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Are There Any Common Genetic Risk Markers for Rheumatoid Arthritis and Periodontal Diseases? A Case-Control Study
Background. Several studies suggest that there is a biologically plausible connection between rheumatoid arthritis (RA) and periodontal diseases (PD). Both disorders are characterized as multifactorial diseases potentially sharing common risk factors. Based on the inflammatory nature of RA and PD, t...
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Published in: | Mediators of inflammation 2019-01, Vol.2019 (2019), p.1-11 |
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description | Background. Several studies suggest that there is a biologically plausible connection between rheumatoid arthritis (RA) and periodontal diseases (PD). Both disorders are characterized as multifactorial diseases potentially sharing common risk factors. Based on the inflammatory nature of RA and PD, the impact of genetic variations of genes of the immune system on both diseases was studied in this study. Materials and Methods. We conducted a case-control study (n=201) comparing 101 RA patients suffering from periodontal disease of different severities (no/mild PD vs. severe PD) with 100 systemically healthy controls without RA and severe PD. The genotype, allele, and haplotype distributions of 22 SNPs of 13 pro- and anti-inflammatory cytokines were assessed applying sequence-specific PCR. Results. Evaluating the impact of cytokine SNPs in RA, we identified the G allele of rs1801275 in IL4Rα (p=0.043) and the G allele of rs361525 in TNFα (p=0.005) as disease-associated risk factors in bivariate analyses. In multivariate analyses, these significant associations could not be proven. The A allele of rs2430561 in IFNγ was indicative for severe periodontitis among the patients with rheumatoid arthritis (p=0.039). Investigating the impact of rs2430561 in IFNγ on comorbidity using binary logistic regression analyses, the A allele was confirmed as an independent risk factor for severe periodontal disease and RA (p=0.024). Conclusions. These results emphasize the association of genetic variations in proinflammatory cytokines (TNFα and IFNγ) and cytokine receptor (IL4Rα) and RA and periodontal diseases. In multivariate analyses, the A allele of IFNγ was proven to be a significant marker of RA and PD comorbidities. The study broadens the knowledge about disease-specific differences in genetic composition and provides an improved understanding of a possible association of both diseases. |
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A Case-Control Study</title><source>Publicly Available Content Database</source><source>Wiley Open Access</source><source>PubMed Central</source><creator>Schaller, Hans-Günter ; Jurianz, Elisa ; Pütz, Natalie ; Schulz, Susanne ; Reichert, Stefan</creator><contributor>Huck, Olivier ; Olivier Huck</contributor><creatorcontrib>Schaller, Hans-Günter ; Jurianz, Elisa ; Pütz, Natalie ; Schulz, Susanne ; Reichert, Stefan ; Huck, Olivier ; Olivier Huck</creatorcontrib><description>Background. Several studies suggest that there is a biologically plausible connection between rheumatoid arthritis (RA) and periodontal diseases (PD). Both disorders are characterized as multifactorial diseases potentially sharing common risk factors. Based on the inflammatory nature of RA and PD, the impact of genetic variations of genes of the immune system on both diseases was studied in this study. Materials and Methods. We conducted a case-control study (n=201) comparing 101 RA patients suffering from periodontal disease of different severities (no/mild PD vs. severe PD) with 100 systemically healthy controls without RA and severe PD. The genotype, allele, and haplotype distributions of 22 SNPs of 13 pro- and anti-inflammatory cytokines were assessed applying sequence-specific PCR. Results. Evaluating the impact of cytokine SNPs in RA, we identified the G allele of rs1801275 in IL4Rα (p=0.043) and the G allele of rs361525 in TNFα (p=0.005) as disease-associated risk factors in bivariate analyses. In multivariate