Evaluating periodontal risk for patients at risk of or suffering from atherosclerosis: recent biological hypotheses and therapeutic consequences.
Identifieur interne : 000323 ( Main/Exploration ); précédent : 000322; suivant : 000324Evaluating periodontal risk for patients at risk of or suffering from atherosclerosis: recent biological hypotheses and therapeutic consequences.
Auteurs : Olivier Huck [France] ; Kenza Saadi-Thiers ; Henri Tenenbaum ; Jean-Luc Davideau ; Christine Romagna ; Yves Laurent ; Yves Cottin ; José G. RoulSource :
- Archives of cardiovascular diseases [ 1875-2128 ] ; 2011.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Appréciation des risques (MeSH), Athérosclérose (immunologie), Athérosclérose (microbiologie), Athérosclérose (prévention et contrôle), Athérosclérose (étiologie), Facteurs de risque (MeSH), Humains (MeSH), Maladies cardiovasculaires (immunologie), Maladies cardiovasculaires (microbiologie), Maladies cardiovasculaires (prévention et contrôle), Maladies cardiovasculaires (étiologie), Maladies parodontales (complications), Maladies parodontales (immunologie), Maladies parodontales (microbiologie), Maladies parodontales (thérapie), Médecine factuelle (MeSH), Médiateurs de l'inflammation (métabolisme), Pronostic (MeSH).
- MESH :
- immunologie : Athérosclérose, Maladies cardiovasculaires, Maladies parodontales.
- microbiologie : Athérosclérose, Maladies cardiovasculaires, Maladies parodontales.
- métabolisme : Maladies parodontales, Médiateurs de l'inflammation.
- prévention et contrôle : Athérosclérose, Maladies cardiovasculaires.
- thérapie : Maladies parodontales.
- étiologie : Athérosclérose, Maladies cardiovasculaires.
- Animaux, Appréciation des risques, Facteurs de risque, Humains, Médecine factuelle, Pronostic.
English descriptors
- KwdEn :
- Animals (MeSH), Atherosclerosis (etiology), Atherosclerosis (immunology), Atherosclerosis (microbiology), Atherosclerosis (prevention & control), Cardiovascular Diseases (etiology), Cardiovascular Diseases (immunology), Cardiovascular Diseases (microbiology), Cardiovascular Diseases (prevention & control), Evidence-Based Medicine (MeSH), Humans (MeSH), Inflammation Mediators (metabolism), Periodontal Diseases (complications), Periodontal Diseases (immunology), Periodontal Diseases (microbiology), Periodontal Diseases (therapy), Prognosis (MeSH), Risk Assessment (MeSH), Risk Factors (MeSH).
- MESH :
- chemical , metabolism : Inflammation Mediators.
- complications : Periodontal Diseases.
- etiology : Atherosclerosis, Cardiovascular Diseases.
- immunology : Atherosclerosis, Cardiovascular Diseases, Periodontal Diseases.
- microbiology : Atherosclerosis, Cardiovascular Diseases, Periodontal Diseases.
- prevention & control : Atherosclerosis, Cardiovascular Diseases.
- therapy : Periodontal Diseases.
- Animals, Evidence-Based Medicine, Humans, Prognosis, Risk Assessment, Risk Factors.
Abstract
Cardiovascular disease, such as atherosclerosis, is the main cause of mortality in developed countries. Most atherosclerosis risk factors have been identified and are treated, improving patient cardiovascular status and reducing mortality, but some remain unknown. Periodontal disease is generally defined as inflammatory disease initiated by accumulation of dental bacterial plaque, leading to the destruction of tissues that support the teeth. Severe forms have a high prevalence (15% of the population) and are associated with the presence of virulent pathogens such as Porphyromonas gingivalis. Epidemiological studies have shown that severe periodontal disease negatively influences cardiovascular status. The aim of this paper was to present a synthesis of the most recent biological data related to the link between periodontal and cardiovascular disease. The potential biological mechanisms involved in these two inflammatory diseases (bacteriological theory, inflammatory theory, immune theory) were developed. According to the observed positive effects of periodontal treatment on systemic conditions, the benefit of a reinforced collaboration between dentists and cardiologists was discussed, especially for patients at risk for cardiovascular disease.
