Impact of tooth loss on oral and systemic health.
Identifieur interne : 000E71 ( PubMed/Corpus ); précédent : 000E70; suivant : 000E72Impact of tooth loss on oral and systemic health.
Auteurs : S. Offenbacher ; S P Barros ; S. Altarawneh ; J D Beck ; Z G LoewySource :
- General dentistry [ 0363-6771 ]
English descriptors
- KwdEn :
- Candidiasis, Oral (immunology), Chronic Disease, Focal Infection, Dental (immunology), Gene Expression Regulation (genetics), Health Status, Humans, Mouth, Edentulous (immunology), Mouth, Edentulous (microbiology), Oral Health, Periodontitis (immunology), Periodontitis (microbiology), Risk Factors, Stomatitis, Denture (immunology), Stomatitis, Denture (microbiology).
- MESH :
- genetics : Gene Expression Regulation.
- immunology : Candidiasis, Oral, Focal Infection, Dental, Mouth, Edentulous, Periodontitis, Stomatitis, Denture.
- microbiology : Mouth, Edentulous, Periodontitis, Stomatitis, Denture.
- Chronic Disease, Health Status, Humans, Oral Health, Risk Factors.
Abstract
Periodontitis is a primarily bacterial infection that is common in dentate individuals, while denture stomatitis is a predominantly fungal infection that is common among denture wearers. Both infections may increase a patient's risk for chronic systemic infection dissemination, and may in turn increase the risk of chronic, inflammatory-based systemic diseases. Systemic diseases for which chronic oral infections are believed to confer attributable risk include atherosclerotic and coronary disease, stroke, chronic obstructive pulmonary disease, diabetes, and hypertension. It appears that invasive oral pathogens trigger a systemic inflammatory response via mediators released by the cardiovascular system and liver, putting the patient at increased risk for these diseases. Data comparing gene expression between denture wearers with and without denture stomatitis (and associated Candida albicans infections) has demonstrated unique up- and down-regulation patterns for a number of genes. It appears that down-regulated genes (whose functions are thereby diminished) are associated with reduced epithelial barrier integrity. By contrast, there appears to be an association between up-regulated genes (which have enhanced function) and inflammatory responses that facilitate the ability of C. albicans to bind with and penetrate the oral mucosa. Molecular biological approaches suggest that future therapeutic development could target reducing either the local inflammatory processor, the binding and attachment of C. albicans to the oral mucosa, or both. Ongoing investigations are attempting to incorporate interventions into matrices, to provide a local and sustained presence to therapeutic interventions.
PubMed: 23220304
Links to Exploration step
pubmed:23220304Le document en format XML
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Altarawneh</name></author><author><name sortKey="Beck, J D" sort="Beck, J D" uniqKey="Beck J" first="J D" last="Beck">J D Beck</name></author><author><name sortKey="Loewy, Z G" sort="Loewy, Z G" uniqKey="Loewy Z" first="Z G" last="Loewy">Z G Loewy</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="????"><PubDate><MedlineDate>2012 Nov-Dec</MedlineDate></PubDate></date><idno type="RBID">pubmed:23220304</idno><idno type="pmid">23220304</idno><idno type="wicri:Area/PubMed/Corpus">000E71</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000E71</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Impact of tooth loss on oral and systemic health.</title><author><name sortKey="Offenbacher, S" sort="Offenbacher, S" uniqKey="Offenbacher S" first="S" last="Offenbacher">S. Offenbacher</name><affiliation><nlm:affiliation>Department of Periodontology, University of North Carolina,School of Dentistry, Chapel Hill, NC, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Barros, S P" sort="Barros, S P" uniqKey="Barros S" first="S P" last="Barros">S P Barros</name></author><author><name sortKey="Altarawneh, S" sort="Altarawneh, S" uniqKey="Altarawneh S" first="S" last="Altarawneh">S. Altarawneh</name></author><author><name sortKey="Beck, J D" sort="Beck, J D" uniqKey="Beck J" first="J D" last="Beck">J D Beck</name></author><author><name sortKey="Loewy, Z G" sort="Loewy, Z G" uniqKey="Loewy Z" first="Z G" last="Loewy">Z G Loewy</name></author></analytic><series><title level="j">General dentistry</title><idno type="ISSN">0363-6771</idno></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Candidiasis, Oral (immunology)</term><term>Chronic Disease</term><term>Focal Infection, Dental (immunology)</term><term>Gene Expression Regulation (genetics)</term><term>Health Status</term><term>Humans</term><term>Mouth, Edentulous (immunology)</term><term>Mouth, Edentulous (microbiology)</term><term>Oral Health</term><term>Periodontitis (immunology)</term><term>Periodontitis (microbiology)</term><term>Risk Factors</term><term>Stomatitis, Denture (immunology)</term><term>Stomatitis, Denture (microbiology)</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Gene Expression Regulation</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Candidiasis, Oral</term><term>Focal Infection, Dental</term><term>Mouth, Edentulous</term><term>Periodontitis</term><term>Stomatitis, Denture</term></keywords><keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Mouth, Edentulous</term><term>Periodontitis</term><term>Stomatitis, Denture</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Chronic Disease</term><term>Health Status</term><term>Humans</term><term>Oral Health</term><term>Risk Factors</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Periodontitis is a primarily bacterial infection that is common in dentate individuals, while denture stomatitis is a predominantly fungal infection that is common among denture wearers. Both infections may increase a patient's risk for chronic systemic infection