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Antibodies to periodontal pathogens are associated with coronary heart disease

Identifieur interne : 000125 ( PascalFrancis/Curation ); précédent : 000124; suivant : 000126

Antibodies to periodontal pathogens are associated with coronary heart disease

Auteurs : Pirkko J. Pussinen [Finlande] ; Pekka Jousilahti [Finlande] ; Georg Alfthan [Finlande] ; Timo Palosuo [Finlande] ; Sirkka Asikainen [Finlande, Suède] ; Veikko Salomaa [Finlande]

Source :

RBID : Pascal:04-0019041

Descripteurs français

English descriptors

Abstract

Objective-We analyzed the association of coronary heart disease (CHD) and serology of periodontitis in a random sample (n=1163) of men (aged 45 to 74 years) by determining serum IgG-antibodies to Actinobacillus actinomvcetemcomitans and Porphyromonas gingivalis. Methods and Results-CHD (n=159) was more prevalent among edentulous than dentate subjects (19.8% and 12.1%, P=0.003). In the dentate population, CHD was more common among subjects seropositive for P. gingivalis compared with those seronegative (14.0% and 9.7%, P=0.029). Accordingly, CHD was more prevalent in subjects with a high combined antibody response than those with a low response (17.4% and 11.1%, P=0.026). When adjusted for age and several CHD risk factors, the subjects with a high combined antibody response had an odds ratio of 1.5 (95% CI, 0.95 to 2.50, P=0.077) for prevalent CHD. In a linear regression model, the combined antibody response was directly associated with prevalent CHD (P=0.046) and inversely with serum HDL cholesterol concentration (P=0.050). Conclusions-In conclusion, edentulousness and serum antibodies to major periodontal pathogens were associated with CHD. This suggests that periodontal infection or response of the host against the infection may play a role in the pathogenesis of CHD.
pA  
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A02 01      @0 ATVBFA
A03   1    @0 Arterioscler. thromb. vasc. biol.
A05       @2 23
A06       @2 7
A08 01  1  ENG  @1 Antibodies to periodontal pathogens are associated with coronary heart disease
A11 01  1    @1 PUSSINEN (Pirkko J.)
A11 02  1    @1 JOUSILAHTI (Pekka)
A11 03  1    @1 ALFTHAN (Georg)
A11 04  1    @1 PALOSUO (Timo)
A11 05  1    @1 ASIKAINEN (Sirkka)
A11 06  1    @1 SALOMAA (Veikko)
A14 01      @1 Institute of Dentistry, University of Helsinki and Department of Oral and Maxillofacial Diseases, Helsinki University Central Hospital @3 FIN @Z 1 aut. @Z 5 aut.
A14 02      @1 Department of Epidemiology and Health Promotion, KTL-National Public Health Institute @2 Helsinki @3 FIN @Z 2 aut. @Z 6 aut.
A14 03      @1 Department of Health and Functional Ability, KTL-National Public Health Institute @2 Helsinki @3 FIN @Z 3 aut. @Z 4 aut.
A14 04      @1 Umeå University @3 SWE @Z 5 aut.
A20       @1 1250-1254
A21       @1 2003
A23 01      @0 ENG
A43 01      @1 INIST @2 19104 @5 354000119956370190
A44       @0 0000 @1 © 2004 INIST-CNRS. All rights reserved.
A45       @0 15 ref.
A47 01  1    @0 04-0019041
A60       @1 P
A61       @0 A
A64 01  1    @0 Arteriosclerosis, thrombosis, and vascular biology
A66 01      @0 USA
