Bone remodeling is inhibited by high load environments such as that in the joints of athletic horses in training. However focal offsetting of remodeling inhibition is observed associated with micro-damage in the subchondral bone (SCB) of these animals either due to targeting of damaged areas by bone remodeling units or local unloading due to loss of articular surface congruity. To test whether local unloading of the articular surface can stimulate focal bone remodeling we arthroscopically created a defect in one surface of the midcarpal joint of six adult horses. Two weeks post-operatively the animals began an eight-week training program following which osteochondral samples were collected from the site of the defect and immediately adjacent to it in both the radial carpal bone (Cr) and the opposing third carpal bone (C3). Control samples were collected from the sham-operated contralateral limb. Samples were imaged with BSEM and cryosections stained for TRAP to identify osteoclasts. In treated joints there was evidence of increased bone turnover (mean difference, active surface: 4.36mm^-1, P<0.01) and osteoclast numbers (28.6cells/mm², P=0.04) in the unloaded subchondral bone below the lesion in Cr, with similar but less marked changes in the opposing unloaded region in C3 (active surface: 1.28mm^-1, P=0.03, osteoclasts: 3.4cells/mm², P=0.03). In the loaded region adjacent to the lesion in Cr there was no change in bone turnover (active surface: 0.35mm^-1, P=0.65) while in the opposing site in C3 there was reduced bone turnover (active surface: -0.66mm^-1, P=0.01). There was no difference in osteoclast numbers in the loaded region in either bone (Cr: 6.2cells/mm², P=0.13; C3: -0.3 cells/mm², P=0.86). Local unloading of the articular surface resulted in increased focal SCB remodeling underlying the intact joint surface in this equine model. This demonstrates a possible mechanism by which focal remodeling may occur in SCB in a high load environment.