analyses, these significant associations could not be proven. The A allele of rs2430561 in IFNγ was indicative for severe periodontitis among the patients with rheumatoid arthritis (p=0.039). Investigating the impact of rs2430561 in IFNγ on comorbidity using binary logistic regression analyses, the A allele was confirmed as an independent risk factor for severe periodontal disease and RA (p=0.024). Conclusions. These results emphasize the association of genetic variations in proinflammatory cytokines (TNFα and IFNγ) and cytokine receptor (IL4Rα) and RA and periodontal diseases. In multivariate analyses, the A allele of IFNγ was proven to be a significant marker of RA and PD comorbidities. The study broadens the knowledge about disease-specific differences in genetic composition and provides an improved understanding of a possible association of both diseases.</description><identifier>ISSN: 0962-9351</identifier><identifier>EISSN: 1466-1861</identifier><identifier>DOI: 10.1155/2019/2907062</identifier><identifier>PMID: 30890897</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Adolescent ; Adult ; Alleles ; Arthritis, Rheumatoid - genetics ; Cardiovascular disease ; Case-Control Studies ; Cytokines ; Female ; Genetic diversity ; Genotype ; Genotypes ; Gum disease ; Haplotypes ; Health risk assessment ; Humans ; Hypotheses ; Immune system ; Inflammation ; Inflammatory diseases ; Interferon-gamma - genetics ; Male ; Multivariate Analysis ; Nonsteroidal anti-inflammatory drugs ; Periodontal diseases ; Periodontal Diseases - genetics ; Periodontitis ; Polymorphism, Single Nucleotide - genetics ; Porphyromonas gingivalis - pathogenicity ; Rheumatoid arthritis ; Rheumatology ; Risk Factors ; Single-nucleotide polymorphism ; Studies ; Teeth ; Tumor Necrosis Factor-alpha - genetics ; Tumor necrosis factor-α ; Young Adult ; γ-Interferon</subject><ispartof>Mediators of inflammation, 2019-01, Vol.2019 (2019), p.1-11</ispartof><rights>Copyright © 2019 Susanne Schulz et al.</rights><rights>Copyright © 2019 Susanne Schulz et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. http://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2019 Susanne Schulz et al. 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c537t-8adbb9cee9a935e38e3c8d4c45505c31525810f84854b8b836515c872285a48b3</citedby><cites>FETCH-LOGICAL-c537t-8adbb9cee9a935e38e3c8d4c45505c31525810f84854b8b836515c872285a48b3</cites><orcidid>0000-0003-4541-666X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2185506617/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2185506617?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25751,27922,27923,37010,37011,44588,53789,53791,74896</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30890897$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Huck, Olivier</contributor><contributor>Olivier Huck</contributor><creatorcontrib>Schaller, Hans-Günter</creatorcontrib><creatorcontrib>Jurianz, Elisa</creatorcontrib><creatorcontrib>Pütz, Natalie</creatorcontrib><creatorcontrib>Schulz, Susanne</creatorcontrib><creatorcontrib>Reichert, Stefan</creatorcontrib><title>Are There Any Common Genetic Risk Markers for Rheumatoid Arthritis and Periodontal Diseases? A Case-Control Study</title><title>Mediators of inflammation</title><addtitle>Mediators Inflamm</addtitle><description>Background. Several studies suggest that there is a biologically plausible connection between rheumatoid arthritis (RA) and periodontal diseases (PD). Both disorders are characterized as multifactorial diseases potentially sharing common risk factors. Based on the inflammatory nature of RA and PD, the impact of genetic variations of genes of the immune system on both diseases was studied in this study. Materials and Methods. We conducted a case-control study (n=201) comparing 101 RA patients suffering from periodontal disease of different severities (no/mild PD vs. severe PD) with 100 systemically healthy controls without RA and severe PD. The genotype, allele, and haplotype distributions of 22 SNPs of 13 pro- and anti-inflammatory cytokines were assessed applying sequence-specific PCR. Results. Evaluating