OBJECTIVE:To evaluate the effectiveness and safety of using the retrosigmoid sinus approach for BONEBRIDGE implantation in patients undergoing auricle reconstruction with tissue expansion flap. METHODS:44 patients who accepted BONEBRIDGE implantation through the retrosigmoid sinus approach were included. Audiological outcomes were measured before and after the BONEBRIDGE implantation. Long-term hearing and complications were also evaluated. RESULTS:After surgery, there was no significant change in bone conduction hearing thresholds compared to pre-surgery levels. Sound field thresholds after being aided with BONEBRIDGE showed a significant decrease of 27.2 dB HL. Speech recognition scores of monosyllabic words, disyllabic words, and short sentences in quiet environments significantly increased to 72 %, 84 %, and 98 %, respectively. During the 8-51 months follow-up, audiological results remained stable, and all patients were satisfied with the aesthetics of auricle reconstruction. CONCLUSION:Patients with bilateral microtia, undergoing auricle reconstruction with expanded postauricular flap, were chosen for the retrosigmoid sinus approach during BONEBRIDGE implantation and achieved safety, good hearing results as well as improved aesthetics.

BackgroundTreacher Collins syndrome (TCS, MIM #154500), a severe congenital disorder, predominantly involves dysplasia of craniofacial bones and is characterized by features such as downslanting palpebral fissures, lower eyelid colobomas, microtia, and other craniofacial anomalies. Despite its clinical importance, the underlying pathogenic mutations in TCS remain largely uncharacterized, representing a critical knowledge gap for researchers in the field.ResultsTo address this, we performed mutation screening on a familial TCS case (trio) and 11 sporadic cases from a Chinese population. We identified 11 mutations predominantly localized to the central repeat domain (CRD) and the C-terminal domain (CTD, including the nuclear localization sequence) of TCOF1. The de novo frameshift mutation identified in the trio led to TCOF1 truncation, disrupting the central repeat domain crucial for binding transcriptional factors. Immunoprecipitation assays revealed that this pathogenic mutation attenuates the interaction between TCOF1 and transcription-related proteins, such as Pol II. Furthermore, cellular luciferase assays demonstrated that the mutation compromises the nuclear localization capability of TCOF1.ConclusionsOur findings establish TCOF1 as the primary pathogenic gene in this Chinese TCS cohort, with mutations predominantly in the CRD and CTD, thereby expanding the known mutation spectrum of TCS and informing its prevention strategies.

Background: This study aims to summarize tear patterns of massive rotator cuff tears (MRCTs) and outline our surgical techniques for complete repair. Methods: From January 2018 to May 2023, 394 shoulders in 389 individuals with consecutive MRCT received arthroscopic MRCT repair. The tear pattern of each case was identified and generalized based on preoperative magnetic resonance imaging and interoperative arthroscopy. To evaluate prognosis of complete repair, outcome scores, comprising the University of California at Los Angeles (UCLA) score, the Constant-Murley Shoulder (CMS) score, the American Shoulder and Elbow Surgeons (ASES) score, the visual analog scale pain score, and the integrity and level of healing were obtained preoperatively and at 6 months, 12 months, and the last visit after surgery. Results: The tear patterns of 394 MRCT cases could be divided into 3 types depending on the number of longitudinal tears between cuffs. The complete repair rate was negatively correlated with age, duration of symptoms and number of longitudinal tears. To evaluate the outcomes of surgical techniques for complete repair, 51 patients (n = 17 men; n = 34 women) with a mean follow-up of 1.7 years (range: 1-4.8 years) and a mean age of 63 years old (range: 48-75 years old) were included. Clinical parameters of ASES, CMS, and UCLA were significantly enhanced at the last follow-up in contrast to those preoperatively (scores of ASES, CMS, and UCLA at the final follow-up were 79.02 ± 13.80, 79.53 ± 15.66, and 28.62 ± 4.21 vs. 36.58 ± 13.04, 51.18 ± 17.63 and 15.71 ± 4.14 preoperatively). Visual analog scale score decreased from 5.00 to 1.00 (P < .01). All 4 scores above reached minimum clinically important difference. Furthermore, postoperative magnetic resonance imaging scans revealed that there was no case of rotator cuff retear (Sugaya types IV and V) in type Ⅰ, 3.23% rotator cuff retear rate in type Ⅱ, and 22.22% rotator cuff retear rate in type Ⅲ. Conclusion: The new geometric classification according to the number of longitudinal tears offers guidance on the treatment of MRCT and prognosis after MRCT repair.

