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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 35 (1983), S. 732-739 
    ISSN: 1432-0827
    Keywords: Mesenchymol cell proliferation ; Chondrogenesis ; Osteogenesis ; Proteoglycans
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The influence of retinoic acid on matrix-induced endochondral bone differentiation was determined. Retinoic acid was administered during discrete stages of endochondral bone formation, specifically, mesenchymal cell proliferation, chondrogenesis, bone formation, and mineralization. In retinoic acid-treated rats examined on day 3 following matrix implantation, biochemical markers for mesenchymal cell proliferation were about 50% of the controls. Chondrogenesis on day 7, assessed by35SO4 incorporation into proteoglycans, was 27% of the control. In addition, dissociative extraction of proteoglycans with 4.0 M guanidine-HCl and chromatography on Sepharose CL-2B revealed the synthesis of a smaller molecular weight proteoglycan when compared to controls which exhibited the cartilage-specific type. Osteogenesis and bone mineralization were monitored by alkaline phosphatase activity and45Ca incorporation. On day 11 alkaline phosphatase activity was decreased by 40% and45Ca incorporation was 48% of the control. These results revealed the multiple foci of the actions of excess vitamin A.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 33 (1981), S. 425-430 
    ISSN: 1432-0827
    Keywords: Bone induction ; Insulin ; Chondrogenesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The influence of somatostatin on discrete stages of collagenous-matrix-induced endochondral bone formation has been investigated. Local injection of somatostatin, i.e., without any measurable systemic effect, resulted in a 75% reduction of cell proliferation as measured by [3H]thymidine incorporation and ornithine decarboxylase activities. The minimum effective inhibitory dose of somatostatin was 0.25 µg/day. Twice daily local injections of the hormone during cartilage formation also resulted in an inhibition, but this was shown to be due to impaired cell proliferation rather than to a direct effect of somatostatin on differentiation. Injection of somatostatin into developing bone tissue after the cartilage stage impaired osteogenesis, assessed by45Ca incorporation and alkaline phosphatase activity. Concurrent injections of insulin and somatostatin obliterated the inhibitory effect of the latter on cell proliferation. Somatostatin can locally regulate the proliferation and differentiation of chondroprogenitor and osteoprogenitor cells in vivo and may directly contribute to the regulation of bone growth by its ability to counteract the stimulatory effect of insulin.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 29 (1979), S. 15-20 
    ISSN: 1432-0827
    Keywords: Alkaline phosphatase ; 45Ca incorporation ; Mineralization ; Bone marrow
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The effect of magnesium deficiency on bone cell differentiation and bone formation was investigated using in vivo matrix-induced endochondral ossification as a test system. Demineralized bone matrix was implanted subcutaneously in young (35-day-old) male Long-Evans rats that had been fed a semisynthetic Mg-deficient diet (50 ppm Mg) for 7 days. Plasma Mg levels were reduced to 25–30% of control values at that time. Control rats were pairfed the same diet, supplemented to contain 1000 ppm Mg. The implants were harvested 7, 9, 11, 15, and 20 days after implantation and analyzed for Mg and Ca content,45Ca incorporation, and alkaline phosphatase levels. At each stage, plaques (implants) removed from Mg-deficient rats showed retardation in cartilage and bone differentiation and matrix calcification. Magnesium content was markedly reduced when compared to the control plaques. Histological appearance of the matrix-induced plaques confirmed the retardation in bone development and mineralization suggested by the chemical indicators. Most marked was the virtual absence of bone marrow in 20-day-old plaques in Mg-depleted rats. These data show that bone cell differentiation can occur in a severely Mg-depleted environment, although the onset of mineralization and bone remodeling was delayed and bone marrow differentiation was impaired.
    Type of Medium: Electronic Resource
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