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Objective:To design a new V-shaped forearm flap and to investigate the possibility of direct donor site closure and its value in the reconstruction of soft tissue defect after resection of buccal carcinoma.Methods:The new V-shaped forearm flap technique was applied in 10 patients with buccal carcinoma from October, 2018 to September, 2019. There were 6 males and 4 females aged from 35 to 63 years (48.3 years in average). Flap size ranged from 3.0 cm×5.0 cm to 4.0 cm×6.0 cm. Wound healing and the appearance forearm were recorded and evaluated three months after the surgery. Radial deviation angle, wrist flexion, ulnar deviation and dorsal extension were measured and calculated 3 months after the surgery. The wrist function was evaluated according to the Gartland-Werley scale. The recovery of wrist function was evaluated by comparing with the preoperative data.Results:Forearm donor sites were successfully closed without skin grafting in all 10 patients. Skin ischemia caused by excessive tension was observed at the incision edge in 3 patients, therefore leading to skin exfoliation and pigment loss without affecting wound healing. All patients were presented a cosmetic outcome during the follow-up period. No scar hyperplasia was observed. No significant difference was observed in perioperative wrist flexion angle, dorsal extension angle, radial deviation angle, ulnar deviation angle ( P>0.05)[data before surgery were (57.8±1.3) °, (58.4±0.7) °, (18.2±0.5) °, (28.5±1.1) ° respectively, and data 3 months after surgery were (53.2±2.1) °, (55.3±1.8) °, (16.4±0.4) °, (25.4±1.4) ° respectively]; Excellent and good rate of Gartland-Werley wrist score before and after surgery were both 100%. Conclusion:The new V-shaped free forearm flap can directly close small to medium forearm flap donor site. This method could avoid the trauma and complications of traditional free skin graft. The postoperative appearance on donor site is satisfactory and will not have adverse effects on wrist function. The new V-shaped free forearm flap is a novel method for repair of the defect of soft tissue defect after buccal cancer and it is worth to be applied in clinical practice.
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<p><b>OBJECTIVE</b>To mimic oral squamous cell carcinoma (OSCC) cell hypoxia by using chemical agent CoCl2 and to investigate its biological behaviour.</p><p><b>METHODS</b>Oral squamous cell carcinoma cell lines HSC-3 and SCC-4 were exposed to different concentration of CoCl2. HSC-3 and SCC-4 cells were treated with 50, 100, 150, 200 µmol/L CoCl2. Expression of hypoxia inducible factor-1α (HIF-1α), vascular endothelial growth factor (VEGF) and B-cell lymphoma-2 (BCL-2) were measured by real time polymerase chain reaction (PCR) and Western blotting in both mRNA and protein level. Cell proliferation, cell apoptosis and cell cycle were detected to analyze its biological behaviour. Both wound healing and Transwell assay were applied to test the ability of cell igration.</p><p><b>RESULTS</b>The result showed that after treatment of 150 µmol/L CoCl2 for 24 h, mRNA level of HIF-1α, VEGF and Bcl-2 was increased by 6.00 ± 0.20, 5.40 ± 0.40, 5.40 ± 0.30 (SCC-4); 5.60 ± 0.30, 5.20 ± 0.60, 5.80 ± 0.40(HSC-3). OSCC cells treated with 150 µmol/L CoCl2 for 24 h were collected. Compared with control group, the growth rate of cells was significantly decreased, P value was less than 0.05 (when HSC-3, SCC-4 cultured for 2 and 3 days). The apoptosis of OSCC cells was increased when treated with 150 µmol/L CoCl2 for 24 h:HSC-3 2.25% (control group) and 5.82% (treatment group); SCC-4 2.58% (control group) and 10.27% (treatment group). The migration ablility of OSCC cells was decreased when using 150 µmol/L CoCl2 for 24 h. The migration area ratio was (31.5 ± 2.3) % (HSC-3), (29.1 ± 1.5) % (SCC-4) in control group and (18.3 ± 1.9) % (HSC-3), (13.2 ± 0.8)% (SCC-4) in treatment group (P < 0.05).</p><p><b>CONCLUSIONS</b>The hypoxic cell model of OSCC could be induced by CoCl2. The expression level of hypoxic markers was up regulated significantly and the cells biological behaviour changed including decreased cell proliferation, increased apoptosis and decreased migration.</p>