Liza J Raggatt, Kylie A Alexander, Simranpreet Kaur, Andy C Wu, Kelli P A MacDonald, Allison R Pettit
University of Queensland Centre for Clinical Research, The University of Queensland, Herston, Brisbane, Australia.
The American journal of pathology 2013 MayPrevious 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 osteoblast-mediated 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 osteocalcin(+) 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. Copyright © 2013 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.
Liza J Raggatt, Kylie A Alexander, Simranpreet Kaur, Andy C Wu, Kelli P A MacDonald, Allison R Pettit. Absence of B cells does not compromise intramembranous bone formation during healing in a tibial injury model. The American journal of pathology. 2013 May;182(5):1501-8
PMID: 23499466
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