Associations Between Periodontal Disease and Risk for Atherosclerosis, Cardiovascular Disease, and Stroke. A Systematic Review

Scannapieco, Frank A.; Bush, Renee B.; Paju, Susanna

doi:10.1902/annals.2003.8.1.38

Cited by 454 publications

(345 citation statements)

References 40 publications

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“…At the very least, inflammatory markers measured by OMT reflect peripheral, localized inflammation in the mouth, a critical site for immune response, as it is a primary avenue by which bacteria and viruses can enter and infect the body. Moreover, oral inflammatory activity is also implicated in the pathogenesis of periodontal disease (61), which is linked to other systemic disease including diabetes and cardiovascular diseases (62,63).…”

Section: Discussionmentioning

confidence: 99%

Negative and competitive social interactions are related to heightened proinflammatory cytokine activity

Chiang¹,

Eisenberger²,

Seeman

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

106

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Research has consistently documented that social relationships influence physical health, a link that may implicate systemic inflammation. We examined whether daily social interactions predict levels of proinflammatory cytokines IL-6 and the soluble receptor for tumor necrosis factor-α (sTNFαRII) and their reactivity to a social stressor. One-hundred twenty-two healthy young adults completed daily diaries for 8 d that assessed positive, negative, and competitive social interactions. Participants then engaged in laboratory stress challenges, and IL-6 and sTNFαRII were collected at baseline and at 25-and 80-min poststressor, from oral mucosal transudate. Negative social interactions predicted elevated sTNFαRII at baseline, and IL-6 and sTNFαRII 25-min poststressor, as well as total output of sTNFαRII. Competitive social interactions predicted elevated baseline levels of IL-6 and sTNFαRII and total output of both cytokines. These findings suggest that daily social interactions that are negative and competitive are associated prospectively with heightened proinflammatory cytokine activity.competition | social stress | immunology

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Section: Discussionmentioning

confidence: 99%

Negative and competitive social interactions are related to heightened proinflammatory cytokine activity

Chiang¹,

Eisenberger²,

Seeman

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

106

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“…The underlying mechanism(s) responsible for the hyperinflammatory neutrophil phenotype seen in chronic periodontitis (the commonest form of the disease) is currently unknown, although analyses indicate that it is not a result of altered adhesion molecule (7) or Phox gene (10) expression, polymorphisms in Fc␥R (8,12), or in vitro priming by cytokines or LPS (13,14). Furthermore, the association of periodontitis with increased relative risk for cardiovascular disease, fatal coronary events (15), and ischemic stroke (16), and the demonstrable medium-term reductions in vascular endothelial dysfunction following aggressive periodontal therapies (17), emphasize the potential impact of inflammatory periodontitis on peripheral macrovascular disease.…”

Section: P Eripheral Blood Neutrophils (Pbn)mentioning

confidence: 99%

Periodontitis Associates with a Type 1 IFN Signature in Peripheral Blood Neutrophils

Wright

Matthews

Chapple

et al. 2008

The Journal of Immunology

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Peripheral blood neutrophils from periodontitis patients exhibit a hyperreactive and hyperactive phenotype (collectively termed hyperresponsivity) in terms of production of reactive oxygen species (ROS). The molecular basis for this phenomenon, however, has yet to be determined. Our objectives were to identify genes differentially expressed in hyperresponsive peripheral blood neutrophils from chronic periodontitis patients relative to periodontally healthy controls and use these data to identify potential contributory pathways to the hyperresponsive neutrophil phenotype. Using microarray technology we demonstrated differential expression of 163 genes (149 increased, 14 decreased) representing a range of ontological classes. There was increased expression of a significant number of IFN-stimulated genes (ISG). RT-PCR analysis of ISG transcripts in individual and pooled samples further corroborated these data, and indicated that levels decreased to near those of controls following successful therapy. Significantly enhanced FcγR-stimulated ROS production was subsequently achieved by priming control neutrophils with IFN-α/-β/-γ, but not LPS, and gene expression analysis indicated that exposure to the type I IFN (in particular IFN-α) better replicated the mRNA profile observed in vivo. Further studies demonstrated that plasma levels of IFN-α were significantly higher in samples from patients relative to unaffected controls. Following successful periodontitis treatment, plasma IFN-α levels, neutrophil ISG expression, and FcγR-stimulated neutrophil ROS output of patients, all decreased to levels comparable with those of controls. In conclusion, although chronic periodontitis is a complex disease, raised IFN-α may be one determinant of the distinct molecular phenotype and hyperresponsivity exhibited by patients’ peripheral blood neutrophils.

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“…It has been reported that 10% to 15% of the periodontal patients had been linked to CVD. [17][18][19] We previously showed that periodontopathic pathogens deteriorated ventricular remodeling after MI 20,21) and other cardiovascular diseases. [22][23][24][25][26] However, a detailed mechanism is still to be elucidated.…”

mentioning

confidence: 99%

<i>Porphyromonas Gingivalis</i> Elevated High-Mobility Group Box 1 Levels After Myocardial Infarction in Mice

et al. 2017

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SummaryHigh mobility group box 1 (HMGB1) is a nuclear protein released from necrotic cells, inducing inflammatory responses. Epidemiological studies suggested a possible association between periodontitis and cardiovascular diseases (CVDs). Due to tissue damage and necrosis of cardiac cells following myocardial infarction (MI), HMGB1 is released, activating an inflammatory reaction. However, it remains unclear whether periodontitis is also involved in myocardial damage. The purpose of this study was to determine the effect of the periodontal pathogen Porphyromonas gingivalis (P.g.) after MI in mice.C57BL/6J wild type mice in post-MI were inoculated with P.g. in the infected group (P.g.-inoculated MI group) and with phosphate buffer saline (PBS) in the control group (PBS-injected MI group). Plasma samples and twelve tissue samples from mice hearts after MI were obtained. We determined the expression of HMGB1 by ELISA and immunohistochemistry.The level of HMGB1 protein in the P.g.-inoculated MI group was significantly higher than in the PBSinjected MI group on day 5, but not on day 14. Immunohistochemistry analysis revealed that HMGB1 was mainly expressed in cardiomyocytes, immune cells, and vascular endothelial cells in the PBS-injected MI group, while HMGB1 was seen broadly in degenerated cardiomyocytes, extracellular fields, immune cells, and vascular endothelial cells in the P.g.-inoculated MI group. A significant increase in the number of HMGB1 positive cells was observed in the P.g.-inoculated MI group compared to the PBS-injected MI group.Infection with P.g. after MI enhanced myocardial HMGB1 expression. There is a possible relationship between periodontitis and post-infarction myocardial inflammation through HMGB-1.(Int Heart J 2017; 58: 762-768)

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Associations Between Periodontal Disease and Risk for Atherosclerosis, Cardiovascular Disease, and Stroke. A Systematic Review

Abstract: 1. Periodontal disease may be modestly associated with atherosclerosis, MI, and CVD. 2. Additional large-scale longitudinal epidemiologic and intervention studies are necessary to validate this association and to determine causality.

Cited by 454 publications

References 40 publications

Negative and competitive social interactions are related to heightened proinflammatory cytokine activity

Negative and competitive social interactions are related to heightened proinflammatory cytokine activity

Periodontitis Associates with a Type 1 IFN Signature in Peripheral Blood Neutrophils

<i>Porphyromonas Gingivalis</i> Elevated High-Mobility Group Box 1 Levels After Myocardial Infarction in Mice

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