{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T18:36:27Z","timestamp":1791311787572,"version":"4.3.1"},"reference-count":23,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2013,6,18]],"date-time":"2013-06-18T00:00:00Z","timestamp":1371513600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Oral Pathology Medicine"],"published-print":{"date-parts":[[2013,11]]},"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p>Recurrent aphthous stomatitis (<jats:styled-content style=\"fixed-case\">RAS<\/jats:styled-content>) is a common oral ulcerative condition. At ulcer sites vascular adhesion molecule\u20101 (<jats:styled-content style=\"fixed-case\">VCAM<\/jats:styled-content>\u20101), <jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>\u2010selectin and intercellular adhesion molecule\u20101 (<jats:styled-content style=\"fixed-case\">ICAM<\/jats:styled-content>\u20101) are strongly expressed on blood vessels, and <jats:styled-content style=\"fixed-case\">ICAM<\/jats:styled-content>\u20101 is expressed on keratinocytes. Expression of these molecules would promote leukocyte accumulation and invasion of the epithelium. Thus, polymorphisms in these candidate genes might contribute to <jats:styled-content style=\"fixed-case\">RAS<\/jats:styled-content> susceptibility. We investigated whether the inheritance of specific selectin, <jats:styled-content style=\"fixed-case\">ICAM<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">VCAM<\/jats:styled-content> gene polymorphisms is associated with <jats:styled-content style=\"fixed-case\">RAS<\/jats:styled-content> susceptibility.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Ninety\u2010six <jats:styled-content style=\"fixed-case\">RAS<\/jats:styled-content> cases and 153 controls were recruited from a <jats:styled-content style=\"fixed-case\">J<\/jats:styled-content>ordanian population. Blood was collected for hematological investigations and genotyping. Six <jats:styled-content style=\"fixed-case\">SNP<\/jats:styled-content>s were genotyped: <jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>\u2010selectin rs5361 and rs1805193, <jats:styled-content style=\"fixed-case\">L<\/jats:styled-content>\u2010selectin, rs2205849, <jats:styled-content style=\"fixed-case\">ICAM<\/jats:styled-content>\u20101 rs5498, <jats:styled-content style=\"fixed-case\">ICAM<\/jats:styled-content>\u20105 rs885743 and <jats:styled-content style=\"fixed-case\">VCAM<\/jats:styled-content>\u20101 rs1800821. Association was determined using chi\u2010square and binary logistic regression analysis after correcting for confounding factors. Linkage disequilibrium was determined using the <jats:styled-content style=\"fixed-case\">EH<\/jats:styled-content> program, and the Phase 2.1 program was used to construct and compare haplotypes between cases and controls.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>There was a significant association of the <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content> allele (<jats:italic>P<\/jats:italic><jats:sub>corr<\/jats:sub>\u00a0=\u00a00.027), <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content> genotypes (<jats:styled-content style=\"fixed-case\">OR<\/jats:styled-content>\u00a0=\u00a010.9 and 9.0, respectively) of the <jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>\u2010selectin rs5361 gene polymorphism and <jats:styled-content style=\"fixed-case\">TAA<\/jats:styled-content> haplotype (rs2205849, rs5361, and rs1805193, respectively; <jats:italic>P<\/jats:italic>\u00a0=\u00a00.03) with <jats:styled-content style=\"fixed-case\">RAS<\/jats:styled-content>. None of the other <jats:styled-content style=\"fixed-case\">SNP<\/jats:styled-content>s showed a significant association.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>This is the first report to link inheritance of the <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content> allele, <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content> genotypes of the <jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>\u2010selectin rs5361 polymorphism with increased risk of <jats:styled-content style=\"fixed-case\">RAS<\/jats:styled-content>. Further studies in different patient cohorts are needed to confirm the association, and functional analyses might clarify the biological significance of the association.