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. The objective of this study was to analyze mechanical, inflammatory, and infectious stump skin complications and justify the role of bacterial and mycological dysbiosis in blocking tissue regeneration. Methods: A critical narrative review guided by SANRA principles was conducted (PubMed/Scopus, 1980–2026). Data were extracted with a structured query focusing on amputation stumps, prosthetic interfaces, and skin/microbiological complications (dysbiosis, biofilms, and inflammatory markers). Evidence was graded using predefined clinical matrices and integrated through structured evidence collations to synthesize stump–prosthesis pathogenesis. The PRISMA method was not applied due to study heterogeneity. 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 liner space creates 100% humidity and alkalization (pH > 6.5). This causes a mycological 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. Conclusions: 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.