Burn wounds can result in the development of hypertrophic scar (HTS). A problematic characteristic of HTS is dyschromia, which is often distressing to patients and has been shown to impact quality of life. There are currently no viable, non-surgical treatment methods for dyschromia, and the mechanisms behind it are not well understood. We aimed to test if the fibrotic microenvironment of the dermis plays a contributing role in the development of epidermal dyschromia. To do this, we focused on reproducing a previously published model of bleomycin-induced dermal fibrosis to add to the replicability of previous findings and establish a reliable model to serve as a basis for understanding post-burn dyschromia development. By treating C57BL/6 mice with intradermal injections of three varying doses of bleomycin for two weeks and conducting histological and molecular analyses of collected data, we were able to assess the adequacy of dermal fibrosis development. Collected data showed evidence of hair follicle obliteration, dermal thickening, and other characteristics of fibrotic architecture within all three bleomycin-treated groups, bust mostly profoundly in the high-dose group. However, qRT-PCR data did not reveal any significant trends in differential expression of genes of interest. In future work, additional qRT-PCR analysis, immunofluorescence visualization, and other molecular assays should be conducted to obtain further molecular confirmation of bleomycin-induced dermal fibrosis before we can attempt to understand the mechanistic relationship between dermal fibrosis and epidermal dyschromia.