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jop.12100","type":"journal-article","created":{"date-parts":[[2013,6,18]],"date-time":"2013-06-18T06:48:24Z","timestamp":1371538104000},"page":"741-746","source":"Crossref","is-referenced-by-count":13,"title":["Association of cell adhesion molecule gene polymorphisms with recurrent aphthous stomatitis"],"prefix":"10.1111","volume":"42","author":[{"given":"Asem","family":"Alkhateeb","sequence":"first","affiliation":[{"name":"Department of Biotechnology and Genetics Jordan University of Science and Technology (JUST) Irbid Jordan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jumana","family":"Karasneh","sequence":"additional","affiliation":[{"name":"Department of Oral Medicine and Oral Surgery JUST Irbid Jordan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hebah","family":"Abbadi","sequence":"additional","affiliation":[{"name":"Department of Biotechnology and Genetics Jordan University of Science and Technology (JUST) Irbid Jordan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ahmad","family":"Hassan","sequence":"additional","affiliation":[{"name":"Department of Oral Medicine and Oral Diagnosis College of Dentistry Al Mustansiriya University Baghdad Iraq"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin","family":"Thornhill","sequence":"additional","affiliation":[{"name":"Unit of Oral and Maxillofacial Medicine and Surgery School of Clinical Dentistry The University of Sheffield Sheffield UK"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2013,6,18]]},"reference":[{"key":"e_1_2_5_2_1","doi-asserted-by":"publisher","DOI":"10.4317\/medoral.16.e33"},{"key":"e_1_2_5_3_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1529-8019.2010.01324.x"},{"key":"e_1_2_5_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/0030-4220(72)90211-3"},{"key":"e_1_2_5_5_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.0904-2512.2004.00089.x"},{"key":"e_1_2_5_6_1","doi-asserted-by":"publisher","DOI":"10.1001\/archderm.134.7.827"},{"key":"e_1_2_5_7_1","doi-asserted-by":"crossref","first-page":"865","DOI":"10.4049\/jimmunol.145.3.865","article-title":"IL\u20104 regulates endothelial cell activation by IL\u20101, TNF or IFN\u2010gamma","volume":"145","author":"Thornhill MH","year":"1990","journal-title":"J Immunol"},{"key":"e_1_2_5_8_1","doi-asserted-by":"crossref","first-page":"2558","DOI":"10.4049\/jimmunol.144.7.2558","article-title":"A monoclonal antibody that detects a novel antigen on endothelial cells that is induced by TNF, IL\u20101 or LPS","volume":"144","author":"Wellicome S","year":"1990","journal-title":"J Immunol"},{"key":"e_1_2_5_9_1","doi-asserted-by":"crossref","first-page":"592","DOI":"10.4049\/jimmunol.146.2.592","article-title":"TNF synergises with IL\u20104 or IFN\u2010gamma to selectively enhance endothelial cell adhesiveness for T cells: the contribution of VCAM\u20101 dependent and independent binding mechanisms","volume":"146","author":"Thornhill MH","year":"1991","journal-title":"J Immunol"},{"key":"e_1_2_5_10_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0714.1999.tb01986.x"},{"key":"e_1_2_5_11_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0714.1997.tb00005.x"},{"key":"e_1_2_5_12_1","first-page":"2650","article-title":"Association of the A561C E\u2010selectin polymorphism with systemic lupus erythematosus in 2 independent populations","volume":"28","author":"El\u2010Magadmi M","year":"2001","journal-title":"J Rheumatol"},{"key":"e_1_2_5_13_1","doi-asserted-by":"publisher","DOI":"10.1086\/383251"},{"key":"e_1_2_5_14_1","first-page":"188","volume-title":"Handbook of human genetic linkage","author":"Terwilliger J","year":"1994"},{"key":"e_1_2_5_15_1","doi-asserted-by":"publisher","DOI":"10.1086\/319501"},{"key":"e_1_2_5_16_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.2466335"},{"key":"e_1_2_5_17_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.27.16160"},{"key":"e_1_2_5_18_1","doi-asserted-by":"publisher","DOI":"10.1002\/1521-4141(200201)32:1<251::AID-IMMU251>3.0.CO;2-0"},{"key":"e_1_2_5_19_1","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.169.10.5860"},{"key":"e_1_2_5_20_1","doi-asserted-by":"publisher","DOI":"10.1515\/BC.1999.082"},{"key":"e_1_2_5_21_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(06)68345-1"},{"key":"e_1_2_5_22_1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.gene.6364222"},{"key":"e_1_2_5_23_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.thromres.2003.10.018"},{"key":"e_1_2_5_24_1","doi-asserted-by":"publisher","DOI":"10.1177\/00220345650440051501"}],"container-title":["Journal of Oral Pathology &amp; 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