Healing of 0.5 or 1.0-millimeter step-off defects associated with displaced intra-articular fractures of the medial femoral condyle was examined in fifty-four adult New Zealand White rabbits. The rabbits were treated with either immobilization for three weeks, intermittent active motion, or continuous passive motion for seven days. At twelve weeks, the healing and remodeling of the step-off defects were examined with use of contact-pressure maps on pressure-sensitive film, light microscopy (with hematoxylin and eosin or safranin-O staining), and scanning electron microscopy. Macroscopically, the sharp profile that had been present initially with both sizes of step-off defect had rounded off; however, there was less residual incongruity with the 0.5-millimeter step-offs than with the 1.0-millimeter step-offs. Among step-off defects of the same size, the method of treatment had no discernible effect on the macroscopic appearance of the surface of the joint. With fresh step-offs (the control group), the contact pressure of the cartilage on the elevated side was approximately three times greater than that at a distance from the step-off. On the depressed side, an unloaded zone extended approximately three times the height of the step-off, with an average width of 3.4 millimeters for the 1.0-millimeter step-offs and 1.6 millimeters for the 0.5-millimeter step-offs. After healing and remodeling, the unloaded zone still averaged 2.5 millimeters in width for the 1.0-millimeter step-offs but had decreased to only 0.35 millimeter in width for the 0.5-millimeter step-offs. For seven of the nine 0.5-millimeter step-offs, the contact pressure in the previously unloaded zone ranged from 0.5 to 1.5 megapascals, with a mean of 0.8 megapascal (40 per cent of the normal mean contact pressure at this location). Under light microscopy, the cartilage on the elevated side of the healed step-offs had decreased in thickness, was displaced toward the defect and tapered toward the depressed side, and ended in a hypocellular tissue flap. In contrast, the cartilage on the depressed side had thickened as a result of hyperplasia of the chondrocytes and hypertrophy of the cartilage and had failed to establish continuity between the sides of the defect. There was a marked increase in the subchondral vascular bed and re-establishment of the subchondral plate. With the exception of the aforementioned hypocellular tissue flap, safranin O stained the cartilage on both levels of the step-off uniformly, which indicated the absence of glycosaminoglycan depletion.(ABSTRACT TRUNCATED AT 400 WORDS)