Technology and product reviews References


39. Supp DM, Boyce ST. Overexpression of vascular


endothelial growth factor accelerates early vascularization and improves healing of genetically modifi ed


cultured skin substitutes. J Burn Care Rehabil 2002; 23: 10–20.


40. Uitto J, Pulkkinen L. Molecular


genetics of heritable blistering disorders. Arch Dermatol 2001; 137: 1458–61.


41. Dellambra E, Vailly J, Pellegrini G et al. Corrective transduction of human epidermal stem cells in laminin-5- dependent junctional epidermolysis bullosa. Hum Gene Ther 1998; 9: 1359–70.


42. Vailly J, Gagnouz-Palacios L, Dell’Ambra E, et al. Corrective gene


transfer of keratinoyctes from patients with junctional epidermolysis bullosa restores assembly of


hemidesmosomes in reconstructed epithelia. Gene Ther 1998; 5: 1322–32.


certain products have been developed for this purpose, the epidermal component is not always successful due to inadequate in-growth of new blood vessels through the underlying dermis to supply the epidermis. Dermal substitutes thicker than 1mm revascularise poorly[25]


, resulting


in inadequate nutrition to the overlying epidermis and consequent epidermal necrosis. Therefore, most dermal substitutes require a two-step approach to help dermal vascularisation and avoid epidermal necrosis — one operation to initially place the dermal substitute and a second to place an STSG as an autograft over this dermis. Research is currently underway to overcome this limitation[26]


.


Irregular pigmentation In intact skin, pigmentation results from the proper distribution and function of melanocytes[27,28]


. In cultures of epidermal


keratinocytes, melanocytes can sometimes unintentionally persist resulting in hyperpigmentation after grafting[29,30]


. By the


Transmission of diseases Although donors’ medical histories are thoroughly evaluated and their blood screened for hepatitis, HIV and syphilis before any tissue is obtained for use in TESSs, products from human sources cannot be terminally sterilised owing to the presence of viable human cells.


same phenomenon, a lack of melanocytes can result in hypopigmentation. Although preclinical studies have shown that uniform pigmentation can be achieved[31]


, irregular


pigmentation after usage of a tissue- engineered product with or without skin graft remains a clinical concern.


Graft contraction and lack of elasticity Most skin substitutes contain only two cell types (fi broblasts and keratinocytes). Thus they lack the connective tissues (extracellular matrix and collagen) that are required for elasticity and pliability of the skin. In addition, the transplanted autograft can ‘contract’, resulting in functional and aesthetic compromise[32]


.


Figure 2 Flow chart demonstrating examples of how products are obtained. AUTOGRAFT Take skin biopsy Isolate cells


Keratinocytes Fibroblasts


Epicel® MySkinTM ReCell®


Culture cells


Cultured skin substitute® Bioseed®-S CellSpray® StrataGraft®


ALLOGRAFT Take skin biopsy Isolate cells


Keratinocytes Fibroblasts


Laserskin® Culture cells


LyphodermTM VivodermTM ICX-SKN


ACELLULAR ALLOGRA


Antigens neutralise


Cells removed, but matrix/ structure left intact


AlloDerm® OASIS® XENOGRAFT (Porcine and Bovine) and BIOSYNTHETIC


PermacolTM Matriderm® EZ-DermTM Biobrane® Integra®


Dermagraft®


33


Wounds International Vol 2 | Issue 1 | ©Wounds International 2011


Patient


Live donor


Cadaver


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