Osteomacs: osteoclast precursors during inflammatory bone disease but regulators of physiologic bone remodelling

Raggatt, L. J., Chang, M. K., Alexander, K. A., Maylin, E. R., Walsh, N. C., Gravallese, E. M., Hume, D. A. and Pettit, A. R. (2009). Osteomacs: osteoclast precursors during inflammatory bone disease but regulators of physiologic bone remodelling. In: Bone. Abstracts from the 2nd Joint Meeting of the International Bone & Mineral Society and the Australian & New Zealand Bone & Mineral Society. 2nd Joint Meeting of the International Bone & Mineral Society and the Australian & New Zealand Bone & Mineral Society, Sydney, Australia, (S136-S137). 21-25 March, 2009. doi:10.1016/j.bone.2009.01.300


Author Raggatt, L. J.
Chang, M. K.
Alexander, K. A.
Maylin, E. R.
Walsh, N. C.
Gravallese, E. M.
Hume, D. A.
Pettit, A. R.
Title of paper Osteomacs: osteoclast precursors during inflammatory bone disease but regulators of physiologic bone remodelling
Conference name 2nd Joint Meeting of the International Bone & Mineral Society and the Australian & New Zealand Bone & Mineral Society
Conference location Sydney, Australia
Conference dates 21-25 March, 2009
Proceedings title Bone. Abstracts from the 2nd Joint Meeting of the International Bone & Mineral Society and the Australian & New Zealand Bone & Mineral Society   Check publisher's open access policy
Journal name Bone   Check publisher's open access policy
Place of Publication New York
Publisher Elsevier Science
Publication Year 2009
DOI 10.1016/j.bone.2009.01.300
ISSN 8756-3282
1873-2763
Volume 44
Issue Supp. 1
Start page S136
End page S137
Total pages 2
Language eng
Abstract/Summary We have identified a population of resident tissue macrophages (OsteoMacs), defined by expression of F4/80 and anatomical location that are present within osteal tissues. OsteoMacs regulate in vitro mineralization by osteoblasts and are required for the maintenance of mature osteoblasts in vivo. The close lineage relationship of macrophages and osteoclasts leads us to investigate whether OsteoMacs function as osteoclast precursors. Primary OsteoMacs isolated from endosteal bone surfaces formed TRAP+ osteoclasts in the presence of RANKL (40 ng/ml) and CSF-1, confirming that like many myeloid cell populations, they can be driven to form osteoclasts in vitro. Interestingly, similar treatment of calvarial digest cultures, that contain both osteoblasts and OsteoMacs, produced two distinct populations: F4/80+/TRAP-OsteoMacs and mononuclear/binuclear F4/80-/TRAP+ cells. Therefore, in this more physiologic mixed culture, OsteoMacs are not osteoclast precursors. Immunohistochemical analysis of the metaphyseal region in bone sections confirmed that F4/80+ OsteoMacs do not express TRAP and mononuclear TRAP+ cells do not express F4/80, indicating that during physiologic bone turnover OsteoMacs are not osteoclast precursors. Comparison of Mac-3 and F4/80 distribution within the metaphyseal zone identified that a Mac-3+/F4/80-myeloid population predominates in the primary spongiosa, a region rich in osteoclasts, confirming that other potential osteoclast precursor populations are present in the appropriate anatomical location. The bone microenvironment during inflammatory bone disease is greatly altered and in response to these conditions the in vivo osteoclast precursor population may change. In adjuvant-induced arthritis mononuclear transition cells expressing both F4/80 and TRAP were associated with sites of resorption indicating that in this pathological setting macrophages contribute to the osteoclast precursor pool. Finally, we identified a canopy structure encapsulating mouse bone remodelling units, similar to that reported in human bone, and demonstrated that the canopy cell is an F4/80+ OsteoMac. These data suggest OsteoMacs, like other tissue macrophages, are highly adaptive and their roles in bone biology change depending on the local microenvironment. Specifically during pathological conditions OsteoMacs may function as osteoclast precursors. However, during physiologic conditions they may be important coordinators of bone remodelling through regulation of osteoclast recruitment, formation and activity as well as osteoblast function.
Subjects 11 Medical and Health Sciences
06 Biological Sciences
Q-Index Code EX
Q-Index Status Provisional Code
Institutional Status Unknown

Document type: Conference Paper
Collection: Institute for Molecular Bioscience - Publications
 
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Created: Wed, 06 Oct 2010, 09:03:23 EST by Laura McTaggart on behalf of Institute for Molecular Bioscience