Tragus Perichondrium-Cartilage Island and Temporalis Muscle Fascia for Repairing Tympanic Membrane Perforation Under the Otoendoscope: A Randomized Controlled Trial.

OBJECTIVE: To compare the clinical effects of repairing tympanic membrane perforation (TMP) with the tragus perichondrium-cartilage island and temporalis muscle fascia (TMF) under the otoendoscope. METHODS: The clinical data of 84 patients (total 84 ears) with TMP repaired by otoendoscopy from March 2019 to April 2021 were analyzed. The patients were randomly divided into the control group (n = 42, TMF repair) and the experimental group (n = 42, perichondrium-cartilage island repair). The intraoperative blood loss, operation time, length of hospital stay, success rate of the TMP repair, mean air-conducted sound, and air-bone gap before and after surgery were compared between the two groups. RESULTS: The mean air-bone gap and mean air-conducted hearing threshold in the experimental group were significantly lower after surgery at all frequencies than those of the control group (all P < .05). The reduction of the mean air-conducted hearing threshold in the experimental group was significantly higher than that of the control group (P < .001). The surgery time of the experimental group was significantly shorter than the control group (78.04 ± 2.23 vs. 84.27 ± 1.67 minutes, P < .001). The success rate of the TMP repair was 95.24% (40/42) in the experimental group and 92.86% (39/42) in the control group, indicating that there was no significant difference in the success rate of TMP repair between the two materials (risk ratio = 1.75; 95% confidence interval: .31-12.04; P = .71). CONCLUSION: Repairs with the tragus perichondrium-cartilage island have a short operation time, high healing rate, and more significant postoperative hearing improvement, which makes it a more effective method of TMP repair.

Proteomic analysis of chondromodulin-I-induced differentiation of mesenchymal stem cells into chondrocytes.

To identify novel proteins that might help clarify the molecular mechanisms underlying chondromodulin-I (ChM-I) induction of mesenchymal stem cells (MSCs) differentiate into chondrocytes. MSCs are triggered to differentiate into chondrocytes, which are recognized as important factors in cartilage tissue engineering. ChM-I is a glycoprotein that stimulates the growth of chondrocytes and inhibits angiogenesis in vitro. In this study, the proteomic approach was used to evaluate protein changes between undifferentiated MSCs and ChM-I-transfected MSCs. The expression of the protein spots was analyzed using two-dimensional gel electrophoresis. Then, 14 protein spots were identified between MSCs and ChM-I-transfected MSCs. 309 proteins were identified using mass spectrometry (MS). The differentially regulated proteins were categorized and annotated using Protein Analysis Through Evolutionary Relationships (PANTHER) analysis with the aid of the Database for Annotation, Visualization and Integrated Discovery (DAVID) tool. These proteins are included in a variety of metabolic pathways and signal transduction pathways, such as focal adhesion, glycolysis, actin cytoskeleton regulation, and ribosome. These results demonstrate novel information about the molecular mechanism by which ChM-I induce MSCs to differentiate into chondrocytes. These results also provide a solid foundation for the development of tissue-engineered cartilage.

Chondrogenic differentiation of ChM-I gene transfected rat bone marrow-derived mesenchymal stem cells on 3-dimensional poly (L-lactic acid) scaffold for cartilage engineering.

We have explored the role of Chondromodulin-I (ChM-I) in chondrogenesis of bone marrow-derived mesenchymal stem cells (BMSCs) in 3-dimensional (3D) scaffold for cartilage tissue engineering. BMSCs of Sprague Dawley (SD) rats were cultured on poly-(L-lactic acid) [PLLA] scaffolds with different pore sizes (80-200 µm, 200-450 µm) with or without surface modification by chitosan. Cell viability, proliferation, and morphology were measured using confocal microscope and the CCK-8 method. Untransfected BMSCs, BMSCs expressing pcDNA3.1(+), BMSCs expressing plasmid pcDNA3.1 (+)/ChM-I were cultured on 3D scaffolds in standard growth medium or transforming growth factor-ß1 (TGF-ß1) supplemented chondrogenic induction medium in vitro for 3 weeks and the expression of collagen type II was determined. Cell-scaffolds constructs were implanted subcutaneously for 3 months in vivo. BMSCs had a higher viability and proliferation in PLLA scaffolds of pore size 200-450 µm than that of 80-200 µm, and surface modification with chitosan did not enhance cell attachment. The ChM-I gene enhanced chondrogenesis and increased collagen type II synthesis. Immunohistochemistry from in vivo study showed enhanced cartilage regeneration in BMSCs expressing pcDNA3.1 (+)/ChM-I on 3D PLLA scaffolds. It also demonstrated that TGF-ß1 might promote chondrogenesis of rat BMSCs by synergizing with the ChM-I gene. ChM-I could be beneficial to future applications in cartilage repair.