Pathogenic coding variants have been identified in thousands of genes, yet the mechanisms underlying the incomplete penetrance in individuals carrying these variants are poorly understood. In this study, in a cohort of 2009 craniofacial microsomia (CFM) patients of Chinese ancestry and 2625 Han Chinese controls, we identified multiple predicted pathogenic coding variants in SHROOM3 in both CFM patients and healthy individuals. We found that the penetrance of CFM correlates with specific haplotype combinations containing likely pathogenic-coding SHROOM3 variants and CFM-associated expression quantitative trait loci (eQTLs) of SHROOM3 expression. Further investigations implicate specific eQTL combinations, such as rs1001322 or rs344131, in combination with other significant CFM-associated eQTLs, which we term combined eQTL phenotype modifiers (CePMods). We additionally show that rs344131, located within a regulatory enhancer region of SHROOM3 , demonstrates allele-specific effects on enhancer activity and thus impacts expression levels of the associated SHROOM3 allele harboring any rare coding variant. Our findings also suggest that CePMods may serve as pathogenic determinants, even in the absence of rare deleterious coding variants in SHROOM3 . This highlights the critical role of allelic expression in determining the penetrance and severity of craniofacial abnormalities, including microtia and facial asymmetry. Additionally, using quantitative phenotyping, we demonstrate that both microtia and facial asymmetry are present in two separate Shroom3 mouse models, the severity of which is dependent on gene dosage. Our study establishes SHROOM3 as a likely pathogenic gene for CFM and demonstrates eQTLs as determinants of modified penetrance in the manifestation of the disease in individuals carrying likely pathogenic rare coding variants.

Pathogenic coding variants have been identified in thousands of genes, yet the mechanisms underlying the incomplete penetrance in individuals carrying these variants are poorly understood. In this study, in a cohort of 2009 craniofacial microsomia (CFM) patients of Chinese ancestry and 2625 Han Chinese controls, we identified multiple predicted pathogenic coding variants in SHROOM3 in both CFM patients and healthy individuals. We found that the penetrance of CFM correlates with specific haplotype combinations containing likely pathogenic-coding SHROOM3 variants and CFM-associated expression quantitative trait loci (eQTLs) of SHROOM3 expression. Further investigations implicate specific eQTL combinations, such as rs1001322 or rs344131, in combination with other significant CFM-associated eQTLs, which we term combined eQTL phenotype modifiers (CePMods). We additionally show that rs344131, located within a regulatory enhancer region of SHROOM3, demonstrates allele-specific effects on enhancer activity and thus impacts expression levels of the associated SHROOM3 allele harboring any rare coding variant. Our findings also suggest that CePMods may serve as pathogenic determinants, even in the absence of rare deleterious coding variants in SHROOM3. This highlights the critical role of allelic expression in determining the penetrance and severity of craniofacial abnormalities, including microtia and facial asymmetry. Additionally, using quantitative phenotyping, we demonstrate that both microtia and facial asymmetry are present in two separate Shroom3 mouse models, the severity of which is dependent on gene dosage. Our study establishes SHROOM3 as a likely pathogenic gene for CFM and demonstrates eQTLs as determinants of modified penetrance in the manifestation of the disease in individuals carrying likely pathogenic rare coding variants.

Enhancers, through the combinatorial action of transcription factors (TFs), dictate both the spatial specificity and the levels of gene expression, and their aberrations can result in diseases. While a HMX1 downstream enhancer is associated with ear malformations, the mechanisms underlying bilateral constricted ear (BCE) remain unclear. Here, we identify a copy number variation (CNV) containing three enhancers-collectively termed the positional identity hierarchical enhancer cluster (PI-HEC)-that drives BCE by coordinately regulating HMX1 expression. Each enhancer exhibits distinct activity-location-structure features, and the dominant enhancer with high mobility group (HMG)-box combined with Coordinator and homeodomain TF motifs modulating its activity and specificity, respectively. Mouse models demonstrate that neural crest-derived fibroblasts with aberrant Hmx1 expression in the basal pinna, along with ectopic distal pinna expression, disrupt outer ear development, affecting cartilage, muscle, and epidermis. Our findings elucidate mammalian ear morphogenesis and underscore the complexity of synergistic regulation among enhancers and between enhancers and transcription factors.

