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Expression of SOST/sclerostin in compressed periodontal ligament cells
BACKGROUND/PURPOSE: Bone resorption and inhibition of bone formation occur on the compressed side during orthodontic tooth movement. Bone formation inhibitory factors such as sclerostin (encoded by SOST) are secreted on the compressed side by periodontal ligament (PDL) cells. PDL cells control bone...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Association for Dental Sciences of the Republic of China
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6395252/ https://www.ncbi.nlm.nih.gov/pubmed/30894984 http://dx.doi.org/10.1016/j.jds.2016.02.006 |
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author | Ueda, Masae Kuroishi, Kayoko N. Gunjigake, Kaori K. Ikeda, Erina Kawamoto, Tatsuo |
author_facet | Ueda, Masae Kuroishi, Kayoko N. Gunjigake, Kaori K. Ikeda, Erina Kawamoto, Tatsuo |
author_sort | Ueda, Masae |
collection | PubMed |
description | BACKGROUND/PURPOSE: Bone resorption and inhibition of bone formation occur on the compressed side during orthodontic tooth movement. Bone formation inhibitory factors such as sclerostin (encoded by SOST) are secreted on the compressed side by periodontal ligament (PDL) cells. PDL cells control bone metabolism, and compressed PDL cells inhibit bone formation during orthodontic tooth movement. The aim of this study was to identify the inhibitory factors of bone formation in PDL cells. MATERIALS AND METHODS: Changes in SOST expression and subsequent protein release from human PDL (hPDL) cells were assessed using the real-time polymerase chain reaction (PCR), semiquantitative PCR, and immunofluorescence in hPDL cells subjected to centrifugal force (40g and 90g). To confirm the effects on bone formation, human alveolar bone-derived osteoblasts (hOBs) were grown with the addition of sclerostin peptide. In vivo, a compressive force was applied using the Waldo method in rats, and the distribution of sclerostin in PDL tissues was examined by immunohistochemistry. RESULTS: SOST expression was downregulated in vitro by centrifugation at 90g for 24 hours but upregulated by centrifugation at 40g based on real-time PCR, as was confirmed by immunofluorescence staining. The addition of sclerostin peptide significantly decreased the mineralized area in hOBs. However, slightly weakly sclerostin-positive PDL cells were observed on the compressed side in vivo. CONCLUSION: These results indicate that PDL cells subjected to light compressive force exhibit increased expression of SOST/sclerostin, which inhibits bone formation on the compressed side during orthodontic tooth movement. |
format | Online Article Text |
id | pubmed-6395252 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Association for Dental Sciences of the Republic of China |
record_format | MEDLINE/PubMed |
spelling | pubmed-63952522019-03-20 Expression of SOST/sclerostin in compressed periodontal ligament cells Ueda, Masae Kuroishi, Kayoko N. Gunjigake, Kaori K. Ikeda, Erina Kawamoto, Tatsuo J Dent Sci Original Article BACKGROUND/PURPOSE: Bone resorption and inhibition of bone formation occur on the compressed side during orthodontic tooth movement. Bone formation inhibitory factors such as sclerostin (encoded by SOST) are secreted on the compressed side by periodontal ligament (PDL) cells. PDL cells control bone metabolism, and compressed PDL cells inhibit bone formation during orthodontic tooth movement. The aim of this study was to identify the inhibitory factors of bone formation in PDL cells. MATERIALS AND METHODS: Changes in SOST expression and subsequent protein release from human PDL (hPDL) cells were assessed using the real-time polymerase chain reaction (PCR), semiquantitative PCR, and immunofluorescence in hPDL cells subjected to centrifugal force (40g and 90g). To confirm the effects on bone formation, human alveolar bone-derived osteoblasts (hOBs) were grown with the addition of sclerostin peptide. In vivo, a compressive force was applied using the Waldo method in rats, and the distribution of sclerostin in PDL tissues was examined by immunohistochemistry. RESULTS: SOST expression was downregulated in vitro by centrifugation at 90g for 24 hours but upregulated by centrifugation at 40g based on real-time PCR, as was confirmed by immunofluorescence staining. The addition of sclerostin peptide significantly decreased the mineralized area in hOBs. However, slightly weakly sclerostin-positive PDL cells were observed on the compressed side in vivo. CONCLUSION: These results indicate that PDL cells subjected to light compressive force exhibit increased expression of SOST/sclerostin, which inhibits bone formation on the compressed side during orthodontic tooth movement. Association for Dental Sciences of the Republic of China 2016-09 2016-04-14 /pmc/articles/PMC6395252/ /pubmed/30894984 http://dx.doi.org/10.1016/j.jds.2016.02.006 Text en Copyright © 2016, Association for Dental Sciences of the Republic of China. Published by Elsevier Taiwan LLC. http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Original Article Ueda, Masae Kuroishi, Kayoko N. Gunjigake, Kaori K. Ikeda, Erina Kawamoto, Tatsuo Expression of SOST/sclerostin in compressed periodontal ligament cells |
title | Expression of SOST/sclerostin in compressed periodontal ligament cells |
title_full | Expression of SOST/sclerostin in compressed periodontal ligament cells |
title_fullStr | Expression of SOST/sclerostin in compressed periodontal ligament cells |
title_full_unstemmed | Expression of SOST/sclerostin in compressed periodontal ligament cells |
title_short | Expression of SOST/sclerostin in compressed periodontal ligament cells |
title_sort | expression of sost/sclerostin in compressed periodontal ligament cells |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6395252/ https://www.ncbi.nlm.nih.gov/pubmed/30894984 http://dx.doi.org/10.1016/j.jds.2016.02.006 |
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