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Objective:To establish silicone cartilage models of donor-sites for the microtia patients by using digital technology, and to explore the application of surgical simulation in auricular reconstruction.Methods:From June 2018 to October 2019, 19 congenital microtia patients underwent thoracic CT scans and following three-dimensional costal cartilage imaging with Mimics software at the Nanfang Hospital, Southern Medical University. Among these patients, 16 were males and 3 were females. The mean age of patients was 16 years (range 8 to 35 years). Silicon cartilage models were produced by 3D printing and used for surgical planning and preoperative simulation in ear framework fabrication. Cartilaginous framework was sculptured according to the simulation during operation. Patients were followed up for a minimum of six months to evaluate the size, outline, height and auriculocephalic angle of the reconstructed ear. The satisfactory outcomes of the patients were scored according to a 5-point Likert scale.Results:All the patients received the surgical simulation and sculpture training with silicone cartilage models before operation. Auricular reconstruction was completed successfully according to the simulation. The duration of sculpture was shortened to 1-1.5 hours. There were no serious complications, such as hematoma, inflammation, skin necrosis and framework exposure. The contour of reconstructed ear was natural and clear over a 6 months follow-up, and all the patients were satisfied with their surgical outcomes.Conclusions:With the application of digital technology and silicone cartilage models by 3D printing to the surgical planning and training in microtia patients, patient-specific framework is fabricated with precisely assembling, which not only shortens the operation time, but also provides the unexperienced surgeons with a safe and effective training of ear framework fabrication.
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<p><b>OBJECTIVE</b>To assess the outcome of large facial defect reconstruction with "partition" pre-expanded cervico-scapulo-dorsal flaps (CSDF) based on the superficial cervical artery (SCA).</p><p><b>METHODS</b>Surgical course consisted of 3 stages. In stage I, a skin flap was designed along the axis of SCA according to the facial defect and an expander was implanted in the cervico-scapulo-dorsal region by means of "partition" expansion. The expanders were implanted beside the flap axis and beneath the posterior half of flaps so as to expand only half area of the flap. During the stage II, expanders were injected with saline regularly for continuous expansion. In stage III, the pre-expanded CSDFs were transferred to cover the facial defect of which the CSDFs included about half of non-expanded area.</p><p><b>RESULTS</b>From November of 2008 to December of 2013, 15 patients with facial hypertrophic scar or scar contracture were reconstructed with pre-expanded CSDF based on the SCA. The expansion lasted for 3 to 4 months, and the expanded volume varied from 680 to 960 ml. One case of 4.0 cm x 1.5 cm epidermal flap necrosis occurred and healed subsequently with superficial scar; and another case of blister formation in the distal part of flap was found, which recovered without scar; the other 13 flaps survived without complications. After a follow-up for 12 to 38 months( average 26. 2 months), patients regained satisfactory appearance of face, with no obvious hypertrophic scar in the donor site.</p><p><b>CONCLUSIONS</b>Partition preexpanded CSDF based on the SCA is a good choice for large facial defect reconstruction, and the partition expansion is an effective strategy for prevention of venous congestion.</p>
Subject(s)
Humans , Arteries , Back , Cicatrix, Hypertrophic , General Surgery , Face , General Surgery , Hyperemia , Surgical Flaps , Transplantation , Tissue ExpansionABSTRACT
Objective To investigate the correlation of HIF-1α and hypoxia in keloids fibroblasts, and to investigate the mechanism that hypoxia promotes abnormal scarring by HIF-1α pathway. Methods Keloid fibroblasts cultured in vitro were placed in an incubator with different O2 concentrations. After 24 h, the keloid fibroblasts were collected for further study. Western blotting was performed to detect the expression of HIF-1α in the keloid fibroblasts. Results Relative amounts of HIF-1α in keloid fibroblasts cultured under O2 concentrations at 20 %, 10 %, 5 % and 1 % were 0. 007 ±0. 006, 0. 133 ±0. 006, 0. 537±0. 015 and 0. 903±0. 021, respectively. It indicated that hypoxia could increase the expression of HIF-lα in keloid fibroblasts. Conclusions Hypoxia can induce the expression of HIF-1α in fibroblasts of keloids. Moreover, there still is a positive relation between hypoxia and the expression of HIF-1α. Therefore, a close relationship exists between abnormal scarring and HIF-1α pathway by hypoxia.
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<p><b>OBJECTIVE</b>To investigate the correlation between the expression of key proto-oncogenes playing major roles in tumorigenic process and abnormal sarring.</p><p><b>METHODS</b>Immunohistochemical technique was performed to detect the expressions of c-myc, c-fos and ras p21 proteins on hypertrophic scars, keloids and normal skin. Image analysis was used to compare their quantitative difference of expression.</p><p><b>RESULTS</b>C-myc and c-fos expressions on the nucleus of fibroblasts of hypertrophic and keloid scars were significantly higher than normal skin controls, and there was no difference between the two lesions. Ras p21 expression was not detected on the fibroblasts of hypertrophic and keloid scars.</p><p><b>CONCLUSION</b>1. c-myc and c-fos oncogenes are activated on hypertrophic and keloid scars, which may contribute to proliferation and differentiation of fibroblasts, synthesis and degradation of collagen and regulation of cytokines and induce abnormal scarring, the mechanisms of their effects remain to be further studied. 2. Ras gene may not mutate or its mutations may not play a major role in the process of abnormal scarring. 3. Only part of proto-oncogenes moderately expressed on abnormal scars. The expression of multiple oncogenes does not coexist in abnormal scars may be the cause of their less chances to induce malignant transformation.</p>