Therapeutic, III.

Introduction The number of perforators required for safe perfusion remains under debate. This study aimed to determine whether a single‐ or multiple‐perforator‐based anterolateral thigh flap yields better flap outcomes in head and neck reconstruction. Patients and Methods Between August 2012 and July 2016, 180 men and 4 women with a mean age of 52.8 ± 9.8 years underwent head and neck anterolateral thigh flap reconstruction for oncologic defect in 181 cases, plate exposure in two cases, and trismus release in one case. The flap was patched for inner or external lining, folded for through–through defect, or tubed for cervical esophageal reconstruction. Of 184 flaps, 136 (73.9%) were based on multiple perforators (range, 2–5 perforators), whereas 48 (26.1%) were based on a single perforator. The demographics, operative findings, and flap outcomes were compared. Results The prevalence of systemic diseases between groups was comparable. The mean flap size in the single‐perforator group was smaller (92.8 ± 36.8 vs. 140.5 ± 99.9 cm2, P < .0001). Twenty‐one flaps (11.4%) required emergency take‐back and 13 (61.9%) were successfully salvaged. Eight flaps failed, yielding a 95.7% flap survival rate. The single‐perforator group had a significantly higher rate of emergency take‐back for vascular compromise (8/48 (16.7%) vs. 8/136 (5.9%), P = .035), a decreased salvage success rate (2/8 (25.0%) vs. 11/13 (84.6%), P = .018), and a corresponding lower flap survival rate (42/48 (87.5%) vs. 134/136 (98.5%), P = .004). Conclusion Whenever possible, we recommend including multiple cutaneous perforators in anterolateral thigh flaps to yield better flap outcomes in head and neck reconstruction.

Keloids are a fibrotic skin disorder caused by abnormal wound healing and featuring the activation and expansion of fibroblasts beyond the original wound margin. Signal transducer and activator of transcription 3 (STAT3) has been found to mediate the biological functions of keloid fibroblasts (KFs). Therefore, we aimed to demonstrate whether ASC-J9, an inhibitor of STAT3 phosphorylation, can suppress the activation of KFs. Western blotting results showed that ASC-J9 inhibited the levels of COL1A1 and FN1 proteins, which were upregulated in KFs, by decreasing the expression of pSTAT3 and STAT3. RNA sequencing and in vitro studies further demonstrated that ASC-J9 treatment of KFs reduced cell division, inflammation, and ROS generation, as well as extracellular matrix (ECM) synthesis. ELISA assays verified that ASC-J9 treatment significantly mitigated IL-6 protein secretion in KFs. Transmission electron microscopy images revealed that ASC-J9 induced the formation of multilamellar bodies in KFs, which is associated with autophagy-related signaling. These results suggested that inhibiting a vicious cycle of the ROS/STAT3/IL-6 axis by ASC-J9 may represent a potential therapeutic approach to suppress cell proliferation and ECM production in KFs.