Natural distribution of 5 bacteria associated with periodontal disease
The purpose of this study was to determine the prevalence and distribution of 5 bacterial pathogens in subgingival plaque, their relationship with each other and probing depth. Plaque was collected from 6905 sites in 938 subjects. A bacterial concentration fluorescence immunoassay and bacterial spec...
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Veröffentlicht in: | Journal of clinical periodontology 1993-11, Vol.20 (10), p.699-706 |
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description | The purpose of this study was to determine the prevalence and distribution of 5 bacterial pathogens in subgingival plaque, their relationship with each other and probing depth. Plaque was collected from 6905 sites in 938 subjects. A bacterial concentration fluorescence immunoassay and bacterial specific monoclonal antibodies were used to determine the presence and level of P. gingivalis (Pg), A. actinomycetemcomitans (Aa), P. intermedia (Pi), E. carrodens (Ec) and F. nucleatum (Fn) in each plaque sample. The prevalence in subjects was lowest for Pg (32%) and highest for Ec (49%). The site‐based frequency distribution of these bacterial species ranged from 10.3% for Pg to 18.7% for Ec. Pi and Ec were the bacterial combination most often found together in a subject (27.2%). While 64.0% of the sites were without any of the 5 bacterial species evaluated, 20.2% had only 1 of the 5 bacterial species evaluated. The remaining 15.8% of sites had at least 2 bacteria species present. There was a general linear association of the detection level of bacterial species and probing depth. The odds ratios were 3.9 (Pg). 3.0 (Aa), 4.0 (Pi). 2.7 (Ec) and 2.8 (Fn) of finding high levels of these bacterial pathogens at > 5 mm probing depth (p≤ 0.01). Mean probing depth at molar sites without a specific bacteria was greater (p≤ 0.01) in subjects wish a specific bacterium compared to molar sites in subjects without the bacteria. The observation that these 5 bacterial species frequently inhabit the subgingival environment, yet are not associated with advanced disease, suggest that a susceptible host is required, in addition to a “pathogenic bacteria”, before disease progression may occur. |
doi_str_mv | 10.1111/j.1600-051X.1993.tb00694.x |
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F. ; Aeppli, D. M. ; Pihlstrom, B. ; Anderson, L. ; Stoltenberg, J. ; Osborn, J. ; Hardie, N. ; Shelburne, C. ; Fischer, G.</creator><creatorcontrib>Wolff, L. F. ; Aeppli, D. M. ; Pihlstrom, B. ; Anderson, L. ; Stoltenberg, J. ; Osborn, J. ; Hardie, N. ; Shelburne, C. ; Fischer, G.</creatorcontrib><description>The purpose of this study was to determine the prevalence and distribution of 5 bacterial pathogens in subgingival plaque, their relationship with each other and probing depth. Plaque was collected from 6905 sites in 938 subjects. A bacterial concentration fluorescence immunoassay and bacterial specific monoclonal antibodies were used to determine the presence and level of P. gingivalis (Pg), A. actinomycetemcomitans (Aa), P. intermedia (Pi), E. carrodens (Ec) and F. nucleatum (Fn) in each plaque sample. The prevalence in subjects was lowest for Pg (32%) and highest for Ec (49%). The site‐based frequency distribution of these bacterial species ranged from 10.3% for Pg to 18.7% for Ec. Pi and Ec were the bacterial combination most often found together in a subject (27.2%). While 64.0% of the sites were without any of the 5 bacterial species evaluated, 20.2% had only 1 of the 5 bacterial species evaluated. The remaining 15.8% of sites had at least 2 bacteria species present. There was a general linear association of the detection level of bacterial species and probing depth. The odds ratios were 3.9 (Pg). 3.0 (Aa), 4.0 (Pi). 2.7 (Ec) and 2.8 (Fn) of finding high levels of these bacterial pathogens at > 5 mm probing depth (p≤ 0.01). Mean probing depth at molar sites without a specific bacteria was greater (p≤ 0.01) in subjects wish a specific bacterium compared to molar sites in subjects without the bacteria. The observation that these 5 bacterial species frequently inhabit the subgingival environment, yet are not associated with advanced disease, suggest that a susceptible host is required, in addition to a “pathogenic bacteria”, before disease progression may occur.