Hypopigmentation in burns is associated with alterations in the architecture of the skin and the dendricity of the melanocytes.

Hypopigmentation is a major problem in deep dermal burns. To date, no standard treatment is available for the post burn hypopigmentation disorder. Therefore, understanding the molecular and cellular events are of benefit for therapeutic intervention. Hematoxylin and Eosin (H&E) and Fontana Masson (FM) staining of post burn hypopigmented skin (PBHS) showed an altered architectural pattern in cellular organization, cornified layer and melanin pigment as compared to the normal skin. This was confirmed by immunohistochemistry (IHC) analysis of PBHS samples using specific marker cytokeratin 5 (CK5) for keratinocytes and melanocortin 1 receptor (MCIR) for melanocytes. Validation of these observations was performed by IHC using proliferation and differentiation markers, Ki67 and Loricrin respectively and the melanocyte specific marker tyrosinase related protein 1 (TRP1). Taking a cue from the IHC study, the interaction of keratinocytes and melanocytes was studied by developing a co-culture model from PBHS and normal skin. Culture data exhibited a change of dendritic structure, reduced proliferation rate, faulty melanin synthesis and transfer of melanin from melanocytes to keratinocytes in PBHS samples. To the best of our knowledge, this is the first study showing structural and functional aberrations of melanocytes and keratinocytes, as a potential cause of hypopigmentation in burned patients. Our study, therefore, provides valuable insight for the basis of hypopigmentation in post burn patients, which may pave the way for clinical intervention in the future.