Influence of alumina shot blasting induced roughness on bacterial adhesion to titanium

To evaluate the influence of different surface roughness levels of titanium disks, induced by alumina blasting, on bacterial adhesion.

Twelve different surface roughnesses, ranging from 0.01 μm to 6 μm, were produced using a shot blasting technique with varying alumina particle sizes. Surface roughness was measured using confocal interferometry, wettability was assessed by contact angle measurements, and compressive residual stress was evaluated by X-ray diffraction. For each roughness level, 720 samples were used to culture Porphyromonas gingivalis (Gram-negative, anaerobic) and Streptococcus sanguinis (Gram-positive, anaerobic). The colonies formed per unit area, the ratio of dead bacteria to total bacteria, and the metabolic activity for each roughness ere determined.

The polished surface (Sa = 0.01 μm) showed the highest bacterial adhesion for both strains compared to the 0.13 μm roughness, which exhibited a antibacterial activity, likely due to nanostructured peaks causing bacterial membrane disruption. For surface roughness values between 0.5 and 3 μm, Gram-positive bacterial colonies increased approximately threefold. When the roughness exceeded 3.8 μm, colony formation rose fivefold. In contrast, Gram-negative bacteria did not exhibit statistically significant changes in adhesion between 0.5 and 2 μm. However, beginning at 2.6 μm, a marked increase was observed, with colony numbers reaching nearly four times the control at 6 μm. The ratio of dead bacteria and metabolic activity confirms bacterial colonization studies (CFU/mm²).

Surface roughness significantly influenced bacterial colonization on titanium implants. An antibacterial effect was observed at a roughness of 0.13 μm. Bacterial adhesion increased moderately up to 2.1 μm for Gram-negative and 3 μm for Gram-positive strains, followed by a sharp rise at higher roughness values. An optimal surface roughness range of 1 to 2 μm appears to promote favorable osteoblastic response while minimizing bacterial adhesion.

These results enhance our understanding of how implant surface roughness influences bacterial adhesion. This knowledge could contribute to the development of clinical approaches designed to lower the risk of peri-implantitis.