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Journal of Clinical Endocrinology & Metabolism, Vol 69, 272-279, Copyright © 1989 by Endocrine Society
ARTICLES |
PJ Marie, A Sabbagh, MC de Vernejoul and A Lomri
Unite 18 INSERM, Lariboisiere Hopital, Paris, France.
The aim of this study was to determine whether abnormal osteoblastic growth and/or differentiation play a role in the decreased bone formation in women with postmenopausal osteoporosis. To do so, we compared bone formation evaluated by histomorphometric methods and the proliferation kinetics and phenotypic expression of osteoblastic cells isolated from the trabecular bone surface. We found that osteoblastic cells isolated from women whose trabecular bone had low double tetracycline-labeled surface and decreased mean wall thickness had a reduced rate of cell proliferation. The peak of [3H]thymidine incorporation into DNA, the maximal DNA synthesis, and the area under the curve of bone cell proliferation were significantly lower in these women than in those with high double tetracycline-labeled surface. In addition, the parameters of bone cell replication correlated with osteoblastic surface and mean wall thickness. By contrast, the initial osteocalcin production and alkaline phosphatase activity and the response to 10 nmol/L 1,25-dihydroxyvitamin D (48 h) in vitro were similar in women with low, normal, or high bone formation. These results indicate that reduction of bone formation in women with postmenopausal osteoporosis results from an impaired proliferative capacity of cells of osteoblastic lineage present at the trabecular bone surface level.
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