Romosozumab monoclonal antibody treatment works by binding sclerostin and causing rapid stimulation of bone formation while decreasing bone resorption. The location and local magnitude of vertebral bone accrual by romosozumab and how it compares to teriparatide remains to be investigated. Here we analysed the data from a study collecting lumbar CT spine scans at enrolment and 12 months post-treatment with romosozumab (210 mg SC QM, n=17), open-label daily teriparatide (20 ug SC, n=19) or placebo (SC QM, n=20). For each of the 56 women, cortical thickness (CtTh), endocortical thickness (EcTh), cortical BMD (CtBMD), cancellous BMD (CnBMD) and cortical mass surface density (CMSD) were measured across the first lumbar vertebral surface. In addition, colour maps of the changes in the lumbar vertebrae structure were statistically analysed and then visualised on the bone surface. At 12 months Romosozumab improved all parameters significantly over placebo and resulted in a mean vertebral CtTh increase of 10.3% versus 4.3% for teriparatide, an EcTh increase of 137.6% versus 47.5% for teriparatide, a CtBMD increase of 2.1% versus a -0.2% decrease for teriparatide, and a CMSD increase of 12.4% versus 3.8% for teriparatide. For all these measurements the differences between romosozumab and teriparatide were statistically significant (p < 0.05). There was no significant difference between the romosozumab-associated CnBMD gains of 22.2% versus 18.1% for teriparatide, but both were significantly greater compared to the change in the placebo group (-4.6%, p < 0.05). Cortical maps showed the topographical locations of the increase in bone in fracture-prone areas of the vertebral shell, walls and endplates. This study confirms widespread vertebral bone accrual with romosozumab or teriparatide treatment, and provides new insights into how the rapid prevention of vertebral fractures is achieved in women with osteoporosis using these anabolic agents.