Kassem M, Brixen K, Mosekilde L, Eriksen E F
Department of Endocrinology and Metabolism, Aarhus University Hospital, Denmark.
Calcif Tissue Int. 1994 Jan;54(1):1-6. doi: 10.1007/BF00316280.
Decreased osteoblastic activity seems to play an important role in the pathogenesis of postmenopausal osteoporosis. The aim of the present study was to examine the direct effects of human growth hormone (GH) on proliferation and differentiation of osteoblastic cells obtained from patients with postmenopausal osteoporosis and age-matched normals and to compare the cellular responses induced by GH between the two groups. Osteoblast cultures (human marrow stromal osteoblast-like cells) were established from bone marrow aspirates obtained from 9 osteoporotic patients and 12 age-matched normals. Effects on cell proliferation and cell differentiation markers [alkaline phosphatase (AP)], procollagen type I propeptide (PICP), and osteocalcin] were assessed. GH stimulated 3H-thymidine incorporation into DNA in cell cultures of osteoporotic patients to a maximum of 158 +/- 14% of no-treatment controls (n = 9, P < 0.001) and to 203 +/- 52% (n = 9, P < 0.001) in normals. GH increased cell number as measured by methylene blue (MB) assay in cells of osteoporotic patients to 138 +/- 10% (P < 0.05, n = 7) and in normals to 138 +/- 12 (P < 0.05, n = 7). GH alone reduced cellular AP production: 61 +/- 3.8% (P < 0.05, n = 7) versus 65 +/- 16% (P < 0.05, n = 7) and cellular PICP production: 79 +/- 6% (P < 0.05, n = 7) versus 69 +/- 16% (n.s., n = 7), in cell cultures of osteoporotics and normals, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)