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Immobilization induced osteopenia is strain specific in mice

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Immobilization induced osteopenia is strain specific in mice. / Lodberg, Andreas; Vegger, Jens Bay; Jensen, Michael Vinkel et al.

I: Bone Reports, Bind 2, 01.06.2015, s. 59-67.

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

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Lodberg A, Vegger JB, Jensen MV, Larsen CM, Thomsen JS, Brüel A. Immobilization induced osteopenia is strain specific in mice. Bone Reports. 2015 jun. 1;2:59-67. doi: 10.1016/j.bonr.2015.04.001

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Lodberg, Andreas ; Vegger, Jens Bay ; Jensen, Michael Vinkel et al. / Immobilization induced osteopenia is strain specific in mice. I: Bone Reports. 2015 ; Bind 2. s. 59-67.

Bibtex

@article{56aed8dde2924f4bb71b7da1297304fc,
title = "Immobilization induced osteopenia is strain specific in mice",
abstract = "Immobilization causes rapid and massive bone loss. By comparing Botulinum Toxin A (BTX)-induced bone loss in mouse strains with different genetic backgrounds we investigated whether the genetic background had an influenceon the severity of the osteopenia. Secondly, we investigated whether BTX had systemic effects on bone. Female mice from four inbred mouse strains (BALB/cJ, C57BL/6 J, DBA/2 J, and C3H/HeN) were injected unilaterally with BTX (n = 10/group) or unilaterally with saline (n = 10/group). Mice were euthanized after 21 days, and the bone properties evaluated using μCT, DXA, bone histomorphometry, and mechanical testing. BTX resulted in substantially lower trabecular bone volume fraction (BV/TV) and trabecular thickness in all mouse strains. The deterioration of BV/TV was significantly greater in C57BL/6 J (−57%) and DBA/2 J (−60%) than in BALB/cJ (−45%) and C3H/HeN (−34%) mice. The loss of femoral neck fracture strength was significantly greater in C57BL/6 J (−47%) and DBA/2 J (−45%) than in C3H (−25%) mice and likewise the loss of mid-femoral fracture strength was greater in C57BL/6 J (−17%), DBA/2 J (−12%), and BALB/cJ (−9%) than in C3H/HeN (−1%) mice, which were unaffected. Using high resolution μCT we found no evidence of a systemic effect on any of the microstructural parameters of the contralateral limb. Likewise, there was no evidence of a systemic effect on the bone strength in any mouse strain. We did, however, find a small systemic effect on aBMD in DBA/2 J and C3H/HeNmice. The present study shows that BTX-induced immobilization causes the greatest loss of cortical and trabecular bone in C57BL/6 J and DBA/2 J mice. A smaller loss of bone microstructure and fracture strength was seen in BALB/cJ mice, while the bone microstructure and fracture strength of C3H/HeN mice were markedly less affected. This indicates that BTX-induced loss of bone is mouse strain dependent. We found only minimal systemic effects of BTX.",
keywords = "Biomechanics, Botox systemic effects, Histomorphometry, Immobilization, MicroCT, Osteopenia, Immobilization, Osteopenia, Botox systemic effects, MicroCT, Biomechanics, Histomorphometry",
author = "Andreas Lodberg and Vegger, {Jens Bay} and Jensen, {Michael Vinkel} and Larsen, {Christian Mirian} and Thomsen, {Jesper Skovhus} and Annemarie Br{\"u}el",
year = "2015",
month = jun,
day = "1",
doi = "10.1016/j.bonr.2015.04.001",
language = "English",
volume = "2",
pages = "59--67",
journal = "Bone Reports",
issn = "2352-1872",
publisher = "Elsevier Inc.",

