Periodontitis and atherosclerotic cardiovascular disease: Consensus report of the Joint EFP/ AAP Workshop on Periodontitis and Systemic Diseases

Working group 1 of the joint EFP/AAP workshop

Research output: Contribution to journalArticle

87 Citations (Scopus)

Abstract

Background: This consensus report is concerned with the association between periodontitis and atherosclerotic cardiovascular disease (ACVD). Periodontitis is a chronic multifactorial inflammatory disease caused by microorganisms and characterized by progressive destruction of the tooth supporting apparatus leading to tooth loss; as such, it is a major public health issue. Aims: This report examined biological plausibility, epidemiology and early results from intervention trials. Plausibility: Periodontitis leads to entry of bacteria in the blood stream. The bacteria activate the host inflammatory response by multiple mechanisms. The host immune response favors atheroma formation, maturation and exacerbation. Epidemiology: In longitudinal studies assessing incident cardiovascular events, statistically significant excess risk for ACVD was reported in individuals with periodontitis. This was independent of established cardiovascular risk factors. The amount of the adjusted excess risk varies by type of cardiovascular outcome and across populations by age and gender. Given the high prevalence of periodontitis, even low to moderate excess risk is important from a public health perspective. Intervention: There is moderate evidence that periodontal treatment: (i) reduces systemic inflammation as evidenced by reduction in C-reactive protein (CRP) and improvement of both clinical and surrogate measures of endothelial function; but (ii) there is no effect on lipid profiles - supporting specificity. Limited evidence shows improvements in coagulation, biomarkers of endothelial cell activation, arterial blood pressure and subclinical atherosclerosis after periodontal therapy. The available evidence is consistent and speaks for a contributory role of periodontitis to ACVD. There are no periodontal intervention studies on primary ACVD prevention and there is only one feasibility study on secondary ACVD prevention. Conclusions: It was concluded that: (i) there is consistent and strong epidemiologic evidence that periodontitis imparts increased risk for future cardiovascular disease; and (ii) while in vitro, animal and clinical studies do support the interaction and biological mechanism, intervention trials to date are not adequate to draw further conclusions. Well-designed intervention trials on the impact of periodontal treatment on prevention of ACVD hard clinical outcomes are needed.

Original languageEnglish (US)
Pages (from-to)S24-S29
JournalJournal of Periodontology
Volume84
Issue number4
DOIs
StatePublished - Apr 1 2013
Externally publishedYes

Fingerprint

Periodontitis
Cardiovascular Diseases
Joints
Education
Epidemiology
Public Health
Bacteria
Tooth Loss
Feasibility Studies
Atherosclerotic Plaques
antiarrhythmic peptide
C-Reactive Protein
Longitudinal Studies
Atherosclerosis
Tooth
Arterial Pressure
Endothelial Cells
Biomarkers
Inflammation
Lipids

Keywords

  • Atherosclerosis
  • Bacteremia
  • C-reactive protein
  • Cardiovascular diseases
  • Clinical trials
  • Epidemiology
  • Inflammation
  • Myocardial infarction
  • Periodontal diseases
  • Periodontitis
  • Stroke

ASJC Scopus subject areas

  • Periodontics

Cite this

Periodontitis and atherosclerotic cardiovascular disease : Consensus report of the Joint EFP/ AAP Workshop on Periodontitis and Systemic Diseases. / Working group 1 of the joint EFP/AAP workshop.

In: Journal of Periodontology, Vol. 84, No. 4, 01.04.2013, p. S24-S29.

