Tailoring the structural evolution, in vitro bioactivity, and gastrointestinal cell cytocompatibility of sol–gel-derived Bi(III)-doped bioactive glasses: The role of bismuth precursors
Bismuth(III)-doped 13–93 silicate bioactive glass powders were synthesized via a sol–gel route with Bi₂O₃ contents ranging from 0.1 to 5 wt% using two different precursors, BiCl₃ and Bi(NO₃)₃.5H2O. Structural characterization by X-ray diffraction and FTIR confirmed the predominantly amorphous nature of the glasses and the formation of a typical silicate network structure. In vitro bioactivity studies performed in simulated body fluid (SBF) and phosphate-buffered saline (PBS) demonstrated the formation of a calcium phosphate–rich apatite layer on the surface of the glasses, confirming their bioactive behavior. FTIR and SEM analyses indicated apatite-like calcium phosphate formation after immersion, with Bi3+-doped compositions showed slightly enhanced apatite formation. Cytocompatibility assessments using multiple gastrointestinal-relevant cell models, including AGS, HIF, HISMC, and HEK-293 cells, showed that high Bi3+ contents (≥1 wt%) resulted in reduced cell viability, whereas low Bi3+ concentrations (0.1–0.5 wt%) maintained excellent cytocompatibility. Overall, the results indicate that low-Bi3+-doped 13–93 bioactive glasses combine bioactivity and cytocompatibility, suggesting their potential as multifunctional biomaterials for localized soft tissue applications. Sol–gel bioactive glasses were synthesized using BiCl₃ and Bi(NO₃)₃. Bismuth precursor chemistry influenced particle morphology and glass structure. Bi3+-doped glasses retained in vitro bioactivity through apatite formation. Bi3+ contents of 0.1–0.5 wt% maintained gastrointestinal cell cytocompatibility. Bi3+ contents ≥1 wt% induced cytotoxicity in gastrointestinal cell models. Sol–gel bioactive glasses were synthesized using BiCl₃ and Bi(NO₃)₃. Bismuth precursor chemistry influenced particle morphology and glass structure. Bi3+-doped glasses retained in vitro bioactivity through apatite formation. Bi3+ contents of 0.1–0.5 wt% maintained gastrointestinal cell cytocompatibility. Bi3+ contents ≥1 wt% induced cytotoxicity in gastrointestinal cell models.