The primary aim of our study was to investigate the genetic correlations, colocalized genes, and causal relationships between craniofacial microsomia (CFM) and 33 diseases (including tumours and respiratory, heart, and kidney diseases). On the basis of extensive summary-level data from genome-wide association studies (GWASs), we evaluated the genetic linkage between CFM and a spectrum of 33 medical conditions using linkage disequilibrium score regression (LDSC). We employed PLACO to identify pleiotropic loci and genes associated with CFM and other diseases. These genes were subsequently subjected to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. Finally, the causal effect of CFM on the 33 diseases was assessed through Mendelian randomization (MR). We observed a genetic association between CFM and malignant lymphoma, thyroid cancer, and chronic obstructive pulmonary disease. The PLACO analysis identified 172 potential multi-effect loci (P < 5 × 10- 8). Furthermore, the MAGMA analysis of colocalized single nucleotide polymorphisms (SNPs) revealed that 1,760 SNPs shared genes (P < 0.05/18,345 = 2.726e-6). KEGG analysis revealed enrichment of these genes in the calcium signalling pathway. Finally, Mendelian randomization (MR) analysis suggested that CFM may reduce the risk of developing urolithiasis (IVW: OR = 0.989, 95% CI = 0.979-0.999, p = 0.034). Our study reveals for the first time the genetic associations of CFM with three diseases (malignant lymphoma, thyroid cancer and chronic obstructive pulmonary disease) in an Asian population. In addition, we found a common calcium signalling pathway between these three diseases and CFM. These results provide new insights into the pathogenesis and research potential of CFM.

BACKGROUND:Bilateral microtia can present with different bilateral classifications. Traditional surgical techniques require prolonged operative time and substantial amounts of costal cartilage. The surgical strategy used in this study was developed with the aim to provide a surgical technique to minimize surgery duration and costal cartilage harvest. METHODS:This retrospective study involved 84 patients in the experimental group (EG) who underwent the new surgery technique, and 65 patients in the control group (CG) who underwent traditional surgery from July 2022 to July 2024 in the Plastic Surgery Hospital. Postoperative follow-up included assessment using the Likert satisfaction scale, costal cartilage harvest number, surgery duration, and ear measurements. RESULTS:Patients were assessed during follow-ups ranging from 12 to 24 months postoperatively. The satisfaction rate of the EG was higher than that of CG (p<0.01). Costal cartilage harvest number and total anesthesia time of the EG were significantly less than that of CG (p<0.01). The ear measurements indicated that our surgical method achieved comparable symmetry in ear size to the traditional technique. CONCLUSIONS:The Nagata two-stage method of auricular reconstruction combined with helix cartilage scaffold ear correction effectively addresses the bilateral microtia of lobule and concha types. This approach conserves cartilage requirement, reduces surgical time, and achieves superior long-term outcomes compared to traditional methods. LEVEL OF EVIDENCE:Therapeutic, IV.

This study aimed to elucidate the genetic aspects of the relationship between sex hormones and cutaneous melanoma risk, providing valuable insights into this complex association. In this study, we used estradiol, bioavailable testosterone, sex hormone-binding globulin, and total testosterone as the exposure and melanoma as the outcome for two-sample Mendelian randomization analysis. In this study, a random-effects inverse-variance weighting (IVW) model was used as the main analysis model, and the corresponding weighted median, simple mode, weighted mode, and Mendelian randomization‒Egger methods were used as supplementary methods. We assessed both heterogeneity and horizontal pleiotropy in our study, scrutinizing whether the analysis results were affected by any individual single nucleotide polymorphism. The random-effects IVW method indicated that estradiol [odds ratio (OR), 1.000; 95% confidence interval (CI), 0.998–1.003; P = 0.658], bioavailable testosterone (OR = 1.001, 95% CI, 0.999–1.003; P = 0.294), sex hormone-binding globulin (IVW: OR, 1.000; 95% CI, 0.998–1.003; P = 0.658), and total testosterone (IVW: OR, 1.002; 95% CI, 0.999–1.005; P = 0.135) were not genetically linked to cutaneous melanoma. No analyses exhibited heterogeneity, horizontal pleiotropy, or deviations. We were unable to find genetic evidence for a causal relationship between sex hormones and the occurrence of cutaneous melanoma in this study. These results are limited by sample size and population, so the causal relationship between sex hormones and cutaneous melanoma needs to be further studied.

