Modulation of osteoclast differentiation by epigallocatechin-3-gallate (EGCG)/type I collagen-coated titanium implant surface in vitro.

BACKGROUND/PURPOSE: Implant osseointegration depends not only on osteogenesis but also on coordinated bone remodeling. Our previous study demonstrated that epigallocatechin-3-gallate (EGCG)/type I collagen-coated titanium (Ti) surfaces enhance angiogenesis and osteogenic differentiation in vitro. However, their influence on osteoclast differentiation remains unclear. This study evaluated the modulatory effects of this coating on osteoclast responses in vitro. MATERIALS AND METHODS: Sandblasted and acid-etched (SLA) Ti surfaces followed by alkaline treatment (SLAA) were prepared. Type I collagen was immobilized onto SLAA surfaces using the natural crosslinker EGCG (10 or 50 μg/mL). Surface morphology, roughness, hydrophilicity, and functional groups were characterized. RAW 264.7 macrophages were used to assess cell adhesion, proliferation, viability, tartrate-resistant acid phosphatase (TRAP) expression, and F-actin ring formation. Osteoclast differentiation was induced using receptor activator of nuclear factor kappa-B ligand (RANKL). Statistical analysis was performed using one-way ANOVA with Dunnett's test. RESULTS: Surface characterization confirmed successful coating without compromising surface stability. Compared with SLA surfaces, collagen-coated surfaces with or without EGCG enhanced initial cell spreading while showing less increase in metabolic activity without cytotoxicity. EGCG- and EGCG/type I collagen-coated surfaces significantly reduced TRAP expression and F-actin ring size relative to SLA surfaces. Although the 50 μg/mL EGCG groups showed lower TRAP expression and smaller F-actin rings than the 10 μg/mL groups, the differences were not statistically significant. CONCLUSION: EGCG/type I collagen surface modification may modulate osteoclast-related cellular responses in RAW 264.7 cells without affecting cell viability, suggesting a potential strategy to modulate peri-implant bone resorption and support long-term implant stability.