C01 01    ENG  @0 Objective-We analyzed the association of coronary heart disease (CHD) and serology of periodontitis in a random sample (n=1163) of men (aged 45 to 74 years) by determining serum IgG-antibodies to Actinobacillus actinomvcetemcomitans and Porphyromonas gingivalis. Methods and Results-CHD (n=159) was more prevalent among edentulous than dentate subjects (19.8% and 12.1%, P=0.003). In the dentate population, CHD was more common among subjects seropositive for P. gingivalis compared with those seronegative (14.0% and 9.7%, P=0.029). Accordingly, CHD was more prevalent in subjects with a high combined antibody response than those with a low response (17.4% and 11.1%, P=0.026). When adjusted for age and several CHD risk factors, the subjects with a high combined antibody response had an odds ratio of 1.5 (95% CI, 0.95 to 2.50, P=0.077) for prevalent CHD. In a linear regression model, the combined antibody response was directly associated with prevalent CHD (P=0.046) and inversely with serum HDL cholesterol concentration (P=0.050). Conclusions-In conclusion, edentulousness and serum antibodies to major periodontal pathogens were associated with CHD. This suggests that periodontal infection or response of the host against the infection may play a role in the pathogenesis of CHD.
C02 01  X    @0 002B12A03
C03 01  X  FRE  @0 Cardiopathie coronaire @5 01
C03 01  X  ENG  @0 Coronary heart disease @5 01
C03 01  X  SPA  @0 Cardiopatía coronaria @5 01
C03 02  X  FRE  @0 Homme @5 02
C03 02  X  ENG  @0 Human @5 02
C03 02  X  SPA  @0 Hombre @5 02
C03 03  X  FRE  @0 Anticorps @5 03
C03 03  X  ENG  @0 Antibody @5 03
C03 03  X  SPA  @0 Anticuerpo @5 03
C03 04  X  FRE  @0 Parodontite @5 04
C03 04  X  ENG  @0 Periodontitis @5 04
C03 04  X  SPA  @0 Parodontitis @5 04
C03 05  X  FRE  @0 Sérologie @5 05
C03 05  X  ENG  @0 Serology @5 05
C03 05  X  SPA  @0 Serología @5 05
C03 06  X  FRE  @0 Actinobacillus actinomycetemcomitans @2 NS @5 06
C03 06  X  ENG  @0 Actinobacillus actinomycetemcomitans @2 NS @5 06
C03 06  X  SPA  @0 Actinobacillus actinomycetemcomitans @2 NS @5 06
C03 07  X  FRE  @0 Porphyromonas gingivalis @2 NS @5 07
C03 07  X  ENG  @0 Porphyromonas gingivalis @2 NS @5 07
C03 07  X  SPA  @0 Porphyromonas gingivalis @2 NS @5 07
C03 08  X  FRE  @0 Bactériose @2 NM @5 08
C03 08  X  ENG  @0 Bacteriosis @2 NM @5 08
C03 08  X  SPA  @0 Bacteriosis @2 NM @5 08
C03 09  X  FRE  @0 Association morbide @5 09
C03 09  X  ENG  @0 Concomitant disease @5 09
C03 09  X  SPA  @0 Asociación morbosa @5 09
C03 10  X  FRE  @0 Physiopathologie @5 10
C03 10  X  ENG  @0 Pathophysiology @5 10
C03 10  X  SPA  @0 Fisiopatología @5 10
C03 11  X  FRE  @0 Pathogénie @5 11
C03 11  X  ENG  @0 Pathogenesis @5 11
C03 11  X  SPA  @0 Patogenia @5 11
C07 01  X  FRE  @0 Pasteurellaceae @2 NS
C07 01  X  ENG  @0 Pasteurellaceae @2 NS
C07 01  X  SPA  @0 Pasteurellaceae @2 NS
C07 02  X  FRE  @0 Bactérie
C07 02  X  ENG  @0 Bacteria
C07 02  X  SPA  @0 Bacteria
C07 03  X  FRE  @0 Bacteroidaceae @2 NS
C07 03  X  ENG  @0 Bacteroidaceae @2 NS
C07 03  X  SPA  @0 Bacteroidaceae @2 NS
C07 04  X  FRE  @0 Infection @2 NM
C07 04  X  ENG  @0 Infection @2 NM
C07 04  X  SPA  @0 Infección @2 NM
C07 05  X  FRE  @0 Appareil circulatoire pathologie @5 37
C07 05  X  ENG  @0 Cardiovascular disease @5 37
C07 05  X  SPA  @0 Aparato circulatorio patología @5 37
C07 06  X  FRE  @0 Stomatologie @5 45
C07 06  X  ENG  @0 Stomatology @5 45
C07 06  X  SPA  @0 Estomatología @5 45
C07 07  X  FRE  @0 Parodontopathie @5 46
C07 07  X  ENG  @0 Periodontal disease @5 46
C07 07  X  SPA  @0 Parodontopatía @5 46
N21       @1 012
N82       @1 PSI

