Absence of B cells does Not compromise intramembranous bone formation during healing in a tibial injury model

Raggatt, Liza J., Alexander, Kylie A., Kaur, Simranpreet, Wu, Andy C., MacDonald, Kelli P. A. and Pettit, Allison R. (2013) Absence of B cells does Not compromise intramembranous bone formation during healing in a tibial injury model. American Journal of Pathology, 182 5: 1501-1508. doi:10.1016/j.ajpath.2013.01.046

Author Raggatt, Liza J.
Alexander, Kylie A.
Kaur, Simranpreet
Wu, Andy C.
MacDonald, Kelli P. A.
Pettit, Allison R.
Title Absence of B cells does Not compromise intramembranous bone formation during healing in a tibial injury model
Journal name American Journal of Pathology   Check publisher's open access policy
ISSN 0002-9440
Publication date 2013-05
Year available 2013
Sub-type Article (original research)
DOI 10.1016/j.ajpath.2013.01.046
Open Access Status DOI
Volume 182
Issue 5
Start page 1501
End page 1508
Total pages 8
Place of publication New York, NY, United States
Publisher Elsevier
Collection year 2014
Language eng
Formatted abstract
Previous studies have generated conflicting results regarding the contribution of B cells to bone
formation during physiology and repair. Here, we have investigated the role of B cells in osteoblastmediated
intramembranous anabolic bone modeling. Immunohistochemistry for CD45 receptor
expression indicated that B cells had no propensity or aversion for endosteal regions or sites of bone
modeling and/or remodeling in wild-type mice. In the endocortical diaphyseal region, quantitative
immunohistology demonstrated that young wild-type and B-cell deficient mice had similar amounts of
osteocalcinþ osteoblast bone modeling surface. The degree of osteoblast-associated osteomac canopy
was also comparable in these mice inferring that bone modeling cellular units were preserved in the
absence of B cells. In a tibial injury model, only rare CD45 receptor positive B cells were located within
areas of high anabolic activity, including minimal association with osterix+ osteoblast-lineage
committed mesenchymal cells in wild-type mice. Quantitative immunohistology demonstrated that
collagen type I matrix deposition and macrophage and osteoclast distribution within the injury site
were not compromised by the absence of B cells. Overall, osteoblast distribution during normal growth
and bone healing via intramembranous ossification proceeded normally in the absence of B cells. These
observations support that in vivo, these lymphoid cells have minimal influence, or at most, make
redundant contributions to osteoblast function during anabolic bone modeling via intramembranous mechanisms.
Keyword In-Vivo
Defect Model
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: UQ Centre for Clinical Research Publications
Official 2014 Collection
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Citation counts: TR Web of Science Citation Count  Cited 2 times in Thomson Reuters Web of Science Article | Citations
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