RESUMEN
Lipomas occurring in the hard palate are extremely rare, and treating lipomas in this area presents challenges due to the thinness of soft tissue and the risk of postoperative bony surface exposure. We present a case of hard palate lipoma that was successfully removed using the partial thickness flap dissection technique. In addition, we reviewed the clinicopathological features of 20 reported cases of hard palate lipomas worldwide and retrospectively analyzed the clinical characteristics and pathological types of 68 oral lipomas in China. The use of a partial thickness flap demonstrates potential effectiveness in excising benign masses located in the hard palate. Regarding 68 patients with oral lipomas, the most commonly affected sites were the buccal region, tongue, and floor of the mouth. Histologically, simple lipomas and fibrolipomas were the predominant types observed.
RESUMEN
Objective: The objective of this study was to investigate the impact of transforming growth factor ß1 (TGF-ß1) on epithelial development using an ex vivo model of submandibular gland (SMG) epithelial-mesenchymal separation. Materials and methods: The ex vivo model was established by separating E13 mouse SMG epithelia and mesenchyme, culturing them independently for 24 h, recombining them, and observing branching morphogenesis. Microarray analysis was performed to evaluate the transcriptome of epithelia treated with and without 1 ng/ml TGF-ß1. Differential gene expression, pathway enrichment, and protein-protein interaction networks were analyzed. Quantitative real-time polymerase chain reaction, Western blot, and immunofluorescence were employed to validate the mRNA and protein levels. Results: Recombined SMGs using separated epithelia and mesenchyme that were cultured for 24 h showed a significant inhibition of epithelial development compared to SMGs recombined immediately after separation. The level of TGF-ß1 decreased in the SMG epithelia after epithelia-mesenchyme separation. Epithelia that were separated from mesenchyme for 24 h and pretreated with 1 ng/ml TGF-ß1 continued to develop after recombination with mesenchyme, while epithelia without 1 ng/ml TGF-ß1 treatment did not. Microarray analysis suggested pathway enrichment related to epithelial development and an upregulation of Sox2 in the 1 ng/ml TGF-ß1-treated epithelia. Further experiments validated the phosphorylation of SMAD2 and SMAD3, upregulation of SOX2 and genes associated with epithelial development, including Prol1, Dcpp1, Bhlha15, Smgc, and Bpifa2. Additionally, 1 ng/ml TGF-ß1 inhibited epithelial apoptosis by improving the BCL2/BAX ratio and reducing cleaved caspase 3. Conclusions: The addition of 1 ng/ml TGF-ß1 maintained the developmental potential of embryonic SMG epithelia separated from mesenchyme for 24 h. This suggests that 1 ng/ml TGF-ß1 may partially compensate for the role of mesenchyme during the separation phase, although its compensation is limited in extent.
RESUMEN
Background/purpose: Fibrosis is present in various physiologic and pathologic conditions of salivary glands (SGs). This study aimed to identify novel biomarkers of SG fibrosis by next-generation sequencing. Materials and methods: We established the SG fibrosis mouse model by excretory main duct ligation. Next-generation sequencing, differentially expressed gene (DEG) analysis, and gene set enrichment analysis was performed by comparing ligated and control SGs. We used algorithms of Cytohubba, molecular complex detection, Lasso logistic regression, and support vector machine to identify the key biomarkers. Selected key biomarkers were verified by the polymerase chain reaction and immunohistochemistry. We also retrieved and analyzed the key gene expression in the fibrosis of the heart, liver, lung, and kidney to ensure the generalization of key biomarkers in SG fibrosis. Results: Both interlobular and intralobular fibrosis was confirmed in the ligated SGs, with improved expressions of collagen I and transforming growth factor ß. Next-generation sequencing identified 2666 upregulated DEGs and 336 downregulated DEGs, which were highly enriched in the extracellular matrix-related pathways. Multiple algorithms identified 15 key biomarkers in SG fibrosis, including Thrombospondin-1 (THBS1) and Prolyl 4-Hydroxylase Subunit Alpha 3 (P4HA3). The mRNA and protein expression of THBS1 and P4HA3 was verified in mice. THBS1 was also highly expressed in lung and kidney fibrosis, whereas P4HA3 was upregulated in liver fibrosis. Conclusion: THBS1 and P4HA3 may be potential biomarkers for SG fibrosis. They may be also applicable in the diagnosis of multi-organ fibrosis.
