Actinic keratoses and the epidermis on which they arise.
The appearance of the epidermis and epidermal autoradiographic labelling indices were compared in actinic keratoses and paralesional skin in seventeen patients after injection of tritiated thymidine. The skin on the buttock area was also studied as a "non-sun exposed" control. Labelling indices obtained from skin removed after 1 hwere as follows: actinic keratoses 17-4%; paralesional skin 11-2%; buttock skin 5-4%. Many of the epidermal cells in the keratoses that incorporated tritiated thymidine were bizarre and not restricted to the basal or suprabasal regions but were scattered through the thickness of the epidermis. Paralesional skin also showed epidermal thickening and cytological abnormalities including the formation of multinucleate epidermal cells. These findings suggest that the development of actinic keratoses takes place in epidermis that is itself abnormal. The changes suggest that there is a gradual stepwise progression of sun damage epidermis via the clinically obvious keratosis to squamous cell epithelioma.
D001345:Autoradiography; D002454:Cell Differentiation; D004247:DNA / Q000096:biosynthesis; D006801:Humans; D007642:Keratosis / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D012867:Skin / Q000166:cytology / Q000378:metabolism / Q000473:pathology*; D013471:Sunburn / Q000473:pathology
D004247:DNA