Fall 2007 Bone Seminar Series

Tuesday October 9 , 2007
CUNY Graduate Center, Room 9207, GC, 7:00 PM
Click here for directions to the CUNY Graduate Center

Image: 3D reconstructions of 1 cm^3 of trabeculae from the medial femoral condyle of a control animal (left), as compared to an animal subjected to 20 minutes per day of low-level mechanical signals

Speakers
—Sheldon Weinbaum, PhD, CUNY Distinguished Professor, The City College of New York
—Clinton Rubin, PhD, SUNY Distinguished Professor; Chair, Department of Biomedical Engineering; Director, Center for Biotechnology—State University of New York at Stony Brook

Host: Susannah Fritton, PhD, The City College of New York

Topic: Low-Level Mechanical Signals as the Basis for a Non-Pharmacologic Treatment for Osteoporosis

Dr. Weinbaum’s Research Interests: Mechanotransduction in all tissues, including bone, kidney, intestines, cardiovascular system, and ear. In the past Dr. Weinbaum has studied transport and heat transfer in the microcirculation and LDL transport across vascular endothelium in atherogenesis.

Dr. Rubin’s Research Interests: How physical (e.g., mechanical, electrical) signals influence the mass and morphology of the musculoskeletal system, and whether these signals can be used as the basis of interventions for the treatment of bone/muscle disease and/or injury

Abstract: Exercise is recognized as a critical regulatory signal to the skeleton, but which specific components are responsible for influencing bone mass and morphology remain unknown. There is mounting evidence that extremely-low-magnitude (<<100 microstrain) mechanical signals can be strongly anabolic to bone if applied at a high frequency (15-60 Hz). Long-term animal studies (1 year) show that such loading, inducing cortical strains of 5 microstrain, can increase cancellous bone volume fraction, thicken trabeculae, increase trabecular number, and enhance bone stiffness and strength. These very low mechanical signals are effective in halting disuse osteoporosis and are most influential in trabecular bone. Studies in the mouse have shown that these low-level signals are anabolic, but extremely complex in terms of their molecular regulators. Considering these strains are far below (<1/1000th) those which may cause damage, they have potential as a nonpharmacologic prophylaxis for osteoporosis.

Several clinical studies have been completed, including reversing low bone density in children with functional disabilities, promoting bone quantity in young women with osteopenia, and preventing osteoporosis in postmenopausal women. Evidence in the animal and human indicates that brief exposure to low-magnitude, high-frequency mechanical signals can benefit bone quantity and quality and perhaps benefit the musculoskeletal “system.” Such a biomechanical intervention is self-targeting, endogenous to bone tissue, and auto-regulated, and provides insight toward a unique, non-pharmacogenic intervention for osteoporosis.

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Tuesday November 13, 2007
The seminar scheduled for this date was cancelled due to a family illness.

Wednesday December 12, 2007
CUNY Graduate Center, Room 9204, GC, 7:00 PM
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Speaker: Stavroula Kousteni, PhD, Assistant Professor of Medicine, Department of
Medicine, College of Physicians and Surgeons, Columbia University Medical
Center

Host: Mitchell Schaffler, PhD, Mount Sinai School of Medicine

Topic: Molecular Mechanisms of Periosteal Expansion

Dr. Kousteni’s Research Interests: Interactions between hormones, cytokines, kinases and bone. Specifically, exploring the cellular and molecular mechanisms of the pathogenesis of osteoporosis due to estrogen or androgen deficiency and old age; mechanisms of parathyroid hormone and steroid hormone receptor action.

Abstract: The periosteum is now widely recognized as a homeostatic and therapeutic target for actions of sex steroids and intermittent parathyroid hormone (PTH) administration. However, the target cells, let alone the mechanisms by which estrogens suppress but androgens and PTH promote periosteal expansion, are not known. We are interested in the molecular mechanisms by which intermittent PTH and sex steroids act and interact to regulate periosteal bone mass. Our studies, using cell and animal models, suggest that the different effects of sex steroids and PTH result from opposing actions on the recruitment of early periosteal osteoblast progenitors. Intermittent PTH and androgens promote osteoblast differentiation from periosteum-derived mesenchymal progenitors. These effects involve rapid activation of specific components of the Wnt or BMP-2 signaling cascades and are also mediated by activation of the cytoplasmic kinases ERK1/2. Estrogens promote the expansion of early osteoblast progenitors but inhibit their differentiation by osteogenic agents such as PTH or BMP-2.

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