Aspects of the Pathogenesis of Skin Complications in the Stump-Prosthesis System in Dynamics: The Role of Bacterial and Mycological Dysbiosis

Background. Lower limb exoprostheses often lead to stump dermatological pathologies. The mechanisms by which mechanical microtraumas progress to non-healing ulcerative defects due to dysbiosis remain poorly understood. Study Objective. To analyze mechanical, inflammatory, and infectious stump skin complications and justify the role of bacterial and mycological dysbiosis in blocking tissue regeneration. Materials and Methods. Scale for the Assessment of Narrative Review Articles principles were used to quality control the narrative review. A targeted search was conducted in PubMed and Scopus databases. Search dates ranged date in January 1980 to May 2026. Results. Skin damage dynamics were categorized into three stages: adaptation (up to 12 months), chronic reactive changes (12–24 months), and late proliferative-infectious destruction (>24 months). The sealed sleeve space creates 100% humidity and alkalization (pH >6.5). This causes a "fungal shift," where resident Malassezia spp. lose dominance to invasive Candida albicans and non-dermatophyte molds (Aspergillus spp., Fusarium spp.). These pathogens form polymicrobial biofilms with Staphylococcus aureus. At the molecular level, delayed regeneration is driven by “frustrated phagocytosis”: macrophages, unable to engulf large fungal hyphae, continuously release reactive oxygen species and enzymes, trapping the wound in the inflammatory phase. Excessive matrix degradation and suppressed angiogenic factors further block epithelialization. Conclusion. The skin under a prosthesis socket forms a unique pathological biotope. Successful regeneration requires preventive mycobiota correction and targeted management of biophysical parameters (pH, humidity) within the “skin-liner” interface.