the impact of cytokine SNPs in RA, we identified the G allele of rs1801275 in IL4Rα (p=0.043) and the G allele of rs361525 in TNFα (p=0.005) as disease-associated risk factors in bivariate analyses. In multivariate analyses, these significant associations could not be proven. The A allele of rs2430561 in IFNγ was indicative for severe periodontitis among the patients with rheumatoid arthritis (p=0.039). Investigating the impact of rs2430561 in IFNγ on comorbidity using binary logistic regression analyses, the A allele was confirmed as an independent risk factor for severe periodontal disease and RA (p=0.024). Conclusions. These results emphasize the association of genetic variations in proinflammatory cytokines (TNFα and IFNγ) and cytokine receptor (IL4Rα) and RA and periodontal diseases. In multivariate analyses, the A allele of IFNγ was proven to be a significant marker of RA and PD comorbidities. The study broadens the knowledge about disease-specific differences in genetic composition and provides an improved understanding of a possible association of both diseases.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Alleles</subject><subject>Arthritis, Rheumatoid - genetics</subject><subject>Cardiovascular disease</subject><subject>Case-Control Studies</subject><subject>Cytokines</subject><subject>Female</subject><subject>Genetic diversity</subject><subject>Genotype</subject><subject>Genotypes</subject><subject>Gum disease</subject><subject>Haplotypes</subject><subject>Health risk assessment</subject><subject>Humans</subject><subject>Hypotheses</subject><subject>Immune system</subject><subject>Inflammation</subject><subject>Inflammatory diseases</subject><subject>Interferon-gamma - genetics</subject><subject>Male</subject><subject>Multivariate Analysis</subject><subject>Nonsteroidal anti-inflammatory drugs</subject><subject>Periodontal diseases</subject><subject>Periodontal Diseases - genetics</subject><subject>Periodontitis</subject><subject>Polymorphism, Single Nucleotide - genetics</subject><subject>Porphyromonas gingivalis - pathogenicity</subject><subject>Rheumatoid arthritis</subject><subject>Rheumatology</subject><subject>Risk Factors</subject><subject>Single-nucleotide polymorphism</subject><subject>Studies</subject><subject>Teeth</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor necrosis factor-α</subject><subject>Young Adult</subject><subject>γ-Interferon</subject><issn>0962-9351</issn><issn>1466-1861</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNqNks9rFDEUxwdR7Fq9eZaAF0HH5udMclGWVWuhotR6Dm8yb7rZzkzaZEbZ_97UXav1JIQkvHz4JN_wiuIpo68ZU-qIU2aOuKE1rfi9YsFkVZVMV-x-saCm4qURih0Uj1LaUEqVlPphcSCoNnnUi-J6GZGcrzHPy3FLVmEYwkiOccTJO3Lm0yX5BPESYyJdiORsjfMAU_AtWcZpHf3kE4GxJV8w-tCGcYKevPMJIWF6S5ZklTflKtdj6MnXaW63j4sHHfQJn-zXw-Lbh_fnq4_l6efjk9XytHRK1FOpoW0a4xAN5AQoNAqnW-mkUlQ5wRRXmtFOS61koxstKsWU0zXnWoHUjTgsTnbeNsDGXkU_QNzaAN7-KoR4YSHmkD3arlbcNJ1Ssquk6wCgrrgBrlrg-T6XXW92rqu5GbB1mPNAf0d692T0a3sRvttKGMqFyYIXe0EM1zOmyQ4-Oex7GDHMyXJmpNJSGZ3R5_-gmzDHMX9VpnROX1WsztSrHeViSClid_sYRu1NX9ibvrD7vsj4s78D3MK_GyEDL3fA2o8t_PD_qcPMYAd_aGZ4LZn4CbMOyOQ</recordid><startdate>20190101</startdate><enddate>20190101</enddate><creator>Schaller, Hans-Günter</creator><creator>Jurianz, Elisa</creator><creator>Pütz, Natalie</creator><creator>Schulz, Susanne</creator><creator>Reichert, Stefan</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0003-4541-666X</orcidid></search><sort><creationdate>20190101</creationdate><title>Are There Any Common Genetic Risk Markers for Rheumatoid Arthritis and Periodontal Diseases? 