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Submitted on April 22, 2005
Accepted on May 27, 2005
Department of Nutrition and Exercise Science, Oregon State University, Corvallis, OR 97331and Life Sciences Division, Universities Space Research Association, Houston, TX 77058
* To whom correspondence should be addressed. E-mail: russell.turner{at}oregonstate.edu.
We examined proliferation of cells associated with parathyroid hormone (PTH)-induced peritrabecular bone marrow fibrosis in rats, as well as the fate of those cells following withdrawal of PTH. Time course studies established that severe fibrosis was present 7 days following initiation of a continuous sc PTH infusion (40 µg/kg/day). To ascertain cell proliferation, rats were co-infused for 1 week with PTH (treated) or vehicle (control) and [3H]thymidine (1.5 mCi/rat). Groups of control and treated rats were killed immediately (day 0) and 1 week (day 7) later. Few osteoblasts (Ob) and osteocytes (Ocy) in treated and control groups were radiolabeled on day 0. Peritrabecular cells expressing a fibroblastic (Fb) phenotype and surrounded by an extracellular matrix were not present in controls on either day 0 or day 7. Multiple cell layers of Fb lined most (70%) of the bone surface on day 0 in treated rats and nearly all (85%) of the Fb were radiolabeled. Fb had entirely disappeared from bone surfaces on day 7. 85% of the Ob on and 73% of the Ocy within the active remodeling sites were radiolabeled. Immunohistochemistry revealed that Fb induced by PTH treatment produced osteocalcin, osteonectin, and core binding factor 
1 (cbfa1). These data provide compelling evidence that Fb recruited to bone surfaces in response to a continuous PTH infusion undergo extensive proliferation, express osteoblast specific proteins and produce an extracellular matrix that is similar to osteoid. Following restoration of normal PTH levels Fb differentiated to Ob, providing further evidence that Fb are preosteoblasts.
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