Pivotal Role of Tenascin-W (-N) in Postnatal Incisor Growth and Periodontal Ligament Remodeling

Show simple item record

dc.contributor University of Helsinki, Institute of Biotechnology en
dc.contributor University of Helsinki, Institute of Biotechnology en
dc.contributor.author Imhof, Thomas
dc.contributor.author Balic, Anamaria
dc.contributor.author Heilig, Juliane
dc.contributor.author Chiquet-Ehrismann, Ruth
dc.contributor.author Chiquet, Matthias
dc.contributor.author Niehoff, Anja
dc.contributor.author Brachvogel, Bent
dc.contributor.author Thesleff, Irma
dc.contributor.author Koch, Manuel
dc.date.accessioned 2021-08-24T10:07:01Z
dc.date.available 2021-08-24T10:07:01Z
dc.date.issued 2021-01-22
dc.identifier.citation Imhof , T , Balic , A , Heilig , J , Chiquet-Ehrismann , R , Chiquet , M , Niehoff , A , Brachvogel , B , Thesleff , I & Koch , M 2021 , ' Pivotal Role of Tenascin-W (-N) in Postnatal Incisor Growth and Periodontal Ligament Remodeling ' , Frontiers in Immunology , vol. 11 , 608223 . https://doi.org/10.3389/fimmu.2020.608223 en
dc.identifier.issn 1664-3224
dc.identifier.other PURE: 161461520
dc.identifier.other PURE UUID: a86a7ce3-0ca5-4ba2-82f2-a2ce27be4e59
dc.identifier.other WOS: 000614762900001
dc.identifier.other ORCID: /0000-0001-6796-1197/work/98919948
dc.identifier.uri http://hdl.handle.net/10138/333478
dc.description.abstract The continuously growing mouse incisor provides a fascinating model for studying stem cell regulation and organ renewal. In the incisor, epithelial and mesenchymal stem cells assure lifelong tooth growth. The epithelial stem cells reside in a niche known as the cervical loop. Mesenchymal stem cells are located in the nearby apical neurovascular bundle and in the neural plexus. So far, little is known about extracellular cues that are controlling incisor stem cell renewal and guidance. The extracellular matrix protein tenascin-W, also known as tenascin-N (TNN), is expressed in the mesenchyme of the pulp and of the periodontal ligament of the incisor, and is closely associated with collagen 3 fibers. Here, we report for the first time the phenotype of tenascin-W/TNN deficient mice, which in a C57BL/6N background exhibit a reduced body weight and lifespan. We found major defects in the alveolar bone and periodontal ligament of the growing rodent incisors, whereas molars were not affected. The alveolar bone around the incisor was replaced by a dense scar-like connective tissue, enriched with newly formed nerve fibers likely leading to periodontal pain, less food intake and reduced body weight. Using soft food to reduce mechanical load on the incisor partially rescued the phenotype. In situ hybridization and Gli1 reporter mouse experiments revealed decreased hedgehog signaling in the incisor mesenchymal stem cell compartment, which coordinates the development of mesenchymal stem cell niche. These results indicate that TNN deficiency in mice affects periodontal remodeling and increases nerve fiber branching. Through periodontal pain the food intake is reduced and the incisor renewal and the neurovascular sonic hedgehog secretion rate are reduced. In conclusion, tenascin-W/TNN seems to have a primary function in rapid periodontal tissue remodeling and a secondary function in mechanosensation. en
dc.format.extent 13
dc.language.iso eng
dc.relation.ispartof Frontiers in Immunology
dc.rights en
dc.subject tenascin-W en
dc.subject tenascin-N en
dc.subject bone en
dc.subject remodeling en
dc.subject periodontal ligament en
dc.subject pain en
dc.subject tenascin en
dc.subject 1182 Biochemistry, cell and molecular biology en
dc.title Pivotal Role of Tenascin-W (-N) in Postnatal Incisor Growth and Periodontal Ligament Remodeling en
dc.type Article
dc.description.version Peer reviewed
dc.identifier.doi https://doi.org/10.3389/fimmu.2020.608223
dc.type.uri info:eu-repo/semantics/other
dc.type.uri info:eu-repo/semantics/publishedVersion

Files in this item

Total number of downloads: Loading...

Files Size Format View
fimmu_11_608223.pdf 11.69Mb PDF View/Open

This item appears in the following Collection(s)

Show simple item record