Background:Microtia with constricted ear features represents a challenging congenital deformity characterized by the variable shape and large volume of the remnant cartilage and skin involved. This study aimed to evaluate the efficacy and safety of a method using helix costal cartilage scaffold and postauricular flap advancement for the correction.Methods:This prospective study analyzed the clinical and postoperative data of 121 patients diagnosed with microtia and constricted ear features, treated at the authors' institution between January of 2020 and January of 2023. All patients underwent helix reconstruction using the eighth or ninth costal cartilage combined with postauricular flap advancement. Outcomes were assessed based on the incidence of postoperative complications and auricular aesthetic scores. The aesthetic evaluation of the reshaped auricle was based on a 4-point Likert scale (ie, 1 = poor, 2 = fair, 3 = good, and 4 = excellent).Results:The postoperative follow-up period ranged from 12 months to 3 years (mean, 18.5 months). All patients achieved successful helix expansion, with reconstructed ears showing improved symmetry and shape comparable to the contralateral normal ears. The average aesthetic score was 3.4 of 4. Complications included suture exposure in 8.3% of cases and cartilage protrusion in 4.1%, both managed without significant issues. There were no instances of skin necrosis, costal cartilage exposure, or infection.Conclusion:The combination of helix costal cartilage scaffold and postauricular advancing flap offers a reliable and effective method for correcting microtia with constricted ear features, providing satisfactory aesthetic outcomes with minimal complications.CLINICAL QUESTION/LEVEL OF EVIDENCE:Therapeutic, IV.

BACKGROUND:Microtia is a prevalent congenital malformation, the precise etiology and pathogenesis of which remain elusive. Mutations in the non-coding region of the HMX1 gene have been implicated in isolated cases of microtia, emerging as a significant focus of contemporary research. Several pathogenic copy number variations (CNVs) proximal to the HMX1 gene have been documented in wild animal populations, whereas only a single large segmental duplication in this region has been identified in humans. However, the absence of a gene-edited animal model has impeded the investigation of the unclear gene function associated with HMX1 mutations in human isolated microtia. In this study, we sought to precisely identify the pathogenic mutation by analyzing three pedigrees alongside population controls. Subsequently, our objective was to develop a CRISPR/Cas9 gene-edited mouse model to elucidate the functional implications of the identified mutation. METHODS:Genomic DNA was collected from 32 affected individuals across three pedigrees, as well as from 2000 control subjects. Comprehensive genomic analyses, including genome-wide linkage analysis, targeted capture, second-generation sequencing, and copy number analysis, were conducted to identify potential mutations associated with congenital auricle malformation. CRISPR/Cas9 gene-edited murine models were generated in response to the identified mutation. The auricular phenotypes of these gene-edited mice were systematically monitored. Small-animal Micro-CT scanning was employed to identify potential craniofacial or skeletal abnormalities. Furthermore, the expression of the HMX1 gene in the PA2 region of mouse embryos was quantified using RT-qPCR. RESULTS:A co-segregated 600 base pair duplication located on chromosome 4 (chr4:8701900-8702500, hg19) was identified in affected individuals across three pedigrees, but was absent in healthy controls. Two types of CRISPR/Cas9 gene-edited mice were subsequently generated. The knock-in (KI) mouse model was engineered by inserting one copy of the duplicated sequence directly adjacent to the mutated site, whereas the knockout (KO) mouse model was created by excising the mutation sequence. The phenotypes of different group of CRISPR/Cas9 gene-edited mice demonstrated distinct auricular deformities. Furthermore, an increase in the copy number of the mutated sequence was associated with elevated expression levels of HMX1 in the gene-edited mouse model. CONCLUSIONS:In this study, we further narrowed down and identified a 600 base pair copy number variation (CNV) located at chr4:8701900-8702500 (hg19), which is implicated in human bilateral, isolated microtia. Utilizing CRISPR/Cas9 technology, we developed novel mouse models harboring the identified mutation. These models serve as a robust platform for the comprehensive investigation of the underlying mechanisms of the disease.

