A bioadhesive sustained-release films for in situ therapy of oral ulcers

A multifunctional adhesive electrospun BG/HPMC film delivers BG-derived bioactive ions (Si, Ca, Na, P) to the oral ulcer site, creating a biomimetic microenvironment. This enables synergistic antimicrobial, pro-proliferative (epithelial/endothelial), ROS-scavenging, and anti-inflammatory effects, accelerating ulcer re-epithelialization. The study demonstrates the effectiveness of a single-component, multi-target strategy for oral ulcer therapy. • Developed an innovative multifunctional electrospun film specifically designed for oral ulcer therapy. • Demonstrated a synergistic therapeutic mechanism that promotes rapid re-epithelialization and comprehensive regulation of ulcer pathology. • Established the scientific validity of a single-component, multi-target strategy for effective oral ulcer treatment. Oral ulcers affect more than 25 % of the global population and are driven by complex pathological mechanisms, including bacterial infection, oxidative stress, and dysregulated inflammation, all of which impede healing. To address the limitations of therapies that target only a single aspect of ulcer pathology, this study developed a multifunctional electrospun film by combining 45S5 bioactive glass (BG) with hydroxypropyl methyl cellulose (HPMC). The BG/HPMC films, fabricated by electrospinning with 5 wt% BG incorporated into HPMC matrices, were thoroughly characterized for their structural and bioactive properties. In a rat oral ulcer model, the BG/HPMC films significantly accelerated re-epithelialization and reduced ulcer size compared to both control and chitosan-treated groups. The films also exhibited strong antibacterial activity against Staphylococcus aureus. In vitro, BG extracts promoted the viability and migration of human oral epithelial cells (HOECs) and human umbilical vein endothelial cells (HUVECs), mitigated hydrogen peroxide-induced oxidative stress, and suppressed the expression of pro-inflammatory cytokines—interleukin-1 alpha (IL-1α), tumor necrosis factor alpha (TNF-α), and interleukin-6 (IL-6)—in lipopolysaccharide-stimulated macrophages.