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Hypertrophic scars (HTS) arise from dysregulated wound healing characterized by excessive inflammation, fibroblast hyperactivity, and extracellular matrix (ECM) imbalance, as described across multiple mechanistic reviews in the included dataset. Several UV-focused articles identify ultraviolet (UV) radiation as a major environmental stressor capable of inducing oxidative DNA damage, cellular injury, and persistent inflammatory signaling. Environmental studies examining outdoor workers report substantial cumulative UV exposure and inadequate photoprotection, underscoring the relevance of occupational risk in high-sun environments. This review aimed to evaluate the potential influence of high occupational UV exposure on hypertrophic scar healing among outdoor workers in sunny climates.

A comprehensive literature review was conducted using PubMed, Embase, Cochrane, CINAHL, OpenEvidence, Consensus AI, and Undermind to identify studies related to high occupational UV exposure and hypertrophic scarring. The search identified 183 articles, which were independently screened by six reviewers using predefined inclusion criteria focusing on adult participants with hypertrophic scars, high occupational sun exposure, and relevance to sunny climates. Of the 183 articles screened, 19 met inclusion criteria.

Across the included literature, UV radiation was consistently associated with biological pathways that overlap with known drivers of hypertrophic scarring. Mechanistic HTS studies emphasized cytokine-mediated inflammation, fibroblast overactivation, and ECM dysregulation, while UV-focused articles detailed oxidative stress, DNA damage, and deep-penetrating UVA1 injury as key consequences of chronic exposure. Environmental studies confirmed high UV burden among outdoor workers, though none directly evaluated hypertrophic scar outcomes in high-UV occupational settings. The evidence base was heterogeneous, with most studies being mechanistic or environmental rather than clinical.

The findings suggest that high UV exposure may exacerbate hypertrophic scar dysregulation through oxidative damage and inflammation. However, the absence of direct clinical studies in high-UV-exposed workers highlights a critical gap for future research.

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