{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T20:05:59Z","timestamp":1790971559713,"version":"4.1.0"},"reference-count":26,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2018,7,23]],"date-time":"2018-07-23T00:00:00Z","timestamp":1532304000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000072","name":"National Institute of Dental and Craniofacial Research","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000072","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81670949"],"award-info":[{"award-number":["81670949"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["R90DE022527"],"award-info":[{"award-number":["R90DE022527"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Oral Diseases"],"published-print":{"date-parts":[[2019,4]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Tooth agenesis (TA) is one of the most common developmental anomalies that affects the number of teeth. An extensive analysis of publicly accessible databases revealed 15 causative genes responsible for nonsyndromic TA, along with their signaling pathways in Wnt\/\u03b2\u2010catenin, TGF\u2010\u03b2\/BMP, and Eda\/Edar\/NF\u2010\u03baB. However, genotype\u2013phenotype correlation analysis showed that most of the causal genes are also responsible for syndromic TA or other conditions. In a total of 198 different mutations of the 15 genes responsible for nonsyndromic TA, 182 mutations (91.9%) are derived from seven genes (\n                    <jats:italic>AXIN2<\/jats:italic>\n                    ,\n                    <jats:italic>EDA<\/jats:italic>\n                    ,\n                    <jats:italic>LRP6<\/jats:italic>\n                    ,\n                    <jats:italic>MSX1<\/jats:italic>\n                    ,\n                    <jats:italic>PAX9<\/jats:italic>\n                    ,\n                    <jats:italic>WNT10A,<\/jats:italic>\n                    and\n                    <jats:italic>WNT10B<\/jats:italic>\n                    ) compared with the remaining 16 mutations (8.1%) identified in the remaining eight genes (\n                    <jats:italic>BMP4<\/jats:italic>\n                    ,\n                    <jats:italic>DKK1<\/jats:italic>\n                    ,\n                    <jats:italic>EDAR<\/jats:italic>\n                    ,\n                    <jats:italic>EDARADD<\/jats:italic>\n                    ,\n                    <jats:italic>GREM2<\/jats:italic>\n                    ,\n                    <jats:italic>KREMEN1<\/jats:italic>\n                    ,\n                    <jats:italic>LTBP3,<\/jats:italic>\n                    and\n                    <jats:italic>SMOC2<\/jats:italic>\n                    ). Furthermore, specificity analysis in terms of the ratio of nonsyndromic TA mutations versus syndromic mutations in each of the aforementioned seven genes showed a 98.2% specificity rate in\n                    <jats:italic>PAX9<\/jats:italic>\n                    , 58.9% in\n                    <jats:italic>WNT10A<\/jats:italic>\n                    , 56.6% in\n                    <jats:italic>MSX1<\/jats:italic>\n                    , 41.2% in\n                    <jats:italic>WNT10B<\/jats:italic>\n                    , 31.4% in\n                    <jats:italic>LRP6<\/jats:italic>\n                    , 23.8% in\n                    <jats:italic>AXIN2%<\/jats:italic>\n                    , and 8.4% in\n                    <jats:italic>EDA<\/jats:italic>\n                    . These findings underscore an important role of the Wnt and Wnt\u2010associated pathways in the genetic etiology of this heterozygous disease and shed new lights on the discovery of novel molecular mechanisms associated with tooth agenesis.\n                  <\/jats:p>","DOI":"10.1111\/odi.12931","type":"journal-article","created":{"date-parts":[[2018,7,3]],"date-time":"2018-07-03T18:49:01Z","timestamp":1530643741000},"page":"646-651","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":137,"title":["Genetic analysis: Wnt and other pathways in nonsyndromic tooth agenesis"],"prefix":"10.1111","volume":"25","author":[{"given":"Miao","family":"Yu","sequence":"first","affiliation":[{"name":"Department of Prosthodontics, National Engineering Laboratory for Digital and Material Technology of Stomatology, Beijing Key Laboratory of Digital Stomatology Peking University School and Hospital of Stomatology Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sing\u2010Wai","family":"Wong","sequence":"additional","affiliation":[{"name":"Oral and Craniofacial Biomedicine Curriculum, School of Dentistry University of North Carolina at Chapel Hill Chapel Hill North Carolina"},{"name":"Immunity, Inflammation, and Disease Laboratory National Institute of Environmental Health Sciences Research Triangle Park North Carolina"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dong","family":"Han","sequence":"additional","affiliation":[{"name":"Department of Prosthodontics, National Engineering Laboratory for Digital and Material Technology of Stomatology, Beijing Key Laboratory of Digital Stomatology Peking University School and Hospital of Stomatology Beijing 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