Epithelial wound closure
After injury wound healing closes the tissue defect and re-establishes the skin barrier. With an intact barrier microorganisms cannot enter, at the same time fluid loss from the body is prevented. The actual barrier is located in the outermost layer of the skin, the epidermis.
In many patients wound healing is delayed. A number of systemic diseases interferes with normal wound healing mechanisms. The longer a wound persists the harder it becomes to achieve wound closure subsequently. These wounds become chronic and show a phenotype of chronic low-level inflammation preventing the next steps in the healing cascade: granulation tissue formation and epithelial wound closure.
There are several therapeutic options. It is consensus that all chronic wounds need to become activated and form a healthy, productive granulation tissue.
This can be achieved by a surgical debridement or specialized protease-modulating wound dressings such as HydroClean.[2,3] But once the granulation tissue is established clinicians expect that epithelial wound closure follows suit.
Most clinicians agree that they have little control or therapeutic options how to speed epithelial wound healing apart from surgical techniques like flap procedures or split thickness skin grafting. However,few patients have access to the surgical procedures. From the research perspective clinical trials with some growth factors showed promise, but these were never developed into prescription drugs. Consequently, clinicians have virtually no therapies at hand to speed epithelial wound closure and shorten healing time.
This can be achieved with a special polymer chemistry in wound dressings. In a series of in vitro tests hydrated polyurethanes, the name of these materials, can concentrate growth factors and increase the response of e.g. epithelial cells (keratinocytes) to close defects faster. This was confirmed in pre-clinical studies resulting in significant faster epithelial cell migration measured at the wound borders.
A radically new concept was developed. Can we boost growth factor activities in the wound bed so that epithelial cells migrate faster to close the wound? In practical terms, this concept would increase the concentration and activity of growth factors the patient is already producing. Epithelial cells would react to the increased concentration with faster healing, getting a boost to close the wound.
This new therapeutic concept gives clinicians for the first time the option to influence and speed wound healing without the need of surgery or recombinant growth factors with all their inherent limitations. For patients it is easy and comfortable, the technology has been optimized to fit into dressings.
 EWMA position document. Wound bed preparation in practice [Internet]. 2004. Available from: http://ewma.org/fileadmin/user_upload/EWMA/pdf/Position_Documents/2004/pos_doc_English_final_04.pdf
 Eming S, Smola H, Hartmann B, Malchau G, Wegner R, Krieg T, et al. The inhibition of matrix metalloproteinase activity in chronic wounds by a polyacrylate superabsorber. Biomaterials. 2008 Jul;29(19):2932–40.
 Humbert P, Faivre B, Véran Y, Debure C, Truchetet F, Bécherel P-A, et al. Protease-modulating polyacrylate-based hydrogel stimulates wound bed preparation in venous leg ulcers--a randomized controlled trial. J Eur Acad Dermatol Venereol JEADV. 2014 Dec;28(12):1742–50.
 Smola H. Stimulation of epithelial migration – novel material based approaches. Oral presentation presented at: EWMA Meeting; 2015; London.