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Periodontal Status and A1C Change: Longitudinal results from the Study of Health in Pomerania (SHIP)

Identifieur interne : 000184 ( PascalFrancis/Checkpoint ); précédent : 000183; suivant : 000185

Periodontal Status and A1C Change: Longitudinal results from the Study of Health in Pomerania (SHIP)

Auteurs : Ryan T. Demmer [États-Unis] ; Henri Wallaschofski [Allemagne] ; Moise Desvarieux [États-Unis, France] ; Matthias Nauck [Allemagne] ; Birte Holtfreter [Allemagne] ; Henry Völzke [Allemagne] ; David R. Jr Jacobs [Norvège] ; Thomas Kocher [Allemagne]

Source :

RBID : Pascal:10-0249261

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English descriptors

Abstract

OBJECTIVE - Infection may be a type 2 diabetes risk factor. Periodontal disease is a chronic infection. We hypothesized that periodontal disease was related to A1C progression in diabetes-free participants. RESEARCH DESIGN AND METHODS - The Study of Health in Pomerania (SHIP) is a population-based cohort in Germany including 2,973 diabetes-free participants (53% women; aged 20-81 years). Participants were categorized into four groups according to increasing baseline periodontal disease levels (percentage of sites per mouth with attachment loss ≥5 mm, determined a priori); sample sizes for each respective category were 1,122, 488, 463, and 479 (241 participants were edentulous). Mean absolute changes (year 5 minus baseline) in A1C (ΔA1C) were regressed across periodontal categories while adjusting for confounders (e.g., age, sex, smoking, obesity, physical activity, and family history). RESULTS - Across baseline periodontal disease categories, ΔA1C ± SEM values were 0.023 ± 0.02, 0.023 ± 0.02, 0.065 ± 0.03, and 0.106 ± 0.03 (Ptrend = 0.02), yielding an approximate fivefold increase in the absolute difference in ΔA1C when dentate participants in the highest versus lowest periodontal disease category were compared; these results were markedly stronger among participants with high-sensitivity C-reactive protein ≥1.0 mg/l (Pinteraction = 0.01). When individuals who had neither baseline periodontal disease nor deterioration in periodontal status at 5 years were compared with individuals with both poor baseline periodontal health and longitudinal periodontal deterioration, mean ΔA1C values were 0.005 vs. 0.143% (P = 0.003). CONCLUSIONS - Periodontal disease was associated with 5-year A1C progression, which was similar to that observed for a 2-SD increase in either waist-to-hip ratio or age in this population.


