Long-Term Pathologic Sequelae In Skin Grafts: A Systematic Review

PURPOSE: Skin grafting (SG) remains a cornerstone in reconstructive surgery for definitive wound coverage. While early graft physiology, take, and contracture are well characterized, the long-term biological behavior of grafted skin has not been comprehensively studied. Emerging reports of delayed-onset pathology at SG sites, sometimes decades after successful graft healing, suggest an underrecognized phase in graft remodeling and immune surveillance. This systematic review synthesizes all available case-level evidence of noninfectious dermatoses arising at skin graft recipient sites, encompassing neoplastic, inflammatory, and autoimmune etiologies, to define their clinical spectrum and mechanistic implications. METHODS: A systematic search of PubMed/MEDLINE, Embase, Web of Science, and Cochrane CENTRAL was conducted in accordance with PRISMA guidelines. Eligible studies included case reports and series documenting noninfectious cutaneous disorders localized to full-thickness (FTSG), split-thickness (STSG), or composite graft recipient sites with supporting clinical or histopathologic data. Donor site-only pathologies were excluded. RESULTS: Forty-one case reports representing forty-one individual patients met inclusion criteria. Of 34 with reported graft type, 25 (74%) were STSGs and 9 (26%) FTSGs. Lesions most frequently involved the lower extremities (n=21), followed by scalp, upper limbs, pubic region, and face. Twenty-nine cases were confined to recipient sites, and 12 involved both donor and recipient areas. The most common pathologies were squamous cell carcinoma (n=10), eczematous dermatitis variants (n=4), erosive pustular dermatosis (n=4), bullous pemphigoid (n=3), and keratoacanthoma (n=2). Rare entities included melanoma, pemphigus vegetans, psoriasis (Koebner phenomenon), keloid, perforating dermatosis, plasmacytoma, and cylindroma. Inflammatory and autoimmune lesions typically manifested within weeks to months postoperatively, whereas neoplasms exhibited latency up to six decades. Several presentations diverged from classical patterns, such as SCC arising in well-healed grafts rather than chronic ulcers and localized autoimmune blistering disease restricted to grafted skin. Notably, one case revealed cutaneous plasmacytoma confined to an FTSG overlying systemic multiple myeloma, implicating graft microenvironments as sentinel sites for systemic disease. CONCLUSION: Skin grafts should be conceptualized as long-term dynamic constructs that remain biologically active and susceptible to diverse dermatoses. Grafted skin represents an immunologically distinct niche where altered vasculature, loss of adnexal structures, and impaired immune surveillance predispose to atypical inflammatory and neoplastic processes. The predominance of STSG involvement likely reflects structural fragility and reduced regenerative capacity, particularly in lower extremity sites prone to venous stasis and chronic inflammation. Surgeons and dermatologists should maintain lifelong vigilance for new or evolving lesions at SG sites and adopt a low threshold for biopsy. Understanding graft-site immune dysregulation may inform strategies to improve long-term graft design and surveillance protocols, reframing SGs not as inert reconstructions but as evolving biological systems. *Source: https://ps-rc.org/meeting/Program/2026/EP108.cgi*