Periodontal Status and A1C Change: Longitudinal results from the Study of Health in Pomerania (SHIP)
Identifieur interne : 000490 ( PascalFrancis/Curation ); précédent : 000489; suivant : 000491Periodontal 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 :
- Diabetes care [ 0149-5992 ] ; 2010.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Santé publique, Nutrition, Homme.
English descriptors
- KwdEn :
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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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">Periodontal Status and A1C Change: Longitudinal results from the Study of Health in Pomerania (SHIP)</title><author><name sortKey="Demmer, Ryan T" sort="Demmer, Ryan T" uniqKey="Demmer R" first="Ryan T." last="Demmer">Ryan T. Demmer</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Epidemiology, Mailman School of Public Health, Columbia University</s1><s2>New York, New York</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ></inist:fA14><country>États-Unis</country></affiliation></author><author><name sortKey="Wallaschofski, Henri" sort="Wallaschofski, Henri" uniqKey="Wallaschofski H" first="Henri" last="Wallaschofski">Henri Wallaschofski</name><affiliation wicri:level="1"><inist:fA14 i1="06"><s1>Institute for Clinical Chemistry and Laboratory Medicine, University of Greifswald</s1><s2>Greifswald</s2><s3>DEU</s3><sZ>2 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Allemagne</country></affiliation></author><author><name sortKey="Desvarieux, Moise" sort="Desvarieux, Moise" uniqKey="Desvarieux M" first="Moise" last="Desvarieux">Moise Desvarieux</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Epidemiology, Mailman School of Public Health, Columbia University</s1><s2>New York, New York</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ></inist:fA14><country>États-Unis</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Institut National de la Santé et de la Recherche Médicale, Unité Mixte de Recherche S707, and Universite Pierre et Marie Curie-Paris 6</s1><s2>Paris</s2><s3>FRA</s3><sZ>3 aut.</sZ></inist:fA14><country>France</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Ecole des Hautes Etudes en Sante Publique, Paris et Rennes</s1><s2>Paris</s2><s3>FRA</s3><sZ>3 aut.</sZ></inist:fA14><country>France</country></affiliation></author><author><name sortKey="Nauck, Matthias" sort="Nauck, Matthias" uniqKey="Nauck M" first="Matthias" last="Nauck">Matthias Nauck</name><affiliation wicri:level="1"><inist:fA14 i1="06"><s1>Institute for Clinical Chemistry and Laboratory Medicine, University of Greifswald</s1><s2>Greifswald</s2><s3>DEU</s3><sZ>2 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Allemagne</country></affiliation></author><author><name sortKey="Holtfreter, Birte" sort="Holtfreter, Birte" uniqKey="Holtfreter B" first="Birte" last="Holtfreter">Birte Holtfreter</name><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Unit of Periodontology, Department of Restorative Dentistry, Periodontology and Endodontology, Ernst-Moritz-Arndt-University Greifswald</s1><s2>Greifswald</s2><s3>DEU</s3><sZ>5 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>Allemagne</country></affiliation></author><author><name sortKey="Volzke, Henry" sort="Volzke, Henry" uniqKey="Volzke H" first="Henry" last="Völzke">Henry Völzke</name><affiliation wicri:level="1"><inist:fA14 i1="07"><s1>Institute for Community Medicine, University of Greifswald</s1><s2>Greifswald</s2><s3>DEU</s3><sZ>6 aut.</sZ></inist:fA14><country>Allemagne</country></affiliation></author><author><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><affiliation wicri:level="1"><inist:fA14 i1="05"><s1>Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, Minnesota, and the Department of Nutrition, University of Oslo</s1><s2>Oslo</s2><s3>NOR</s3><sZ>7 aut.