DOI: 10.1016/j.acvd.2011.02.002
PubMed: 21693372
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Most atherosclerosis risk factors have been identified and are treated, improving patient cardiovascular status and reducing mortality, but some remain unknown. Periodontal disease is generally defined as inflammatory disease initiated by accumulation of dental bacterial plaque, leading to the destruction of tissues that support the teeth. Severe forms have a high prevalence (15% of the population) and are associated with the presence of virulent pathogens such as Porphyromonas gingivalis. Epidemiological studies have shown that severe periodontal disease negatively influences cardiovascular status. The aim of this paper was to present a synthesis of the most recent biological data related to the link between periodontal and cardiovascular disease. The potential biological mechanisms involved in these two inflammatory diseases (bacteriological theory, inflammatory theory, immune theory) were developed. According to the observed positive effects of periodontal treatment on systemic conditions, the benefit of a reinforced collaboration between dentists and cardiologists was discussed, especially for patients at risk for cardiovascular disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21693372</PMID><DateCompleted><Year>2011</Year><Month>10</Month><Day>25</Day></DateCompleted><DateRevised><Year>2011</Year><Month>06</Month><Day>22</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1875-2128</ISSN><JournalIssue CitedMedium="Internet"><Volume>104</Volume><Issue>5</Issue><PubDate><Year>2011</Year><Month>May</Month></PubDate></JournalIssue><Title>Archives of cardiovascular diseases</Title><ISOAbbreviation>Arch Cardiovasc Dis</ISOAbbreviation></Journal><ArticleTitle>Evaluating periodontal risk for patients at risk of or suffering from atherosclerosis: recent biological hypotheses and therapeutic consequences.</ArticleTitle><Pagination><MedlinePgn>352-8</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.acvd.2011.02.002</ELocationID><Abstract><AbstractText>Cardiovascular disease, such as atherosclerosis, is the main cause of mortality in developed countries. Most atherosclerosis risk factors have been identified and are treated, improving patient cardiovascular status and reducing mortality, but some remain unknown. Periodontal disease is generally defined as inflammatory disease initiated by accumulation of dental bacterial plaque, leading to the destruction of tissues that support the teeth. Severe forms have a high prevalence (15% of the population) and are associated with the presence of virulent pathogens such as Porphyromonas gingivalis. Epidemiological studies have shown that severe periodontal disease negatively influences cardiovascular status. The aim of this paper was to present a synthesis of the most recent biological data related to the link between periodontal and cardiovascular disease. The potential biological mechanisms involved in these two inflammatory diseases (bacteriological theory, inflammatory theory, immune theory) were developed. According to the observed positive effects of periodontal treatment on systemic conditions, the benefit of a reinforced collaboration between dentists and cardiologists was discussed, especially for patients at risk for cardiovascular disease.</AbstractText><CopyrightInformation>Copyright © 2011 Elsevier Masson SAS. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Huck</LastName><ForeName>Olivier</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>Service de parodontologie, faculté de chirurgie dentaire, Strasbourg, France. huck.olivier@gmail.com</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Saadi-Thiers</LastName><ForeName>Kenza</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Tenenbaum</LastName><ForeName>Henri</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Davideau</LastName><ForeName>Jean-Luc</ForeName><Initials>JL</Initials></Author><Author ValidYN="Y"><LastName>Romagna</LastName><ForeName>Christine</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Laurent</LastName><ForeName>Yves</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Cottin</LastName><ForeName>Yves</ForeName><Initials>Y</Initials></Author><Author 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UI="Q000209" MajorTopicYN="Y">etiology</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002318" MajorTopicYN="N">Cardiovascular Diseases</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019317" MajorTopicYN="N">Evidence-Based Medicine</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018836" MajorTopicYN="N">Inflammation Mediators</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010510" MajorTopicYN="N">Periodontal Diseases</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011379" MajorTopicYN="N">Prognosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018570" MajorTopicYN="N">Risk Assessment</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2010</Year><Month>04</Month><Day>17</Day></PubMedPubDate><PubMedPubDate 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Est</li></region><settlement><li>Strasbourg</li></settlement></list><tree><noCountry><name sortKey="Cottin, Yves" sort="Cottin, Yves" uniqKey="Cottin Y" first="Yves" last="Cottin">Yves Cottin</name><name sortKey="Davideau, Jean Luc" sort="Davideau, Jean Luc" uniqKey="Davideau J" first="Jean-Luc" last="Davideau">Jean-Luc Davideau</name><name sortKey="Laurent, Yves" sort="Laurent, Yves" uniqKey="Laurent Y" first="Yves" last="Laurent">Yves Laurent</name><name sortKey="Romagna, Christine" sort="Romagna, Christine" uniqKey="Romagna C" first="Christine" last="Romagna">Christine Romagna</name><name sortKey="Roul, Jose G" sort="Roul, Jose G" uniqKey="Roul J" first="José G" last="Roul">José G. Roul</name><name sortKey="Saadi Thiers, Kenza" sort="Saadi Thiers, Kenza" uniqKey="Saadi Thiers K" first="Kenza" last="Saadi-Thiers">Kenza Saadi-Thiers</name><name sortKey="Tenenbaum, Henri" sort="Tenenbaum, Henri" uniqKey="Tenenbaum H" first="Henri" last="Tenenbaum">Henri Tenenbaum</name></noCountry><country name="France"><region name="Grand Est"><name sortKey="Huck, Olivier" sort="Huck, Olivier" uniqKey="Huck O" first="Olivier" last="Huck">Olivier Huck</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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