Steven Tommasini, PhD

My research focuses on understanding the complementary contributions of bone mass, geometry and tissue material properties to whole-bone structural behavior. Specifically, this work assesses bone quality and bone mechanical properties at the tissue and organ level both during homeostasis as well as in response to either catabolic or anabolic stimuli. I am interested in the relationship between bone quality, metabolism, and mechanosensitivity, especially how changes in metabolism (as a result of diet, age, drug treatment, or estrogen withdrawal) alter the morphology of the osteocyte lacunar-canalicular network potentially affecting bone’s response to biomechanical stimuli. A combination of state-of-the-art techniques to assess bone quality such as nanoindentation, Fourier Transform Infrared imaging, synchrotron radiation-based computerized tomography, and finite element modeling are being used to explore the hypothesis that mechanical and biochemical stimuli may cause osteocytes to directly contribute to the modulation of bone quality and quantity by directly remodeling their surrounding environment. Previously, using high resolution computed-tomography, we observed that the number, size, and distribution of microporosities in lamellar bone can be altered by conditions such as estrogen withdrawal and pharmaceutical treatment of osteoporosis in an OVX rat model. Currently, different genetic strains of inbred mice, both with normal phenotype and impaired mineralization are being used to investigate the relationship between mineral ion homeostasis, osteocyte biology, and skeletal adaptation.