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).