Abstract
Pressure ulcers are areas of soft tissue breakdown that result from sustained mechanical loading of the skin and underlying tissues. Today, little is known with respect to the aetiology of these ulcers. This study introduces an in vitro model system to study the effects of clinically relevant loading regimes on damage progression in the epidermis, the uppermost skin layer. Engineered epidermal equivalents (EpiDerm) were subjected to 6.7 and 13.3 kPa for either 2 or 20 h using a custom-built loading device. Tissue damage was assessed by (1) histological examination, (2) tissue viability evaluation, and (3) by the release of a pro-inflammatory mediator, interleukin-1alpha (IL-1alpha). Loading the EpiDerm samples for 2 h increased the IL-1alpha release, although no visible tissue damage was observed. However, in the 20 h loading experiments visible tissue damage and a small decrease in tissue viability were observed. Furthermore, in these experiments the IL-1alpha release increased with magnitude of loading. It is concluded that this in vitro model system can be applied to improve insight in the epidermal damage process due to prolonged mechanical loading and can serve as a sound basis for effective clinical identification and prevention of pressure ulcers.
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