Peak strain magnitudes and rates in the tibia exceed greatly those in the skull: An in vivo study in a human subject

Bone mass and architecture are the result of a genetically determined baseline structure, modified by the effect of internal hormonal/biochemical regulators and the effect of mechanical loading. Bone strain is thought to drive a feedback mechanism to regulate bone formation and resorption to maintai...

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Published inJournal of biomechanics Vol. 48; no. 12; pp. 3292 - 3298
Main Authors Hillam, Richard A, Goodship, Allen E, Skerry, Tim M
Format Journal Article
LanguageEnglish
Published United States Elsevier Ltd 18.09.2015
Elsevier Limited
Elsevier Science
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Abstract Bone mass and architecture are the result of a genetically determined baseline structure, modified by the effect of internal hormonal/biochemical regulators and the effect of mechanical loading. Bone strain is thought to drive a feedback mechanism to regulate bone formation and resorption to maintain an optimal, but not excessive mass and organisation of material at each skeletal location. Because every site in the skeleton has different functions, we have measured bone strains induced by physiological and more unusual activities, at two different sites, the tibia and cranium of a young human male in vivo. During the most vigorous activities, tibial strains were shown to exceed 0.2%, when ground reaction exceeded 5 times body weight. However in the skull the highest strains recorded were during heading a heavy medicine/exercise ball where parietal strains were up to 0.0192%. Interestingly parietal strains during more physiological activities were much lower, often below 0.01%. Strains during biting were not dependent upon bite force, but could be induced by facial contortions of similar appearance without contact between the teeth. Rates of strain change in the two sites were also very different, where peak tibial strain rate exceeded rate in the parietal bone by more than 5 fold. These findings suggest that the skull and tibia are subject to quite different regulatory influences, as strains that would be normal in the human skull would be likely to lead to profound bone loss by disuse in the long bones.
AbstractList Abstract Bone mass and architecture are the result of a genetically determined baseline structure, modified by the effect of internal hormonal/biochemical regulators and the effect of mechanical loading. Bone strain is thought to drive a feedback mechanism to regulate bone formation and resorption to maintain an optimal, but not excessive mass and organisation of material at each skeletal location. Because every site in the skeleton has different functions, we have measured bone strains induced by physiological and more unusual activities, at two different sites, the tibia and cranium of a young human male in vivo. During the most vigorous activities, tibial strains were shown to exceed 0.2%, when ground reaction exceeded 5 times body weight. However in the skull the highest strains recorded were during heading a heavy medicine/exercise ball where parietal strains were up to 0.0192%. Interestingly parietal strains during more physiological activities were much lower, often below 0.01%. Strains during biting were not dependent upon bite force, but could be induced by facial contortions of similar appearance without contact between the teeth. Rates of strain change in the two sites were also very different, where peak tibial strain rate exceeded rate in the parietal bone by more than 5 fold. These findings suggest that the skull and tibia are subject to quite different regulatory influences, as strains that would be normal in the human skull would be likely to lead to profound bone loss by disuse in the long bones.
Bone mass and architecture are the result of a genetically determined baseline structure, modified by the effect of internal hormonal/biochemical regulators and the effect of mechanical loading. Bone strain is thought to drive a feedback mechanism to regulate bone formation and resorption to maintain an optimal, but not excessive mass and organisation of material at each skeletal location. Because every site in the skeleton has different functions, we have measured bone strains induced by physiological and more unusual activities, at two different sites, the tibia and cranium of a young human male in vivo. During the most vigorous activities, tibial strains were shown to exceed 0.2%, when ground reaction exceeded 5 times body weight. However in the skull the highest strains recorded were during heading a heavy medicine/exercise ball where parietal strains were up to 0.0192%. Interestingly parietal strains during more physiological activities were much lower, often below 0.01%. Strains during biting were not dependent upon bite force, but could be induced by facial contortions of similar appearance without contact between the teeth. Rates of strain change in the two sites were also very different, where peak tibial strain rate exceeded rate in the parietal bone by more than 5 fold. These findings suggest that the skull and tibia are subject to quite different regulatory influences, as strains that would be normal in the human skull would be likely to lead to profound bone loss by disuse in the long bones.
