Oral infection, hyperglycemia, and endothelial dysfunction
Identifieur interne : 006670 ( Main/Exploration ); précédent : 006669; suivant : 006671Oral infection, hyperglycemia, and endothelial dysfunction
Auteurs : Sok-Ja Janket ; Judith A. Jones ; Jukka H. Meurman ; Alison E. Baird ; Thomas E. Van DykeSource :
- Oral surgery, oral medicine, oral pathology, oral radiology, and endodontics [ 1079-2104 ] ; 2007.
Abstract
Metabolic syndrome and type 2 diabetes (T2DM) resulting from sustained hyperglycemia are considered as risk factors for cardiovascular disease (CVD) but the mechanism for their contribution to cardiopathogenesis is not well understood. Hyperglycemia induces nonenzymatic glycation of protein-yielding advanced glycation end products (AGE), which are postulated to stimulate interleukin-6 (IL-6) expression, triggering the liver to secrete tissue necrosis factor α (TNF-α) and C-reactive protein (CRP) that contribute to CVD pathogenesis. Although the high prevalence of periodontitis among individuals with diabetes is well known by dental researchers, it is relatively unrecognized in the medical community. The expression of the same proinflammatory mediators implicated in hyperglycemia (i.e., IL-6, TNF-α, and CRP) have been reported to be associated with periodontal disease and increased risk for CVD. We will review published evidence related to these 2 pathways and offer a consensus.
Url:
DOI: 10.1016/j.tripleo.2007.06.027
PubMed: 17905606
PubMed Central: 2574939
Affiliations:
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Jones</name><affiliation><nlm:aff id="A2">Professor and Chair, Department of General Dentistry, Boston University School of Dental Medicine.</nlm:aff><wicri:noCountry code="subfield">Boston University School of Dental Medicine.</wicri:noCountry></affiliation></author><author><name sortKey="Meurman, Jukka H" sort="Meurman, Jukka H" uniqKey="Meurman J" first="Jukka H." last="Meurman">Jukka H. Meurman</name><affiliation><nlm:aff id="A3">Professor, Institute of Dentistry, University of Helsinki Central Hospital and Institute of Dentistry.</nlm:aff><wicri:noCountry code="subfield">University of Helsinki Central Hospital and Institute of Dentistry.</wicri:noCountry></affiliation></author><author><name sortKey="Baird, Alison E" sort="Baird, Alison E" uniqKey="Baird A" first="Alison E." last="Baird">Alison E. 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Jones</name><affiliation><nlm:aff id="A2">Professor and Chair, Department of General Dentistry, Boston University School of Dental Medicine.</nlm:aff><wicri:noCountry code="subfield">Boston University School of Dental Medicine.</wicri:noCountry></affiliation></author><author><name sortKey="Meurman, Jukka H" sort="Meurman, Jukka H" uniqKey="Meurman J" first="Jukka H." last="Meurman">Jukka H. Meurman</name><affiliation><nlm:aff id="A3">Professor, Institute of Dentistry, University of Helsinki Central Hospital and Institute of Dentistry.</nlm:aff><wicri:noCountry code="subfield">University of Helsinki Central Hospital and Institute of Dentistry.</wicri:noCountry></affiliation></author><author><name sortKey="Baird, Alison E" sort="Baird, Alison E" uniqKey="Baird A" first="Alison E." last="Baird">Alison E. Baird</name><affiliation><nlm:aff id="A4">Chief, Stroke Division, National Institutes of Neurologic Disorders and Stroke, National Institutes of Health.</nlm:aff><wicri:noCountry code="subfield">National Institutes of Health.</wicri:noCountry></affiliation></author><author><name sortKey="Van Dyke, Thomas E" sort="Van Dyke, Thomas E" uniqKey="Van Dyke T" first="Thomas E." last="Van Dyke">Thomas E. Van Dyke</name><affiliation><nlm:aff id="A5">Professor, Department of Periodontology and Oral Biology, Department of Periodontology and Oral Biology, Boston University School of Dental Medicine.</nlm:aff><wicri:noCountry code="subfield">Boston University School of Dental Medicine.</wicri:noCountry></affiliation></author></analytic><series><title level="j">Oral surgery, oral medicine, oral pathology, oral radiology, and endodontics</title><idno type="ISSN">1079-2104</idno><idno type="eISSN">1528-395X</idno><imprint><date when="2007">2007</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">Metabolic syndrome and type 2 diabetes (T2DM) resulting from sustained hyperglycemia are considered as risk factors for cardiovascular disease (CVD) but the mechanism for their contribution to cardiopathogenesis is not well understood. Hyperglycemia induces nonenzymatic glycation of protein-yielding advanced glycation end products (AGE), which are postulated to stimulate interleukin-6 (IL-6) expression, triggering the liver to secrete tissue necrosis factor α (TNF-α) and C-reactive protein (CRP) that contribute to CVD pathogenesis. Although the high prevalence of periodontitis among individuals with diabetes is well known by dental researchers, it is relatively unrecognized in the medical community. The expression of the same proinflammatory mediators implicated in hyperglycemia (i.e., IL-6, TNF-α, and CRP) have been reported to be associated with periodontal disease and increased risk for CVD. We will review published evidence related to these 2 pathways and offer a consensus.</p></div></front></TEI><affiliations><list></list><tree><noCountry><name sortKey="Baird, Alison E" sort="Baird, Alison E" uniqKey="Baird A" first="Alison E." last="Baird">Alison E. Baird</name><name sortKey="Janket, Sok Ja" sort="Janket, Sok Ja" uniqKey="Janket S" first="Sok-Ja" last="Janket">Sok-Ja Janket</name><name sortKey="Jones, Judith A" sort="Jones, Judith A" uniqKey="Jones J" first="Judith A." last="Jones">Judith A. Jones</name><name sortKey="Meurman, Jukka H" sort="Meurman, Jukka H" uniqKey="Meurman J" first="Jukka H." last="Meurman">Jukka H. Meurman</name><name sortKey="Van Dyke, Thomas E" sort="Van Dyke, Thomas E" uniqKey="Van Dyke T" first="Thomas E." last="Van Dyke">Thomas E. Van Dyke</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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