Accelerated tooth movement in Rsk2-deficient mice with impaired cementum formation
Abstract Coffin–Lowry–Syndrome (CLS) is a X-linked mental retardation characterized by skeletal dysplasia and premature tooth loss. We and others have previously demonstrated that the ribosomal S6 kinase RSK2, mutated in CLS, is essential for bone and cementum formation; however, it remains to be es...
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Nature Publishing Group
2020-12-01
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Series: | International Journal of Oral Science |
Online Access: | https://doi.org/10.1038/s41368-020-00102-4 |
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author | Cita Nottmeier Maximilian G. Decker Julia Luther Simon von Kroge Bärbel Kahl-Nieke Michael Amling Thorsten Schinke Julian Petersen Till Koehne |
author_facet | Cita Nottmeier Maximilian G. Decker Julia Luther Simon von Kroge Bärbel Kahl-Nieke Michael Amling Thorsten Schinke Julian Petersen Till Koehne |
author_sort | Cita Nottmeier |
collection | DOAJ |
description | Abstract Coffin–Lowry–Syndrome (CLS) is a X-linked mental retardation characterized by skeletal dysplasia and premature tooth loss. We and others have previously demonstrated that the ribosomal S6 kinase RSK2, mutated in CLS, is essential for bone and cementum formation; however, it remains to be established whether RSK2 plays also a role in mechanically induced bone remodeling during orthodontic tooth movement (OTM). We, therefore, performed OTM in wild-type (WT) mice and Rsk2-deficient mice using Nitinol tension springs that were fixed between the upper left molars and the incisors. The untreated contralateral molars served as internal controls. After 12 days of OTM, the jaws were removed and examined by micro-computed tomography (µCT), decalcified histology, and immunohistochemistry. Our analysis of the untreated teeth confirmed that the periodontal phenotype of Rsk2-deficient mice is characterized by alveolar bone loss and hypoplasia of root cementum. Quantification of OTM using µCT revealed that OTM was more than two-fold faster in Rsk2-deficient mice as compared to WT. We also observed that OTM caused alveolar bone loss and root resorptions in WT and Rsk2-deficient mice. However, quantification of these orthodontic side effects revealed no differences between WT and Rsk2-deficient mice. Taken together, Rsk2 loss-of-function accelerates OTM in mice without causing more side effects. |
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issn | 1674-2818 2049-3169 |
language | English |
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series | International Journal of Oral Science |
spelling | doaj.art-5f7eea3ea2da47208cb6a699110d50d62022-12-21T23:21:51ZengNature Publishing GroupInternational Journal of Oral Science1674-28182049-31692020-12-011211810.1038/s41368-020-00102-4Accelerated tooth movement in Rsk2-deficient mice with impaired cementum formationCita Nottmeier0Maximilian G. Decker1Julia Luther2Simon von Kroge3Bärbel Kahl-Nieke4Michael Amling5Thorsten Schinke6Julian Petersen7Till Koehne8Department of Orthodontics, University Medical Center Hamburg-EppendorfDepartment of Orthodontics, University Medical Center Hamburg-EppendorfInstitute of Osteology and Biomechanics, University Medical Center Hamburg-EppendorfInstitute of Osteology and Biomechanics, University Medical Center Hamburg-EppendorfDepartment of Orthodontics, University Medical Center Hamburg-EppendorfInstitute of Osteology and Biomechanics, University Medical Center Hamburg-EppendorfInstitute of Osteology and Biomechanics, University Medical Center Hamburg-EppendorfInstitute of Osteology and Biomechanics, University Medical Center Hamburg-EppendorfDepartment of Orthodontics, University Medical Center Hamburg-EppendorfAbstract Coffin–Lowry–Syndrome (CLS) is a X-linked mental retardation characterized by skeletal dysplasia and premature tooth loss. We and others have previously demonstrated that the ribosomal S6 kinase RSK2, mutated in CLS, is essential for bone and cementum formation; however, it remains to be established whether RSK2 plays also a role in mechanically induced bone remodeling during orthodontic tooth movement (OTM). We, therefore, performed OTM in wild-type (WT) mice and Rsk2-deficient mice using Nitinol tension springs that were fixed between the upper left molars and the incisors. The untreated contralateral molars served as internal controls. After 12 days of OTM, the jaws were removed and examined by micro-computed tomography (µCT), decalcified histology, and immunohistochemistry. Our analysis of the untreated teeth confirmed that the periodontal phenotype of Rsk2-deficient mice is characterized by alveolar bone loss and hypoplasia of root cementum. Quantification of OTM using µCT revealed that OTM was more than two-fold faster in Rsk2-deficient mice as compared to WT. We also observed that OTM caused alveolar bone loss and root resorptions in WT and Rsk2-deficient mice. However, quantification of these orthodontic side effects revealed no differences between WT and Rsk2-deficient mice. Taken together, Rsk2 loss-of-function accelerates OTM in mice without causing more side effects.https://doi.org/10.1038/s41368-020-00102-4 |
spellingShingle | Cita Nottmeier Maximilian G. Decker Julia Luther Simon von Kroge Bärbel Kahl-Nieke Michael Amling Thorsten Schinke Julian Petersen Till Koehne Accelerated tooth movement in Rsk2-deficient mice with impaired cementum formation International Journal of Oral Science |
title | Accelerated tooth movement in Rsk2-deficient mice with impaired cementum formation |
title_full | Accelerated tooth movement in Rsk2-deficient mice with impaired cementum formation |
title_fullStr | Accelerated tooth movement in Rsk2-deficient mice with impaired cementum formation |
title_full_unstemmed | Accelerated tooth movement in Rsk2-deficient mice with impaired cementum formation |
title_short | Accelerated tooth movement in Rsk2-deficient mice with impaired cementum formation |
title_sort | accelerated tooth movement in rsk2 deficient mice with impaired cementum formation |
url | https://doi.org/10.1038/s41368-020-00102-4 |
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