</sZ></inist:fA14><country>Norvège</country></affiliation></author><author><name sortKey="Kocher, Thomas" sort="Kocher, Thomas" uniqKey="Kocher T" first="Thomas" last="Kocher">Thomas Kocher</name><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Unit of Periodontology, Department of Restorative Dentistry, Periodontology and Endodontology, Ernst-Moritz-Arndt-University Greifswald</s1><s2>Greifswald</s2><s3>DEU</s3><sZ>5 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>Allemagne</country></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">10-0249261</idno><date when="2010">2010</date><idno type="stanalyst">PASCAL 10-0249261 INIST</idno><idno type="RBID">Pascal:10-0249261</idno><idno type="wicri:Area/PascalFrancis/Corpus">000211</idno><idno type="stanalyst">FRANCIS 10-0249261 INIST</idno><idno type="wicri:Area/PascalFrancis/Corpus">000247</idno><idno type="wicri:Area/PascalFrancis/Curation">000490</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Periodontal Status and A1C Change: Longitudinal results from the Study of Health in Pomerania (SHIP)</title><author><name sortKey="Demmer, Ryan T" sort="Demmer, Ryan T" uniqKey="Demmer R" first="Ryan T." last="Demmer">Ryan T. Demmer</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Epidemiology, Mailman School of Public Health, Columbia University</s1><s2>New York, New York</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ></inist:fA14><country>États-Unis</country></affiliation></author><author><name sortKey="Wallaschofski, Henri" sort="Wallaschofski, Henri" uniqKey="Wallaschofski H" first="Henri" last="Wallaschofski">Henri Wallaschofski</name><affiliation wicri:level="1"><inist:fA14 i1="06"><s1>Institute for Clinical Chemistry and Laboratory Medicine, University of Greifswald</s1><s2>Greifswald</s2><s3>DEU</s3><sZ>2 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Allemagne</country></affiliation></author><author><name sortKey="Desvarieux, Moise" sort="Desvarieux, Moise" uniqKey="Desvarieux M" first="Moise" last="Desvarieux">Moise Desvarieux</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Epidemiology, Mailman School of Public Health, Columbia University</s1><s2>New York, New York</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ></inist:fA14><country>États-Unis</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Institut National de la Santé et de la Recherche Médicale, Unité Mixte de Recherche S707, and Universite Pierre et Marie Curie-Paris 6</s1><s2>Paris</s2><s3>FRA</s3><sZ>3 aut.</sZ></inist:fA14><country>France</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Ecole des Hautes Etudes en Sante Publique, Paris et Rennes</s1><s2>Paris</s2><s3>FRA</s3><sZ>3 aut.</sZ></inist:fA14><country>France</country></affiliation></author><author><name sortKey="Nauck, Matthias" sort="Nauck, Matthias" uniqKey="Nauck M" first="Matthias" last="Nauck">Matthias Nauck</name><affiliation wicri:level="1"><inist:fA14 i1="06"><s1>Institute for Clinical Chemistry and Laboratory Medicine, University of Greifswald</s1><s2>Greifswald</s2><s3>DEU</s3><sZ>2 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Allemagne</country></affiliation></author><author><name sortKey="Holtfreter, Birte" sort="Holtfreter, Birte" uniqKey="Holtfreter B" first="Birte" last="Holtfreter">Birte Holtfreter</name><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Unit of Periodontology, Department of Restorative Dentistry, Periodontology and Endodontology, Ernst-Moritz-Arndt-University Greifswald</s1><s2>Greifswald</s2><s3>DEU</s3><sZ>5 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>Allemagne</country></affiliation></author><author><name sortKey="Volzke, Henry" sort="Volzke, Henry" uniqKey="Volzke H" first="Henry" last="Völzke">Henry Völzke</name><affiliation wicri:level="1"><inist:fA14 i1="07"><s1>Institute for Community Medicine, University of Greifswald</s1><s2>Greifswald</s2><s3>DEU</s3><sZ>6 aut.