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Dental and extra‐oral clinical features in 41 patients with WNT10A gene mutations: A multicentric genotype–phenotype study
WNT10A gene encodes a canonical wingless pathway signaling molecule involved in cell fate specification as well as morphogenetic patterning of the developing ectoderm, nervous system, skeleton, and tooth. In patients, WNT10A mutations are responsible for ectodermal‐derived pathologies including isol...
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Published in: | Clinical genetics 2017-11, Vol.92 (5), p.477-486 |
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creator | Tardieu, C. Jung, S. Niederreither, K. Prasad, M. Hadj‐Rabia, S. Philip, N. Mallet, A. Consolino, E. Sfeir, E. Noueiri, B. Chassaing, N. Dollfus, H. Manière, M.C. Bloch‐Zupan, A. Clauss, F. |
description | WNT10A gene encodes a canonical wingless pathway signaling molecule involved in cell fate specification as well as morphogenetic patterning of the developing ectoderm, nervous system, skeleton, and tooth. In patients, WNT10A mutations are responsible for ectodermal‐derived pathologies including isolated hypo‐oligodontia, tricho‐odonto‐onycho‐dermal dysplasia and Schöpf‐Schulz‐Passarge syndrome (SSPS). Here we describe the dental, ectodermal, and extra‐ectodermal phenotypic features of a cohort of 41 patients from 32 unrelated families. Correlations with WNT10A molecular status (heterozygous carrier, compound heterozygous, homozygous) and patient's phenotypes were performed. Mild to severe oligodontia was observed in all patients bearing biallelic WNT10A mutations. However, patients with compound heterozygous mutations presented no significant difference in phenotypes compared with homozygous individuals. Anomalies in tooth morphology were frequently observed with heterozygous patients displaying hypodontia. No signs of SSPS, especially eyelids cysts, were detected in our cohort. Interestingly, extra‐ectodermal signs consisted of skeletal, neurological and vascular anomalies, the latter suggesting a wider phenotypic spectrum associated with WNT10A mutations. Indeed, the Wnt pathway plays a crucial role in skeletal development, lipid metabolism, and neurogenesis, potentially explaining patient's clinical manifestations. |
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In patients, WNT10A mutations are responsible for ectodermal‐derived pathologies including isolated hypo‐oligodontia, tricho‐odonto‐onycho‐dermal dysplasia and Schöpf‐Schulz‐Passarge syndrome (SSPS). Here we describe the dental, ectodermal, and extra‐ectodermal phenotypic features of a cohort of 41 patients from 32 unrelated families. Correlations with WNT10A molecular status (heterozygous carrier, compound heterozygous, homozygous) and patient's phenotypes were performed. Mild to severe oligodontia was observed in all patients bearing biallelic WNT10A mutations. However, patients with compound heterozygous mutations presented no significant difference in phenotypes compared with homozygous individuals. Anomalies in tooth morphology were frequently observed with heterozygous patients displaying hypodontia. No signs of SSPS, especially eyelids cysts, were detected in our cohort. Interestingly, extra‐ectodermal signs consisted of skeletal, neurological and vascular anomalies, the latter suggesting a wider phenotypic spectrum associated with WNT10A mutations. Indeed, the Wnt pathway plays a crucial role in skeletal development, lipid metabolism, and neurogenesis, potentially explaining patient's clinical manifestations.