The Link Between Periodontal Disease and Rheumatoid Arthritis: An Updated Review
Porphyromonas gingivalis is a leading pathogen in chronic periodontitis, a disease process involving progressive destruction of the tissues that support the teeth. Recently, the organism has been reported to produce a unique bacterial enzyme, P. gingivalis peptidyl-arginine deiminase (PPAD), which h...
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| Veröffentlicht in: | Current rheumatology reports 2014-03, Vol.16 (3), p.408-408, Article 408 |
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| creator | Koziel, Joanna Mydel, Piotr Potempa, Jan |
| description | Porphyromonas gingivalis
is a leading pathogen in chronic periodontitis, a disease process involving progressive destruction of the tissues that support the teeth. Recently, the organism has been reported to produce a unique bacterial enzyme,
P. gingivalis
peptidyl-arginine deiminase (PPAD), which has the ability to convert arginine residues in proteins to citrulline. Protein citrullination alters protein structure and function; hence, PPAD may be involved in deregulation of the host’s signalling network and immune evasion. Further, accumulating evidence suggests a role for autoimmunity against citrullinated proteins in the development of rheumatoid arthritis (RA). As inflammatory conditions in the lungs of cigarette smokers contribute to the breakdown of immune tolerance to citrullinated epitopes, chronic exposure to citrullinated proteins at periodontitis sites may also predispose susceptible individuals to the development of autoantibodies and the initiation of RA. In this review, we discuss evidence that PPAD may represent a mechanistic link between periodontitis and RA, diseases that are known to be significantly associated at the epidemiological level. |
| doi_str_mv | 10.1007/s11926-014-0408-9 |
| format | Article |
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is a leading pathogen in chronic periodontitis, a disease process involving progressive destruction of the tissues that support the teeth. Recently, the organism has been reported to produce a unique bacterial enzyme,
P. gingivalis
peptidyl-arginine deiminase (PPAD), which has the ability to convert arginine residues in proteins to citrulline. Protein citrullination alters protein structure and function; hence, PPAD may be involved in deregulation of the host’s signalling network and immune evasion. Further, accumulating evidence suggests a role for autoimmunity against citrullinated proteins in the development of rheumatoid arthritis (RA). As inflammatory conditions in the lungs of cigarette smokers contribute to the breakdown of immune tolerance to citrullinated epitopes, chronic exposure to citrullinated proteins at periodontitis sites may also predispose susceptible individuals to the development of autoantibodies and the initiation of RA. In this review, we discuss evidence that PPAD may represent a mechanistic link between periodontitis and RA, diseases that are known to be significantly associated at the epidemiological level.</description><identifier>ISSN: 1523-3774</identifier><identifier>EISSN: 1534-6307</identifier><identifier>DOI: 10.1007/s11926-014-0408-9</identifier><identifier>PMID: 24458478</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Arthritis, Rheumatoid - immunology ; Arthritis, Rheumatoid - microbiology ; Autoantibodies - blood ; Bacteroidaceae Infections - complications ; Bacteroidaceae Infections - immunology ; Citrulline - immunology ; Humans ; Hydrolases - immunology ; Immune Evasion - immunology ; Medicine ; Medicine & Public Health ; Periodontitis - complications ; Periodontitis - immunology ; Porphyromonas gingivalis ; Protein-Arginine Deiminases ; Rheumatoid Arthritis (Lw Moreland ; Rheumatoid Arthritis (Lw Moreland, Section Editor) ; Rheumatology ; Section Editor ; Topical Collection on Rheumatoid Arthritis</subject><ispartof>Current rheumatology reports, 