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Systemic alendronate prevents resorption of necrotic bone during revascularization. A bone chamber study in rats

Åstrand, Jörgen LU and Aspenberg, Per LU (2002) In BMC Musculoskeletal Disorders 3.
Abstract
Background: Avascular necrosis of bone (osteonecrosis) can cause structural failure and subsequent deformation, leading to joint dysfunction and pain. Structural failure is the result of resorption of necrotic bone during revascularization, before new bone has formed or consolidated enough for loadbearing. Bone resorption can be reduced by bisphosphonates. If resorption of the necrotic bone could be reduced during the revascularization phase until sufficient new bone has formed, it would appear that structural failure could be avoided. Methods: To test whether resorption of necrotic bone can be prevented, structural grafts were subjected to new bone ingrowth during systemic bisphosphonate treatment in a rat model. Results: In rats treated... (More)
Background: Avascular necrosis of bone (osteonecrosis) can cause structural failure and subsequent deformation, leading to joint dysfunction and pain. Structural failure is the result of resorption of necrotic bone during revascularization, before new bone has formed or consolidated enough for loadbearing. Bone resorption can be reduced by bisphosphonates. If resorption of the necrotic bone could be reduced during the revascularization phase until sufficient new bone has formed, it would appear that structural failure could be avoided. Methods: To test whether resorption of necrotic bone can be prevented, structural grafts were subjected to new bone ingrowth during systemic bisphosphonate treatment in a rat model. Results: In rats treated with alendronate the necrotic bone was not resorbed, whereas it was almost entirely resorbed in the controls. Conclusion: Systemic alendronate treatment prevents resorption of necrotic bone during revascularization. In patients with osteonecrosis, bisphosphonates may therefore prevent collapse of the necrotic bone. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
BMC Musculoskeletal Disorders
volume
3
publisher
BioMed Central
external identifiers
  • pmid:12165099
  • wos:000181476500019
  • scopus:34248400391
ISSN
1471-2474
DOI
10.1186/1471-2474-3-19
language
English
LU publication?
yes
id
c50be297-6b08-4774-8217-e7d59de7b912 (old id 317062)
date added to LUP
2007-08-07 16:22:03
date last changed
2017-12-03 03:46:10
@article{c50be297-6b08-4774-8217-e7d59de7b912,
  abstract     = {Background: Avascular necrosis of bone (osteonecrosis) can cause structural failure and subsequent deformation, leading to joint dysfunction and pain. Structural failure is the result of resorption of necrotic bone during revascularization, before new bone has formed or consolidated enough for loadbearing. Bone resorption can be reduced by bisphosphonates. If resorption of the necrotic bone could be reduced during the revascularization phase until sufficient new bone has formed, it would appear that structural failure could be avoided. Methods: To test whether resorption of necrotic bone can be prevented, structural grafts were subjected to new bone ingrowth during systemic bisphosphonate treatment in a rat model. Results: In rats treated with alendronate the necrotic bone was not resorbed, whereas it was almost entirely resorbed in the controls. Conclusion: Systemic alendronate treatment prevents resorption of necrotic bone during revascularization. In patients with osteonecrosis, bisphosphonates may therefore prevent collapse of the necrotic bone.},
  author       = {Åstrand, Jörgen and Aspenberg, Per},
  issn         = {1471-2474},
  language     = {eng},
  publisher    = {BioMed Central},
  series       = {BMC Musculoskeletal Disorders},
  title        = {Systemic alendronate prevents resorption of necrotic bone during revascularization. A bone chamber study in rats},
  url          = {http://dx.doi.org/10.1186/1471-2474-3-19},
  volume       = {3},
  year         = {2002},
}