Background: Non-invasive assessment methods such as measurement of the transepidermal water loss (TEWL) allow a continuous follow-up of cutaneous processes with impairment of the epidermal barrier function. Objective: The aim of the trial was to establish an in vivo model for the assessment of drug effects on epidermal regeneration. Methods: Twenty healthy volunteers were included in this double-blind randomized trial. After setting four suction blisters on the volar aspect of the forearm, the epidermis was removed to create a standardized subepidermal wound. Thereafter the wounds were treated topically for 6 h daily during 14 days. The following treatments were to be compared: a clo-betasol 17-propionate preparation under occlusion, a corticoid-free cream under occlusion, no treatment and occlusion (aluminium chamber), no treatment and no occlusion. Daily measurement of TEWL above the wounds was performed. Results: The 0.05% clobetasol 17-propionate preparation caused a dramatic delay in TEWL decrease, whereby the untreated unoccluded field showed a continuous decrease over the observed period of 14 days. Occlusion and corticoid-free treatment led to a weak but significant delay of TEWL decrease when compared to the untreated unoccluded test field. Conclusion: This model seems to describe re-epithelialization in a reliable manner and can be used for in vivo assessment of drug effects on migrating and proliferating epithelial cells.

In this study, we investigated the effect of calcipotriol, prednicarbate and clobetasol 17-propionate on skin thickness over a treatment period of 6 weeks. The study was conducted as a controlled, randomized, double-blind comparison. The influence of these drugs on normal skin under occlusive conditions was assessed visually and by measuring skin thickness using 20 MHz B mode ultrasound. Both topically applied glucocorticosteroids lead to a significant decrease in skin thickness. In contrast to the glucocorticosteroid-induced atrophy, calcipotriol application on normal skin leads to an increase in skin thickness in all volunteers. The effect remains constant for the duration of treatment. The cause of this increase seems to be an irritative reaction of the skin which was histologically investigated in one volunteer. The histological features of this reaction are characteristic for a subacute dermatitis. The implications of these findings for the therapeutic mechanism of calcipotriol are discussed.

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