title: Absence of B cells does not compromise intramembranous bone formation during healing in a tibial injury model.
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 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.
authors.affiliation: University of Queensland Centre for Clinical Research, The University of Queensland, Herston, Brisbane, Australia.
authors.forename: Liza J
authors.initials: LJ
authors.lastname: Raggatt
authors.forename: Kylie A
authors.initials: KA
authors.lastname: Alexander
authors.forename: Simranpreet
authors.initials: S
authors.lastname: Kaur
authors.forename: Andy C
authors.initials: AC
authors.lastname: Wu
authors.forename: Kelli P A
authors.initials: KP
authors.lastname: MacDonald
authors.forename: Allison R
authors.initials: AR
authors.lastname: Pettit
mesh_terms: D000818:Animals; D001402:B-Lymphocytes / Q000473:pathology*; D001853:Bone Marrow / Q000473:pathology; D016723:Bone Remodeling; D060833:Cellular Microenvironment; D018483:Diaphyses / Q000473:pathology; D004195:Disease Models, Animal; D017493:Leukocyte Common Antigens / Q000378:metabolism; D008212:Lymphocyte Depletion; D008566:Membranes / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D009999:Ossification, Heterotopic / Q000473:pathology / Q000503:physiopathology; D010012:Osteogenesis; D013977:Tibia / Q000293:injuries* / Q000473:pathology* / Q000503:physiopathology; D014945:Wound Healing
chemical_list: D017493:Leukocyte Common Antigens