EPIDERMAL PROLIFERATION IS NOT IMPAIRED IN CHRONIC VENOUS ULCERS

In this study we have investigated epidermal growth and differentiatio n during wound healing in human skin. The studies were performed in ex cisional wounds in normal skin and in chronic venous ulcers. Tissues w ere analyzed by immunohistochemical staining for proliferation-associa ted nuclear antigens (PCNA and Ki-67 antigen) and cytokeratin 16, Heal ing of excisional wounds was studied from day 2 to 14. Recruitment of resting (G(0)) epidermal cells started within 2 days after wounding; t he number of cycling cells was maximal at day 4 and continued to be in creased (compared to baseline levels in normal skin) after wound closu re (7-14 days). Cytokeratin 16, a proliferation-associated keratin, wa s induced within 48 h and was expressed in the suprabasal keratinocyte s of the wound edge. Cytokeratin 16 expression was maximal at day 4 an d was still present in the neo-epidermis after restoration of epiderma l continuity (7-14 days), Surprisingly, in chronic venous ulcers, cycl ing cells were present in the wound edges of all stages of the leg ulc ers studied. Both the number and localization of cycling cells were si milar to those in normal wound healing. Cytokeratin 16 was strongly ex pressed in all these ulcers. Our in vivo data demonstrate that recruit ment of G(0)-cells into the cell cycle is not impaired in venous ulcer s, which suggests that epidermal proliferation is not a limiting facto r in the healing process of chronic venous ulcers.