Parathyroid hormone stimulates cancellous bone formation at skeletal sites regardless of marrow composition in ovariectomized rats

The purpose of the current report is to compare the skeletal effects of PTH treatment at red (hematopoietic) and yellow (fatty) marrow sites in ovariectomized (ovx) rats. In the first study, mature, slowly growing ovx rats that were 4 months of age and 4 weeks postovariectomy were treated with human parathyroid hormone [hPTH(134)] (80 mu g/kg, 5 days/week) for 6 weeks. In the second study, aged ovx rats that were 15 months of age and 1 year postovariectomy were treated with PTH according to the same regimen for 10 weeks, The proximal tibial metaphysis (PTM) and first lumbar vertebra (LV), bone sites with red marrow, as well as the distal tibial metaphysis (DTM) and fifth caudal vertebra (CV), bone sites with yellow marrow, were processed undecalcified for quantitative bone histomorphometry, At the end of the first study in mature ovx rats, estrogen depletion induced a 73% loss of cancellous bone in the PTM and a 15% loss in the LV, In contrast, not even a trend for cancellous bone loss was observed in the DTM and CV of vehicle-treated ovx rats. PTH treatment of ovx rats increased cancellous bone volume by 191% in the PTM, 56% in the DTM, 47% in the LV, and 22% in the CV, compared with vehicle treatment of ovx rats. In addition, the hormone markedly increased cancellous bone formation by 177% in the PTM, 679% in the DTM, 309% in the LV, and 833% in the CV, Aged ovx rats (second study) exhibited moderate cancellous osteopenia in the LV but not the CV, PTH treatment increased cancellous bone volume by 67% and 37% and bone formation rate by 635% and 359% in the LV and CV, respectively, compared with vehicle treatment of ovx rats. Although the magnitude of the anabolic response to PTH may vary somewhat within the skeleton, the results indicate that PTH augments cancellous bone mass and markedly stimulates bone formation at skeletal sites, regardless of marrow composition, (Bone 24: 95-100; 1999) (C) 1999 by Elsevier Science Inc. All rights reserved.