Background The remnant ear is a very important material in auricular reconstruction surgery; its dimension, position, and shape determine how it is used. However, the local conditions of microtia patients are complex and variable. Situations may be encountered where a series of abnormal remnant ears cannot be utilized in clinical practice. Currently, there are no literature that elaborates on this type of microtia and provides systematic treatment methods. The purpose of this article is to systematically classify them and optimize the two-stage method auricular reconstruction, to provide an effective surgical method for these patients. Methods Based on the size, shape, and relative position of the residual ears, the unusable remnant ears were classified into three types: tiny size, abnormal shape, and relative position anomaly (over 1-cm higher than the contralateral earlobe). Fifty-three microtia patients with unusable remnant ear (54 ears) who underwent two-stage auricular reconstruction from August 2020 to August 2023 were reviewed. All patients had experienced earlobe reconstruction by using autologous rib cartilage during the first stage of surgery. Aesthetic assessments were evaluated from the naturalness of the earlobe reconstructed with autologous rib cartilage and the connection with the overall framework. The data on any complications that occurred during the follow-up period and patient satisfaction were collected. Results Among all patients, 31 had tiny size, 14 had abnormal shape, and 8 had excessively high positions. Patients were followed up for an average period of 9.2 months (6 to 12 months). No complex complications such as infection, skin necrosis, or cartilage exposure occurred. Fifty patients (94.3%) achieved excellent or good aesthetic outcomes. Fifty-one patients (96.2%) were satisfied with the reconstruction outcomes. Conclusions An accurate assessment of the residual ear preoperatively is essential. Reconstructing and splicing the earlobe with autologous rib cartilage in cases where the residual ear cannot be utilized compensate for the defect that the soft tissue cannot provide the earlobe flap. This is an effective surgical method for the ear reconstruction in such patients.

Objectives: Soft tissue expansion is one of the main methods for autologous cartilage auricular reconstruction. The aim of this study was to analyze the risk factors for cartilage exposure after this method and to describe a surgical method for this complication. Methods: From January 2018 to December 2020, 853 patients (908 sides) underwent auricular reconstruction with an expanded two-flap method at our center. Thirty-two patients experienced cartilage exposure postoperatively. These patients were set as the case group, and 1:1 matched sampling was performed among patients who did not have cartilage exposure. The matched sample of 32 cases was set as the control group. All 64 patients were evaluated according to the Orbit, Mandible, Ear, Nerve, and Soft tissue (OMENS) classification system to analyze the correlation between cartilage exposure and hemifacial microsomia (HFM) and OMENS subtypes. The complication was repaired with superficial temporal fascial flap combined with skin graft. Results: HFM might be a risk factor for scaffold cartilage exposure, and there was a significant correlation between cartilage exposure and orbital malformation, facial nerve dysplasia, and soft tissue developmental malformation. The use of a superficial temporal fascial flap combined with a split-thickness skin graft to repair the complication achieved satisfactory outcomes. Conclusions: There is a correlation between cartilage scaffold exposure and the severity of HFM. Temporoparietal fascial flap transfer combined with skin grafting proved to be an effective method for cartilage exposure.

Background: Congenital microtia usually lead to impairment of both appearance and hearing especially for patients with bilateral microtia. The simultaneous combination of auricular reconstruction and bone bridge implantation has been proved effective and satisfied with the patients. We retrospectively analyzed this method and the complication of it. We summarized and found the application of superficial temporal island flap for repairing the bone bridge exposure. Methods: From January 2017 to December 2020, there were 84 patients who underwent the surgery of auricular reconstruction simultaneously combined with bone bridge implantation in the Plastic Surgery Hospital of Chinese Academy of Medical Sciences. And after 12 months follow-up, we evaluated the postoperative effect and collected data on the patients who had bone bridge exposure. We analyzed the reason of the complication and covered the exposed bone bridge with superficial temporal island flap. Results: There were 3 cases (3.6%) of implant exposure and the surgical outcome was satisfactory using the repairment of superficial temporal island flap. All 3 patients were healed in 1-stage surgery, and no further implant exposure occurred after another 12-month follow-up. Conclusions: The method of auricular reconstruction simultaneously combined with bone bridge implant is an optional choice for patients with bilateral microtia, and has a low incidence of implant exposure. The superficial temporal island flap could well fill the dead space and increase the wear resistance of the tissue, and the scar was not obvious. We found and summarized a satisfactory method of repairing the implantation exposure using the superficial temporal island flap. Level of Evidence: Level IV, cases study.

Extensive skin graft necrosis after auricle reconstruction surgery is a thorny problem for plastic surgeons. Four unilateral microtia patients were enrolled for extensive skin graft necrosis after ear elevation surgery. Early debridement and daily dressing changes were important for preoperative preparation. Surgical treatments involved local flaps and secondary split-thickness skin graft. After 3 to 12 months of follow-up, clear surface structures and obvious auricular sulcus were shown in all 4 patients. No cartilage exposure, skin necrosis, healing impairment, or other complications were found. We attribute the cause of extensive skin graft necrosis to subcutaneous hematoma. Local skin flaps and split-thickness skin grafting can be effective treatments for such situations. The use of temporoparietal fascial flap is unnecessary when poor graft survival is caused by subcutaneous hematoma.

