• Jia Tan and Jin-feng Fu.
• Burn Institute of Yunnan Province, Department of Burns, the Second Affiliated Hospital of Kunming Medical University, Kunming 650000, China.
• Zhonghua Shao Shang Za Zhi. 2013 Dec 1;29(6):509-15.

ObjectiveTo explore the effects of pressure therapy on proliferation and apoptosis of cells in hypertrophic scar (HS) of burn patients.MethodsTwenty patients who were hospitalized from September 2010 to September 2012 and started to wear pressure garment tailored by rehabilitation therapists over 20 hours a day beginning from two weeks after healing of burn wounds with the depth from deep partial-thickness to full-thickness (early stage of formation of HS) were set as pressure treatment group (PT). Another group of patients who were hospitalized in the same period with HS formed 3, 6, 12, 24 months (with 5 patients at each time point) after deep partial-thickness to full-thickness burns without receiving any treatment were set as control group. HS tissue samples from limbs and face were excised at post treatment month (PTM) 3, 6, 12, 24 in group PT (with 5 patients at each time point), and 2 to 3 days after admission in control group. Five patients out of the above-mentioned 40 patients were selected according to the random number table, and normal skin tissue samples from abdomen and thigh were also obtained to serve as normal control. The expressions of proliferating cell nuclear antigen (PCNA) in HS and normal skin tissue were determined with immunohistochemical staining. The apoptosis status was detected with situ end labeling technique. The mRNA expressions of P57(kip2) and Cyclin E were determined with real-time fluorescence quantification PCR. Data were processed with t test, one-way analysis of variance, or LSD test.Results(1) In normal skin tissue, PCNA-positive cells were observed in the epidermal basal layer and prickle cell layer. In group PT and control group, PCNA-positive cells were observed in the epidermal basal layer, prickle cell layer, lower part of the granular cell layer, and dermis of HS. The percentages of PCNA-positive cells in HS in group PT were respectively (40.4 ± 2.9)%, (28.2 ± 6.2)%, (9.9 ± 0.7)% at PTM 3, 6, 12, which were significantly lower than those of HS formed 3, 6, 12 months after wound healing in control group [(48.3 ± 4.7)%, (36.2 ± 3.2)%, (11.4 ± 0.9)%, with t values respectively 3.186, 2.559, 2.880, P values all below 0.05]. (2) In normal skin tissue, apoptotic cells were observed in the epidermal basal layer. In group PT and control group, apoptotic cells were observed in each layer of epidermis of HS. The apoptotic indexes of HS in group PT were respectively (20.4 ± 1.2)%, (26.1 ± 0.4)%, (26.6 ± 1.0)% at PTM 6, 12, 24, which were significantly higher than those of HS formed 6, 12, 24 months after wound healing in control group [(16.2 ± 1.5)%, (23.1 ± 2.0)%, (24.8 ± 1.1)%, with t values respectively -4.904, -3.366, -2.606, P < 0.05 or P < 0.01]. (3) The mRNA expressions of P57(kip2) of HS in group PT were respectively 3.87 ± 0.20, 8.60 ± 0.78, 10.00 ± 0.57 at PTM 3, 6, 12, which were significantly higher than those of HS formed 3, 6, 12 months after wound healing in control group (3.34 ± 0.15, 6.36 ± 0.29, 9.34 ± 0.12, with t values respectively -4.880, -6.014, -2.375, P < 0.05 or P < 0.01). The mRNA expression of P57(kip2) in normal skin tissue was close to those of HS in group PT at PTM 12, 24 and those of HS formed 12, 24 months after wound healing in control group (with P values all above 0.05). (4) The mRNA expressions of Cyclin E of HS in group PT were respectively 19.30 ± 0.18, 12.77 ± 0.30, 9.21 ± 0.18 at PTM 3, 6, 12, which were significantly higher than those of HS formed 3, 6, 12 months after wound healing in control group (19.79 ± 0.34, 15.41 ± 0.26, 9.47 ± 0.17, with t values respectively 3.186, 2.559, 2.880, P < 0.05 or P < 0.01). The mRNA expression of Cyclin E in normal skin tissue was close to those of HS in group PT at PTM 12, 24 and those of HS formed 12, 24 months after wound healing in control group (with P values all above 0.05).ConclusionsPressure therapy can accelerate the evolution process of HS through accelerating apoptosis and inhibition of cell proliferation, thereby scar proliferation is inhibited.

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