Lack Of Bmi-adiponectin Association S-m Kuo and MM Halpernmentioning

confidence: 87%

Lack of association between body mass index and plasma adiponectin levels in healthy adults

Kuo

2011

Int J Obes

View full text Add to dashboard Cite

Objectives: To test the hypothesis that obesity (increase in fat mass) independently affects the level of adipokines: adiponectin, tumor necrosis factor-a (TNFa) and interleukin (IL)-6. Methods: Publications in the past decade reporting adult plasma adiponectin, leptin, TNFa and/or IL-6 levels were compiled. Mean gender-specific values were extracted from studies that included medical screening to confirm physical health (43 groups, total 4852 subjects). Correlation analysis was conducted between adipokine levels and body mass index (BMI), a widely used estimate of adiposity. Results: For healthy lean to obese adults of both genders, no significant correlation between plasma adiponectin and BMI was detected. There was also no gender difference in plasma adiponectin level. In contrast, leptin levels showed a positive correlation with BMI in both genders, and women had significantly higher levels of plasma leptin consistent with a higher percentage of body fat. The proinflammatory cytokine TNFa failed to show correlation with BMI. Although IL-6 showed a positive correlation with BMI in women, the obesity-related increase was very limited. Conclusions: Data analysis based on studies performed on healthy adults did not support the hypothesis that obesity independently affects the plasma level of adiponectin and TNFa. Reported obesity-related changes in plasma adipokine levels may be a consequence of obesity-related metabolic disorders. Future studies are especially needed to understand the homeostasis of adiponectin.

show abstract

Section: Lack Of Bmi-adiponectin Association S-m Kuo and MM Halpernmentioning

confidence: 87%

Lack of association between body mass index and plasma adiponectin levels in healthy adults

Kuo

2011

Int J Obes

View full text Add to dashboard Cite

show abstract

“…Thus, in periodontitis, overgrowth of gram-negative bacteria may cause endotoxemia and systemic inflammation leading to CVD (70). Periodontal disease may represent a risk factor for atherosclerosis and thromboembolic events (71).…”

Section: Poor Oral Health As a Contributor To Atherosclerotic Complicmentioning

confidence: 99%

Systemic Consequences of Poor Oral Health in Chronic Kidney Disease Patients

Akar

Carrero

et al. 2011

Clinical Journal of the American Society of Nephrology

168

136

View full text Add to dashboard Cite

SummaryChanges in the oral cavity, such as periodontitis and other manifestations of poor oral health, are common in patients with chronic kidney disease (CKD) and may contribute to increased morbidity and mortality because of systemic consequences such as inflammation, infections, protein-energy wasting, and atherosclerotic complications. Poor oral health in CKD patients may thus represent an important, but often overlooked, problem. Several studies show that uremic patients have higher rates of decayed, missing, and filled teeth, loss of attachment, and periapical and mucosal lesions than the general population. The consequences of poor oral health may be more severe in CKD patients because of advanced age, common comorbidities such as diabetes, concurrent medications, and a state of immune dysfunction that may increase the risk for systemic consequences of periodontitis and other oral and dental pathologic conditions. Poor dentition and other signs of poor oral health should be an alarm clock also at early stages of CKD. However, it remains to be determined whether more successful management of poor oral health and periodontitis will reduce the risk of inflammation, infection, protein-energy wasting, and atherosclerotic complications in CKD patients. This review explores etiological factors and potential systemic consequences of poor oral health in CKD patients as well as possible preventive and therapeutic strategies.

show abstract

“…Furthermore, Gram-negative pathogens associated with periodontal disease have also been linked to atherosclerotic plaque formation (104,105). In this regard, it is thought that periodontal disease can lead frequent bacteremia thereby inducing a systemic inflammatory response (106,107).…”

Section: Cardiovascular Diseasementioning

confidence: 99%

Diabetic complications and dysregulated innate immunity

Graves

Kayal²

2008

Front Biosci

227

188

View full text Add to dashboard Cite

Diabetes mellitus is a metabolic disorder that leads to the development of a number of complications. The etiology of each diabetic complication is undoubtedly multifactorial. We will focus on one potential component that may be common in many diabetic complications, dysregulation of innate immunity associated with an increased inflammatory response. High glucose levels lead to shunting through the polyol pathway, an increase in diacylglycerol which activates protein kinase C, an increase in the release of electrons that react with oxygen molecules to form superoxides, and the non-enzymatic glycosylation of proteins that result in greater formation of advanced glycation end products. Each of these can lead to aberrant cell signalling that affects innate immunity for example, by activating the MAP kinase pathway or inducing activation of transcription factors such as NF-kappaB. This may be a common feature of several complications including periodontal disease, atherosclerosis, nephropathy, impaired healing and retinopathy. These complications are frequently associated with increased expression of inflammatory cytokines such as TNF-alpha, IL-1beta and IL-6 and enhanced generation of reactive oxygen species. Cause and effect relationship between dysregulation of key components of innate immunity and diabetic complications in many instances have been demonstrated with the use of cytokine blockers and antioxidants.

show abstract

Endotoxemia, Immune Response to Periodontal Pathogens, and Systemic Inflammation Associate With Incident Cardiovascular Disease Events

Cited by 224 publications

References 35 publications

Lack of association between body mass index and plasma adiponectin levels in healthy adults

Lack of association between body mass index and plasma adiponectin levels in healthy adults

Systemic Consequences of Poor Oral Health in Chronic Kidney Disease Patients

Diabetic complications and dysregulated innate immunity

Contact Info

Product

Resources

About