</sZ></inist:fA14><country>Allemagne</country></affiliation></author><author><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><affiliation wicri:level="1"><inist:fA14 i1="05"><s1>Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, Minnesota, and the Department of Nutrition, University of Oslo</s1><s2>Oslo</s2><s3>NOR</s3><sZ>7 aut.</sZ></inist:fA14><country>Norvège</country></affiliation></author><author><name sortKey="Kocher, Thomas" sort="Kocher, Thomas" uniqKey="Kocher T" first="Thomas" last="Kocher">Thomas Kocher</name><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Unit of Periodontology, Department of Restorative Dentistry, Periodontology and Endodontology, Ernst-Moritz-Arndt-University Greifswald</s1><s2>Greifswald</s2><s3>DEU</s3><sZ>5 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>Allemagne</country></affiliation></author></analytic><series><title level="j" type="main">Diabetes care</title><title level="j" type="abbreviated">Diabetes care</title><idno type="ISSN">0149-5992</idno><imprint><date when="2010">2010</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Diabetes care</title><title level="j" type="abbreviated">Diabetes care</title><idno type="ISSN">0149-5992</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Change</term><term>Endocrinology</term><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><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Santé publique</term><term>Nutrition</term><term>Homme</term></keywords></textClass></profileDesc></teiHeader><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></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0149-5992</s0></fA01><fA02 i1="01"><s0>DICAD2</s0></fA02><fA03 i2="1"><s0>Diabetes care</s0></fA03><fA05><s2>33</s2></fA05><fA06><s2>5</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Periodontal Status and A1C Change: Longitudinal results from the Study of Health in Pomerania (SHIP)</s1></fA08><fA11 i1="01" i2="1"><s1>DEMMER (Ryan T.)</s1></fA11><fA11 i1="02" i2="1"><s1>WALLASCHOFSKI (Henri)</s1></fA11><fA11 i1="03" i2="1"><s1>DESVARIEUX (Moise)</s1></fA11><fA11 i1="04" i2="1"><s1>NAUCK (Matthias)</s1></fA11><fA11 i1="05" i2="1"><s1>HOLTFRETER (Birte)</s1></fA11><fA11 i1="06" i2="1"><s1>VÖLZKE (Henry)</s1></fA11><fA11 i1="07" i2="1"><s1>JACOBS (David R. JR)</s1></fA11><fA11 i1="08" i2="1"><s1>KOCHER (Thomas)</s1></fA11><fA14 i1="01"><s1>Department of Epidemiology, Mailman School of Public Health, Columbia University</s1><s2>New York, New York</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ></fA14><fA14 i1="02"><s1>Institut National de la Santé et de la Recherche Médicale, Unité Mixte de Recherche S707, and Universite Pierre et Marie Curie-Paris 6</s1><s2>Paris</s2><s3>FRA</s3><sZ>3 aut.</sZ></fA14><fA14 i1="03"><s1>Ecole des Hautes Etudes en Sante Publique, Paris et Rennes</s1><s2>Paris</s2><s3>FRA</s3><sZ>3 aut.</sZ></fA14><fA14 i1="04"><s1>Unit of Periodontology, Department of Restorative Dentistry, Periodontology and Endodontology, Ernst-Moritz-Arndt-University Greifswald</s1><s2>Greifswald</s2><s3>DEU</s3><sZ>5 aut.</sZ><sZ>8 aut.</sZ></fA14><fA14 i1="05"><s1>Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, Minnesota, and the Department of Nutrition, University of Oslo</s1><s2>Oslo</s2><s3>NOR</s3><sZ>7 aut.</sZ></fA14><fA14 i1="06"><s1>Institute for Clinical Chemistry and Laboratory Medicine, University of Greifswald</s1><s2>Greifswald</s2><s3>DEU</s3><sZ>2 aut.</sZ><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></record>Pour manipuler ce document sous Unix (Dilib)
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|texte= Periodontal Status and A1C Change: Longitudinal results from the Study of Health in Pomerania (SHIP)
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