}

RIS

TY - JOUR

T1 - Immobilization induced osteopenia is strain specific in mice

AU - Lodberg, Andreas

AU - Vegger, Jens Bay

AU - Jensen, Michael Vinkel

AU - Larsen, Christian Mirian

AU - Thomsen, Jesper Skovhus

AU - Brüel, Annemarie

PY - 2015/6/1

Y1 - 2015/6/1

N2 - Immobilization causes rapid and massive bone loss. By comparing Botulinum Toxin A (BTX)-induced bone loss in mouse strains with different genetic backgrounds we investigated whether the genetic background had an influenceon the severity of the osteopenia. Secondly, we investigated whether BTX had systemic effects on bone. Female mice from four inbred mouse strains (BALB/cJ, C57BL/6 J, DBA/2 J, and C3H/HeN) were injected unilaterally with BTX (n = 10/group) or unilaterally with saline (n = 10/group). Mice were euthanized after 21 days, and the bone properties evaluated using μCT, DXA, bone histomorphometry, and mechanical testing. BTX resulted in substantially lower trabecular bone volume fraction (BV/TV) and trabecular thickness in all mouse strains. The deterioration of BV/TV was significantly greater in C57BL/6 J (−57%) and DBA/2 J (−60%) than in BALB/cJ (−45%) and C3H/HeN (−34%) mice. The loss of femoral neck fracture strength was significantly greater in C57BL/6 J (−47%) and DBA/2 J (−45%) than in C3H (−25%) mice and likewise the loss of mid-femoral fracture strength was greater in C57BL/6 J (−17%), DBA/2 J (−12%), and BALB/cJ (−9%) than in C3H/HeN (−1%) mice, which were unaffected. Using high resolution μCT we found no evidence of a systemic effect on any of the microstructural parameters of the contralateral limb. Likewise, there was no evidence of a systemic effect on the bone strength in any mouse strain. We did, however, find a small systemic effect on aBMD in DBA/2 J and C3H/HeNmice. The present study shows that BTX-induced immobilization causes the greatest loss of cortical and trabecular bone in C57BL/6 J and DBA/2 J mice. A smaller loss of bone microstructure and fracture strength was seen in BALB/cJ mice, while the bone microstructure and fracture strength of C3H/HeN mice were markedly less affected. This indicates that BTX-induced loss of bone is mouse strain dependent. We found only minimal systemic effects of BTX.

AB - Immobilization causes rapid and massive bone loss. By comparing Botulinum Toxin A (BTX)-induced bone loss in mouse strains with different genetic backgrounds we investigated whether the genetic background had an influenceon the severity of the osteopenia. Secondly, we investigated whether BTX had systemic effects on bone. Female mice from four inbred mouse strains (BALB/cJ, C57BL/6 J, DBA/2 J, and C3H/HeN) were injected unilaterally with BTX (n = 10/group) or unilaterally with saline (n = 10/group). Mice were euthanized after 21 days, and the bone properties evaluated using μCT, DXA, bone histomorphometry, and mechanical testing. BTX resulted in substantially lower trabecular bone volume fraction (BV/TV) and trabecular thickness in all mouse strains. The deterioration of BV/TV was significantly greater in C57BL/6 J (−57%) and DBA/2 J (−60%) than in BALB/cJ (−45%) and C3H/HeN (−34%) mice. The loss of femoral neck fracture strength was significantly greater in C57BL/6 J (−47%) and DBA/2 J (−45%) than in C3H (−25%) mice and likewise the loss of mid-femoral fracture strength was greater in C57BL/6 J (−17%), DBA/2 J (−12%), and BALB/cJ (−9%) than in C3H/HeN (−1%) mice, which were unaffected. Using high resolution μCT we found no evidence of a systemic effect on any of the microstructural parameters of the contralateral limb. Likewise, there was no evidence of a systemic effect on the bone strength in any mouse strain. We did, however, find a small systemic effect on aBMD in DBA/2 J and C3H/HeNmice. The present study shows that BTX-induced immobilization causes the greatest loss of cortical and trabecular bone in C57BL/6 J and DBA/2 J mice. A smaller loss of bone microstructure and fracture strength was seen in BALB/cJ mice, while the bone microstructure and fracture strength of C3H/HeN mice were markedly less affected. This indicates that BTX-induced loss of bone is mouse strain dependent. We found only minimal systemic effects of BTX.

KW - Biomechanics

KW - Botox systemic effects

KW - Histomorphometry

KW - Immobilization

KW - MicroCT

KW - Osteopenia

KW - Immobilization

KW - Osteopenia

KW - Botox systemic effects

KW - MicroCT

KW - Biomechanics

KW - Histomorphometry

UR - http://www.scopus.com/inward/record.url?scp=84928657612&partnerID=8YFLogxK

U2 - 10.1016/j.bonr.2015.04.001

DO - 10.1016/j.bonr.2015.04.001

M3 - Journal article

C2 - 28377955

AN - SCOPUS:84928657612

VL - 2

SP - 59

EP - 67

JO - Bone Reports

JF - Bone Reports

SN - 2352-1872

ER -