Silk-Derived Antibacterial Hydrogels: Material Identity, Mechanistic Evidence, and Translation

Silk fibroin (SF)- and silk sericin (SS)-based antibacterial hydrogels are increasingly engineered as local antimicrobial platforms, yet cross-study interpretation is limited by inconsistent material reporting and by conflation of bacterial inhibition with tissue repair. We performed a structured evidence-mapping and critical synthesis of a frozen 2020-July 2026 corpus of 94 references. The original 46-record core map was re-audited at the original-article level: 43 full-text-verified, non-retracted primary studies were retained for detailed evidence grading, 2 records available only at abstract/database level were retained descriptively but not graded, and 1 subsequently retracted study was excluded from quantitative synthesis. Among the 43 graded studies, metal-ion/nanozyme/catalytic systems were most common (12/43, 27.9%), followed by release-mediated (11/43, 25.6%), multimodal (9/43, 20.9%), contact-active/anti-adhesive (6/43, 14.0%), and light-responsive systems (5/43, 11.6%). Sixteen studies (37.2%) used deliberately infected animal models, whereas only 4 (9.3%) reached a biofilm or adherent-bacteria-level endpoint in the graded map. Biological claim ceilings (C0-C5) are assessed independently from translation gates spanning material identity, reproducibility, mechanism, host safety, sterilization/storage, resistance, long-term fate, and deployment. Across mechanisms, SF and SS most often function as structural, interfacial, or transport-regulating matrices; direct silk-dependent bactericidal causality remains uncommon. The central translational deficit is failure to quantitatively link silk molecular identity and network architecture to antimicrobial exposure, bacterial killing, host selectivity, and long-term material fate.