Diabetes mellitus is a global burden that affects wound healing at nearly every stage, transforming what should be a coordinated and self-limited repair process into a chronic, non-healing state. In diabetic patients, sustained hyperglycemia drives persistent inflammation, impaired angiogenesis, fibroblast dysfunction and extracellular matrix instability, resulting in refractory ulcers and often causing severe complications such as infection, hospitalisation, amputation and premature death. This review integrates mechanistic insights with dermatological advancements providing a comprehensive picture of diabetic wound pathophysiology and emerging therapeutic approaches. The normal sequence of wound healing is outlined and contrasted with the cellular and molecular derailments seen in diabetes, with a focus on macrophage polarisation, neutrophil dysfunction, mast cell and dendritic cell dysregulation, impaired regulatory T cell function, pericyte loss, disrupted neuroimmunomodulation, oxidative stress and defective tissue remodelling. Current and novel interventions including hyperbaric oxygen therapy, negative pressure wound therapy, advanced dressings, biologic grafts, phototherapy, as well as regenerative strategies involving stem cells, nanomaterials and exosome-based treatments are critically examined for their clinical utility, limitations and translational promise. No single modality fully addresses the multifactorial nature of diabetic wounds, but multimodal, mechanism-driven strategies hold potential to synergistically restore tissue repair. Bridging basic science with innovative dermatological interventions remains essential to reduce the global burden of diabetic wounds and improving quality of life for diabetics.
Jreije et al. (Mon,) studied this question.