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Amniotic membrane induces epithelialization in massive posttraumatic wounds
Author(s) -
Insausti Carmen L.,
Alcaraz Antonia,
GarcíaVizcaíno Eva M.,
Mrowiec Anna,
LópezMartínez María C.,
Blanquer Miguel,
Piñero Antonio,
Majado María J.,
Moraleda José M.,
Castellanos Gregorio,
Nicolás Francisco J.
Publication year - 2010
Publication title -
wound repair and regeneration
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.847
H-Index - 109
eISSN - 1524-475X
pISSN - 1067-1927
DOI - 10.1111/j.1524-475x.2010.00604.x
Subject(s) - hacat , wound healing , keratinocyte , keratinocyte growth factor , immunogenicity , medicine , foreskin , epidermis (zoology) , immunology , growth factor , immune system , biology , cell culture , anatomy , receptor , genetics
Large‐surface or deep wounds often become senescent in the inflammatory or proliferation stages and cannot progress to reepithelialization. This failure makes intervention necessary to provide the final sealing epithelial layer. The best current treatment is autologous skin graft, although there are other choices such as allogenic or autologous skin substitutes and synthetic dressings. Amniotic membrane (AM) is a tissue of interest as a biological dressing due to its biological properties and immunologic characteristics. It has low immunogenicity and beneficial reepithelialization effects, with antiinflammatory, antifibrotic, antimicrobial, and nontumorigenic properties. These properties are related to its capacity to synthesize and release cytokines and growth factors. We report the use of AM as a wound dressing in two patients with large and deep traumatic wounds. Negative pressure wound therapy followed by AM application was capable of restoring skin integrity avoiding the need for skin graft reconstruction. AM induced the formation of a well‐structured epidermis. To understand this effect, we designed some assays on human keratinocyte‐derived HaCaT cells. AM treatment of HaCaT induced ERK1/2 and SAP/JNK kinases phosphorylation and c‐jun expression, a gene critical for keratinocytes migration; however, it did not affect cell cycle distribution. These data suggest that AM substantially modifies the behavior of keratinocytes in chronic wounds, thereby allowing effective reepithelialization.