2014-03, Vol.16 (3), p.408-408, Article 408</ispartof><rights>The Author(s) 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c442t-346aff04cee22da5d5d65b4544216d82d820d8d7e755bbe4adb5a1997bd8b61d3</citedby><cites>FETCH-LOGICAL-c442t-346aff04cee22da5d5d65b4544216d82d820d8d7e755bbe4adb5a1997bd8b61d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11926-014-0408-9$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11926-014-0408-9$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24458478$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Koziel, Joanna</creatorcontrib><creatorcontrib>Mydel, Piotr</creatorcontrib><creatorcontrib>Potempa, Jan</creatorcontrib><title>The Link Between Periodontal Disease and Rheumatoid Arthritis: An Updated Review</title><title>Current rheumatology reports</title><addtitle>Curr Rheumatol Rep</addtitle><addtitle>Curr Rheumatol Rep</addtitle><description>Porphyromonas gingivalis
is a leading pathogen in chronic periodontitis, a disease process involving progressive destruction of the tissues that support the teeth. Recently, the organism has been reported to produce a unique bacterial enzyme,
P. gingivalis
peptidyl-arginine deiminase (PPAD), which has the ability to convert arginine residues in proteins to citrulline. Protein citrullination alters protein structure and function; hence, PPAD may be involved in deregulation of the host’s signalling network and immune evasion. Further, accumulating evidence suggests a role for autoimmunity against citrullinated proteins in the development of rheumatoid arthritis (RA). As inflammatory conditions in the lungs of cigarette smokers contribute to the breakdown of immune tolerance to citrullinated epitopes, chronic exposure to citrullinated proteins at periodontitis sites may also predispose susceptible individuals to the development of autoantibodies and the initiation of RA. In this review, we discuss evidence that PPAD may represent a mechanistic link between periodontitis and RA, diseases that are known to be significantly associated at the epidemiological level.</description><subject>Arthritis, Rheumatoid - immunology</subject><subject>Arthritis, Rheumatoid - microbiology</subject><subject>Autoantibodies - blood</subject><subject>Bacteroidaceae Infections - complications</subject><subject>Bacteroidaceae Infections - immunology</subject><subject>Citrulline - immunology</subject><subject>Humans</subject><subject>Hydrolases - immunology</subject><subject>Immune Evasion - immunology</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Periodontitis - complications</subject><subject>Periodontitis - immunology</subject><subject>Porphyromonas gingivalis</subject><subject>Protein-Arginine Deiminases</subject><subject>Rheumatoid Arthritis (Lw Moreland</subject><subject>Rheumatoid Arthritis (Lw Moreland, Section Editor)</subject><subject>Rheumatology</subject><subject>Section Editor</subject><subject>Topical Collection on Rheumatoid Arthritis</subject><issn>1523-3774</issn><issn>1534-6307</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><recordid>eNp9kUtrGzEUhUVJaBy3P6CbomU2k-g5muki4KTNAwwNJV4Lzeg6ljuWHEmT0H8fGaeh2RQEEpzvnivOQegLJaeUEHWWKG1ZXREqKiJIU7Uf0IRKLqqaE3WwezNecaXEETpOaU0II6ThH9ERE0I2QjUTdHe_Ajx3_je-gPwM4PEdRBds8NkM-LtLYBJg4y3-tYJxY3JwFs9iXkWXXfqGZx4vttZkKAA8OXj-hA6XZkjw-fWeosXVj_vLm2r-8_r2cjaveiFYrriozXJJRA_AmDXSSlvLTsgi0to2rBxiG6tASdl1IIztpKFtqzrbdDW1fIrO977bsduA7cHnaAa9jW5j4h8djNPvFe9W-iE8ad7yEgItBievBjE8jpCy3rjUwzAYD2FMmoqSbVu3ihWU7tE-hpQiLN_WUKJ3Teh9E7o0oXdN6LbMfP33f28Tf6MvANsDqUj-AaJehzH6ktl_XF8AmwyU8w</recordid><startdate>20140301</startdate><enddate>20140301</enddate><creator>Koziel, Joanna</creator><creator>Mydel, Piotr</creator><creator>Potempa, Jan</creator><general>Springer US</general><scope>C6C</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><scope>5PM</scope></search><sort><creationdate>20140301</creationdate><title>The Link Between Periodontal Disease and Rheumatoid Arthritis: An Updated