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Pascal:04-0019041

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<name sortKey="Salomaa, Veikko" sort="Salomaa, Veikko" uniqKey="Salomaa V" first="Veikko" last="Salomaa">Veikko Salomaa</name>
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<term>Actinobacillus actinomycetemcomitans</term>
<term>Antibody</term>
<term>Bacteriosis</term>
<term>Concomitant disease</term>
<term>Coronary heart disease</term>
<term>Human</term>
<term>Pathogenesis</term>
<term>Pathophysiology</term>
<term>Periodontitis</term>
<term>Porphyromonas gingivalis</term>
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<term>Cardiopathie coronaire</term>
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<term>Parodontite</term>
<term>Sérologie</term>
<term>Actinobacillus actinomycetemcomitans</term>
<term>Porphyromonas gingivalis</term>
<term>Bactériose</term>
<term>Association morbide</term>
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<div type="abstract" xml:lang="en">Objective-We analyzed the association of coronary heart disease (CHD) and serology of periodontitis in a random sample (n=1163) of men (aged 45 to 74 years) by determining serum IgG-antibodies to Actinobacillus actinomvcetemcomitans and Porphyromonas gingivalis. Methods and Results-CHD (n=159) was more prevalent among edentulous than dentate subjects (19.8% and 12.1%, P=0.003). In the dentate population, CHD was more common among subjects seropositive for P. gingivalis compared with those seronegative (14.0% and 9.7%, P=0.029). Accordingly, CHD was more prevalent in subjects with a high combined antibody response than those with a low response (17.4% and 11.1%, P=0.026). When adjusted for age and several CHD risk factors, the subjects with a high combined antibody response had an odds ratio of 1.5 (95% CI, 0.95 to 2.50, P=0.077) for prevalent CHD. In a linear regression model, the combined antibody response was directly associated with prevalent CHD (P=0.046) and inversely with serum HDL cholesterol concentration (P=0.050). Conclusions-In conclusion, edentulousness and serum antibodies to major periodontal pathogens were associated with CHD. This suggests that periodontal infection or response of the host against the infection may play a role in the pathogenesis of CHD.</div>
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<s0>Objective-We analyzed the association of coronary heart disease (CHD) and serology of periodontitis in a random sample (n=1163) of men (aged 45 to 74 years) by determining serum IgG-antibodies to Actinobacillus actinomvcetemcomitans and Porphyromonas gingivalis. Methods and Results-CHD (n=159) was more prevalent among edentulous than dentate subjects (19.8% and 12.1%, P=0.003). In the dentate population, CHD was more common among subjects seropositive for P. gingivalis compared with those seronegative (14.0% and 9.7%, P=0.029). Accordingly, CHD was more prevalent in subjects with a high combined antibody response than those with a low response (17.4% and 11.1%, P=0.026). When adjusted for age and several CHD risk factors, the subjects with a high combined antibody response had an odds ratio of 1.5 (95% CI, 0.95 to 2.50, P=0.077) for prevalent CHD. In a linear regression model, the combined antibody response was directly associated with prevalent CHD (P=0.046) and inversely with serum HDL cholesterol concentration (P=0.050). Conclusions-In conclusion, edentulousness and serum antibodies to major periodontal pathogens were associated with CHD. This suggests that periodontal infection or response of the host against the infection may play a role in the pathogenesis of CHD.</s0>
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</fC03>
<fC03 i1="01" i2="X" l="SPA">
<s0>Cardiopatía coronaria</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE">
<s0>Homme</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG">
<s0>Human</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA">
<s0>Hombre</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE">
<s0>Anticorps</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG">
<s0>Antibody</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA">
<s0>Anticuerpo</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE">
<s0>Parodontite</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG">
<s0>Periodontitis</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA">
<s0>Parodontitis</s0>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE">
<s0>Sérologie</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG">
<s0>Serology</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA">
<s0>Serología</s0>
<s5>05</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE">
<s0>Actinobacillus actinomycetemcomitans</s0>
<s2>NS</s2>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG">
<s0>Actinobacillus actinomycetemcomitans</s0>
<s2>NS</s2>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA">
<s0>Actinobacillus actinomycetemcomitans</s0>
<s2>NS</s2>
<s5>06</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE">
<s0>Porphyromonas gingivalis</s0>
<s2>NS</s2>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG">
<s0>Porphyromonas gingivalis</s0>
<s2>NS</s2>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA">
<s0>Porphyromonas gingivalis</s0>
<s2>NS</s2>
<s5>07</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE">
<s0>Bactériose</s0>
<s2>NM</s2>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG">
<s0>Bacteriosis</s0>
<s2>NM</s2>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA">
<s0>Bacteriosis</s0>
<s2>NM</s2>
<s5>08</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE">
<s0>Association morbide</s0>
<s5>09</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG">
<s0>Concomitant disease</s0>
<s5>09</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA">
<s0>Asociación morbosa</s0>
<s5>09</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE">
<s0>Physiopathologie</s0>
<s5>10</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG">
<s0>Pathophysiology</s0>
<s5>10</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA">
<s0>Fisiopatología</s0>
<s5>10</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE">
<s0>Pathogénie</s0>
<s5>11</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG">
<s0>Pathogenesis</s0>
<s5>11</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA">
<s0>Patogenia</s0>
<s5>11</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Pasteurellaceae</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Pasteurellaceae</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Pasteurellaceae</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Bactérie</s0>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Bacteria</s0>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Bacteria</s0>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Bacteroidaceae</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Bacteroidaceae</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Bacteroidaceae</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Infection</s0>
<s2>NM</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Infection</s0>
<s2>NM</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Infección</s0>
<s2>NM</s2>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Appareil circulatoire pathologie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Cardiovascular disease</s0>
<s5>37</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Aparato circulatorio patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE">
<s0>Stomatologie</s0>
<s5>45</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Stomatology</s0>
<s5>45</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA">
<s0>Estomatología</s0>
<s5>45</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE">
<s0>Parodontopathie</s0>
<s5>46</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG">
<s0>Periodontal disease</s0>
<s5>46</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA">
<s0>Parodontopatía</s0>
<s5>46</s5>
</fC07>
<fN21>
<s1>012</s1>
</fN21>
<fN82>
<s1>PSI</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

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