Periodontitis and diabetes: a two-way relationship
Identifieur interne : 004099 ( Main/Merge ); précédent : 004098; suivant : 004100Periodontitis and diabetes: a two-way relationship
Auteurs : P. M. Preshaw ; A. L. Alba [Espagne] ; D. Herrera [Espagne] ; S. Jepsen [Allemagne] ; A. Konstantinidis [Grèce] ; K. Makrilakis [Grèce] ; R. Taylor [Royaume-Uni]Source :
- Diabetologia [ 0012-186X ] ; 2011.
Abstract
Periodontitis is a common chronic inflammatory disease characterised by destruction of the supporting structures of the teeth (the periodontal ligament and alveolar bone). It is highly prevalent (severe periodontitis affects 10–15% of adults) and has multiple negative impacts on quality of life. Epidemiological data confirm that diabetes is a major risk factor for periodontitis; susceptibility to periodontitis is increased by approximately threefold in people with diabetes. There is a clear relationship between degree of hyperglycaemia and severity of periodontitis. The mechanisms that underpin the links between these two conditions are not completely understood, but involve aspects of immune functioning, neutrophil activity, and cytokine biology. There is emerging evidence to support the existence of a two-way relationship between diabetes and periodontitis, with diabetes increasing the risk for periodontitis, and periodontal inflammation negatively affecting glycaemic control. Incidences of macroalbuminuria and end-stage renal disease are increased twofold and threefold, respectively, in diabetic individuals who also have severe periodontitis compared to diabetic individuals without severe periodontitis. Furthermore, the risk of cardiorenal mortality (ischaemic heart disease and diabetic nephropathy combined) is three times higher in diabetic people with severe periodontitis than in diabetic people without severe periodontitis. Treatment of periodontitis is associated with HbA1c reductions of approximately 0.4%. Oral and periodontal health should be promoted as integral components of diabetes management.
Url:
DOI: 10.1007/s00125-011-2342-y
PubMed: 22057194
PubMed Central: 3228943
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M." last="Preshaw">P. M. Preshaw</name><affiliation><nlm:aff id="Aff1">School of Dental Sciences and Institute of Cellular Medicine, Newcastle University, Framlington Place, Newcastle upon Tyne, NE2 4BW UK</nlm:aff><wicri:noCountry code="subfield">NE2 4BW UK</wicri:noCountry></affiliation></author><author><name sortKey="Alba, A L" sort="Alba, A L" uniqKey="Alba A" first="A. L." last="Alba">A. L. Alba</name><affiliation wicri:level="1"><nlm:aff id="Aff2">Endocrinology Department, Hospital de Jove, Gijon, Spain</nlm:aff><country xml:lang="fr">Espagne</country><wicri:regionArea>Endocrinology Department, Hospital de Jove, Gijon</wicri:regionArea><wicri:noRegion>Gijon</wicri:noRegion></affiliation></author><author><name sortKey="Herrera, D" sort="Herrera, D" uniqKey="Herrera D" first="D." last="Herrera">D. 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Jepsen</name><affiliation wicri:level="3"><nlm:aff id="Aff4">Department of Periodontology, Operative and Preventive Dentistry, University of Bonn, Bonn, Germany</nlm:aff><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Periodontology, Operative and Preventive Dentistry, University of Bonn, Bonn</wicri:regionArea><placeName><region type="land" nuts="1">Rhénanie-du-Nord-Westphalie</region><region type="district" nuts="2">District de Cologne</region><settlement type="city">Bonn</settlement></placeName></affiliation></author><author><name sortKey="Konstantinidis, A" sort="Konstantinidis, A" uniqKey="Konstantinidis A" first="A." last="Konstantinidis">A. 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Makrilakis</name><affiliation wicri:level="3"><nlm:aff id="Aff6">Department of Internal Medicine, University of Athens Medical School, Athens, Greece</nlm:aff><country xml:lang="fr">Grèce</country><wicri:regionArea>Department of Internal Medicine, University of Athens Medical School, Athens</wicri:regionArea><placeName><settlement type="city">Athènes</settlement><region nuts="2" type="region">Attique (région)</region></placeName></affiliation></author><author><name sortKey="Taylor, R" sort="Taylor, R" uniqKey="Taylor R" first="R." last="Taylor">R. Taylor</name><affiliation wicri:level="1"><nlm:aff id="Aff7">School of Medical Sciences and Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>School of Medical Sciences and Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne</wicri:regionArea><wicri:noRegion>Newcastle upon Tyne</wicri:noRegion></affiliation></author></analytic><series><title level="j">Diabetologia</title><idno type="ISSN">0012-186X</idno><idno type="eISSN">1432-0428</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Periodontitis is a common chronic inflammatory disease characterised by destruction of the supporting structures of the teeth (the periodontal ligament and alveolar bone). It is highly prevalent (severe periodontitis affects 10–15% of adults) and has multiple negative impacts on quality of life. Epidemiological data confirm that diabetes is a major risk factor for periodontitis; susceptibility to periodontitis is increased by approximately threefold in people with diabetes. There is a clear relationship between degree of hyperglycaemia and severity of periodontitis. The mechanisms that underpin the links between these two conditions are not completely understood, but involve aspects of immune functioning, neutrophil activity, and cytokine biology. There is emerging evidence to support the existence of a two-way relationship between diabetes and periodontitis, with diabetes increasing the risk for periodontitis, and periodontal inflammation negatively affecting glycaemic control. Incidences of macroalbuminuria and end-stage renal disease are increased twofold and threefold, respectively, in diabetic individuals who also have severe periodontitis compared to diabetic individuals without severe periodontitis. Furthermore, the risk of cardiorenal mortality (ischaemic heart disease and diabetic nephropathy combined) is three times higher in diabetic people with severe periodontitis than in diabetic people without severe periodontitis. Treatment of periodontitis is associated with HbA<sub>1c</sub> reductions of approximately 0.4%. Oral and periodontal health should be promoted as integral components of diabetes management.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Fox, Ch" uniqKey="Fox C">CH Fox</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Fox, Ch" uniqKey="Fox C">CH Fox</name></author><author><name sortKey="Jette, Am" uniqKey="Jette A">AM Jette</name></author><author><name sortKey="Mcguire, Sm" uniqKey="Mcguire S">SM McGuire</name></author><author><name sortKey="Feldman, Ha" uniqKey="Feldman H">HA Feldman</name></author><author><name sortKey="Douglass, Cw" uniqKey="Douglass C">CW Douglass</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kelly, M" uniqKey="Kelly M">M Kelly</name></author><author><name sortKey="Steele, J" uniqKey="Steele J">J Steele</name></author><author><name sortKey="Nuttall, N" uniqKey="Nuttall N">N 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Syrjala</name></author><author><name sortKey="Knuuttila, Ml" uniqKey="Knuuttila M">ML Knuuttila</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Soskolne, Wa" uniqKey="Soskolne W">WA Soskolne</name></author><author><name sortKey="Klinger, A" uniqKey="Klinger A">A Klinger</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Preshaw, Pm" uniqKey="Preshaw P">PM Preshaw</name></author></analytic></biblStruct></listBibl></div1></back></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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