Total tooth loss and systemic correlates of inflammation: role of obesity.
Identifieur interne : 001266 ( PubMed/Corpus ); précédent : 001265; suivant : 001267Total tooth loss and systemic correlates of inflammation: role of obesity.
Auteurs : Peter Meisel ; Peter Wilke ; Reiner Biffar ; Birte Holtfreter ; Henry Wallaschofski ; Thomas KocherSource :
- Obesity (Silver Spring, Md.) [ 1930-739X ] ; 2012.
English descriptors
- KwdEn :
- Adult, Aged, Aged, 80 and over, Biomarkers (blood), Body Mass Index, C-Reactive Protein (metabolism), Cross-Sectional Studies, Female, Germany (epidemiology), Humans, Inflammation (blood), Inflammation (complications), Inflammation (epidemiology), Inflammation Mediators (metabolism), Male, Middle Aged, Mouth, Edentulous (epidemiology), Mouth, Edentulous (etiology), Obesity (complications), Obesity (epidemiology), Obesity (etiology), Risk Factors, Tooth Loss (epidemiology), Tooth Loss (etiology), Waist-Hip Ratio, Young Adult.
- MESH :
- chemical , blood : Biomarkers.
- chemical , metabolism : C-Reactive Protein, Inflammation Mediators.
- geographic , epidemiology : Germany.
- blood : Inflammation.
- complications : Inflammation, Obesity.
- epidemiology : Inflammation, Mouth, Edentulous, Obesity, Tooth Loss.
- etiology : Mouth, Edentulous, Obesity, Tooth Loss.
- Adult, Aged, Aged, 80 and over, Body Mass Index, Cross-Sectional Studies, Female, Humans, Male, Middle Aged, Risk Factors, Waist-Hip Ratio, Young Adult.
Abstract
Obesity and edentulism are both associated with multiple systemic disorders with an inflammatory background including periodontal diseases. This study aimed to evaluate the different impact of obesity on inflammation in dentate and toothless subjects. The data came from the population-based, cross-sectional study SHIP (Study of Health in Pomerania). We determined anthropometric measures including BMI, waist-to-hip ratio (WHR), diagnostic periodontal parameters, and systemic metabolites. It was shown that measures of systemic markers of inflammation and lipid or glucose metabolism (P < 0.001) were increased with higher WHR. When adjusted for age, sex, smoking, diabetes, education, physical activity, and last dentist's appointment, C-reactive protein (CRP), fibrinogen, and leukocyte count were significantly related to WHR increasing from the first to the fourth WHR quartile (P < 0.001) as well as to the BMI. In both dentate and edentulous subjects higher WHR contributes significantly to increasing systemic CRP and fibrinogen with sex differences. In toothless subjects, while still dependent on increasing WHR, the inflammatory markers CRP and fibrinogen were higher than in dentate subjects, thereby revealing effect modification between sex and edentulism (P < 0.010). In conclusion, subjects with total tooth loss, although devoid of periodontal inflammation, may exhibit increased levels of systemic inflammatory mediators. Possible implications are discussed with respect to obesity and its relationship to inflammation.
DOI: 10.1038/oby.2011.218
PubMed: 21760638
Links to Exploration step
pubmed:21760638Le document en format XML
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first="Henry" last="Wallaschofski">Henry Wallaschofski</name></author><author><name sortKey="Kocher, Thomas" sort="Kocher, Thomas" uniqKey="Kocher T" first="Thomas" last="Kocher">Thomas Kocher</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2012">2012</date><idno type="RBID">pubmed:21760638</idno><idno type="pmid">21760638</idno><idno type="doi">10.1038/oby.2011.218</idno><idno type="wicri:Area/PubMed/Corpus">001266</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001266</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Total tooth loss and systemic correlates of inflammation: role of obesity.</title><author><name sortKey="Meisel, Peter" sort="Meisel, Peter" uniqKey="Meisel P" first="Peter" last="Meisel">Peter Meisel</name><affiliation><nlm:affiliation>Dental Clinics, Department of Periodontology, Ernst Moritz Arndt University Greifswald, Greifswald, Germany. meiselp@uni-greifswald.de</nlm:affiliation></affiliation></author><author><name sortKey="Wilke, Peter" sort="Wilke, Peter" uniqKey="Wilke P" first="Peter" last="Wilke">Peter Wilke</name></author><author><name sortKey="Biffar, Reiner" sort="Biffar, Reiner" uniqKey="Biffar R" first="Reiner" last="Biffar">Reiner Biffar</name></author><author><name sortKey="Holtfreter, Birte" sort="Holtfreter, Birte" uniqKey="Holtfreter B" first="Birte" last="Holtfreter">Birte Holtfreter</name></author><author><name sortKey="Wallaschofski, Henry" sort="Wallaschofski, Henry" uniqKey="Wallaschofski H" first="Henry" last="Wallaschofski">Henry Wallaschofski</name></author><author><name sortKey="Kocher, Thomas" sort="Kocher, Thomas" uniqKey="Kocher T" first="Thomas" last="Kocher">Thomas Kocher</name></author></analytic><series><title level="j">Obesity (Silver Spring, Md.)