Filling the empty holes in peri-articular locking plates may improve the fatigue strength of the fixation. The purpose of this in vitro study was to investigate the effect of plugging the unused holes on the fatigue life of peri-articular distal femoral plates used to fix a comminuted supracondylar fracture model.

A locking/compression plate was applied to 33 synthetic femurs and then a 6 cm metaphyseal defect was created (AO Type 33-A3). The specimens were then divided into three groups: unplugged, plugged with locking screw only and fully plugged holes. They were then tested using a stepwise or run-out fatigue protocol, each applying cyclic physiological multiaxial loads.

All specimens in the stepwise group failed at the 770 N load level. The mean number of cycles to failure for the stepwise specimen was 25 500 cycles (sd 1500), 28 800 cycles (sd 6300), and 26 400 cycles (sd 2300) cycles for the unplugged, screw only and fully plugged configurations, respectively (p = 0.16). The mean number of cycles to failure for the run-out specimens was 42 800 cycles (sd 10 700), 36 000 cycles (sd 7200), and 36 600 cycles (sd 10 000) for the unplugged, screw only and fully plugged configurations, respectively (p = 0.50). There were also no differences in axial or torsional stiffness between the constructs. The failures were through the screw holes at the level of comminution.

In conclusion, filling the empty combination locking/compression holes in peri-articular distal femur locking plates at the level of supracondylar comminution does not increase the fatigue life of the fixation in a comminuted supracondylar femoral fracture model (AO 33-A3) with a 6 cm gap.

Bone growth into cementless prosthetic components is compromised by osteoporosis, by any gap between the implant and the bone, by micromotion, and after the revision of failed prostheses. Recombinant human transforming growth factor-β1 (rhTGF-β1) has recently been shown to be a potent stimulator of bone healing and bone formation in various models in vivo.

We have investigated the potential of rhTGF-β1, adsorbed on to weight-loaded tricalcium phosphate (TCP) coated implants, to enhance bone ongrowth and mechanical fixation. We inserted cylindrical grit-blasted titanium alloy implants bilaterally into the weight-bearing part of the medial femoral condyles of ten skeletally mature dogs. The implants were mounted on special devices which ensured stable weight-loading during each gait cycle. All implants were initially surrounded by a 0.75 mm gap and were coated with TCP ceramic.

Each animal received two implants, one with 0.3 μg rhTGF-β1 adsorbed on the ceramic surface and the other without growth factor. Histological analysis showed that bone ongrowth was significantly increased from 22 ± 5.6% bone-implant contact in the control group to 36 ± 2.9% in the rhTGF-β stimulated group, an increase of 59%. The volume of bone in the gap was increased by 16% in rhTGF-β1-stimulated TCP-coated implants, but this difference was not significant. Mechanical push-out tests showed no difference in fixation of the implant between the two groups. Our study suggests that rhTGF-β1 adsorbed on TCP-ceramic-coated implants can enhance bone ongrowth.