| First Author | Raggatt LJ | Year | 2013 |
| Journal | Am J Pathol | Volume | 182 |
| Issue | 5 | Pages | 1501-8 |
| PubMed ID | 23499466 | Mgi Jnum | J:195537 |
| Mgi Id | MGI:5484730 | Doi | 10.1016/j.ajpath.2013.01.046 |
| Citation | Raggatt LJ, et al. (2013) Absence of B Cells Does Not Compromise Intramembranous Bone Formation during Healing in a Tibial Injury Model. Am J Pathol 182(5):1501-8 |
| abstractText | 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 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. |