Bone mass and architecture are the result of a genetically determined baseline structure, modified by the effect of internal hormonal/biochemical regulators and the effect of mechanical loading. Bone strain is thought to drive a feedback mechanism to regulate bone formation and resorption to maintain an optimal, but not excessive mass and organisation of material at each skeletal location. Because every site in the skeleton has different functions, we have measured bone strains induced by physiological and more unusual activities, at two different sites, the tibia and cranium of a young human male in vivo. During the most vigorous activities, tibial strains were shown to exceed 0.2%, when ground reaction exceeded 5 times body weight. However in the skull the highest strains recorded were during heading a heavy medicine/exercise ball where parietal strains were up to 0.0192%. Interestingly parietal strains during more physiological activities were much lower, often below 0.01%. Strains during biting were not dependent upon bite force, but could be induced by facial contortions of similar appearance without contact between the teeth. Rates of strain change in the two sites were also very different, where peak tibial strain rate exceeded rate in the parietal bone by more than 5 fold. These findings suggest that the skull and tibia are subject to quite different regulatory influences, as strains that would be normal in the human skull would be likely to lead to profound bone loss by disuse in the long bones.Bone mass and architecture are the result of a genetically determined baseline structure, modified by the effect of internal hormonal/biochemical regulators and the effect of mechanical loading. Bone strain is thought to drive a feedback mechanism to regulate bone formation and resorption to maintain an optimal, but not excessive mass and organisation of material at each skeletal location. Because every site in the skeleton has different functions, we have measured bone strains induced by physiological and more unusual activities, at two different sites, the tibia and cranium of a young human male in vivo. During the most vigorous activities, tibial strains were shown to exceed 0.2%, when ground reaction exceeded 5 times body weight. However in the skull the highest strains recorded were during heading a heavy medicine/exercise ball where parietal strains were up to 0.0192%. Interestingly parietal strains during more physiological activities were much lower, often below 0.01%. Strains during biting were not dependent upon bite force, but could be induced by facial contortions of similar appearance without contact between the teeth. Rates of strain change in the two sites were also very different, where peak tibial strain rate exceeded rate in the parietal bone by more than 5 fold. These findings suggest that the skull and tibia are subject to quite different regulatory influences, as strains that would be normal in the human skull would be likely to lead to profound bone loss by disuse in the long bones.
Author Goodship, Allen E
Hillam, Richard A
Skerry, Tim M
AuthorAffiliation University of Bristol, UK
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  surname: Hillam
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  givenname: Allen E
  surname: Goodship
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  givenname: Tim M
  surname: Skerry
  fullname: Skerry, Tim M
  email: t.skerry@sheffield.ac.uk
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Issue 12
Keywords Human
Bone strain
In vivo
Cranium
Tibia
Language English
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Copyright © 2015 The Authors. Published by Elsevier Ltd.. All rights reserved.
This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
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Present address: School of Veterinary Science, University of Bristol, Southwell Street Bristol BS2 8EJ, UK.
Present address: Churchdown Veterinary Centre, Cheltenham Road East, Gloucester GL3 1HX, UK.
Present address: Centre for Integrated Musculoskeletal research into Ageing, Mellanby Bone Centre, Department of Human Metabolism, University of Sheffield, Beech Hill Road, Sheffield S10 2RX, UK.
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SSID ssj0007479
Score 2.2645323
Snippet Bone mass and architecture are the result of a genetically determined baseline structure, modified by the effect of internal hormonal/biochemical regulators...
Abstract Bone mass and architecture are the result of a genetically determined baseline structure, modified by the effect of internal hormonal/biochemical...
SourceID pubmedcentral
proquest
pubmed
crossref
elsevier
SourceType Open Access Repository
Aggregation Database
Index Database
Enrichment Source
Publisher
StartPage 3292
SubjectTerms Adult
Biomechanical Phenomena
Biomedical materials
Bite Force
Bone strain
Bones
Conflicts of interest
Cranium
Data analysis
Human
Humans
In vivo
In vivo tests
Male
Muscle Strength
Osteoporosis
Physical Exertion
Physical Medicine and Rehabilitation
Physiology
Skull
Skull - physiology
Software
Strain
Strain gauges
Surgery
Surgical implants
Tibia
Tibia - physiology
Walking - physiology
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Title Peak strain magnitudes and rates in the tibia exceed greatly those in the skull: An in vivo study in a human subject
URI https://www.clinicalkey.com/#!/content/1-s2.0-S0021929015003589
https://www.clinicalkey.es/playcontent/1-s2.0-S0021929015003589
https://dx.doi.org/10.1016/j.jbiomech.2015.06.021
https://www.ncbi.nlm.nih.gov/pubmed/26232812
https://www.proquest.com/docview/1718120101
https://www.proquest.com/docview/1718909724
https://www.proquest.com/docview/1751214333
https://www.proquest.com/docview/1778027678
https://pubmed.ncbi.nlm.nih.gov/PMC4601046
Volume 48
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