</description><identifier>ISSN: 0009-9163</identifier><identifier>EISSN: 1399-0004</identifier><identifier>DOI: 10.1111/cge.12972</identifier><identifier>PMID: 28105635</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adolescent ; Adult ; bone ; Cell fate ; Child ; Cohort Studies ; Cone-Beam Computed Tomography ; Cysts ; dental phenotype ; Dysplasia ; Ectoderm ; Ectoderm - pathology ; extra‐ectodermal signs ; Genetic Association Studies ; Genetics ; Genotype & phenotype ; Heterozygote ; Homozygote ; Human genetics ; Humans ; Life Sciences ; Lipid metabolism ; Mandible - pathology ; Middle Aged ; Mutation ; Mutation - genetics ; Nervous system ; Neurogenesis ; oligodontia ; Patients ; Pattern formation ; Phenotype ; Skeleton ; Skin ; Teeth ; Tooth - diagnostic imaging ; Tooth - pathology ; Wnt protein ; Wnt Proteins - genetics ; WNT10A mutation ; Young Adult</subject><ispartof>Clinical genetics, 2017-11, Vol.92 (5), p.477-486</ispartof><rights>2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd</rights><rights>2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3872-77285264c95f1d690a978f943d8775de433216f23ccd682b0b0e9317815a50d13</citedby><cites>FETCH-LOGICAL-c3872-77285264c95f1d690a978f943d8775de433216f23ccd682b0b0e9317815a50d13</cites><orcidid>0000-0002-8078-2406</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fcge.12972$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fcge.12972$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,315,786,790,891,27957,27958,50923,51032</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28105635$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-01741735$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Tardieu, C.</creatorcontrib><creatorcontrib>Jung, S.</creatorcontrib><creatorcontrib>Niederreither, K.</creatorcontrib><creatorcontrib>Prasad, M.</creatorcontrib><creatorcontrib>Hadj‐Rabia, S.</creatorcontrib><creatorcontrib>Philip, N.</creatorcontrib><creatorcontrib>Mallet, A.</creatorcontrib><creatorcontrib>Consolino, E.</creatorcontrib><creatorcontrib>Sfeir, E.</creatorcontrib><creatorcontrib>Noueiri, B.</creatorcontrib><creatorcontrib>Chassaing, N.</creatorcontrib><creatorcontrib>Dollfus, H.</creatorcontrib><creatorcontrib>Manière, M.C.</creatorcontrib><creatorcontrib>Bloch‐Zupan, A.</creatorcontrib><creatorcontrib>Clauss, F.</creatorcontrib><title>Dental and extra‐oral clinical features in 41 patients with WNT10A gene mutations: A multicentric genotype–phenotype study</title><title>Clinical genetics</title><addtitle>Clin Genet</addtitle><description>WNT10A gene encodes a canonical wingless pathway signaling molecule involved in cell fate specification as well as morphogenetic patterning of the developing ectoderm, nervous system, skeleton, and tooth. In patients, WNT10A mutations are responsible for ectodermal‐derived pathologies including isolated hypo‐oligodontia, tricho‐odonto‐onycho‐dermal dysplasia and Schöpf‐Schulz‐Passarge syndrome (SSPS). Here we describe the dental, ectodermal, and extra‐ectodermal phenotypic features of a cohort of 41 patients from 32 unrelated families. Correlations with WNT10A molecular status (heterozygous carrier, compound heterozygous, homozygous) and patient's phenotypes were performed. Mild to severe oligodontia was observed in all patients bearing biallelic WNT10A mutations. However, patients with compound heterozygous mutations presented no significant difference in phenotypes compared with homozygous individuals. Anomalies in tooth morphology were frequently observed with heterozygous patients displaying hypodontia. No signs of SSPS, especially eyelids cysts, were detected in our cohort. Interestingly, extra‐ectodermal signs consisted of skeletal, neurological and vascular anomalies, the latter suggesting a wider phenotypic spectrum associated with WNT10A mutations. Indeed, the Wnt pathway plays a crucial role in skeletal development, lipid metabolism, and neurogenesis, potentially explaining patient's clinical manifestations.