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Updated: May 13, 2026

Multi-Scale Modification of Metallic Implants With Pore Gradients, Polyelectrolytes and Their Indirect Monitoring In vivo
Published on: July 1, 2013
Titanium Particles Released from Dental Implants Under Fluoride Exposure Interact with Macrophages
Waad Kheder1, Soumya Sheela2, A R Samsudin1
1College of Dental Medicine, University of Sharjah,PO Box: 27272, Sharjah, UAE.
Abstract:
This study is designed to investigate the influence of fluoride and pH value on the release of titanium particles from Ti6Al4V dental implants with hydrophobic microrough surface produced by sandblasting and acid-etching techniques; and correlate particle size to their uptake by macrophages and expression of inflammatory cytokines. Fifteen dental implants were immersed in five test solutions with different fluoride concentrations and pH values. Three control implants were scanned using a scanning electron microscope and fifteen test implants were also scanned after their immersion in the test solutions. The immersion solutions were analyzed for titanium particles/ions size-range and amount. The uptake of titanium particles by macrophages and expression of Il-1 β and IL-8 following their exposure to titanium particles were investigated. Test solutions with high fluoride and acidity resulted in the release of micro-size titanium particles (4551.7 ± 114.5 nm and 2783 ± 101.13 nm); while those with low fluoride, neutral pH, and alkaline environment resulted in the release of nano-size titanium particles (431.2 ± 80.6 nm, 448.3 ± 112 nm, and 484.5 ± 85.3 nm respectively). There was an increase in the uptake of nanoparticles by macrophages without altering their membrane integrity. The increase in expression of IL-1β and IL-8 by M0 macrophages after exposure to titanium dioxide particles may facilitate our understanding of immune cell population-specific molecular events deriving the peri-implant inflammation in response to titanium particles. Fluoride and pH values influence the release of titanium particles from the implant's surface. The activated inflammatory mediators are key to imbalance in osteoblast-osteoclast activity and failure of implant osseointegration.
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