Enhancers, through the combinatorial action of transcription factors (TFs), dictate both the spatial specificity and the levels of gene expression, and their aberrations can result in diseases. The association between HMX1 and its downstream enhancer with ear deformities has been previously documented. However, the pathogenic variations and molecular mechanisms underlying the bilateral constricted ear (BCE) malformations remain unclear. This study identifies a copy number variation (CNV) encompassing three enhancers that induces BCE. These enhancers, collectively termed the positional identity hierarchical enhancer cluster (PI-HEC), co-regulate spatiotemporal expression of the HMX1 gene in a coordinated and synergistic mode, each displaying unique activity-location-structure characteristics. A thorough exploration of this regulatory locus reveals that specific motif clusters within the PI-HEC variably modulate its activity and specificity, with the high mobility group (HMG) box combined with Coordinator and homeodomain (HD)-TFs notably influencing them respectively. Our findings based on various types of mouse models, reveal that both aberrant Hmx1 expression in the fibroblasts of the basal pinna, originating from neural crest cells, and ectopic expression in the distal pinna structures contribute to the abnormal development of the outer ear, including the cartilage, muscle, and epidermis tissues. This study deepens our understanding of mammalian ear morphogenesis and sheds light on the complexity of gene expression regulation by enhancers and specific sequence motifs.### Competing Interest StatementThe authors have declared no competing interest.

ABSTRACT:Congenital microtia is the second most common congenital craniofacial deformity, and limb malformation is the most common birth defect. The combination of the 2 deformities is rare. In this study, the authors present 3 cases with a rare combination of congenital microtia and limb malformations and analyze the etiology and treatment of the malformations. There may be genetic homology between these two malformations, and they can be associated with abnormal ectodermal migration. LEVEL OF EVIDENCE:Level IV-case study.

Background: Question mark ear is a rare congenital deformity, mainly characterized the interruption of the natural continuity between the lower border of the helix and the earlobe. In severe cases, the earlobe may be absent. In addition, there may be protrusion and outward expansion of the upper part of the auricle, with partial or complete disappearance of the antihelix. This article aims to introduce a technique that combines autologous costal cartilage carving with auricular cartilage folding to achieve a stable and aesthetic auricle. Method: This study included 26 patients with sporadic question mark ear deformity who were treated at our clinical center from January 2020 to December 2022. Based on the different appearances of the lower part of the auricle, they were divided into 2 categories:11 cases showed a natural continuity interruption between the helix and the earlobe, while 15 cases showed the absence of the earlobe. All patients underwent corrective surgery using costal cartilage transplantation combined with the upper part of the auricular cartilage folding, performed by senior surgeons. Results: Question mark ear was effectively improved and with no significant rebound. The average follow-up period was 8.4 months (ranging from 6 to 12 months). A satisfaction survey showed that 23 patients (88%) were satisfied, 3 patients (12%) were partially satisfied, and no patients were dissatisfied. Most patients experienced temporary swelling after surgery, which resolved within 3 months to half a year. Conclusion: Autologous costal cartilage transplantation combined with folding of the auricular cartilage is an ideal surgical method to correct question mark ear.

Objective For microtia patients with excessively insufficient postauricular skin, it is difficult to obtain a satisfied outcome with existing strategies. In this study, we developed a modified tissue expander method for auricular reconstruction. Methods The modified tissue expander method divided into 4 stages. In the first stage, a 30 ml or 50 ml kidney-shaped tissue expander was implanted in the mastoid region. A short time expansion (average 33.5 days) was conducted subsequently. In the second stage, the expander was removed and a modified cartilage framework without tragus was inserted through the same incision. A crescent-shaped cartilage pad was inserted into the incision of cartilage-harvest site at the same time. In the third stage, the reconstructed ear was elevated. Lobule rotation and remanent modification were performed in the fourth stage. The patients were followed up between half a year and 10 years. The outcomes of the reconstructed ears were scored with evaluation criteria. Results From January 2010 to December 2019, a total of 45 microtia patients with excessively insufficient postauricular skin were performed the modified tissue expander method. Fourty-two patients showed satisfied outcomes. Complications such as hyperpigmentation in the skin graft area (3, 6.7%), scar hyperplasia (3, 6.7%) and folliculitis (1, 2.2%) were found. There were no complications related to the tissue expander. Conclusion The modified tissue expander method is an effective and safe technique for auricular reconstruction in patients having excessively insufficient postauricular skin, with satisfying medium-term results.