Background: In East Asia, intraoral facial skeletal contour surgeries (intraoral FSCSs), including reduction gonioplasty, reduction malarplasty, and genioplasty, have become increasingly popular. Nonetheless, intraoral FSCSs are technically difficult and have a steep learning curve. An effective simulator could be beneficial for intraoral FSCS training. However, there is no intraoral FSCS simulator available. We introduced an intraoral FSCS simulator and assessed its effectiveness. Methods: An intraoral FSCS simulator was established by covering a 3-dimensional printed skull with elastic cloth. Twenty residents were enrolled and randomly divided into experimental group A and control group B. Group A performed the intraoral FSCS on the simulator for 3 times. Group B performed the intraoral FSCS on skull model for 3 times. The intraoral FSCS simulator and trainees' performance were evaluated by a trainee-reported questionnaire before and after training, the surgical outcomes were graded by 3 senior attending physicians. All questions and the surgical outcome were scored based on a 5-point Likert scale (1 = very poor, 5 = very good). The surgical times were recorded. Results: The intraoral FSCS simulator (4.13 ± 0.64) simulated the surgical reality significantly better than the skull (2.6 ± 0.63). In intraoral FSCS simulator training, the restriction and compliance of the facial soft tissue were vividly mimicked (4.4 ± 0.51); the intraoral approach was vividly mimicked (4.07 ± 0.59). The intraoral FSCS simulator is significantly superior to the skull in improving participants' confidence in performing intraoral FSCS, power system control, and intraoral approach adoption (<0.001). The average surgical outcome score was 3.11 ± 0.45 in group A and 3.91 ± 0.24 in group B. The average surgical time was 177.78 ± 28.38 minutes in group A and 65.26 ± 15.38 minutes in group B. Conclusions: We developed the first intraoral FSCS simulator and proved its effectiveness preliminarily. Randomized controlled study with clinical cases is needed to further test its effectiveness.

Orbital hypertelorism correction is still a less precise procedure, with a simple preoperative design and surgical results often depending on the operator’s experience. In recent years, computer-assisted technology has been fully utilized in craniofacial surgery. This article aims to explore the clinical results of computer-assisted technology in orbital hypertelorism correction and discuss its advantages and effects on treatment. Four patients with orbital hypertelorism underwent intracranial and extracranial combined box osteotomy correction. Preoperative computed tomography scans were performed, and 3-dimensional 3D digital technology was used to measure the orbital spacing, virtually design the 3D cutting scheme, and guide the intraoperative 3D cutting to improve the accuracy of periorbital osteotomy and reduce the surgical risk. Four patients underwent successful surgery, and the average distance of the medial orbital wall was decreased from 43.6 to 23.4 mm. Computer-assisted box osteotomy shortens the operative time and provides better corrective results.

Reduction malarplasty is a popular facial skeletal contour surgery in East Asia. Zygomatic nonunion is a reported complication. However, it is often misunderstood and misdiagnosed. Here we present typical misdiagnosed zygomatic nonunion cases, propose and preliminarily clarify 4 major misunderstandings of zygomatic nonunion: diagnostic standard, the cause, the incidence, and the prognosis of zygomatic nonunion.

Keloids are characterized by excessive fibrosis driven by interactions between fibroblasts and macrophages. Carboxylesterase 1 (CES1) is associated with fibrosis, but its role in keloid pathogenesis remains unclear. The present study aimed to explore the role of CES1 in keloid fibrosis and its regulation of macrophage‑fibroblast interactions. Differential expression analysis was performed on keloid datasets (GSE92566, GSE121618 and GSE158766). KEL FIB cells and M0 macrophages or M2 macrophages were co‑cultured. Cellular interactions were evaluated using the Cell Counting Kit‑8 assay to assess proliferation, while flow cytometry was used to assess apoptosis. Additionally, fibrosis‑related markers (collagen III, collagen I, TGF‑β, vimentin, α‑smooth muscle actin and fibronectin), M2 macrophage polarization markers (CD206 and CD163) and components of the JAK/STAT signaling pathway were assessed using western blotting, immunofluorescence and reverse transcription‑quantitative PCR. Bioinformatics analysis showed that CES1 expression was downregulated in keloid tissues compared with normal skin tissues. Co‑culture with M0 macrophages enhanced KEL FIB cell proliferation and reduced apoptosis while upregulating fibrotic markers. Conversely, KEL FIB cells induced M2‑like polarization of M0 macrophages, as characterized by the increased expression of CD163 and CD206. CES1 overexpression in KEL FIB cells was associated with reduced phosphorylated STAT5 levels, suggesting a potential modulatory effect on the JAK/STAT signaling pathway, accompanied by decreased expression of fibrotic markers in KEL FIB cells and M2 polarization markers in co‑cultured M0 macrophages. CES1 knockdown resulted in the opposite effects, which was mitigated by the STAT5 inhibitor AC‑4‑130. However, CES1 overexpression did not notably alter fibrotic markers in KEL FIB cells co‑cultured with M2 macrophages. The results of the present study suggested a key role for CES1 in modulating keloid fibrosis, possibly by modulating M2 polarization through the JAK/STAT signaling pathway in vitro. Targeting CES1 and macrophage‑fibroblast interactions may provide a novel research direction and a promising therapeutic strategy for keloid treatment.