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  • 1
    ISSN: 1432-0827
    Keywords: Growth hormone ; Resorption ; Bone ; Cartilage ; Tartrate-resistant acid phosphatase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Young male Sprague-Dawley rats (5–7 weeks old, 80–120 g) were hypophysectomized (HX) and maintained on thyroxin and dexamethasone replacement therapies. Ten days after surgery, some HX rats received a single injection of human growth hormone (hGH), and others five daily injections of hGH. Tartrate-resistant acid phosphatase (TRAP) histochemistry was employed in order to evaluate the number of cells of resorptive potential in the metaphyseal bone of the proximal tibiae of HX rats and was compared with normal rats and HX rats that further received hGH replacement therapy. In normal rats, two populations of TRAP-positive cells were identified: multinuclear cells, which showed histological characteristics of osteoclasts, and small mononuclear cells, the number of which was overwhelming when compared with the number of TRAP-positive multinuclear cells. Both populations were reduced in the HX rat, but more so the mononuclear cells, which were assumed to represent the precursor pool of mature osteoclasts and chondroclasts (P〈0.005). Five daily injections of hGH to HX rats brought about a significant increase in the number of TRAP-positive multinuclear cells, the number of nuclei of these cells, and the number of mononuclear TRAP-positive cells, throughout the metaphyseal bone (P〈0.05). A single injection of hGH increased only the number of TRAP-positive multinuclear cells in the trabecula/bone marrow interface (P〈0.05), indicating a very rapid fusion of precursor cells into mature osteoclasts in that particular location. It was concluded that GH depletion caused a major reduction in the number of cells presenting resorption capacity and that a short hGH replacement regimen resulted in a gradual restoration of these cells n the metaphyseal bone of the proximal tibia of the HX rat.
    Type of Medium: Electronic Resource
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