Research output: Contribution to journalArticle

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abstract = "Background: This consensus report is concerned with the association between periodontitis and atherosclerotic cardiovascular disease (ACVD). Periodontitis is a chronic multifactorial inflammatory disease caused by microorganisms and characterized by progressive destruction of the tooth supporting apparatus leading to tooth loss; as such, it is a major public health issue. Aims: This report examined biological plausibility, epidemiology and early results from intervention trials. Plausibility: Periodontitis leads to entry of bacteria in the blood stream. The bacteria activate the host inflammatory response by multiple mechanisms. The host immune response favors atheroma formation, maturation and exacerbation. Epidemiology: In longitudinal studies assessing incident cardiovascular events, statistically significant excess risk for ACVD was reported in individuals with periodontitis. This was independent of established cardiovascular risk factors. The amount of the adjusted excess risk varies by type of cardiovascular outcome and across populations by age and gender. Given the high prevalence of periodontitis, even low to moderate excess risk is important from a public health perspective. Intervention: There is moderate evidence that periodontal treatment: (i) reduces systemic inflammation as evidenced by reduction in C-reactive protein (CRP) and improvement of both clinical and surrogate measures of endothelial function; but (ii) there is no effect on lipid profiles - supporting specificity. Limited evidence shows improvements in coagulation, biomarkers of endothelial cell activation, arterial blood pressure and subclinical atherosclerosis after periodontal therapy. The available evidence is consistent and speaks for a contributory role of periodontitis to ACVD. There are no periodontal intervention studies on primary ACVD prevention and there is only one feasibility study on secondary ACVD prevention. Conclusions: It was concluded that: (i) there is consistent and strong epidemiologic evidence that periodontitis imparts increased risk for future cardiovascular disease; and (ii) while in vitro, animal and clinical studies do support the interaction and biological mechanism, intervention trials to date are not adequate to draw further conclusions. Well-designed intervention trials on the impact of periodontal treatment on prevention of ACVD hard clinical outcomes are needed.",
keywords = "Atherosclerosis, Bacteremia, C-reactive protein, Cardiovascular diseases, Clinical trials, Epidemiology, Inflammation, Myocardial infarction, Periodontal diseases, Periodontitis, Stroke",
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AU - Bouchard, Philippe

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AU - Dietrich, Thomas

AU - Eke, Paul

AU - Graziani, Filippo

AU - Gunsolley, John

AU - Herrera, David

AU - Hart, Thomas

AU - Shearer, Barbara

AU - Jepsen, Søren

AU - Kantarci, Alpdogan

AU - Loos, Bruno G.

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AU - Schenkein, Harvey

AU - Renvert, Stefan

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N2 - Background: This consensus report is concerned with the association between periodontitis and atherosclerotic cardiovascular disease (ACVD). Periodontitis is a chronic multifactorial inflammatory disease caused by microorganisms and characterized by progressive destruction of the tooth supporting apparatus leading to tooth loss; as such, it is a major public health issue. Aims: This report examined biological plausibility, epidemiology and early results from intervention trials. Plausibility: Periodontitis leads to entry of bacteria in the blood stream. The bacteria activate the host inflammatory response by multiple mechanisms. The host immune response favors atheroma formation, maturation and exacerbation. Epidemiology: In longitudinal studies assessing incident cardiovascular events, statistically significant excess risk for ACVD was reported in individuals with periodontitis. This was independent of established cardiovascular risk factors. The amount of the adjusted excess risk varies by type of cardiovascular outcome and across populations by age and gender. Given the high prevalence of periodontitis, even low to moderate excess risk is important from a public health perspective. Intervention: There is moderate evidence that periodontal treatment: (i) reduces systemic inflammation as evidenced by reduction in C-reactive protein (CRP) and improvement of both clinical and surrogate measures of endothelial function; but (ii) there is no effect on lipid profiles - supporting specificity. Limited evidence shows improvements in coagulation, biomarkers of endothelial cell activation, arterial blood pressure and subclinical atherosclerosis after periodontal therapy. The available evidence is consistent and speaks for a contributory role of periodontitis to ACVD. There are no periodontal intervention studies on primary ACVD prevention and there is only one feasibility study on secondary ACVD prevention. Conclusions: It was concluded that: (i) there is consistent and strong epidemiologic evidence that periodontitis imparts increased risk for future cardiovascular disease; and (ii) while in vitro, animal and clinical studies do support the interaction and biological mechanism, intervention trials to date are not adequate to draw further conclusions. Well-designed intervention trials on the impact of periodontal treatment on prevention of ACVD hard clinical outcomes are needed.

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KW - Cardiovascular diseases

KW - Clinical trials

KW - Epidemiology

KW - Inflammation

KW - Myocardial infarction

KW - Periodontal diseases

KW - Periodontitis

KW - Stroke

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