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Hypertrophic scars resulting from severe burns are usually treated by continuous elastic compression. Although pressure therapy reaches success rates of 60-85% its mechanisms of action are still poorly understood. In this study, apoptosis induction and release of interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) were evaluated in normal (n = 3) and hypertrophic (=7) scars from burns after in vitro mechanical compression. In the absence of compression (basal condition) apoptotic cells, scored using terminal deoxyribonucleotidyl transferase assay, were present after 24 hours in the derma of both normal scar (23 +/- 0.4% of total cell) and hypertrophic scar (11.3 +/- 1.4%). Mechanical compression (constant pressure of 35 mmHg for 24 hours) increased apoptotic cell percentage both in normal scar (29.5 +/- 0.4%) and hypertrophic scar (29 +/- 1.7%). IL-1beta released in the medium was undetectable in normal scar under basal conditions while in hypertrophic scar the IL-1beta concentration was 3.48 +/- 0.2 ng/g. Compression in hypertrophic scar-induced secretion of IL-1beta twofold higher compared to basal condition. (7.72 +/- 0.2 ng/g). TNF-alpha basal concentration measured in normal scar medium was 8.52 +/- 4.01 ng/g and compression did not altered TNF-alpha release (12.86 +/- 7.84 ng/g). TNF-alpha basal release was significantly higher in hypertrophic scar (14.74 +/- 1.42 ng/g) compared to normal scar samples and TNF-alpha secretion was diminished (3.52 +/- 0.97 ng/g) after compression. In conclusion, in our in vitro model, mechanical compression resembling the clinical use of elastocompression was able to strongly increase apoptosis in the hypertrophic scar derma as observed during granulation tissue regression in normal wound healing. Moreover, the observed modulation of IL-1beta and TNF-alpha release by mechanical loading could play a key role in hypertrophy regression induced by elastocompression.

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Epilysin, designated matrix metalloproteinase (MMP)-28, is the newest member of this family of proteases expressed by keratinocytes in response to an injury. MMP-28's physiological role and specific substrates are unknown, but its expression pattern suggests that it may serve a role in both tissue homeostasis and wound healing. The aim of this preliminary study was to observe the presence of MMP-28 protein in normotrophic and hypertrophic scars and to evaluate the effect of in vitro mechanical compression on its expression. Biopsies from normotrophic and hypertrophic scars resulting from burns were divided into two samples, one to be used as control (uncompressed) and the other to be compressed in an oxygenated organ chamber for 24 hours in the presence of a serum-free medium, using an electromechanical load transducer (stable pressure = 35 mmHg). Analysis of MMP-28 protein secretion, assessed by Western blot and beta-casein zymography in scar conditioned media, revealed that normotrophic scar did not release MMP-28 in any condition while hypertrophic scar released active MMP-28 both in control conditions and after compression. MMP-28 immunohistochemistry revealed a light protein presence in normotrophic scar keratinocytes and a strong MMP-28 positivity in hypertrophic scar keratinocytes in control conditions, while compression increased MMP-28 staining in normotrophic scar and induced a significant reduction of the protein presence in hypertrophic scar keratinocytes. As it has been suggested that MMP-28 may restructure the skin basal membrane (Saarialho-Kere et al., 2002), our data indicate that mechanical compression directly acts to modulate the remodeling phase of wound healing, altering release and activity of MMP-28 in hypertrophic scars.