</description><subject>Adolescent</subject><subject>Adult</subject><subject>bone</subject><subject>Cell fate</subject><subject>Child</subject><subject>Cohort Studies</subject><subject>Cone-Beam Computed Tomography</subject><subject>Cysts</subject><subject>dental phenotype</subject><subject>Dysplasia</subject><subject>Ectoderm</subject><subject>Ectoderm - pathology</subject><subject>extra‐ectodermal signs</subject><subject>Genetic Association Studies</subject><subject>Genetics</subject><subject>Genotype & phenotype</subject><subject>Heterozygote</subject><subject>Homozygote</subject><subject>Human genetics</subject><subject>Humans</subject><subject>Life Sciences</subject><subject>Lipid metabolism</subject><subject>Mandible - pathology</subject><subject>Middle Aged</subject><subject>Mutation</subject><subject>Mutation - genetics</subject><subject>Nervous system</subject><subject>Neurogenesis</subject><subject>oligodontia</subject><subject>Patients</subject><subject>Pattern formation</subject><subject>Phenotype</subject><subject>Skeleton</subject><subject>Skin</subject><subject>Teeth</subject><subject>Tooth - diagnostic imaging</subject><subject>Tooth - pathology</subject><subject>Wnt protein</subject><subject>Wnt Proteins - genetics</subject><subject>WNT10A mutation</subject><subject>Young Adult</subject><issn>0009-9163</issn><issn>1399-0004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><recordid>eNp1kctuEzEUhq0K1IbCoi9QWWJTFtP62OOxzS4KvSBFsCliaTkeT-NqMjPYnpZsUB8BqW_YJ8EhoUhIeHNu3_lt60foCMgp5HNmb9wpUCXoHpoAU6oghJQv0CQHVSio2AF6FeNtLpngah8dUAmEV4xP0I8Prkumxaarsfuegnl6-NmH3LCt77zNSeNMGoOL2He4BDyY5PNKxPc-LfHXT9dApvjGdQ6vxpRnfRff42ku2uRtBoO3m3Gf1oN7engclrscxzTW69foZWPa6N7s4iH6cnF-Pbsq5p8vP86m88IyKWghBJWcVqVVvIG6UsQoIRtVsloKwWtXMkahaiiztq4kXZAFcYqBkMANJzWwQ_Ruq7s0rR6CX5mw1r3x-mo615seAVGCYPxuw55s2SH030YXk175aF3bms71Y9QgK-BSghQZffsPetuPocs_0aBKyUpJKf97uQ19jME1zy8AojcG6myg_m1gZo93iuNi5epn8o9jGTjbAve-dev_K-nZ5flW8hdP16Q8</recordid><startdate>201711</startdate><enddate>201711</enddate><creator>Tardieu, C.</creator><creator>Jung, S.</creator><creator>Niederreither, K.</creator><creator>Prasad, M.</creator><creator>Hadj‐Rabia, S.</creator><creator>Philip, N.</creator><creator>Mallet, A.</creator><creator>Consolino, E.</creator><creator>Sfeir, E.</creator><creator>Noueiri, B.</creator><creator>Chassaing, N.</creator><creator>Dollfus, H.</creator><creator>Manière, M.C.</creator><creator>Bloch‐Zupan, A.</creator><creator>Clauss, F.</creator><general>Blackwell Publishing Ltd</general><general>Wiley</general><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>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0002-8078-2406</orcidid></search><sort><creationdate>201711</creationdate><title>Dental and extra‐oral clinical features in 41 patients with WNT10A gene mutations: A multicentric genotype–phenotype study</title><author>Tardieu, C. ; Jung, S. ; Niederreither, K. ; Prasad, M. ; Hadj‐Rabia, S. ; Philip, N. ; Mallet, A. ; Consolino, E. ; Sfeir, E. ; Noueiri, B. ; Chassaing, N. ; Dollfus, H. ; Manière, M.C. ; Bloch‐Zupan, A. ; Clauss, F.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3872-77285264c95f1d690a978f943d8775de433216f23ccd682b0b0e9317815a50d13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>bone</topic><topic>Cell fate</topic><topic>Child</topic><topic>Cohort Studies</topic><topic>Cone-Beam Computed Tomography</topic><topic>Cysts</topic><topic>dental phenotype</topic><topic>Dysplasia</topic><topic>Ectoderm</topic><topic>Ectoderm - pathology</topic><topic>extra‐ectodermal signs</topic><topic>Genetic Association Studies</topic><topic>Genetics</topic><topic>Genotype & phenotype</topic><topic>Heterozygote</topic><topic>Homozygote</topic><topic>Human genetics</topic><topic>Humans</topic><topic>Life Sciences</topic><topic>Lipid metabolism</topic><topic>Mandible - pathology</topic><topic>Middle Aged</topic><topic>Mutation</topic><topic>Mutation - genetics</topic><topic>Nervous system</topic><topic>Neurogenesis</topic><topic>oligodontia</topic><topic>Patients</topic><topic>Pattern formation</topic><topic>Phenotype</topic><topic>Skeleton</topic><topic>Skin</topic><topic>Teeth</topic><topic>Tooth - diagnostic imaging</topic><topic>Tooth - pathology</topic><topic>Wnt protein</topic><topic>Wnt Proteins - genetics</topic><topic>WNT10A mutation</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tardieu, C.