**5. Clinical evolution**

CTSCAs have initial engraftment, similar to an autologous skin graft, subsequently evolving to rejection. The rejection is clinically manifested as a gradual color change and formation of a necrotic scar in a 21-day average interval, when removed, exposing a vital tissue adhered to the receptor (**Figures 1**–**3**). The latter is histologically evidenced in the CTSCA as necrotis foci with mainly neutrophils and the receptor bedding exposing an interface rich in fibroblasts and neoformation vessels.

CTSCA acts as a scaffold and biological inductor, which becomes colonized by cells from the receptor, creating a neodermis. This model has been verified in xenograft models, where CTSCAs promote angiogenesis and collagen type 1 production without causing a significant fibrotic response.

Secondary to an immunologic phenomenon, the cellular elements of the skin allografts are rejected; however, the dermal components can persist and incorporate into the healing dermis of the receptor. The biologic mechanisms underlying this integration are not fully understood [56, 57].