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genetics</topic><topic>Periodontitis</topic><topic>Polymorphism, Single Nucleotide - genetics</topic><topic>Porphyromonas gingivalis - pathogenicity</topic><topic>Rheumatoid arthritis</topic><topic>Rheumatology</topic><topic>Risk Factors</topic><topic>Single-nucleotide polymorphism</topic><topic>Studies</topic><topic>Teeth</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor necrosis factor-α</topic><topic>Young Adult</topic><topic>γ-Interferon</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schaller, Hans-Günter</creatorcontrib><creatorcontrib>Jurianz, Elisa</creatorcontrib><creatorcontrib>Pütz, Natalie</creatorcontrib><creatorcontrib>Schulz, Susanne</creatorcontrib><creatorcontrib>Reichert, Stefan</creatorcontrib><collection>الدوريات العلمية والإحصائية - e-Marefa Academic and Statistical Periodicals</collection><collection>معرفة - المحتوى العربي الأكاديمي المتكامل - e-Marefa Academic Complete</collection><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Mediators of inflammation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schaller, Hans-Günter</au><au>Jurianz, Elisa</au><au>Pütz, Natalie</au><au>Schulz, Susanne</au><au>Reichert, Stefan</au><au>Huck, Olivier</au><au>Olivier Huck</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Are There Any Common Genetic Risk Markers for Rheumatoid Arthritis and Periodontal Diseases? A Case-Control Study</atitle><jtitle>Mediators of inflammation</jtitle><addtitle>Mediators Inflamm</addtitle><date>2019-01-01</date><risdate>2019</risdate><volume>2019</volume><issue>2019</issue><spage>1</spage><epage>11</epage><pages>1-11</pages><issn>0962-9351</issn><eissn>1466-1861</eissn><abstract>Background. Several studies suggest that there is a biologically plausible connection between rheumatoid arthritis (RA) and periodontal diseases (PD). Both disorders are characterized as multifactorial diseases potentially sharing common risk factors. Based on the inflammatory nature of RA and PD, the impact of genetic variations of genes of the immune system on both diseases was studied in this study. Materials and Methods. We conducted a case-control study (n=201) comparing 101 RA patients suffering from periodontal disease of different severities (no/mild PD vs. severe PD) with 100 systemically healthy controls without RA and severe PD. The genotype, allele, and haplotype distributions of 22 SNPs of 13 pro- and anti-inflammatory cytokines were assessed applying sequence-specific PCR. Results. Evaluating the impact of cytokine SNPs in RA, we identified the G allele of rs1801275 in IL4Rα (p=0.043) and the G allele of rs361525 in TNFα (p=0.005) as disease-associated risk factors in bivariate analyses. In multivariate analyses, these significant associations could not be proven. The A allele of rs2430561 in IFNγ was indicative for severe periodontitis among the patients with rheumatoid arthritis (p=0.039). Investigating the impact of rs2430561 in IFNγ on comorbidity using binary logistic regression analyses, the A allele was confirmed as an independent risk factor for severe periodontal disease and RA (p=0.024). Conclusions. These results emphasize the association of genetic variations in proinflammatory cytokines (TNFα and IFNγ) and cytokine receptor (IL4Rα) and RA and periodontal diseases. In multivariate analyses, the A allele of IFNγ was proven to be a significant marker of RA and PD comorbidities. The study broadens the knowledge about disease-specific differences in genetic composition and provides an improved understanding of a possible association of both diseases.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>30890897</pmid><doi>10.1155/2019/2907062</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0003-4541-666X</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Adolescent Adult Alleles Arthritis, Rheumatoid - genetics Cardiovascular disease Case-Control Studies Cytokines Female Genetic diversity Genotype Genotypes Gum disease Haplotypes Health risk assessment Humans Hypotheses Immune system Inflammation Inflammatory diseases Interferon-gamma - genetics Male Multivariate Analysis Nonsteroidal anti-inflammatory drugs Periodontal diseases Periodontal Diseases - genetics Periodontitis Polymorphism, Single Nucleotide - genetics Porphyromonas gingivalis - pathogenicity Rheumatoid arthritis Rheumatology Risk Factors Single-nucleotide polymorphism Studies Teeth Tumor Necrosis Factor-alpha - genetics Tumor necrosis factor-α Young Adult γ-Interferon |
title | Are There Any Common Genetic Risk Markers for Rheumatoid Arthritis and Periodontal Diseases? A Case-Control Study |
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