Purpose: This dog study sought to evaluate guided bone regeneration (GBR) in peri-implant defects following implantation of b-tricalcium phosphate (b-TCP) with and without osteoinductive recombinant human growth/differentiation factor-5 (rhGDF-5). Materials and Methods: In five beagle dogs, all mandibular premolars and the first molar were extracted. After 2 months, six buccolingual critical-size defects were created, and an implant was inserted into the center of each defect. One defect was filled with b-TCP coated with rhGDF-5 (600 µg/g b-TCP) and covered with a titanium-reinforced e-PTFE membrane (GDF group). A second defect received the same treatment, but pure uncoated b-TCP was used (TCP group). A third defect was filled with b-TCP mixed with autograft and not protected with a membrane (control group). The remaining three defects were filled with other biomaterials. After 2 months, total new bone area, regenerated bone height, and residual amount of b-TCP were determined histomorphometrically. Results: All implants osseointegrated. One membrane in each group became exposed. Mean new bone area for GDF, TCP, and control sites was 43.9 ± 18.7 mm2, 32.3 ± 16.1 mm2, and 13.1 ± 4.0 mm2, respectively, with a significant difference between GDF and control groups. Mean regenerated bone height was 103.8 ± 29.7%, 75.4 ± 36.6%, and 67.2 ± 19.1% for the GDF, TCP, and control groups, respectively. Mean residual matrix volumes were 25.9 ± 13.6%, 30.0 ± 13.0%, and 13.4 ± 6.5%, respectively. Membrane protection of peri-implant defects filled with b-TCP resulted in a stronger effect on bone regeneration, although this was not statistically significant. The most pronounced regenerative results were achieved in rhGDF-5/b-TCP filled membrane-protected defects. Conclusion: Delivery of rhGDF-5 on b-TCP might have the potential to enhance the results of GBR in peri-implant defects. Schlagwörter: autogenous bone, barrier membrane, b-tricalcium phosphate, dental implants, guided bone regeneration, recombinant human growth/differentiation factor-5