Available at: https://digitalcommons.calpoly.edu/theses/1124
Date of Award
MS in Biomedical Engineering
Biomedical and General Engineering
Scott J. Hazelwood
In the human genome, the SOST gene codes for a protein sclerostin. Sclerostin is an osteocyte-expressed negative regulator of bone formation. When the SOST gene is not coded, bone formation is reduced in individuals during skeletal maturation. This study utilizes nanoindentation methods to test for the mechanical properties of bones that both express and do not express the SOST gene. 100 transgenic murine femurs were obtained from Lawrence Livermore Labs in the form of 6 and 8 month SOST transgenic mice, 6 and 12 month SOST knockout mice, and wild type control littermates for each of the 4 age groups. Prior to nanoindentation the bones were broken in a previous experiment under three-point bending tests. Samples were embedded in epoxy and polished to a 0.05 micron level before indentation. Results showed significant difference amongst the treatment group effects for maximum load, hardness and elastic modulus. SOST KO mice had significantly higher values for these properties in comparison to the transgenic and wild type littermates. Additionally, side by side limb differences were examined in which there was a significant difference found amongst the treatment groups. Indentations were conducted in the 4 anatomical regions of each femur in expectation of examining any differences amongst them which resulted with no significant findings amongst them. Data from this study will support research which may result in potential new gene therapies targeted for the treatment of bone diseases such as osteoporosis.