{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T20:51:59Z","timestamp":1787863919371,"version":"build-2784847793"},"reference-count":48,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2022,9,28]],"date-time":"2022-09-28T00:00:00Z","timestamp":1664323200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Periodontal Research"],"published-print":{"date-parts":[[2022,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>Single\u2010cell transcriptomics was used to determine the possible cell\u2010type specificity of periodontitis susceptibility genes.<\/jats:p><\/jats:sec><jats:sec><jats:title>Background<\/jats:title><jats:p>The last decade has witnessed remarkable advances in the field of human genomics. Despite many advances, the genetic factors associated with or contributing to the periodontitis pathogenesis have only been identified to a limited extent and are often poorly validated. Confirming whether a given single nucleotide polymorphism has an association with periodontitis requires a robust mechanistic explanation on the functional consequences of a given genetic variant.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We globally assessed the expression of 26 disease\u2010associated genes identified by GWAS within the gingival mucosa. A total of 12\u2009411 cells from 4 different donors were analysed. Differentially expressed genes were analysed using Seurat, a non\u2010parametric Wilcoxon rank sum test. The minimum threshold for significance was defined as <jats:italic>p<\/jats:italic>\u2009&lt;\u2009.05.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>This exploration at a cellular\u2010level suggests diverse populations contributing to disease pathogenesis, with macrophages expressing a higher number of the analysed disease\u2010associated genes. <jats:italic>IL1B<\/jats:italic>, <jats:italic>PTGS2<\/jats:italic>, <jats:italic>FCGR2A<\/jats:italic>, <jats:italic>IL10<\/jats:italic> and <jats:italic>IL1A<\/jats:italic> specifically showed a more restricted expression in the myeloid lineages.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>This short report combines human genetics and single\u2010cell genomics to better understand periodontitis by mapping variants to predict their cells of action and putative functions. These findings seem to suggest that innate cell dysfunction is linked to disease susceptibility.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jre.13057","type":"journal-article","created":{"date-parts":[[2022,9,28]],"date-time":"2022-09-28T17:50:42Z","timestamp":1664387442000},"page":"1210-1218","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["Expression of periodontitis susceptibility genes in human gingiva using single\u2010cell <scp>RNA<\/scp> sequencing"],"prefix":"10.1111","volume":"57","author":[{"given":"Ana J.","family":"Caetano","sequence":"first","affiliation":[{"name":"Faculty of Dentistry, Oral &amp; Craniofacial Sciences, Centre for Craniofacial and Regenerative Biology King's College London  London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eleanor M.","family":"D'Agostino","sequence":"additional","affiliation":[{"name":"Unilever R&amp;D  Sharnbrook UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul","family":"Sharpe","sequence":"additional","affiliation":[{"name":"Faculty of Dentistry, Oral &amp; 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