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Pascal:10-0249261

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<name sortKey="Nauck, Matthias" sort="Nauck, Matthias" uniqKey="Nauck M" first="Matthias" last="Nauck">Matthias Nauck</name>
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<name sortKey="Volzke, Henry" sort="Volzke, Henry" uniqKey="Volzke H" first="Henry" last="Völzke">Henry Völzke</name>
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<name sortKey="Jacobs, David R Jr" sort="Jacobs, David R Jr" uniqKey="Jacobs D" first="David R. Jr" last="Jacobs">David R. Jr Jacobs</name>
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<name sortKey="Kocher, Thomas" sort="Kocher, Thomas" uniqKey="Kocher T" first="Thomas" last="Kocher">Thomas Kocher</name>
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<title level="j" type="main">Diabetes care</title>
<title level="j" type="abbreviated">Diabetes care</title>
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<date when="2010">2010</date>
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<term>Change</term>
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<term>Follow up study</term>
<term>Hemoglobin A1c</term>
<term>Human</term>
<term>Inositol-1,4,5-trisphosphate 5-phosphatase</term>
<term>Metabolic diseases</term>
<term>Nutrition</term>
<term>Public health</term>
<term>Result</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr">
<term>Hémoglobine A1c</term>
<term>Changement</term>
<term>Etude longitudinale</term>
<term>Résultat</term>
<term>Santé publique</term>
<term>Inositol-1,4,5-trisphosphate 5-phosphatase</term>
<term>Endocrinologie</term>
<term>Maladie métabolique</term>
<term>Nutrition</term>
<term>Homme</term>
</keywords>
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<term>Santé publique</term>
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<front>
<div type="abstract" xml:lang="en">OBJECTIVE - Infection may be a type 2 diabetes risk factor. Periodontal disease is a chronic infection. We hypothesized that periodontal disease was related to A1C progression in diabetes-free participants. RESEARCH DESIGN AND METHODS - The Study of Health in Pomerania (SHIP) is a population-based cohort in Germany including 2,973 diabetes-free participants (53% women; aged 20-81 years). Participants were categorized into four groups according to increasing baseline periodontal disease levels (percentage of sites per mouth with attachment loss ≥5 mm, determined a priori); sample sizes for each respective category were 1,122, 488, 463, and 479 (241 participants were edentulous). Mean absolute changes (year 5 minus baseline) in A1C (ΔA1C) were regressed across periodontal categories while adjusting for confounders (e.g., age, sex, smoking, obesity, physical activity, and family history). RESULTS - Across baseline periodontal disease categories, ΔA1C ± SEM values were 0.023 ± 0.02, 0.023 ± 0.02, 0.065 ± 0.03, and 0.106 ± 0.03 (P
<sub>trend</sub>
= 0.02), yielding an approximate fivefold increase in the absolute difference in ΔA1C when dentate participants in the highest versus lowest periodontal disease category were compared; these results were markedly stronger among participants with high-sensitivity C-reactive protein ≥1.0 mg/l (P
<sub>interaction</sub>
= 0.01). When individuals who had neither baseline periodontal disease nor deterioration in periodontal status at 5 years were compared with individuals with both poor baseline periodontal health and longitudinal periodontal deterioration, mean ΔA1C values were 0.005 vs. 0.143% (P = 0.003). CONCLUSIONS - Periodontal disease was associated with 5-year A1C progression, which was similar to that observed for a 2-SD increase in either waist-to-hip ratio or age in this population.</div>
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<s3>DEU</s3>
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<sZ>7 aut.</sZ>
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<s1>Institute for Clinical Chemistry and Laboratory Medicine, University of Greifswald</s1>
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<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="07">
<s1>Institute for Community Medicine, University of Greifswald</s1>
<s2>Greifswald</s2>
<s3>DEU</s3>
<sZ>6 aut.</sZ>
</fA14>
<fA20>
<s1>1037-1043</s1>
</fA20>
<fA21>
<s1>2010</s1>
</fA21>
<fA23 i1="01">
<s0>ENG</s0>
</fA23>
<fA43 i1="01">
<s1>INIST</s1>
<s2>18054</s2>
<s5>354000182087110180</s5>
</fA43>
<fA44>
<s0>0000</s0>
<s1>© 2010 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45>
<s0>25 ref.</s0>
</fA45>
<fA47 i1="01" i2="1">
<s0>10-0249261</s0>
</fA47>
<fA60>
<s1>P</s1>
</fA60>
<fA61>
<s0>A</s0>
</fA61>
<fA64 i1="01" i2="1">
<s0>Diabetes care</s0>
</fA64>
<fA66 i1="01">
<s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG">
<s0>OBJECTIVE - Infection may be a type 2 diabetes risk factor. Periodontal disease is a chronic infection. We hypothesized that periodontal disease was related to A1C progression in diabetes-free participants. RESEARCH DESIGN AND METHODS - The Study of Health in Pomerania (SHIP) is a population-based cohort in Germany including 2,973 diabetes-free participants (53% women; aged 20-81 years). Participants were categorized into four groups according to increasing baseline periodontal disease levels (percentage of sites per mouth with attachment loss ≥5 mm, determined a priori); sample sizes for each respective category were 1,122, 488, 463, and 479 (241 participants were edentulous). Mean absolute changes (year 5 minus baseline) in A1C (ΔA1C) were regressed across periodontal categories while adjusting for confounders (e.g., age, sex, smoking, obesity, physical activity, and family history). RESULTS - Across baseline periodontal disease categories, ΔA1C ± SEM values were 0.023 ± 0.02, 0.023 ± 0.02, 0.065 ± 0.03, and 0.106 ± 0.03 (P
<sub>trend</sub>
= 0.02), yielding an approximate fivefold increase in the absolute difference in ΔA1C when dentate participants in the highest versus lowest periodontal disease category were compared; these results were markedly stronger among participants with high-sensitivity C-reactive protein ≥1.0 mg/l (P
