Early detection of melanoma is critical to preventing advanced, difficult-to-treat disease, yet we know little about why areas of skin with similar levels of UV exposure do, or do not, develop into de novo melanoma. Even visually-normal skin is awash with somatic mutations that drive proliferation and turn skin into a patchwork of competing clones. We used 3D total body imaging to select precise locations with 1) photodamaged but otherwise normal skin immediately adjacent to melanoma excision sites, 2) skin with a similar level of photodamage 5cm away from melanoma excision sites and 3) photoprotected skin distant from melanoma sites, in 19 participants, to determine whether there were detectable histopathological differences that might predispose one area of skin to melanoma more than other areas. We examined H&E-stained biopsies from each site to assess solar elastosis, the gold standard for assessing photodamage, and SOX10 staining to assess melanocyte density and presence of confluent melanocytes. Confluent melanocytes would indicate clonal proliferation and an area of potentially greater melanoma potential. Each biopsy site was also assessed for clinical photodamage, and the total body photodamage pattern was determined using a photonumeric scale and compared to a general population cohort not enriched for skin cancer.