肌肉量增加对小鼠矢状缝形态和力学的影响。

Craig D Byron, James Borke, Jack Yu, David Pashley, Christopher J Wingard, Mark Hamrick
{"title":"肌肉量增加对小鼠矢状缝形态和力学的影响。","authors":"Craig D Byron,&nbsp;James Borke,&nbsp;Jack Yu,&nbsp;David Pashley,&nbsp;Christopher J Wingard,&nbsp;Mark Hamrick","doi":"10.1002/ar.a.20055","DOIUrl":null,"url":null,"abstract":"<p><p>The purpose of this study is to test predicted form-function relationships between cranial suture complexity and masticatory muscle mass and biomechanics in a mouse model. Specifically, to test the hypothesis that increased masticatory muscle mass increases sagittal suture complexity, we measured the fractal dimension (FD), temporalis mass, and temporalis bite force in myostatin-deficient (GDF8(-/-)) mice and wild-type CD-1 mice (all male, 6 months old). Myostatin is a negative regulator of muscle mass, and myostatin-deficient mice show a marked increase in muscle mass compared to normal mice. We predicted that increased sagittal suture complexity would decrease suture stiffness. The data presented here demonstrate that increased suture complexity (measured as FD) was observed in a hypermuscular mouse model (GDF8(-/-)) with significantly increased temporalis muscle mass and bite forces. Hypermuscular mice were also found to possess suture connective tissue that was less stiff (i.e., underwent more displacement before failure occurred) when loaded in tension. By decreasing stiffness, suture complexity apparently helps to dissipate mechanical loads within the cranium that are related to chewing. These results suggest that cranial suture connective tissue locally adapts to functional demands of the biomechanical suture environment. As such, cranial sutures provide a novel model for studies in connective tissue mechanotransduction.</p>","PeriodicalId":85633,"journal":{"name":"The anatomical record. Part A, Discoveries in molecular, cellular, and evolutionary biology","volume":"279 1","pages":"676-84"},"PeriodicalIF":0.0000,"publicationDate":"2004-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/ar.a.20055","citationCount":"120","resultStr":"{\"title\":\"Effects of increased muscle mass on mouse sagittal suture morphology and mechanics.\",\"authors\":\"Craig D Byron,&nbsp;James Borke,&nbsp;Jack Yu,&nbsp;David Pashley,&nbsp;Christopher J Wingard,&nbsp;Mark Hamrick\",\"doi\":\"10.1002/ar.a.20055\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The purpose of this study is to test predicted form-function relationships between cranial suture complexity and masticatory muscle mass and biomechanics in a mouse model. Specifically, to test the hypothesis that increased masticatory muscle mass increases sagittal suture complexity, we measured the fractal dimension (FD), temporalis mass, and temporalis bite force in myostatin-deficient (GDF8(-/-)) mice and wild-type CD-1 mice (all male, 6 months old). Myostatin is a negative regulator of muscle mass, and myostatin-deficient mice show a marked increase in muscle mass compared to normal mice. We predicted that increased sagittal suture complexity would decrease suture stiffness. The data presented here demonstrate that increased suture complexity (measured as FD) was observed in a hypermuscular mouse model (GDF8(-/-)) with significantly increased temporalis muscle mass and bite forces. Hypermuscular mice were also found to possess suture connective tissue that was less stiff (i.e., underwent more displacement before failure occurred) when loaded in tension. By decreasing stiffness, suture complexity apparently helps to dissipate mechanical loads within the cranium that are related to chewing. These results suggest that cranial suture connective tissue locally adapts to functional demands of the biomechanical suture environment. As such, cranial sutures provide a novel model for studies in connective tissue mechanotransduction.</p>\",\"PeriodicalId\":85633,\"journal\":{\"name\":\"The anatomical record. Part A, Discoveries in molecular, cellular, and evolutionary biology\",\"volume\":\"279 1\",\"pages\":\"676-84\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2004-07-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1002/ar.a.20055\",\"citationCount\":\"120\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"The anatomical record. Part A, Discoveries in molecular, cellular, and evolutionary biology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1002/ar.a.20055\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"The anatomical record. Part A, Discoveries in molecular, cellular, and evolutionary biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1002/ar.a.20055","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 120

摘要

本研究的目的是在小鼠模型中测试预测的颅缝线复杂性与咀嚼肌质量和生物力学之间的形式-功能关系。具体来说,为了验证咀嚼肌质量增加会增加矢状缝复杂性的假设,我们测量了肌生成抑制素缺乏(GDF8(-/-))小鼠和野生型CD-1小鼠(均为雄性,6个月大)的分形维数(FD)、颞肌质量和颞肌咬合力。肌生长抑制素是肌肉质量的负调节因子,与正常小鼠相比,肌生长抑制素缺乏的小鼠肌肉质量显着增加。我们预测矢状面缝合复杂性的增加会降低缝合刚度。本文提供的数据表明,在肌肉发达的小鼠模型(GDF8(-/-))中观察到缝线复杂性(以FD测量)的增加,颞肌质量和咬合力显著增加。研究还发现,在张力载荷下,肌肉过度发达的小鼠具有较不僵硬的缝合结缔组织(即在失效发生前发生更多位移)。通过降低刚度,缝合复杂性显然有助于消散头盖骨内与咀嚼有关的机械负荷。这些结果表明颅缝合结缔组织局部适应了生物力学缝合环境的功能需求。因此,颅缝为结缔组织力学转导的研究提供了一种新的模型。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Effects of increased muscle mass on mouse sagittal suture morphology and mechanics.

The purpose of this study is to test predicted form-function relationships between cranial suture complexity and masticatory muscle mass and biomechanics in a mouse model. Specifically, to test the hypothesis that increased masticatory muscle mass increases sagittal suture complexity, we measured the fractal dimension (FD), temporalis mass, and temporalis bite force in myostatin-deficient (GDF8(-/-)) mice and wild-type CD-1 mice (all male, 6 months old). Myostatin is a negative regulator of muscle mass, and myostatin-deficient mice show a marked increase in muscle mass compared to normal mice. We predicted that increased sagittal suture complexity would decrease suture stiffness. The data presented here demonstrate that increased suture complexity (measured as FD) was observed in a hypermuscular mouse model (GDF8(-/-)) with significantly increased temporalis muscle mass and bite forces. Hypermuscular mice were also found to possess suture connective tissue that was less stiff (i.e., underwent more displacement before failure occurred) when loaded in tension. By decreasing stiffness, suture complexity apparently helps to dissipate mechanical loads within the cranium that are related to chewing. These results suggest that cranial suture connective tissue locally adapts to functional demands of the biomechanical suture environment. As such, cranial sutures provide a novel model for studies in connective tissue mechanotransduction.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
The submicroscopic morphology of protoplasm. 1956. Cortical complexity in cetacean brains. Nature's experiments in brain diversity. Diversity of mammalian photoreceptor properties: adaptations to habitat and lifestyle? Aberrant retinal projections in congenitally deaf mice: how are phenotypic characteristics specified in development and evolution?
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1