Wound Healing Variability across Skin Phototypes: Melanocyte–Fibroblast Crosstalk and Implications for Individualized Scar Management

Scar formation reflects the combined influence of fibroblast activity, inflammatory signaling, mechanical forces, and the broader cellular environment involved in wound healing. Pigmentation biology has received growing attention as a potential contributor to interindividual differences in scar phenotypes. Melanocytes are not simply pigment-producing cells; they secrete a range of cytokines and growth factors that may influence neighboring fibroblasts and keratinocytes during tissue repair. Such interactions have been proposed as a partial explanation for the higher prevalence of hypertrophic scars and keloids in individuals with darker Fitzpatrick skin types. This focused narrative review examines the evidence linking skin phototype, melanocyte-associated signaling, and fibrosis-related wound-healing responses. Key pathways discussed include transforming growth factor-β1, endothelin-1, and mechanotransduction signals mediated by focal adhesion kinase and the Yes-associated protein/transcriptional coactivator with PDZ-binding motif axis. The bidirectional nature of melanocyte–fibroblast crosstalk is explored, along with the role of oxidative stress and reactive oxygen species in sustaining wound inflammation. Post-inflammatory hyperpigmentation is examined as both a clinical marker and a potential mechanistic link between melanocyte overactivation and fibroproliferative scar formation. The clinical implications of phototype-specific adjustments in laser therapy, intralesional corticosteroid injections, botulinum toxin use, and adjuvant radiation therapy are discussed in detail. A conceptual framework for phototype-informed, individualized scar prevention and treatment is proposed. Priorities for future investigations, including phototype-stratified clinical trials and molecular profiling of wound-site biopsies, are outlined.