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Related Concept Videos

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Osteoclasts in Bone Remodeling

Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during bone...
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Glucocorticoids modulate macrophage surface oligosaccharides and their bone binding activity.

Z Bar-Shavit, A J Kahn, L E Pegg

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    Glucocorticoids (GC) enhance macrophage attachment to bone, stimulating bone resorption. This effect involves changes in cell surface sugars and can be blocked by progesterone.

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    Area of Science:

    • Endocrinology
    • Cell Biology
    • Bone Biology

    Background:

    • Glucocorticoids (GC) are suspected to stimulate bone resorption in vivo.
    • Previous studies showed GC increase resorptive cell activity in vitro.
    • Osteoclasts and macrophages are key resorptive cells.

    Purpose of the Study:

    • To investigate the mechanism by which GC stimulate bone resorption.
    • To determine if GC affect cell attachment to bone surfaces.
    • To elucidate the role of cell surface oligosaccharides in GC-mediated effects.

    Main Methods:

    • Assessed macrophage (MO) attachment to bone and other surfaces after GC treatment.
    • Utilized glycosylation inhibitors (tunicamycin, swainsonine) and a GC antagonist (progesterone).
    • Employed flow cytometry with lectins to analyze cell surface oligosaccharides.

    Main Results:

    • Dexamethasone and cortisol significantly enhanced MO attachment to bone by 80% in a dose-dependent manner.
    • GC treatment did not alter MO binding to plastic, collagen, or hydroxyapatite.
    • Glycosylation inhibitors blocked GC-enhanced cell-bone attachment, implicating asparagine-linked oligosaccharides.
    • Flow cytometry revealed increased exposure of N-acetylglucosamine and N-acetylgalactosamine on GC-treated cells.
    • Progesterone inhibited GC-stimulated MO-bone binding and oligosaccharide changes, suggesting receptor-mediated action.

    Conclusions:

    • Glucocorticoids stimulate macrophage resorptive activity by enhancing initial cell-bone attachment.
    • This enhancement is mediated by alterations in cell surface glycoproteins, specifically N-acetylglucosamine and N-acetylgalactosamine residues.
    • The findings suggest a receptor-mediated mechanism involving GC-induced changes in cell surface oligosaccharides.