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Recurrent critical hemorrhage is not sufficient to alter bone remodeling in mice

Bone remodeling is established by the balanced activity of bone-forming osteoblasts and bone- resorbing osteoclasts, which tightly interact with resident hematopoietic stem cells (HSCs) within the endosteal region of the bone. Mobilization and differentiation of HSCs can be induced by some stress conditions including hemorrhage that enhances hematopoiesis to compensate the loss of blood cells. It has been proposed that in such conditions osteoclast activity may be promoted to provide more space within the BM niche. We established a model where mice were subjected to recurrent hemorrhage during several weeks to examine the long-term effect of enhanced hematopoiesis on OC activity. We found no significant changes in any of bone parameters including bone mineral density and trabecular number and thickness, by using uCT analysis and Goldner staining. Number of TRAP positive OC on bone surface and serum levels of C terminal Telopeptides of type l collagen were comparable with control, indicating unaffected osteoclast differentiation and activity. Mineral apposition rate confirmed sustained coupling of bone cells, since OB activity was neither altered. These results confirmed our previous postulate that fine tuning within the niche is sufficient to prevent major changes in bone remodeling following blood loss and facilitate physiological bone density even in recurrent stress conditions.

Hemorrhage; Hematopoiesis; Hematopoietic stem cells; Osteoblast; Osteoclast

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