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Expression of vascular antigens by bone cells during bone regeneration in a membranous bone distraction system.

Authors: Lewinson, D  Maor, G  Rozen, N  Rabinovich, I  Stahl, S  Rachmiel, A 
Citation: Lewinson D, etal., Histochem Cell Biol. 2001 Nov;116(5):381-8. Epub 2001 Oct 18.
Pubmed: (View Article at PubMed) PMID:11735002
DOI: Full-text: DOI:10.1007/s004180100331

An in vivo system of membranous bone formation during distraction has been investigated in order to follow cells that express vascular markers with the objective of understanding the neovascularization process. Concomitantly, sustained proliferation of preskeletal cells was achieved through the application of mechanical force. New capillaries and leading edges that arose by angiogenesis from the periosteal and mucosal surfaces and invaded the central zone of the regenerating distraction tissue temporally preceded the growth of delicate woven bone trabeculae from both edges of the cut bone. Concentrically arranged 'onion-like' configurations were abundant in paracentral zones and in association with mesenchymal condensations, suggesting their de novo formation in situ. Vascular specific markers, the angiopoietin receptor Tie-2 and factor VIII-related antigen (FVIIIrAg), were localized immunohistochemically in order to follow cells of vascular origin. Endothelial cells of the new capillaries, centrally located cells of the concentric configurations, pericytes, and most of the adjacent polygonal mesenchymal cells stained positively with specific antibodies to both antigens. Moreover, preosteoblasts and osteoblasts that lie adjacent to or already embedded in the osteiod of the newly formed trabeculae were also FVIIIrAg and Tie-2 immunopositive. As the source of the bone-forming cells in regenerating tissue during distraction is not yet fully understood, this observation might support the possibility of their vascular origin.


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CRRD Object Information
CRRD ID: 1601509
Created: 2007-04-24
Species: All species
Last Modified: 2007-04-24
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.