</creatorcontrib><creatorcontrib>Jung, S.</creatorcontrib><creatorcontrib>Niederreither, K.</creatorcontrib><creatorcontrib>Prasad, M.</creatorcontrib><creatorcontrib>Hadj‐Rabia, S.</creatorcontrib><creatorcontrib>Philip, N.</creatorcontrib><creatorcontrib>Mallet, A.</creatorcontrib><creatorcontrib>Consolino, E.</creatorcontrib><creatorcontrib>Sfeir, E.</creatorcontrib><creatorcontrib>Noueiri, B.</creatorcontrib><creatorcontrib>Chassaing, N.</creatorcontrib><creatorcontrib>Dollfus, H.</creatorcontrib><creatorcontrib>Manière, M.C.</creatorcontrib><creatorcontrib>Bloch‐Zupan, A.</creatorcontrib><creatorcontrib>Clauss, F.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Clinical genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tardieu, C.</au><au>Jung, S.</au><au>Niederreither, K.</au><au>Prasad, M.</au><au>Hadj‐Rabia, S.</au><au>Philip, N.</au><au>Mallet, A.</au><au>Consolino, E.</au><au>Sfeir, E.</au><au>Noueiri, B.</au><au>Chassaing, N.</au><au>Dollfus, H.</au><au>Manière, M.C.</au><au>Bloch‐Zupan, A.</au><au>Clauss, F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dental and extra‐oral clinical features in 41 patients with WNT10A gene mutations: A multicentric genotype–phenotype study</atitle><jtitle>Clinical genetics</jtitle><addtitle>Clin Genet</addtitle><date>2017-11</date><risdate>2017</risdate><volume>92</volume><issue>5</issue><spage>477</spage><epage>486</epage><pages>477-486</pages><issn>0009-9163</issn><eissn>1399-0004</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>WNT10A gene encodes a canonical wingless pathway signaling molecule involved in cell fate specification as well as morphogenetic patterning of the developing ectoderm, nervous system, skeleton, and tooth. In patients, WNT10A mutations are responsible for ectodermal‐derived pathologies including isolated hypo‐oligodontia, tricho‐odonto‐onycho‐dermal dysplasia and Schöpf‐Schulz‐Passarge syndrome (SSPS). Here we describe the dental, ectodermal, and extra‐ectodermal phenotypic features of a cohort of 41 patients from 32 unrelated families. Correlations with WNT10A molecular status (heterozygous carrier, compound heterozygous, homozygous) and patient's phenotypes were performed. Mild to severe oligodontia was observed in all patients bearing biallelic WNT10A mutations. However, patients with compound heterozygous mutations presented no significant difference in phenotypes compared with homozygous individuals. Anomalies in tooth morphology were frequently observed with heterozygous patients displaying hypodontia. No signs of SSPS, especially eyelids cysts, were detected in our cohort. Interestingly, extra‐ectodermal signs consisted of skeletal, neurological and vascular anomalies, the latter suggesting a wider phenotypic spectrum associated with WNT10A mutations. Indeed, the Wnt pathway plays a crucial role in skeletal development, lipid metabolism, and neurogenesis, potentially explaining patient's clinical manifestations.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>28105635</pmid><doi>10.1111/cge.12972</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-8078-2406</orcidid></addata></record> |
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subjects | Adolescent Adult bone Cell fate Child Cohort Studies Cone-Beam Computed Tomography Cysts dental phenotype Dysplasia Ectoderm Ectoderm - pathology extra‐ectodermal signs Genetic Association Studies Genetics Genotype & phenotype Heterozygote Homozygote Human genetics Humans Life Sciences Lipid metabolism Mandible - pathology Middle Aged Mutation Mutation - genetics Nervous system Neurogenesis oligodontia Patients Pattern formation Phenotype Skeleton Skin Teeth Tooth - diagnostic imaging Tooth - pathology Wnt protein Wnt Proteins - genetics WNT10A mutation Young Adult |
title | Dental and extra‐oral clinical features in 41 patients with WNT10A gene mutations: A multicentric genotype–phenotype study |
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