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.
Extensive Research Description
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.
- Wang M, VanHouten JN, Nasiri AR, Tommasini SM, Broadus AE. 2014. Periosteal PTHrP regulates cortical bone modeling during linear growth in mice. J Anat. 225(1):71-82.
- Yao C, Yao GQ, Sun BH, Zhang C, Tommasini SM, Insogna K. 2014. The transcription factor T-box 3 regulates colony-stimulating factor 1-dependent Jun dimerization protein 2 expression and plays an important role in osteoclastogenesis. J Biol Chem. 289(10):6
- Wang M, Nasiri A, VanHouten JN, Tommasini SM, Broadus AE. 2014. The remarkable migration of the medial collateral ligament. J Anat. 224(4):490-8.
- Wallace IJ, Tommasini SM, Judex S, Garland T Jr, Demes B. 2012. Functional loading history cannot be easily inferred from limb bone morphology. Am J Phys Anthropol. 20(1):21-33.
- Tommasini SM, Trinward A, Acerbo A, Miller LM, Judex S. 2012. Changes in intracortical microporosities induced by pharmaceutical treatment of osteoporosis as detected by high resolution synchrotron radiation-based micro-CT. Bone. 50(3):596-604.
- Tommasini SM, Hu B, Nadeau JH, Jepsen KJ 2009 Phenotypic integration among trabecular and cortical bone traits establishes mechanical functionality of inbred mouse vertebrae. J Bone Miner Res 24(4):606-20.
- Tommasini SM, Wearne SL, Hof PR, Jepsen KJ 2007 Percolation theory relates corticocancellous architecture to mechanical function in vertebrae of inbred mouse strains. Bone 42(4):743-50.
- Tommasini SM, Nasser P, Hu B, Jepsen KJ 2008 Biological co-adaptation of morphological and composition traits contributes to mechanical functionality and skeletal fragility. J Bone Miner Res 23(2):236-46.
- Tommasini SM, Nasser P, Jepsen KJ 2007 Sexual dimorphism affects tibia size and shape but not tissue-level mechanical properties. Bone 40:498-505.
- Tommasini SM, Morgan TG, van der Meulen MCH, Jepsen KJ 2005 Genetic variation in structure-function relationships for the inbred mouse lumbar vertebral body. J Bone Miner Res 20(5):817-27.