The ability to stimulate bone growth has the potential to save the medical industry billions of dollars, annually, by not only reducing healing time of fractures that have occurred, but also helping prevent fractures in osteoporotic bone and loosening of orthopedic implants. Mice lacking the protein developed by the Pten gene have been shown to have a marked increase in bone density, volume, stiffness throughout life. Similarly the mice lacking Pten have shown a more rapid fracture healing time. The goal of this research is to validate the development of a future therapy that would locally inhibit the production of Pten to stimulate bone growth.
Mid-diaphyseal fractures were induced in two groups of mice with and without Pten. Micro-computed tomography (µCT) scans were taken and mechanical 4-point bend testing of the bone callus was conducted at several times during the healing process. This data is being used to develop a finite element model to predict the differences in area moment of inertia, density, stress, and strain between normal mice and those lacking Pten at different stages of healing.