Review</title><author>Koziel, Joanna ; Mydel, Piotr ; Potempa, Jan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c442t-346aff04cee22da5d5d65b4544216d82d820d8d7e755bbe4adb5a1997bd8b61d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Arthritis, Rheumatoid - immunology</topic><topic>Arthritis, Rheumatoid - microbiology</topic><topic>Autoantibodies - blood</topic><topic>Bacteroidaceae Infections - complications</topic><topic>Bacteroidaceae Infections - immunology</topic><topic>Citrulline - immunology</topic><topic>Humans</topic><topic>Hydrolases - immunology</topic><topic>Immune Evasion - immunology</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Periodontitis - complications</topic><topic>Periodontitis - immunology</topic><topic>Porphyromonas gingivalis</topic><topic>Protein-Arginine Deiminases</topic><topic>Rheumatoid Arthritis (Lw Moreland</topic><topic>Rheumatoid Arthritis (Lw Moreland, Section Editor)</topic><topic>Rheumatology</topic><topic>Section Editor</topic><topic>Topical Collection on Rheumatoid Arthritis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Koziel, Joanna</creatorcontrib><creatorcontrib>Mydel, Piotr</creatorcontrib><creatorcontrib>Potempa, Jan</creatorcontrib><collection>Springer Nature OA Free 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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Current rheumatology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Koziel, Joanna</au><au>Mydel, Piotr</au><au>Potempa, Jan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Link Between Periodontal Disease and Rheumatoid Arthritis: An Updated Review</atitle><jtitle>Current rheumatology reports</jtitle><stitle>Curr Rheumatol Rep</stitle><addtitle>Curr Rheumatol Rep</addtitle><date>2014-03-01</date><risdate>2014</risdate><volume>16</volume><issue>3</issue><spage>408</spage><epage>408</epage><pages>408-408</pages><artnum>408</artnum><issn>1523-3774</issn><eissn>1534-6307</eissn><abstract>Porphyromonas gingivalis
is a leading pathogen in chronic periodontitis, a disease process involving progressive destruction of the tissues that support the teeth. Recently, the organism has been reported to produce a unique bacterial enzyme,
P. gingivalis
peptidyl-arginine deiminase (PPAD), which has the ability to convert arginine residues in proteins to citrulline. Protein citrullination alters protein structure and function; hence, PPAD may be involved in deregulation of the host’s signalling network and immune evasion. Further, accumulating evidence suggests a role for autoimmunity against citrullinated proteins in the development of rheumatoid arthritis (RA). As inflammatory conditions in the lungs of cigarette smokers contribute to the breakdown of immune tolerance to citrullinated epitopes, chronic exposure to citrullinated proteins at periodontitis sites may also predispose susceptible individuals to the development of autoantibodies and the initiation of RA. In this review, we discuss evidence that PPAD may represent a mechanistic link between periodontitis and RA, diseases that are known to be significantly associated at the epidemiological level.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>24458478</pmid><doi>10.1007/s11926-014-0408-9</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Arthritis, Rheumatoid - immunology Arthritis, Rheumatoid - microbiology Autoantibodies - blood Bacteroidaceae Infections - complications Bacteroidaceae Infections - immunology Citrulline - immunology Humans Hydrolases - immunology Immune Evasion - immunology Medicine Medicine & Public Health Periodontitis - complications Periodontitis - immunology Porphyromonas gingivalis Protein-Arginine Deiminases Rheumatoid Arthritis (Lw Moreland Rheumatoid Arthritis (Lw Moreland, Section Editor) Rheumatology Section Editor Topical Collection on Rheumatoid Arthritis |
| title | The Link Between Periodontal Disease and Rheumatoid Arthritis: An Updated Review |
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