In situ pedicle lengthening and perforator shifting technique for overcoming the perforator variation of the anterolateral thigh free flap during head and neck reconstruction.

BACKGROUND: Anterolateral thigh (ALT) free flap is one of the most popular options for surgeons when reconstructing head and neck defects. When the recipient vessels are located in a remote site, a flap with adequate pedicle length is essential. The conventional methods of either pedicle elongation or fabricating combined flap increase the total surgical time. We present the experience on the use of what in situ pedicle lengthening and perforator shifting technique to overcome these problems. METHODS: Fifteen patients with an age range of 38-65 years underwent in situ vascular transposition microsurgery of the ALT free flap harvest during head and neck reconstruction. Fourteen patients were male and one was female. Indications for reconstruction were malignant neoplasm in 14 patients and osteoradionecrosis in one patient. In this series, the descending branch of the lateral circumflex femoral vessels was used for interposition grafts. If the pedicle length was insufficient, the interposition grafts were used to lengthen the pedicle. The interposition grafts could also bridge different perforasomes in the thigh region in complex head and neck reconstruction. RESULTS: Of the 15 patients, 11 received the in situ pedicle lengthening technique, while four patients received in situ fabricated combined techniques. After surgery, all of the patients were followed up for at least 3 months. Two partial wounds involving poor healing occurred but finally healed after debridement. There were two major complications: one case involved venous thrombosis of the anastomosis and the other suffered from hematoma. Both cases were salvaged. All of the 15 free ALT flaps were successful. CONCLUSIONS: The alternative method employed in this series was able to solve the ALT flap perforator variation. Although the enrolled cases were confined to only head and neck reconstruction in the series, the in situ technique of the ALT flaps could be administered during reconstruction in other regions.

Recipient vessel selection for multiple free flap transfers in head and neck reconstruction at different periods.

BACKGROUND: Treatment decisions can be challenging in patients undergoing multiple oropharyngeal microsurgical reconstructions at different periods by various causes. We, retrospectively, reviewed patients with at least three consecutive free flap reconstructions to determine the optimal strategy for selecting recipient vessels. METHODS: Then, 36 patients (33 men and 3 women) who underwent at least 3 microsurgical reconstructions with a total of 51 free flap transfers for head and neck defects were included in this report. The most common reason for multiple microsurgical reconstructions was recurrent disease. For reconstructions, recipient vessel candidates on the same side of the head and neck were prioritized; if ipsilateral vessels were unavailable, contralateral recipient vessels, which might necessitate vein grafts, were used. RESULTS: The most common reconstructions were anterolateral thigh flaps (19 cases). The most commonly used contralateral recipient vessels were the superior thyroid artery, facial artery, and external jugular vein. All vessel anastomoses were performed using the end-to-end method. Postoperative complications occurred at the sites of 26 free flap reconstructions. The overall flap reconstruction success rate in patients with at least three surgeries was 90.2%. The median follow-up duration was 25.8 months. During follow-up, 26 patients survived until the end of follow-up. CONCLUSIONS: In patients undergoing multiple free flap reconstructions, recipient vessels on the ipsilateral side that have not been subjected to radiation should be selected first. Recipient vessels contralateral to the reconstruction side can then be selected; however, they may require vein grafts. Finally, distant healthy recipient vessels can be selected through vein grafting.

Nitric oxide: Is it the culprit for the continued expansion of keloids?

Keloids are characterized by excessive proliferation of fibroblasts and invasion of surrounding healthy skin. High levels of Nitric Oxide (NO) are thought to be the crucial factor within the micro-environment in promoting keloid formation. However, the effects and mechanisms of NO on the proliferation of Keloid Fibroblasts (KDFs) remain unclear. In this study, we investigated the effect of NO on KDFs proliferation by Sodium Nitroprusside (SNP), an NO donor. Our results show that SNP significantly enhanced KDFs proliferation. Moreover, with prolonged treatment with SNP after cell confluence, the growth of KDFs escape contact inhibition and experience significant pile up growth. Furthermore, PTIO, an NO scavenger, attenuated SNP-enhanced cell proliferation effectively. The mechanism involved in SNP-induced KDFs proliferation was soluble Guanylyl Cyclase (sGC) and cGMP independent. ODQ, a specific sGC inhibitor, failed to suppress SNP-enhanced KDFs proliferation. 8-Bromo-c GMP, a cell-permeable cGMP analogue, could not stimulate KDFs proliferation. Erk and Akt provide important signaling for cell growth. U0126 and LY294002, inhibitors of Erk and Akt respectively, block SNP-enhanced KDFs proliferation effectively. As expected, a Western blot showed that SNP up-regulated the phosphorylation levels of Erk and Akt. Moreover, it decreased the expression of p27, a cell cycle inhibitor. Our results reveal that SNP induced KDFs proliferation and loss contact inhibition led to pile up growth via activation of the Erk and Akt pathways, as well as a decreased expression of p27. Thus, we speculate that the pathological feature of continuous expansion in keloids is caused by NO-induced KDFs sustained growth.

Gallic acid attenuates TGF-ß1-stimulated collagen gel contraction via suppression of RhoA/Rho-kinase pathway in hypertrophic scar fibroblasts.

AIMS: To examine the effect and molecular mechanism of gallic acid (GA) on transforming growth factor-ß1 (TGF-ß1)-stimulated hypertrophic scar fibroblast (HSF) contraction. MATERIALS AND METHODS: A fibroblast-populated collagen lattice (FPCL) was developed to examine the effect of GA on TGF-ß1-enhanced HSF contraction. The changes in crucial factors related to cell contraction including α-smooth muscle actin (α-SMA), F-actin, and the phosphorylation level of myosin light chain (MLC) were evaluated using western blot and immunostaining. The activation and expression of RhoA/ROCK after the TGF-ß1 challenge and GA insult were evaluated using RhoA-G-LISA and RhoA-ELISA kit while the phosphorylation level of MYPT1 and the expression of ROCK1 and ROCK2 were examined by western blot, respectively. KEY FINDINGS: GA significantly suppressed TGF-ß1-stimulated HSF contraction in a dose- and time-dependent manner. Moreover, the TGF-ß1-enhanced α-SMA expression, F-actin formation, and MLC phosphorylation were obviously attenuated by GA. TGF-ß1 significantly stimulated RhoA activation but did not alter the expression of RhoA in the HSFs. However, both the activation and expression of RhoA decreased obviously with GA pretreatment followed by TGF-ß1 stimulation. Furthermore, GA inhibited ROCK activity but did not affect its expression after TGF-ß1 stimulation. SIGNIFICANCE: These results suggest that GA exhibited the potential to prevent HSF contraction after TGF-ß1 stimulation by down regulating the RhoA/ROCK signal cascade, followed by the inhibition of the expression of α-SMA, F-actin formation, and phosphorylation of MLC.