Available at: http://digitalcommons.calpoly.edu/theses/748
Date of Award
MS in Biomedical Engineering
Biomedical and General Engineering
Sclerostin, a protein coded for by the SOST gene, is an osteocyte-expressed negative regulator of bone formation. The absence of SOST in the genome may have an effect on bone formation both during skeletal maturation and full maturity. This study attempts to determine significant differences in the mechanical properties of bone that expresses SOST compared to bone that does not. One hundred femur samples from 6, 8, and 12 month old mice were obtained from Lawrence Livermore National Labs and loaded until failure using three-point bending. Results showed significant differences in treatment group effects for cross sectional area, yield force, and ultimate force. SOST knockout (KO) mice were found to have significantly higher values for these properties in comparison to transgenic (TG) and wildtype (WT) littermates. In addition, there was a noted effect dependent on the primary axis of loading, anterior-posterior versus medial-lateral. Lastly, data from this study support the existing hypothesis that there is no systematic side-to-side (left-right) difference in bone formation. This data may aid understanding of the role SOST has in bone formation. If the structural integrity and quality of bone resulting from the removal of the SOST gene is shown to be comparable to that of normal, healthy bone, the use of gene therapy to combat diseases/disorders such as osteoporosis may lead to important contributions to medical therapy.