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<title>2</title>
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<short_title>3</short_title>
<subject>Literature &amp; Humanities</subject>
<web_url>http://idai.ir</web_url>
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<journal_hbi_system_user>admin</journal_hbi_system_user>
<journal_id_issn>9</journal_id_issn>
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<journal_id_doi>7</journal_id_doi>
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<journal_id_nlai>8888</journal_id_nlai>
<journal_id_science>13</journal_id_science>
<language>fa</language>
<pubdate>
	<type>jalali</type>
	<year>1390</year>
	<month>10</month>
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	<type>gregorian</type>
	<year>2012</year>
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<volume>6</volume>
<number>6</number>
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<articleset>
	<article>


	<language>en</language>
	<article_id_doi></article_id_doi>
	<title_fa></title_fa>
	<title>Levels of Serum Immunoglobulin G Specific to Bacterial Surface Protein A of Tannerella forsythia are Related to Periodontal Status</title>
	<subject_fa>پریودنتولوژی</subject_fa>
	<subject>Periodontology</subject>
	<content_type_fa>پژوهشي</content_type_fa>
	<content_type>Research</content_type>
	<abstract_fa></abstract_fa>
	<abstract>&lt;p&gt; &lt;strong&gt;Background:&lt;/strong&gt; &lt;i&gt;Tannerella forsythia&lt;/i&gt; (&lt;i&gt;Tf&lt;/i&gt;) is a Gram-negative anaerobe implicated in the development of periodontal disease. Bacterial surface protein A (BspA) is a surface-expressed and -secreted protein that is recognized as an important virulence factor of &lt;i&gt;Tf&lt;/i&gt;. This study was undertaken to determine whether &lt;i&gt;Tf&lt;/i&gt; BspA induces an antibody response in periodontal disease. We hypothesized that serum immunoglobulin (Ig)G antibody levels against BspA correlate with the disease of patients.&lt;/p&gt;&lt;p&gt; &lt;strong&gt;Methods:&lt;/strong&gt; Sera were obtained from 100 patients with cardiac disorders and periodontal disease and 73 patients who experienced myocardial infarction but were periodontally healthy. Sera samples were assayed for anti-BspA antibody (total IgG and IgG subtypes) by enzyme-linked immunosorbent assay (ELISA). Antibody levels were measured in ELISA units by using an arbitrary patient as a standard.&lt;/p&gt;&lt;p&gt; &lt;strong&gt;Results:&lt;/strong&gt; A negative correlation was found with BspA-specific total IgG antibody titers and the severity of disease measured as the clinical attachment level (CAL) when healthy and diseased groups were analyzed separately (healthy group: [−0.23, correlation value] Student's &lt;i&gt;t&lt;/i&gt; value [73 degrees of freedom] = 1.99 &lt;i&gt;P&lt;/i&gt; = 0.05 diseased group: [−0.21] &lt;i&gt;t&lt;/i&gt; [100 degrees of freedom] = 2.12 &lt;i&gt;P&lt;/i&gt; = 0.03]). However, there was a positive correlation ([0.18 correlation value] Student's &lt;i&gt;t&lt;/i&gt; value [173 degrees of freedom] = 2.39 &lt;i&gt;P&lt;/i&gt; = 0.017) when healthy and diseased groups were combined. A strong positive correlation ([0.338 correlation value] Student's &lt;i&gt;t&lt;/i&gt; value [173 degrees of freedom] = 4.69 &lt;i&gt;P&lt;/i&gt; &lt;0.0001) between the BspA-specific IgG titers and periodontal probing depth was observed when healthy and disease groups were combined.&lt;/p&gt;&lt;p&gt; &lt;strong&gt;Conclusions:&lt;/strong&gt; Data demonstrated that antibodies to &lt;i&gt;Tf&lt;/i&gt; BspA were elicited in patients with periodontal disease, and antibody levels were associated with the disease severity. Furthermore, data suggested that anti-BspA IgG might have a protective function in periodontal disease by minimizing the loss of tooth attachment tissue. &lt;/p&gt;&lt;hr&gt;&lt;p&gt;&lt;/p&gt;&lt;p&gt; &lt;strong&gt; Source &lt;/strong&gt;: Journal of Periodentology &lt;/p&gt;&lt;p&gt;&lt;a href=&quot;http://www.joponline.org/doi/abs/10.1902/jop.2011.110116&quot; target=&quot;_blank&quot;&gt;&lt;font color=&quot;#0000cc&quot;&gt;  Full text &lt;/font&gt;&lt;/a&gt;&lt;/p&gt;</abstract>
	<keyword_fa></keyword_fa>
	<keyword> Immunoglobulin G, periodontitis</keyword>
	<start_page>0</start_page>
	<end_page>0</end_page>
	<web_url>http://idai.ir/browse.php?a_code=A-10-32-273&amp;slc_lang=en&amp;sid=1</web_url>


<author_list>
	<author>
	<first_name>Lindsay</first_name>
	<middle_name></middle_name>
	<last_name>M. Hall</last_name>
	<suffix></suffix>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>10031947532846001108</code>
	<orcid>10031947532846001108</orcid>
	<coreauthor>No</coreauthor>
	<affiliation>School of Dental Medicine, University at Buffalo, Buffalo, NY</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Robert</first_name>
	<middle_name></middle_name>
	<last_name>G. Dunford</last_name>
	<suffix></suffix>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>10031947532846001109</code>
	<orcid>10031947532846001109</orcid>
	<coreauthor>No</coreauthor>
	<affiliation>School of Dental Medicine, University at Buffalo, Buffalo, NY</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Robert</first_name>
	<middle_name></middle_name>
	<last_name>J. Genco</last_name>
	<suffix></suffix>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>10031947532846001110</code>
	<orcid>10031947532846001110</orcid>
	<coreauthor>No</coreauthor>
	<affiliation>School of Dental Medicine, University at Buffalo, Buffalo, NY</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Ashu</first_name>
	<middle_name></middle_name>
	<last_name>Sharma</last_name>
	<suffix></suffix>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email>sharmaa@buffalo.edu</email>
	<code>10031947532846001111</code>
	<orcid>10031947532846001111</orcid>
	<coreauthor>Yes
</coreauthor>
	<affiliation>School of Dental Medicine, University at Buffalo, Buffalo, NY</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


</author_list>


	</article>
</articleset>
</journal>
