Mechanical force is important for modeling, remodeling and bone regeneration. It stimulates the osteocytes, causing an alteration in the production and secretion of signaling molecules that regulate osteoblast and osteoclast activity. The present study aims to evaluate the effect of the conditioned medium of mechanically stimulated mouse osteocytic cells on the proliferative and migratory capacity of mesenchymal cells and bone cells. For this, the proliferation and migration of mouse pre-osteoblastic cells, human pre-adult mesenchymal cells and mouse macrophages in the presence of the conditioned medium of osteocytic cells were analyzed, after 6 and 24 hours after being subjected to a mechanical stress of 10 dynes/cm 2 by fluid flow (FF) for 10 minutes. The migration of pre-osteoblastic cells has been found to increase significantly in the presence of conditioned media of osteocytic cells compared to the static control group (SC) (SC=12.63±5.44, FF6h=23.03±11.57, FF24h=29.72±15.76, p<0.0001). In the same way, the pre-adipose cells also significantly increased their migration in the presence of this conditioned media (SC=11.48±4.75, FF6h=18.43±9.94, FF24h=18.80±10.03; p≤0.0007). However, macrophage migration decreased in the presence of the conditioned medium collected at 24 hours with respect to the static control group (SC=69±22.71, FF24h=26.57±5.47, p<0.0001). These effects were associated with decreased protein expression of certain chemokines, such as the monocyte chemotactic protein type I (SC=0.25±0.06, FF24h=0.09±0.005, p=0.0262), the protein of group I of high mobility (SC=0.25±0.04, FF24h=0.15±0.05, p=0.0159) and the regulatory protein of the activation of T lymphocytes and monocytes (SC=3.29±0.88, FF6h=1.33±1.09, FF24h=0.97±0.66, p≤0.0314), by the osteocytes in the presence of mechanical stimulation with respect to the static control group. In conclusion, this in vitro study demonstrates that osteocyte mechanotransduction enhances recruitment of osteoblasts and pre-adipose mesenchymal cells while reducing the migration of macrophages.