Volume 84, Issue 4S p. S106-S112
Article

Diabetes and periodontal diseases: consensus report of the Joint EFP/AAP Workshop on Periodontitis and Systemic Diseases

Iain L. C. Chapple

Corresponding Author

Iain L. C. Chapple

Periodontal Research Group & MRC Centre for Immune Regulation, University of Birmingham School of Dentistry, Birmingham, UK

Address:

Iain L. C. Chapple

School of Dentistry

College of Medical and Dental Sciences

The University of Birmingham

St Chads Queensway

Birmingham, B4 6NN, UK

E-mail: [email protected].

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Robert Genco

Robert Genco

University at Buffalo, Oral Biology and Microbiology and Immunology, Buffalo, NY, USA

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on behalf of working group 2 of the joint EFP/AAP workshop*

on behalf of working group 2 of the joint EFP/AAP workshop*

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First published: 01 April 2013
Citations: 256

The proceedings of the workshop were jointly and simultaneously published in the Journal of Clinical Periodontology and Journal of Periodontology. www.joponline.org/doi/abs/10.1902/jop.2013.1340011 http://onlinelibrary.wiley.com/doi/10.1111/jcpe.12077/abstract

Abstract

Background: Diabetes and periodontitis are complex chronic diseases with an established bidirectional relationship. There is long-established evidence that hyperglycaemia in diabetes is associated with adverse periodontal outcomes. However, given the ubiquity of periodontal diseases and the emerging global diabetes epidemic, the complications of which contribute to significant morbidity and premature mortality, it is timely to review the role of periodontitis in diabetes.

Aims: To report the epidemiological evidence from cross-sectional, prospective and intervention studies for the impact of periodontal disease on diabetes incidence, control and complications and to identify potential underpinning mechanisms.

Epidemiology: Over the last 20 years, consistent and robust evidence has emerged that severe periodontitis adversely affects glycaemic control in diabetes and glycaemia in non-diabetes subjects. In diabetes patients, there is a direct and dose-dependent relationship between periodontitis severity and diabetes complications. Emerging evidence supports an increased risk for diabetes onset in patients with severe periodontitis.

Biological mechanisms: Type 2 diabetes is preceded by systemic inflammation, leading to reduced pancreatic b-cell function, apoptosis and insulin resistance.Increasing evidence supports elevated systemic inflammation (acute-phase and oxidative stress biomarkers) resulting from the entry of periodontal organisms and their virulence factors into the circulation, providing biological plausibility for the effects of periodontitis on diabetes. AGE (Advanced Glycation Endproducts)–RAGE (Receptor for AGEs) interactions and oxidative-stress-mediated pathways provide plausible mechanistic links in the diabetes to periodontitis direction.

Interventions: Randomized controlled trials (RCTs) consistently demonstrate that mechanical periodontal therapy associates with approximately a 0.4% reduction in HbA1C at 3 months, a clinical impact equivalent to adding a second drug to a pharmacological regime for diabetes. RCTs are needed with larger numbers of subjects and longer term follow-up, and if results are substantiated, adjunctive periodontal therapies subsequently need to be evaluated. There is no current evidence to support adjunctive use of antimicrobials for periodontal management of diabetes patients.

Guidelines: Given the current evidence, it is timely to provide guidelines for periodontal care in diabetes patients for medical and dental professionals and recommendations for patients/the public.