dissemination, and may in turn increase the risk of chronic, inflammatory-based systemic diseases. Systemic diseases for which chronic oral infections are believed to confer attributable risk include atherosclerotic and coronary disease, stroke, chronic obstructive pulmonary disease, diabetes, and hypertension. It appears that invasive oral pathogens trigger a systemic inflammatory response via mediators released by the cardiovascular system and liver, putting the patient at increased risk for these diseases. Data comparing gene expression between denture wearers with and without denture stomatitis (and associated Candida albicans infections) has demonstrated unique up- and down-regulation patterns for a number of genes. It appears that down-regulated genes (whose functions are thereby diminished) are associated with reduced epithelial barrier integrity. By contrast, there appears to be an association between up-regulated genes (which have enhanced function) and inflammatory responses that facilitate the ability of C. albicans to bind with and penetrate the oral mucosa. Molecular biological approaches suggest that future therapeutic development could target reducing either the local inflammatory processor, the binding and attachment of C. albicans to the oral mucosa, or both. Ongoing investigations are attempting to incorporate interventions into matrices, to provide a local and sustained presence to therapeutic interventions.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23220304</PMID><DateCompleted><Year>2013</Year><Month>03</Month><Day>12</Day></DateCompleted><DateRevised><Year>2012</Year><Month>12</Month><Day>11</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0363-6771</ISSN><JournalIssue CitedMedium="Internet"><Volume>60</Volume><Issue>6</Issue><PubDate><MedlineDate>2012 Nov-Dec</MedlineDate></PubDate></JournalIssue><Title>General dentistry</Title><ISOAbbreviation>Gen Dent</ISOAbbreviation></Journal><ArticleTitle>Impact of tooth loss on oral and systemic health.</ArticleTitle><Pagination><MedlinePgn>494-500; quiz p. 501-2</MedlinePgn></Pagination><Abstract><AbstractText>Periodontitis is a primarily bacterial infection that is common in dentate individuals, while denture stomatitis is a predominantly fungal infection that is common among denture wearers. Both infections may increase a patient's risk for chronic systemic infection dissemination, and may in turn increase the risk of chronic, inflammatory-based systemic diseases. Systemic diseases for which chronic oral infections are believed to confer attributable risk include atherosclerotic and coronary disease, stroke, chronic obstructive pulmonary disease, diabetes, and hypertension. It appears that invasive oral pathogens trigger a systemic inflammatory response via mediators released by the cardiovascular system and liver, putting the patient at increased risk for these diseases. Data comparing gene expression between denture wearers with and without denture stomatitis (and associated Candida albicans infections) has demonstrated unique up- and down-regulation patterns for a number of genes. It appears that down-regulated genes (whose functions are thereby diminished) are associated with reduced epithelial barrier integrity. By contrast, there appears to be an association between up-regulated genes (which have enhanced function) and inflammatory responses that facilitate the ability of C. albicans to bind with and penetrate the oral mucosa. Molecular biological approaches suggest that future therapeutic development could target reducing either the local inflammatory processor, the binding and attachment of C. albicans to the oral mucosa, or both. Ongoing investigations are attempting to incorporate interventions into matrices, to provide a local and sustained presence to therapeutic interventions.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Offenbacher</LastName><ForeName>S</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Periodontology, University of North Carolina,School of Dentistry, Chapel Hill, NC, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Barros</LastName><ForeName>S P</ForeName><Initials>SP</Initials></Author><Author ValidYN="Y"><LastName>Altarawneh</LastName><ForeName>S</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Beck</LastName><ForeName>J D</ForeName><Initials>JD</Initials></Author><Author ValidYN="Y"><LastName>Loewy</LastName><ForeName>Z G</ForeName><Initials>ZG</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Gen Dent</MedlineTA><NlmUniqueID>7610466</NlmUniqueID><ISSNLinking>0363-6771</ISSNLinking></MedlineJournalInfo><CitationSubset>D</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D002180" MajorTopicYN="N">Candidiasis, Oral</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002908" MajorTopicYN="N">Chronic Disease</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005491" MajorTopicYN="N">Focal Infection, Dental</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006304" MajorTopicYN="Y">Health Status</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009066" MajorTopicYN="N">Mouth, Edentulous</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000382" MajorTopicYN="Y">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009909" MajorTopicYN="Y">Oral Health</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010518" MajorTopicYN="N">Periodontitis</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013282" MajorTopicYN="N">Stomatitis, Denture</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2012</Year><Month>12</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2012</Year><Month>12</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2013</Year><Month>3</Month><Day>13</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">23220304</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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