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High-fat diet-induced obesity triggers alveolar bone loss and spontaneous periodontal disease in growing mice

BACKGROUND: The relationship between high-fat food consumption and obesity is well-established. However, it is as yet unclear whether high-fat diet (HFD)-induced obesity in childhood and adolescence determines age-related changes in jaw bone health. The aim of this study is to examine the age-relate...

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Autores principales: Fujita, Yuko, Maki, Kenshi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4705635/
https://www.ncbi.nlm.nih.gov/pubmed/26793316
http://dx.doi.org/10.1186/s40608-016-0082-8
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author Fujita, Yuko
Maki, Kenshi
author_facet Fujita, Yuko
Maki, Kenshi
author_sort Fujita, Yuko
collection PubMed
description BACKGROUND: The relationship between high-fat food consumption and obesity is well-established. However, it is as yet unclear whether high-fat diet (HFD)-induced obesity in childhood and adolescence determines age-related changes in jaw bone health. The aim of this study is to examine the age-related influence of HFD-induced obesity on mandibular bone architecture and the structure of the periodontium in growing mice. METHODS: Male C57BL/6 J mice (6-weeks-old) were divided into two groups (n = 6 each): the control group received a control diet and the experimental group a HFD. After treatment for 4, 8, or 12 weeks, trabecular and cortical bone architecture was assessed using micro-computed tomography. The periodontium and alveolar bone structure were evaluated by histopathology. RESULTS: In HFD mice, body weight, serum total cholesterol, and serum leptin levels were significantly higher than those in age-matched control mice (p < 0.05, all comparisons). Reductions in trabecular bone volume and in cortical bone growth (measured as the thickness and cross sectional area) in HFD mice were significant compared with the control mice after 4 weeks of treatment (p < 0.05, both comparisons). Significant decreases in cortical bone density in HFD-fed vs. age-matched control mice were determined after 12 weeks (p < 0.05). In the HFD mice, the periodontal ligament fibres were disrupted, having lost their orientation with respect to the bone surface, and constriction of the periodontal ligament space was inhibited. CONCLUSIONS: These results suggest that HFD-induced obesity during growth not only triggers mandibular osteoporosis but also increases the risk of spontaneous periodontal disease.
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spelling pubmed-47056352016-01-20 High-fat diet-induced obesity triggers alveolar bone loss and spontaneous periodontal disease in growing mice Fujita, Yuko Maki, Kenshi BMC Obes Research Article BACKGROUND: The relationship between high-fat food consumption and obesity is well-established. However, it is as yet unclear whether high-fat diet (HFD)-induced obesity in childhood and adolescence determines age-related changes in jaw bone health. The aim of this study is to examine the age-related influence of HFD-induced obesity on mandibular bone architecture and the structure of the periodontium in growing mice. METHODS: Male C57BL/6 J mice (6-weeks-old) were divided into two groups (n = 6 each): the control group received a control diet and the experimental group a HFD. After treatment for 4, 8, or 12 weeks, trabecular and cortical bone architecture was assessed using micro-computed tomography. The periodontium and alveolar bone structure were evaluated by histopathology. RESULTS: In HFD mice, body weight, serum total cholesterol, and serum leptin levels were significantly higher than those in age-matched control mice (p < 0.05, all comparisons). Reductions in trabecular bone volume and in cortical bone growth (measured as the thickness and cross sectional area) in HFD mice were significant compared with the control mice after 4 weeks of treatment (p < 0.05, both comparisons). Significant decreases in cortical bone density in HFD-fed vs. age-matched control mice were determined after 12 weeks (p < 0.05). In the HFD mice, the periodontal ligament fibres were disrupted, having lost their orientation with respect to the bone surface, and constriction of the periodontal ligament space was inhibited. CONCLUSIONS: These results suggest that HFD-induced obesity during growth not only triggers mandibular osteoporosis but also increases the risk of spontaneous periodontal disease. BioMed Central 2016-01-08 /pmc/articles/PMC4705635/ /pubmed/26793316 http://dx.doi.org/10.1186/s40608-016-0082-8 Text en © Fujita and Maki. 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Fujita, Yuko
Maki, Kenshi
High-fat diet-induced obesity triggers alveolar bone loss and spontaneous periodontal disease in growing mice
title High-fat diet-induced obesity triggers alveolar bone loss and spontaneous periodontal disease in growing mice
title_full High-fat diet-induced obesity triggers alveolar bone loss and spontaneous periodontal disease in growing mice
title_fullStr High-fat diet-induced obesity triggers alveolar bone loss and spontaneous periodontal disease in growing mice
title_full_unstemmed High-fat diet-induced obesity triggers alveolar bone loss and spontaneous periodontal disease in growing mice
title_short High-fat diet-induced obesity triggers alveolar bone loss and spontaneous periodontal disease in growing mice
title_sort high-fat diet-induced obesity triggers alveolar bone loss and spontaneous periodontal disease in growing mice
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4705635/
https://www.ncbi.nlm.nih.gov/pubmed/26793316
http://dx.doi.org/10.1186/s40608-016-0082-8
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