In vitro mechanical compression induces apoptosis and regulates cytokines release in hypertrophic scars.

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-1b (IL-1b) and tumor necrosis factor-a (TNF-a) were evaluated in normal (n ¼ 3) and hypertrophic (¼7) 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-1b released in the medium was undetectable in normal scar under basal conditions while in hypertrophic scar the IL-1b concentration was 3.48 ± 0.2 ng/g. Compression in hypertrophic scar-induced secretion of IL-1b twofold higher compared to basal condition. (7.72 ± 0.2 ng/g). TNF-a basal concentration measured in normal scar medium was 8.52 ± 4.01 ng/g and compression did not altered TNF-a release (12.86 ± 7.84 ng/g). TNF-a basal release was significantly higher in hypertrophic scar (14.74 ± 1.42 ng/g) compared to normal scar samples and TNF-a 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-1b and TNF-a release by mechanical loading could play a key role in hypertrophy regression induced by elastocompression. (WOUND REP REG 2003;11:331–336) Hypertrophic scars (HSs) are the result of alterations in the normal processes of cutaneous wound healing occurring as a consequence of injury of the skin, especially burns. HSs are characterized by excessive deposition of fibroblast-derived extracellular matrix (ECM) proteins, especially collagen, in the derma over long periods of time, 1 by