</description><identifier>ISSN: 0303-6979</identifier><identifier>EISSN: 1600-051X</identifier><identifier>DOI: 10.1111/j.1600-051X.1993.tb00694.x</identifier><identifier>PMID: 8276979</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adult ; Age Factors ; Aged ; Aggregatibacter actinomycetemcomitans - isolation & purification ; Bacteria - isolation & purification ; bacterial pathogens ; Bacteroidaceae - isolation & purification ; Dental Plaque - microbiology ; Dentistry ; Eikenella corrodens - isolation & purification ; Female ; Humans ; immunoassay ; Linear Models ; Male ; Middle Aged ; Odds Ratio ; periodontal disease ; Periodontal Diseases - etiology ; Periodontal Diseases - microbiology ; Periodontal Pocket - microbiology ; Prevalence ; Sex Factors</subject><ispartof>Journal of clinical periodontology, 1993-11, Vol.20 (10), p.699-706</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4379-158b74a5e2a678398534a29004cf9170b67ae27006b37b4aa5464ed6be9306103</citedby><cites>FETCH-LOGICAL-c4379-158b74a5e2a678398534a29004cf9170b67ae27006b37b4aa5464ed6be9306103</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1600-051X.1993.tb00694.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1600-051X.1993.tb00694.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8276979$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wolff, L. F.</creatorcontrib><creatorcontrib>Aeppli, D. M.</creatorcontrib><creatorcontrib>Pihlstrom, B.</creatorcontrib><creatorcontrib>Anderson, L.</creatorcontrib><creatorcontrib>Stoltenberg, J.</creatorcontrib><creatorcontrib>Osborn, J.</creatorcontrib><creatorcontrib>Hardie, N.</creatorcontrib><creatorcontrib>Shelburne, C.</creatorcontrib><creatorcontrib>Fischer, G.</creatorcontrib><title>Natural distribution of 5 bacteria associated with periodontal disease</title><title>Journal of clinical periodontology</title><addtitle>J Clin Periodontol</addtitle><description>The purpose of this study was to determine the prevalence and distribution of 5 bacterial pathogens in subgingival plaque, their relationship with each other and probing depth. Plaque was collected from 6905 sites in 938 subjects. A bacterial concentration fluorescence immunoassay and bacterial specific monoclonal antibodies were used to determine the presence and level of P. gingivalis (Pg), A. actinomycetemcomitans (Aa), P. intermedia (Pi), E. carrodens (Ec) and F. nucleatum (Fn) in each plaque sample. The prevalence in subjects was lowest for Pg (32%) and highest for Ec (49%). The site‐based frequency distribution of these bacterial species ranged from 10.3% for Pg to 18.7% for Ec. Pi and Ec were the bacterial combination most often found together in a subject (27.2%). While 64.0% of the sites were without any of the 5 bacterial species evaluated, 20.2% had only 1 of the 5 bacterial species evaluated. The remaining 15.8% of sites had at least 2 bacteria species present. There was a general linear association of the detection level of bacterial species and probing depth. The odds ratios were 3.9 (Pg). 3.0 (Aa), 4.0 (Pi). 2.7 (Ec) and 2.8 (Fn) of finding high levels of these bacterial pathogens at > 5 mm probing depth (p≤ 0.01). Mean probing depth at molar sites without a specific bacteria was greater (p≤ 0.01) in subjects wish a specific bacterium compared to molar sites in subjects without the bacteria. The observation that these 5 bacterial species frequently inhabit the subgingival environment, yet are not associated with advanced disease, suggest that a susceptible host is required, in addition to a “pathogenic bacteria”, before disease progression may occur.</description><subject>Adult</subject><subject>Age Factors</subject><subject>Aged</subject><subject>Aggregatibacter actinomycetemcomitans - isolation & purification</subject><subject>Bacteria - isolation & purification</subject><subject>bacterial pathogens</subject><subject>Bacteroidaceae - isolation & purification</subject><subject>Dental Plaque - microbiology</subject><subject>Dentistry</subject><subject>Eikenella corrodens - isolation & purification</subject><subject>Female</subject><subject>Humans</subject><subject>immunoassay</subject><subject>Linear Models</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Odds Ratio</subject><subject>periodontal disease</subject><subject>Periodontal Diseases - etiology</subject><subject>Periodontal Diseases - microbiology</subject><subject>Periodontal Pocket - microbiology</subject><subject>Prevalence</subject><subject>Sex Factors</subject><issn>0303-6979</issn><issn>1600-051X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkMtu2zAQRYkigesk_YQCQhbZSRmaFClmUxRubOcBp4sU7Y4YSjRKV7ZckoKdv48EGd6HGwJz5x6Ch5BrChntzu06owIghZz-yahSLIsGQCieHT6R8Sk6I2NgwFKhpPpMLkJYA1DJGBuRUTGR_XhMZkuMrcc6qVyI3pk2umabNKskTwyW0XqHCYbQlA6jrZK9i3-TXTdtqmYbh5rFYK_I-QrrYL8c70vya3b_Ol2kzy_zh-n357TkTKqU5oWRHHM7QSELpoqccZwoAF6uFJVghEQ7kd1nDJOGI-ZccFsJYxUDQYFdkpuBu_PN_9aGqDculLaucWubNmgpKC8ELbrFu2Gx9E0I3q70zrsN-jdNQfcS9Vr3pnRvSvcS9VGiPnTlr8dXWrOx1al6tNbl34Z872r79gGyfpz-vBeqJ6QDobNuDycC-n9aSCZz_Xs5169PP5YLUAvN2DvGHpCU</recordid><startdate>199311</startdate><enddate>199311</enddate><creator>Wolff, L. F.</creator><creator>Aeppli, D. M.</creator><creator>Pihlstrom, B.</creator><creator>Anderson, L.</creator><creator>Stoltenberg, J.</creator><creator>Osborn, J.</creator><creator>Hardie, N.</creator><creator>Shelburne, C.</creator><creator>Fischer, G.