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Both implant surface characteristics and mechanical loading are known to affect implant osseointegration. Their interaction and the underlying mechanisms by which they affect peri-implant healing processes are still unknown. The aim of this study is therefore to investigate the influence of a turned versus a rough (Plus®, Dentsply Friadent) implant surface on peri-implant bone formation in case of unloaded or loaded implant healing. Material and Methods: Bone formation was evaluated around screw-shaped implants under four experimental conditions using a repeated sampling bone chamber methodology: (1) unloaded turned implant (CU), (2) unloaded implant with a rough surface (TU), (3) loaded turned implant (CL), and (4) loaded implant with a rough surface (TL). Peri-implant tissue samples were paraffin embedded after implant removal and examined histologically and histomorphometrically. A mixed model was used for statistical analysis. Results: The surface of bone tissue relative to the total tissue area (bone area fraction) was not affected by the experimental conditions. The areas of bone trabeculae relative to the bone area (bone fraction) were significantly higher for TL compared with CU and TU. The bone fraction in the vicinity (100 μm zone) of the implant (BFZ) was significantly the highest around the loaded roughened implants (TL). Conclusion: Implant loading did not affect bone formation in the absence of surface roughness, and implant surface roughness had no effect in the absence of loading. However, a bone-stimulating effect in the implant's vicinity was assigned to the rough surface when the implant was loaded.

The effects of recombinant human fibroblast growth factor-2 in the presence of eroding 50:50 poly(DL-lactide-co-glycolide) on angiogenesis during acute bone defect healing were studied in the optical bone chamber. Bone chambers were loaded with disks of poly(DL-lactide-co-glycolide) surrounded by one of four doses of recombinant human fibroblast growth factor-2. Fifty-two female rabbit right tibias were implanted. Commencing with the third postimplantation week, healing into the bone chamber compartment was observed weekly, with use of intravital microscopy, until week 8. The treatment groups were as follows: unloaded, loaded with polymer only, and loaded with polymer plus-0.5, -1.0, and -10 microg recombinant human fibroblast growth factor-2. Videotaped and photographed bone images were measured and analyzed with a frame-grabber digitizing system. Comparison with controls or polymer alone revealed that angiogenesis rates were significantly above normal in rabbits loaded with polymer plus either of the two highest recombinant human fibroblast growth factor-2 doses. The effects of these doses were not, however, significantly different from each other, indicating a plateauing rather than monotonically increasing response. It was concluded that recombinant human fibroblast growth factor-2 in the dose- range studied can effectively overcome the retarding effects of eroding polymer on angiogenesis in bone, which has been reported previously by this laboratory. In contrast to these results, no statistically significant differences in angiogenesis rate as a function of time could be detected. It is suggested that this apparent lack of variation is linked to observed alterations in vessel patterns from week-to-week. The clinical relevance of these results is that inhibitory carrier effects can be compensated for by increasing the dose of loaded agent where the effect being inhibited is the one being treated, or by adding an agent specific for the inhibited effect. In either case, geometry of the carrier must be considered when programming for delivery rate.