Actinic keratosis: do we have clinicopathological criteria to select lesions for therapy?

Actinic keratoses (AKs) are defined clinically as erythematous and scaly plaques occurring on chronically sun-damaged skin as a result to exposure to ultraviolet radiation. They are typically located on the face, the scalp, the neck, and the extremities. It is said that ‘their potential for malignant transformation is well documented’ (1), because of several mechanisms of ultraviolet-induced damage on DNA (mutations through pirimidine dimer formation), cell membranes (proinflammatory prostaglandin synthesis from damaged phospholipids), and immune suppression (cytokine dysregulation). The relative risk of progression of AKs to SCC increases with the increasing number of AKs (1-5 facial AKs = 1.7; 6-20 facial AKs = 4.2; >20 facial AKs = 11) (2); these data, however must be balanced with the potential of AKs to spontaneously regress (rates of regression of single lesions estimated between 15% and 63% after 1 year) (3).