</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>199311</creationdate><title>Natural distribution of 5 bacteria associated with periodontal disease</title><author>Wolff, L. F. ; Aeppli, D. M. ; Pihlstrom, B. ; Anderson, L. ; Stoltenberg, J. ; Osborn, J. ; Hardie, N. ; Shelburne, C. ; Fischer, G.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4379-158b74a5e2a678398534a29004cf9170b67ae27006b37b4aa5464ed6be9306103</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Adult</topic><topic>Age Factors</topic><topic>Aged</topic><topic>Aggregatibacter actinomycetemcomitans - isolation & purification</topic><topic>Bacteria - isolation & purification</topic><topic>bacterial pathogens</topic><topic>Bacteroidaceae - isolation & purification</topic><topic>Dental Plaque - microbiology</topic><topic>Dentistry</topic><topic>Eikenella corrodens - isolation & purification</topic><topic>Female</topic><topic>Humans</topic><topic>immunoassay</topic><topic>Linear Models</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Odds Ratio</topic><topic>periodontal disease</topic><topic>Periodontal Diseases - etiology</topic><topic>Periodontal Diseases - microbiology</topic><topic>Periodontal Pocket - microbiology</topic><topic>Prevalence</topic><topic>Sex Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wolff, L. F.</creatorcontrib><creatorcontrib>Aeppli, D. M.</creatorcontrib><creatorcontrib>Pihlstrom, B.</creatorcontrib><creatorcontrib>Anderson, L.</creatorcontrib><creatorcontrib>Stoltenberg, J.</creatorcontrib><creatorcontrib>Osborn, J.</creatorcontrib><creatorcontrib>Hardie, N.</creatorcontrib><creatorcontrib>Shelburne, C.</creatorcontrib><creatorcontrib>Fischer, G.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of clinical periodontology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wolff, L. F.</au><au>Aeppli, D. M.</au><au>Pihlstrom, B.</au><au>Anderson, L.</au><au>Stoltenberg, J.</au><au>Osborn, J.</au><au>Hardie, N.</au><au>Shelburne, C.</au><au>Fischer, G.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Natural distribution of 5 bacteria associated with periodontal disease</atitle><jtitle>Journal of clinical periodontology</jtitle><addtitle>J Clin Periodontol</addtitle><date>1993-11</date><risdate>1993</risdate><volume>20</volume><issue>10</issue><spage>699</spage><epage>706</epage><pages>699-706</pages><issn>0303-6979</issn><eissn>1600-051X</eissn><abstract>The purpose of this study was to determine the prevalence and distribution of 5 bacterial pathogens in subgingival plaque, their relationship with each other and probing depth. Plaque was collected from 6905 sites in 938 subjects. A bacterial concentration fluorescence immunoassay and bacterial specific monoclonal antibodies were used to determine the presence and level of P. gingivalis (Pg), A. actinomycetemcomitans (Aa), P. intermedia (Pi), E. carrodens (Ec) and F. nucleatum (Fn) in each plaque sample. The prevalence in subjects was lowest for Pg (32%) and highest for Ec (49%). The site‐based frequency distribution of these bacterial species ranged from 10.3% for Pg to 18.7% for Ec. Pi and Ec were the bacterial combination most often found together in a subject (27.2%). While 64.0% of the sites were without any of the 5 bacterial species evaluated, 20.2% had only 1 of the 5 bacterial species evaluated. The remaining 15.8% of sites had at least 2 bacteria species present. There was a general linear association of the detection level of bacterial species and probing depth. The odds ratios were 3.9 (Pg). 3.0 (Aa), 4.0 (Pi). 2.7 (Ec) and 2.8 (Fn) of finding high levels of these bacterial pathogens at > 5 mm probing depth (p≤ 0.01). Mean probing depth at molar sites without a specific bacteria was greater (p≤ 0.01) in subjects wish a specific bacterium compared to molar sites in subjects without the bacteria. The observation that these 5 bacterial species frequently inhabit the subgingival environment, yet are not associated with advanced disease, suggest that a susceptible host is required, in addition to a “pathogenic bacteria”, before disease progression may occur.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>8276979</pmid><doi>10.1111/j.1600-051X.1993.tb00694.x</doi><tpages>8</tpages></addata></record> |
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subjects | Adult Age Factors Aged Aggregatibacter actinomycetemcomitans - isolation & purification Bacteria - isolation & purification bacterial pathogens Bacteroidaceae - isolation & purification Dental Plaque - microbiology Dentistry Eikenella corrodens - isolation & purification Female Humans immunoassay Linear Models Male Middle Aged Odds Ratio periodontal disease Periodontal Diseases - etiology Periodontal Diseases - microbiology Periodontal Pocket - microbiology Prevalence Sex Factors |
title | Natural distribution of 5 bacteria associated with periodontal disease |
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