Osteoporosis, the most common degenerative disease in the Western Hemisphere, is characterized by a decrease in bone density. The disease comes in two varieties: post-menopausal, primarily affecting post-menopausal women, and age-related, affecting older men as well as women. A study published this week in the early online edition of the Proceedings of the National Academy of Sciences found that mice genetically engineered to lack a molecule called Stem Cell Antigen-1 (Sca-1) experienced normal bone development and maintained normal bone density well into adulthood but exhibited dramatically decreased bone mass and brittle bones as they aged - similar to the symptoms of age-related osteoporosis in humans.

"In these Sca-1-deficient mice, the number of stem cells that normally give rise to new bone cells - called mesenchymal stem cells - declined with age, leading to fewer bone-forming cells," says lead author, Mortaza Bonyadi, a post-doctoral fellow who conducted the research in the labs of senior co-authors and U of T professors William Stanford and Jane Aubin. "We believe that one reason for age-dependent osteoporosis in humans may be defective maintenance of these stem cells. If we can learn how Sca-1 influences the number of stem cells, we may be able to develop new drugs to combat this disabling disease."

Understanding of the causes of age-related osteoporosis is poor compared to the hormonally driven post-menopausal variety, although age-related osteoporosis has a greater mortality and morbidity rate, says Aubin, a professor in the Department of Molecular and Medical Genetics, the Department of Medical Biophysics and the Department of Medical Biophysics and the Institute of Biomaterials and Biomedical Engineering (IBBME).

"While previous studies have suggested that old
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Contact: Jessica Whiteside
jessica.whiteside@utoronto.ca
416-978-5948
University of Toronto
1-May-2003