<sub>interaction</sub>
= 0.01). When individuals who had neither baseline periodontal disease nor deterioration in periodontal status at 5 years were compared with individuals with both poor baseline periodontal health and longitudinal periodontal deterioration, mean ΔA1C values were 0.005 vs. 0.143% (P = 0.003). CONCLUSIONS - Periodontal disease was associated with 5-year A1C progression, which was similar to that observed for a 2-SD increase in either waist-to-hip ratio or age in this population.</s0>
</fC01>
<fC02 i1="01" i2="X">
<s0>002B21E01</s0>
</fC02>
<fC02 i1="02" i2="X">
<s0>002B22</s0>
</fC02>
<fC02 i1="03" i2="X">
<s0>002B30A11</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE">
<s0>Hémoglobine A1c</s0>
<s5>02</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG">
<s0>Hemoglobin A1c</s0>
<s5>02</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA">
<s0>Hemoglobina A1c</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE">
<s0>Changement</s0>
<s5>03</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG">
<s0>Change</s0>
<s5>03</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA">
<s0>Cambio</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE">
<s0>Etude longitudinale</s0>
<s5>05</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG">
<s0>Follow up study</s0>
<s5>05</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA">
<s0>Estudio longitudinal</s0>
<s5>05</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE">
<s0>Résultat</s0>
<s5>06</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG">
<s0>Result</s0>
<s5>06</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA">
<s0>Resultado</s0>
<s5>06</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE">
<s0>Santé publique</s0>
<s5>08</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG">
<s0>Public health</s0>
<s5>08</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA">
<s0>Salud pública</s0>
<s5>08</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE">
<s0>Inositol-1,4,5-trisphosphate 5-phosphatase</s0>
<s2>FE</s2>
<s5>09</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG">
<s0>Inositol-1,4,5-trisphosphate 5-phosphatase</s0>
<s2>FE</s2>
<s5>09</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA">
<s0>Inositol-1,4,5-trisphosphate 5-phosphatase</s0>
<s2>FE</s2>
<s5>09</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE">
<s0>Endocrinologie</s0>
<s5>11</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG">
<s0>Endocrinology</s0>
<s5>11</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA">
<s0>Endocrinología</s0>
<s5>11</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE">
<s0>Maladie métabolique</s0>
<s5>12</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG">
<s0>Metabolic diseases</s0>
<s5>12</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA">
<s0>Metabolismo patología</s0>
<s5>12</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE">
<s0>Nutrition</s0>
<s5>17</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG">
<s0>Nutrition</s0>
<s5>17</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA">
<s0>Nutrición</s0>
<s5>17</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE">
<s0>Homme</s0>
<s5>25</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG">
<s0>Human</s0>
<s5>25</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA">
<s0>Hombre</s0>
<s5>25</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Phosphoric monoester hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Phosphoric monoester hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Phosphoric monoester hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Esterases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Esterases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Esterases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Enzima</s0>
<s2>FE</s2>
</fC07>
<fN21>
<s1>165</s1>
</fN21>
<fN44 i1="01">
<s1>OTO</s1>
</fN44>
<fN82>
<s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
<affiliations>
<list>
<country>
<li>Allemagne</li>
<li>France</li>
<li>Norvège</li>
<li>États-Unis</li>
</country>
<region>
<li>État de New York</li>
<li>Île-de-France</li>
<li>Østlandet</li>
</region>
<settlement>
<li>New York</li>
<li>Oslo</li>
<li>Paris</li>
</settlement>
<orgName>
<li>Université Columbia</li>
</orgName>
</list>
<tree>
<country name="États-Unis">
<region name="État de New York">
<name sortKey="Demmer, Ryan T" sort="Demmer, Ryan T" uniqKey="Demmer R" first="Ryan T." last="Demmer">Ryan T. Demmer</name>
</region>
<name sortKey="Desvarieux, Moise" sort="Desvarieux, Moise" uniqKey="Desvarieux M" first="Moise" last="Desvarieux">Moise Desvarieux</name>
</country>
<country name="Allemagne">
<noRegion>
<name sortKey="Wallaschofski, Henri" sort="Wallaschofski, Henri" uniqKey="Wallaschofski H" first="Henri" last="Wallaschofski">Henri Wallaschofski</name>
</noRegion>
<name sortKey="Holtfreter, Birte" sort="Holtfreter, Birte" uniqKey="Holtfreter B" first="Birte" last="Holtfreter">Birte Holtfreter</name>
<name sortKey="Kocher, Thomas" sort="Kocher, Thomas" uniqKey="Kocher T" first="Thomas" last="Kocher">Thomas Kocher</name>
<name sortKey="Nauck, Matthias" sort="Nauck, Matthias" uniqKey="Nauck M" first="Matthias" last="Nauck">Matthias Nauck</name>
<name sortKey="Volzke, Henry" sort="Volzke, Henry" uniqKey="Volzke H" first="Henry" last="Völzke">Henry Völzke</name>
</country>
<country name="France">
<region name="Île-de-France">
<name sortKey="Desvarieux, Moise" sort="Desvarieux, Moise" uniqKey="Desvarieux M" first="Moise" last="Desvarieux">Moise Desvarieux</name>
</region>
<name sortKey="Desvarieux, Moise" sort="Desvarieux, Moise" uniqKey="Desvarieux M" first="Moise" last="Desvarieux">Moise Desvarieux</name>
</country>
<country name="Norvège">
<region name="Østlandet">
<name sortKey="Jacobs, David R Jr" sort="Jacobs, David R Jr" uniqKey="Jacobs D" first="David R. Jr" last="Jacobs">David R. Jr Jacobs</name>
</region>
</country>
</tree>
</affiliations>
</record>

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