In vivo impact of S1PR2 on bone remodeling. (A) Morphohistometric analyses of control and S1PR2-deficient (S1PR2^−/−) littermates. Femoral bone samples were analyzed by cone-beam µCT (top) and conventional histological examination (bottom). Bars: (top) 1 mm; (bottom) 200 µm. (B) Summary of the data of bone matrix density (bone volume/tissue volume = B.V./T.V.), trabecular thickness (Tb.Th.), trabecular density (Tb.N.; calculated from µCT images), osteoblast surface per bone surface (Ob.S./B.S.), and osteoclastic erosion surface per bone surface (E.S./B.S.; calculated by conventional morphohistometrical analyses). Error bars represent SD. n = 3 for each (from three littermates). (C) Therapeutic effect of S1PR2 antagonist JTE013 on osteoclastic bone resorptive changes. Femurs were collected from each mouse (wild-type and S1PR2^−/−) after three different treatments: PBS + vehicle, RANKL + vehicle, and RANKL + JTE013. RANKL was dissolved in PBS, and JTE013 was dissolved in a vehicle (PBS containing 5% acidified DMSO and 3% fatty acid–free BSA). Mice were i.p. injected with PBS or RANKL, and with JTE or vehicle, every day for 2 d. Bone samples were analyzed by cone-beam µCT and conventional morphohistological examination. Data of bone matrix density (B.V./T.V.) calculated from µCT images (left) and osteoclastic erosion surface per bone surface (E.S./B.S.) calculated by conventional morphohistometrical analyses (right) were shown. Error bars represent SD. n = 3 for each (from three littermates).