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Intraosseous pressure during loading and with vascular occlusion in an animal model

OBJECTIVES: We studied subchondral intraosseous pressure (IOP) in an animal model during loading, and with vascular occlusion. We explored bone compartmentalization by saline injection. MATERIALS AND METHODS: Needles were placed in the femoral condyle and proximal tibia of five anaesthetized rabbits...

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Autores principales: Beverly, M., Mellon, S., Kennedy, J. A., Murray, D. W.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6138809/
https://www.ncbi.nlm.nih.gov/pubmed/30258570
http://dx.doi.org/10.1302/2046-3758.78.BJR-2017-0343.R2
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author Beverly, M.
Mellon, S.
Kennedy, J. A.
Murray, D. W.
author_facet Beverly, M.
Mellon, S.
Kennedy, J. A.
Murray, D. W.
author_sort Beverly, M.
collection PubMed
description OBJECTIVES: We studied subchondral intraosseous pressure (IOP) in an animal model during loading, and with vascular occlusion. We explored bone compartmentalization by saline injection. MATERIALS AND METHODS: Needles were placed in the femoral condyle and proximal tibia of five anaesthetized rabbits and connected to pressure recorders. The limb was loaded with and without proximal vascular occlusion. An additional subject had simultaneous triple recordings at the femoral head, femoral condyle and proximal tibia. In a further subject, saline injections at three sites were carried out in turn. RESULTS: Loading alone caused a rise in subchondral IOP from 11.7 mmHg (sd 7.1) to 17.9 mmHg (sd 8.1; p < 0.0002). During arterial occlusion, IOP fell to 5.3 mmHg (sd 4.1), then with loading there was a small rise to 7.6 mmHg (sd 4.5; p < 0.002). During venous occlusion, IOP rose to 20.2 mmHg (sd 5.8), and with loading there was a further rise to 26.3 mmHg (sd 6.3; p < 0.003). The effects were present at three different sites along the limb simultaneously. Saline injections showed pressure transmitted throughout the length of the femur but not across the knee joint. CONCLUSION: This is the first study to report changes in IOP in vivo during loading and with combinations of vascular occlusion and loading. Intraosseous pressure is not a constant. It is reduced during proximal arterial occlusion and increased with proximal venous occlusion. Whatever the perfusion state, in vivo load is transferred partly by hydraulic pressure. We propose that joints act as hydraulic pressure barriers. An understanding of subchondral physiology may be important in understanding osteoarthritis and other bone diseases. Cite this article: M. Beverly, S. Mellon, J. A. Kennedy, D. W. Murray. Intraosseous pressure during loading and with vascular occlusion in an animal model. Bone Joint Res 2018;7:511–516. DOI: 10.1302/2046-3758.78.BJR-2017-0343.R2.
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spelling pubmed-61388092018-09-26 Intraosseous pressure during loading and with vascular occlusion in an animal model Beverly, M. Mellon, S. Kennedy, J. A. Murray, D. W. Bone Joint Res Research OBJECTIVES: We studied subchondral intraosseous pressure (IOP) in an animal model during loading, and with vascular occlusion. We explored bone compartmentalization by saline injection. MATERIALS AND METHODS: Needles were placed in the femoral condyle and proximal tibia of five anaesthetized rabbits and connected to pressure recorders. The limb was loaded with and without proximal vascular occlusion. An additional subject had simultaneous triple recordings at the femoral head, femoral condyle and proximal tibia. In a further subject, saline injections at three sites were carried out in turn. RESULTS: Loading alone caused a rise in subchondral IOP from 11.7 mmHg (sd 7.1) to 17.9 mmHg (sd 8.1; p < 0.0002). During arterial occlusion, IOP fell to 5.3 mmHg (sd 4.1), then with loading there was a small rise to 7.6 mmHg (sd 4.5; p < 0.002). During venous occlusion, IOP rose to 20.2 mmHg (sd 5.8), and with loading there was a further rise to 26.3 mmHg (sd 6.3; p < 0.003). The effects were present at three different sites along the limb simultaneously. Saline injections showed pressure transmitted throughout the length of the femur but not across the knee joint. CONCLUSION: This is the first study to report changes in IOP in vivo during loading and with combinations of vascular occlusion and loading. Intraosseous pressure is not a constant. It is reduced during proximal arterial occlusion and increased with proximal venous occlusion. Whatever the perfusion state, in vivo load is transferred partly by hydraulic pressure. We propose that joints act as hydraulic pressure barriers. An understanding of subchondral physiology may be important in understanding osteoarthritis and other bone diseases. Cite this article: M. Beverly, S. Mellon, J. A. Kennedy, D. W. Murray. Intraosseous pressure during loading and with vascular occlusion in an animal model. Bone Joint Res 2018;7:511–516. DOI: 10.1302/2046-3758.78.BJR-2017-0343.R2. 2018-09-15 /pmc/articles/PMC6138809/ /pubmed/30258570 http://dx.doi.org/10.1302/2046-3758.78.BJR-2017-0343.R2 Text en © 2018 Author(s) et al. This is an open-access article distributed under the terms of the Creative Commons Attributions licence (CC-BY-NC), which permits unrestricted use, distribution, and reproduction in any medium, but not for commercial gain, provided the original author and source are credited.
spellingShingle Research
Beverly, M.
Mellon, S.
Kennedy, J. A.
Murray, D. W.
Intraosseous pressure during loading and with vascular occlusion in an animal model
title Intraosseous pressure during loading and with vascular occlusion in an animal model
title_full Intraosseous pressure during loading and with vascular occlusion in an animal model
title_fullStr Intraosseous pressure during loading and with vascular occlusion in an animal model
title_full_unstemmed Intraosseous pressure during loading and with vascular occlusion in an animal model
title_short Intraosseous pressure during loading and with vascular occlusion in an animal model
title_sort intraosseous pressure during loading and with vascular occlusion in an animal model
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6138809/
https://www.ncbi.nlm.nih.gov/pubmed/30258570
http://dx.doi.org/10.1302/2046-3758.78.BJR-2017-0343.R2
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