Injectable Thermogel‐Loaded Bi2S3 Nanorods for Synergistic Photothermal Bacterial Elimination and Anti‑Inflammation to Remodel Periodontitis Microenvironment

Why It Matters

The platform offers a drug‑free, dual‑function therapy that tackles infection and chronic inflammation simultaneously, addressing antibiotic resistance and improving outcomes for periodontal disease and other persistent wounds.

Key Takeaways

• Injectable hydrogel delivers Bi2S3 nanorods locally.
• NIR triggers photothermal heating, ROS, GSH depletion.
• Synergistic antibacterial effect eliminates periodontitis pathogens.
• Hydrogel modulates macrophages, reduces inflammation.
• Promotes collagen deposition and alveolar bone regeneration.

Pulse Analysis

Periodontitis affects a large share of adults, driven by biofilm‑induced inflammation that destroys gingival tissue and alveolar bone. Conventional therapy relies on mechanical debridement and systemic antibiotics, but persistent bacterial reservoirs and chronic inflammation often limit healing, especially in diabetic patients. Researchers have therefore turned to multifunctional biomaterials that can both eradicate pathogens and orchestrate tissue repair. In this context, an injectable, thermosensitive hydrogel loaded with bismuth sulfide nanorods offers a platform that merges photothermal therapy with drug‑free antimicrobial action.

The Bi2S3@Gel system combines hyaluronic acid‑Pluronic F127 matrix with Bi2S3 nanorods that absorb near‑infrared light. Upon NIR exposure, the nanorods generate mild hyperthermia (≈45 °C) while catalyzing reactive oxygen species production and depleting intracellular glutathione, creating a hostile environment for oral pathogens. Simultaneously, the hydrogel prolongs residence time, suppresses M1 macrophage polarization, and encourages extracellular matrix deposition. In vitro assays confirm high biocompatibility, >99 % bacterial kill rates, and a shift toward anti‑inflammatory cytokine profiles.

In vivo, the formulation accelerated wound closure in diabetic mouse models and restored alveolar bone in periodontitis lesions to a degree comparable with minocycline, but without systemic drug exposure. This dual‑action approach could reduce antibiotic resistance pressures while delivering regenerative outcomes, positioning it for dental and broader chronic wound markets. Commercialization will hinge on scalable nanorod synthesis, regulatory safety data, and integration with existing periodontal treatment workflows, paving the way for next‑generation, minimally invasive therapies.