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Comprehensive analyses of how tubule occlusion and advanced glycation end-products diminish strength of aged dentin
In clinical dentistry, since fracture is a major cause of tooth loss, better understanding of mechanical properties of teeth structures is important. Dentin, the major hard tissue of teeth, has similar composition to bone. In this study, we investigated the mechanical properties of human dentin not...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4726429/ https://www.ncbi.nlm.nih.gov/pubmed/26797297 http://dx.doi.org/10.1038/srep19849 |
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author | Shinno, Yuko Ishimoto, Takuya Saito, Mitsuru Uemura, Reo Arino, Masumi Marumo, Keishi Nakano, Takayoshi Hayashi, Mikako |
author_facet | Shinno, Yuko Ishimoto, Takuya Saito, Mitsuru Uemura, Reo Arino, Masumi Marumo, Keishi Nakano, Takayoshi Hayashi, Mikako |
author_sort | Shinno, Yuko |
collection | PubMed |
description | In clinical dentistry, since fracture is a major cause of tooth loss, better understanding of mechanical properties of teeth structures is important. Dentin, the major hard tissue of teeth, has similar composition to bone. In this study, we investigated the mechanical properties of human dentin not only in terms of mineral density but also using structural and quality parameters as recently accepted in evaluating bone strength. Aged crown and root dentin (age ≥ 40) exhibited significantly lower flexural strength and toughness than young dentin (age < 40). Aged dentin, in which the dentinal tubules were occluded with calcified material, recorded the highest mineral density; but showed significantly lower flexural strength than young dentin. Dentin with strong alignment of the c-axis in hydroxyapatite exhibited high fracture strength, possibly because the aligned apatite along the collagen fibrils may reinforce the intertubular dentin. Aged dentin, showing a high advanced glycation end-products (AGEs) level in its collagen, recorded low flexural strength. We first comprehensively identified significant factors, which affected the inferior mechanical properties of aged dentin. The low mechanical strength of aged dentin is caused by the high mineral density resulting from occlusion of dentinal tubules and accumulation of AGEs in dentin collagen. |
format | Online Article Text |
id | pubmed-4726429 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-47264292016-01-27 Comprehensive analyses of how tubule occlusion and advanced glycation end-products diminish strength of aged dentin Shinno, Yuko Ishimoto, Takuya Saito, Mitsuru Uemura, Reo Arino, Masumi Marumo, Keishi Nakano, Takayoshi Hayashi, Mikako Sci Rep Article In clinical dentistry, since fracture is a major cause of tooth loss, better understanding of mechanical properties of teeth structures is important. Dentin, the major hard tissue of teeth, has similar composition to bone. In this study, we investigated the mechanical properties of human dentin not only in terms of mineral density but also using structural and quality parameters as recently accepted in evaluating bone strength. Aged crown and root dentin (age ≥ 40) exhibited significantly lower flexural strength and toughness than young dentin (age < 40). Aged dentin, in which the dentinal tubules were occluded with calcified material, recorded the highest mineral density; but showed significantly lower flexural strength than young dentin. Dentin with strong alignment of the c-axis in hydroxyapatite exhibited high fracture strength, possibly because the aligned apatite along the collagen fibrils may reinforce the intertubular dentin. Aged dentin, showing a high advanced glycation end-products (AGEs) level in its collagen, recorded low flexural strength. We first comprehensively identified significant factors, which affected the inferior mechanical properties of aged dentin. The low mechanical strength of aged dentin is caused by the high mineral density resulting from occlusion of dentinal tubules and accumulation of AGEs in dentin collagen. Nature Publishing Group 2016-01-22 /pmc/articles/PMC4726429/ /pubmed/26797297 http://dx.doi.org/10.1038/srep19849 Text en Copyright © 2016, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Shinno, Yuko Ishimoto, Takuya Saito, Mitsuru Uemura, Reo Arino, Masumi Marumo, Keishi Nakano, Takayoshi Hayashi, Mikako Comprehensive analyses of how tubule occlusion and advanced glycation end-products diminish strength of aged dentin |
title | Comprehensive analyses of how tubule occlusion and advanced glycation end-products diminish strength of aged dentin |
title_full | Comprehensive analyses of how tubule occlusion and advanced glycation end-products diminish strength of aged dentin |
title_fullStr | Comprehensive analyses of how tubule occlusion and advanced glycation end-products diminish strength of aged dentin |
title_full_unstemmed | Comprehensive analyses of how tubule occlusion and advanced glycation end-products diminish strength of aged dentin |
title_short | Comprehensive analyses of how tubule occlusion and advanced glycation end-products diminish strength of aged dentin |
title_sort | comprehensive analyses of how tubule occlusion and advanced glycation end-products diminish strength of aged dentin |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4726429/ https://www.ncbi.nlm.nih.gov/pubmed/26797297 http://dx.doi.org/10.1038/srep19849 |
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