Effect of Aluminum Oxide-Blasted Implant Surface on the Bone Healing Around Implants in Rats Submitted to Continuous Administration of Selective Cyclooxygenase-2 Inhibitors

Purpose: The continual use of selective cyclooxygenase-2 (COX-2) inhibitors may have a negative impact on bone repair around titanium implants. Because modified implant surfaces could be considered an important strategy to increase success rates in some conditions that interfere in bone healing, the aim of this study was to investigate whether an aluminum oxide (Al2O3)-blasted implant surface could reduce the negative action promoted by the continuous administration of selective COX-2 inhibitors on bone healing around implants. Materials and Methods: Thirty Wistar rats received one titanium implant (machined or Al2O3-blasted surface) in each tibia and were randomly assigned to one of the following groups: saline (n = 14) or meloxicam (n = 16); each was administered daily for 60 days. Bone-to-implant contact (BIC), bone area (BA) within the limits of threads, and bone density (BD) in a zone lateral to the implant were examined in undecalcified sections. Results: The Al2O3-blasted surface resulted in significantly increased BIC in both groups, and meloxicam significantly reduced bone healing around implants (P .05). For the machined surface, significant differences were observed for BIC (39.48 ± 10.18; 25.23 ± 9.29), BA (60.62 ± 4.09; 42.94 ± 8.12), and BD (56.31 ± 3.64; 49.30 ± 3.15) in the saline and meloxicam groups, respectively. For the Al2O3-blasted surface, data analysis also demonstrated significant differences for BIC (45.92 ± 11.34; 33.30 ± 7.56), BA (61.04 ± 4.39; 44.89 ± 7.11), and BD (58.77 ± 2.93; 50.04 ± 3.94) for the saline and meloxicam groups, respectively. Conclusions: The Al2O3-blasted surface may increase BIC; however, it does not reverse the negative effects promoted by a selective COX-2 inhibitor on bone healing around implants. Keywords: anti-inflammatory agents, dental implants, osseointegration, selective cyclooxygenase-2 inhibitors, wound healing