TY - JOUR
T1 - Diabetes and periodontal diseases
T2 - Consensus report of the Joint EFP/AAP Workshop on Periodontitis and Systemic Diseases
AU - Working group 2 of the joint EFP/AAP workshop
AU - Chapple, Iain L.C.
AU - Genco, Robert
AU - Berglundh, Tord
AU - Eickholz, Peter
AU - Engebretson, Steven
AU - Graves, Dana
AU - Grossi, Sarah
AU - Hasturk, Hatice
AU - Kocher, Thomas
AU - Lalla, Evanthia
AU - Lamster, Ira
AU - Lang, Niklaus
AU - Mealey, Brian
AU - Meyle, Joerg
AU - Nesse, Willem
AU - Paquette, David
AU - Preshaw, Philip
AU - Taylor, George
AU - Taylor, John
AU - Van Der Velden, Ubele
AU - Walter, Clemens
AU - Wenche, Borgnakke
AU - Ylöstalo, Pekka
N1 - Publisher Copyright:
© 2013 European Federation of Periodontology and American Academy of Periodontology.
PY - 2013/4
Y1 - 2013/4
N2 - 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 β-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.
AB - 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 β-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.
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U2 - 10.1902/jop.2013.1340011
DO - 10.1902/jop.2013.1340011
M3 - Article
C2 - 23631572
AN - SCOPUS:84877071822
SN - 0022-3492
VL - 84
SP - S106-S112
JO - Journal of Periodontology
JF - Journal of Periodontology
IS - 4
ER -