In Vivo Reflectance Confocal Microscopy Assessment of Wound Induction and Repair of a Skin Injury Produced by Liquid Nitrogen: An Atlas

The cascade of events following an injury that significantly alters epidermal structures and leads to epidermal necrosis depends on the type of injury. We have studied epidermal necrosis caused by solar-simulated radiation, laser therapy, and liquid nitrogen (N2) with reflectance laser scanning confocal microscopy in vivo. In the present study we investigated injuries produced with liquid nitrogen (N2), or cryotherapy, a common therapeutic modality for solar lentigines, warts, and others. A 3 mm diameter skin site on the forearm of 7 healthy human volunteers was treated with liquid nitrogen for approximately 20 s, following written informed consent. The site was monitored by confocal microscopy and digital imaging until the epidermis appeared clinically fully repaired (>4 weeks). During the first 3 days following exposure to liquid nitrogen (N2), the epidermal cellular organization appears slightly perturbed and the epidermal cellular architecture becomes lost. The pigment distribution in the keratinocytes that line the papillae maintains its appearance and does not spread as the cell boundaries become imperceptible. The dead epidermis remains intact for approximately 2 weeks and protects the new restructuring epidermis under it. The wound repairs from the periphery. Approximately 2 weeks after injury, the new epidermis is infiltrated by large dendritic cells localized in the area where papillae form. The papillae appear to grow and produce the typical invaginations and surrounding structures of the dermal-epidermal junction, and the enclosed capillaries are fully engorged with flowing erythrocytes. These dendritic cells begin to disappear as the epidermis returns to normal appearance and pigment. The dendritic cells appear to play a role in tissue restructuring post-injury, as they are also present for a limited time following UV injury starting at 14 days as in the present case.