| First Author | Gijbels MJ | Year | 1995 |
| Journal | Ultrastruct Pathol | Volume | 19 |
| Issue | 2 | Pages | 107-11 |
| PubMed ID | 7792947 | Mgi Jnum | J:27806 |
| Mgi Id | MGI:75289 | Doi | 10.3109/01913129509014610 |
| Citation | Gijbels MJ, et al. (1995) Ultrastructure of epidermis of mice with chronic proliferative dermatitis. Ultrastruct Pathol 19(2):107-11 |
| abstractText | C57BL/Ka mice with chronic proliferative dermatitis (cpdm/cpdm) develop chronic persistent skin lesions characterized by epidermal hyperplasia, infiltration by granulocytes and macrophages, and vascular dilatation. Similar lesions are present in other orthokeratotic epithelia in affected mice, in particular the esophagus and forestomach. Here, we report on further characterization of epidermal hyperplasia and the granulocytes. Keratinocytes of lesional skin, but not of normal skin, show round and electron-dense mitochondrial inclusions that are present in 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 keratinocyte-derived apoptotic bodies in the epidermis, esophagus, and forestomach was frequently observed in the lesions, which is consistent with previous light microscopic observations of single cell death of keratinocytes. The granulocytes present in the skin, esophagus, and forestomach were mainly eosinophils. There were widespread gaps observed in the lamina densa in the epidermis that were mostly directly associated with dermal or epidermal eosinophils. This type of gap is also observed in psoriasiform diseases in humans. This electron microscopic study demonstrated that this mouse model should be useful to screen potential therapeutic strategies for psoriasiform and other inflammatory skin disorders. |
