ULTRASTRUCTURE OF EPIDERMIS OF MICE WITH CHRONIC PROLIFERATIVE DERMATITIS

C57BL/Ka mice with chronic proliferative dermatitis (cpdm/cpdm) develo p chronic persistent skin lesions characterized by epidermal hyperplas ia, infiltration by granulocytes and macrophages, and vascular dilatat ion. Similar lesions are present in other orthokeratotic epithelia in affected mice, in particular the esophagus and forestomach. Here, we r eport on further characterization of epidermal hyperplasia and the gra nulocytes. Keratinocytes of lesional skin, but not of normal skin, sho w round and electron-dense mitochondrial inclusions that are present i n all layers of the epidermis. Similar inclusions are also present in the esophagus and forestomach of affected mice. There appears to be a direct relation between the presence of intramitochondrial inclusions and epidermal hyperplasia in the mouse. Furthermore, the presence of k eratinocyte-derived apoptotic bodies in the epidermis, esophagus, and forestomach was frequently observed in the lesions, which is consisten t with previous light microscopic observations of single cell death of keratinocytes. The granulocytes present in the skin, esophagus, and f orestomach were mainly eosinophils. There were widespread gaps observe d in the lamina densa in the epidermis that were mostly directly assoc iated with dermal or epidermal eosinophils. This type of gap is also o bserved in psoriasiform diseases in humans. This electron microscopic study demonstrated that this mouse model should be useful to screen po tential therapeutic strategies for psoriasiform and other inflammatory skin disorders.