</title><idno type="eISSN">1930-739X</idno><imprint><date when="2012" 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type="chemical" qualifier="blood" xml:lang="en"><term>Biomarkers</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>C-Reactive Protein</term><term>Inflammation Mediators</term></keywords><keywords scheme="MESH" type="geographic" qualifier="epidemiology" xml:lang="en"><term>Germany</term></keywords><keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Inflammation</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Inflammation</term><term>Obesity</term></keywords><keywords scheme="MESH" qualifier="epidemiology" xml:lang="en"><term>Inflammation</term><term>Mouth, Edentulous</term><term>Obesity</term><term>Tooth Loss</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Mouth, Edentulous</term><term>Obesity</term><term>Tooth Loss</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Body Mass Index</term><term>Cross-Sectional Studies</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Risk Factors</term><term>Waist-Hip Ratio</term><term>Young Adult</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Obesity and edentulism are both associated with multiple systemic disorders with an inflammatory background including periodontal diseases. This study aimed to evaluate the different impact of obesity on inflammation in dentate and toothless subjects. The data came from the population-based, cross-sectional study SHIP (Study of Health in Pomerania). We determined anthropometric measures including BMI, waist-to-hip ratio (WHR), diagnostic periodontal parameters, and systemic metabolites. It was shown that measures of systemic markers of inflammation and lipid or glucose metabolism (P < 0.001) were increased with higher WHR. When adjusted for age, sex, smoking, diabetes, education, physical activity, and last dentist's appointment, C-reactive protein (CRP), fibrinogen, and leukocyte count were significantly related to WHR increasing from the first to the fourth WHR quartile (P < 0.001) as well as to the BMI. In both dentate and edentulous subjects higher WHR contributes significantly to increasing systemic CRP and fibrinogen with sex differences. In toothless subjects, while still dependent on increasing WHR, the inflammatory markers CRP and fibrinogen were higher than in dentate subjects, thereby revealing effect modification between sex and edentulism (P < 0.010). In conclusion, subjects with total tooth loss, although devoid of periodontal inflammation, may exhibit increased levels of systemic inflammatory mediators. Possible implications are discussed with respect to obesity and its relationship to inflammation.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21760638</PMID><DateCompleted><Year>2012</Year><Month>06</Month><Day>12</Day></DateCompleted><DateRevised><Year>2015</Year><Month>11</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1930-739X</ISSN><JournalIssue CitedMedium="Internet"><Volume>20</Volume><Issue>3</Issue><PubDate><Year>2012</Year><Month>Mar</Month></PubDate></JournalIssue><Title>Obesity (Silver Spring, Md.)</Title><ISOAbbreviation>Obesity (Silver Spring)</ISOAbbreviation></Journal><ArticleTitle>Total tooth loss and systemic correlates of inflammation: role of obesity.</ArticleTitle><Pagination><MedlinePgn>644-50</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/oby.2011.218</ELocationID><Abstract><AbstractText>Obesity and edentulism are both associated with multiple systemic disorders with an inflammatory background including periodontal diseases. This study aimed to evaluate the different impact of obesity on inflammation in dentate and toothless subjects. The data came from the population-based, cross-sectional study SHIP (Study of Health in Pomerania). We determined anthropometric measures including BMI, waist-to-hip ratio (WHR), diagnostic periodontal parameters, and systemic metabolites. It was shown that measures of systemic markers of inflammation and lipid or glucose metabolism (P < 0.001) were increased with higher WHR. When adjusted for age, sex, smoking, diabetes, education, physical activity, and last dentist's appointment, C-reactive protein (CRP), fibrinogen, and leukocyte count were significantly related to WHR increasing from the first to the fourth WHR quartile (P < 0.001) as well as to the BMI. In both dentate and edentulous subjects higher WHR contributes significantly to increasing systemic CRP and fibrinogen with sex differences. In toothless subjects, while still dependent on increasing WHR, the inflammatory markers CRP and fibrinogen were higher than in dentate subjects, thereby revealing effect modification between sex and edentulism (P < 0.010). In conclusion, subjects with total tooth loss, although devoid of periodontal inflammation, may exhibit increased levels of systemic inflammatory mediators. Possible implications are discussed with respect to obesity and its relationship to inflammation.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Meisel</LastName><ForeName>Peter</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Dental Clinics, Department of Periodontology, Ernst Moritz Arndt University Greifswald, Greifswald, Germany. meiselp@uni-greifswald.de</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wilke</LastName><ForeName>Peter</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Biffar</LastName><ForeName>Reiner</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Holtfreter</LastName><ForeName>Birte</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Wallaschofski</LastName><ForeName>Henry</ForeName><Initials>H</Initials></Author><Author 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