Suppressed inflammatory gene expression during human hypertrophic scar compared to normotrophic scar formation.

Hypertrophic scar formation is a result of adverse cutaneous wound healing. The pathogenesis of hypertrophic scar formation is still poorly understood. A problem next to the lack of suitable animal models is that often normal skin is compared to hypertrophic scar (HTscar) and not to normotrophic scar (NTscar) tissue.

Time course of the angiogenic response during normotrophic and hypertrophic scar formation in humans.

Previous research suggests that in hypertrophic scars (HSs), an excess of microvessels is present compared with normotrophic scars (NSs). The aim of our study was to quantify vascular densities in HSs and normotrophic scars and to provide an insight into the kinetics of changes in the expression of angiogenic factors in time during wound healing and HS formation. Human presternal wound healing after cardiothoracic surgery through a sternotomy incision was investigated in a standardized manner.

Perioperative conditions affect long-term hypertrophic scar formation.

Corticosteroids are widely used as treatment for excessive scarring by intralesional injection with variable success rates. It is conceivable that systemically administered corticosteroids affect a wider range of inflammatory processes that influence wound healing and may be more successful in preventing hypertrophic scar formation. To study this presumption, we have used a standardized model of presternal scars caused by cardiothoracic surgery through a median sternotomy incision.