Bone mesenchymal stem/ stromal cells (BMSC) reside in bone marrow and can give rise to several cell lineages, including lipid forming adipocytes, cartilage forming chondrocytes and bone forming osteoblasts. Osteoblastic differentiation, driven by Runx2, is a key pathway for the development and maintenance of healthy bone tissue. Altered expression of osteogenic associated genes can lead to bone deficiencies such as Type I and II osteoporosis, resulting in a higher incidence of major fractures. While a common pathology, only 10% of the genetic risk factors for osteoporosis have been uncovered, implying that epigenetic deregulation may be a crucial component. The DNA hydroxymethylases, Tet1 and Tet2 are epigenetic modifiers that have been found to be downregulated during osteoporosis, implicating Tet molecules in the onset and progression of osteoporosis. Investigation into the roles of Tet1 and Tet2 during bone development, as well as the changes in genome wide occupancy of Tet molecules and methylation status of key osteogenic genes during ageing were assessed using conditional double knockout (DKO) of Tet1 and Tet2 in Prrx-1 positive BMSC. Analysis of bone parameters including bone and tissue volume, trabeculae size and osteoblast/ osteoclast number were assessed by 3D mCT and histomorphometric analyses, at various ages (embryonic, new born, 1, 3 and 12 months) to determine the effects of Tet1 and Tet2 on bone density and integrity over time. Preliminary studies found a decreased bone volume and changes in trabecular number in 3 month old Tet 1 and Tet2 DKO animals compared to controls, with the effect being most prevalent in males. Further elucidation of the mechanisms driving Tet1 and Tet2 regulation of bone formation and maintenance may help develop new prognostic indicators of fracture risk and therapeutic strategies to reverse bone loss during ageing.