The effect of barrier recovery using topical steroid and systemic steroid after acetone-application in hairless mice

Background: Acetone disrupts the cutaneous permeability barrier through the removal of stratum corneum lipids. This pertubation of barrier integrity stimulates a variety of homeostatic repair that ultimately results in the normalization of barrier function. Object: To measure the effect of steroid on the barrier recovery of acetone applied skin. Material and Methods: The flank skin of 8-10 week old hairless mice was treated with acetone and then topical and systemic steroids were applied. Transepidermal water loss(TEWL) was checked after 0, 3, 6, 12 and 24 hours. Electron and light microscopic examination and ion capture cytochemistry were performed after 3, 6, 12 and 24 hours after systemic and topical steroids had been applied. Results: The results were as follows; 1) During 3-6 hours after experiment, the recovery rate of TEWL was most prominent in the group of acetone applied animal than other groups. 2) After 12 hours after acetone applied, formation of new stratum corneum was found in the groups of acetone applied or acetone applied skin with topical steroid application. But loss of stratum corneum was observed in the groups of high or low dose steroid injection. 3) Ruthenium tetroxide staining of acetone alone or topical steroid treated specimens after 12 hours experiment revealed that the lipid bilayer was partly impaired and fragmented. Intercellular spaces were widening and the lipid bilayer disappeared or was damaged in the groups of high or low dose steroid injection. 4) Six hours after acetone application, pattern of calcium distribution had been partially reestabilished in the group of acetone alone or topical steroid treated animals. But calcium content was still sparse and decreased from the stratum granulosum to basale in the groups of high or low dose steroid injection. Conclusion: In summary the present study demonstrates that steroid treatment acutely delays recovery rate of TEWL, inhibits normalization of calcium gradient or epidermal lipid synthesis that leads to abnormalities in permeability barrier homeostasis.