Journal
JOURNAL OF CLINICAL PERIODONTOLOGY
Volume 40, Issue -, Pages S85-S105Publisher
WILEY
DOI: 10.1111/jcpe.12061
Keywords
periodontitis; CVD; biomarkers; CRP; FMD; IMT; Inflammation; Oxidative Stress; Blood Pressure; Coagulation
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Funding
- UK Clinical Research Collaboration
- Johnson and Johnson Consumer Services EAME Limited
- Department of Health's National Institute of Health Research (NIHR) Biomedical Research Centres funding scheme
- Colgate-Palmolive
- American Academy of Periodontology
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Aim The aim of this review was to critically appraise the evidence on the impact of periodontal treatment of cardiovascular diseases (CVDs) biomarkers and outcomes. Methods A systematic search was performed in Cinhal, Cochrane, Embase and Medline for relevant articles up to July 2012. Duplicate screening and reference hand searching were performed. Data were then summarized and evidence graded in tables. Results The search resulted in: (a) no evidence on the effects of periodontal therapy on subclinical atherosclerosis, serum levels of CD40 ligand, serum amyloid A and monocyte chemoattractant protein-1, (b) limited evidence on the effects of periodontal therapy on arterial blood pressure, leucocyte counts, fibrinogen, tissue necrosis factor-, sE-selectin, von Willebrand factors, d-dimers, matrix metalloproteinases, oxidative stress and CVD events, and (c) moderate evidence suggesting a negligible effect of periodontal therapy in reducing interleukin-6 and lipids levels, whilst a positive effect in reducing serum C-reactive protein levels and improving endothelial function. Conclusions Periodontal therapy triggers a short-term inflammatory response followed by (a) a progressive and consistent reduction of systemic inflammation and (b) an improvement in endothelial function. There is however limited evidence that these acute and chronic changes will either increase or reduce CVD burden of individuals suffering from periodontitis in the long term.
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