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Purpose: This study proposes the Lamella Ostium Extent Mucosa (LOEM) system as a compact and user-friendly classification for endoscopic sinus surgery (ESS), based on surgical bone extension and mucosal management, aiming to resolve inconsistencies in describing surgical techniques and extension levels, and to enhance comparability of outcomes in chronic rhinosinusitis (CRS)., Methods: LOEM uses a lettering system representing a specific topographical level: L identifies the lamellae, O the ostia, E the opening of the sinus walls, and M the mucosal approach. Eleven CRS surgical cases were independently evaluated by seven rhinologists following a Delphi method in two consecutive rounds. Consensus was assessed using Cohen's kappa., Results: A substantial agreement was found among the experts (κ = 0.77) in the first round, although the M item only showed fair agreement (κ = 0.37). Clarifications for this item were given in the second round, after which, the overall agreement increased to κ = 0.81 and to κ = 0.79 for the M item. A decrease in agreement from substantial to moderate for O and E items in the second round was found. Test-retest analysis showed an almost perfect agreement (92.96%, κ = 0.82). In this study, a web-based app is provided to assist with the regular use of the LOEM system., Conclusions: The LOEM system provides a compact, comprehensive code for ESS, integrating anatomical and functional aspects to represent surgical techniques described so far. This system may be suitable for facilitating communication between surgeons and collecting robust labeled data, hopefully leading to further standardization and validation of surgical approaches in future CRS studies., Competing Interests: Declarations. Conflict of interest: The authors report no conflict of interest., (© 2024. The Author(s).)

Introduction: The aim of this study is to assess the impact of lymph node ratio (LNR) and number of positive lymph nodes (NPLN) on mortality and recurrence rates in patients with laryngeal squamous cell carcinoma., Materials and Methods: We conducted a retrospective multicenter international study involving 24 Otorhinolaryngology-Head and Neck Surgery divisions. Disease-specific survival (DSS) and disease-free survival (DFS) were evaluated as the main outcomes. The curves for DSS and DFS according to NPLN and LNR were analyzed to identify significant variations and establish specific cut-off values., Results: 2507 patients met the inclusion criteria. DSS and DFS were significantly different in the groups of patients stratified according to LNR and NPLN. The 5-year DSS and DFS based on LNR and NPLN demonstrated an improved ability to stratify patients when compared to pN staging., Conclusion: Our data demonstrate the potential prognostic value of NPLN and LNR in laryngeal squamous cell carcinoma., (© 2023 Wiley Periodicals LLC.)

Background: Fibroblasts and others mesenchymal cells have recently been identified as critical cells triggering tissue-specific inflammatory responses. Persistent activation of fibroblasts inflammatory program has been suggested as an underlying cause of chronic inflammation in a wide range of tissues and pathologies. Nevertheless, the role of fibroblasts in the emergence of chronic inflammation in the upper airway has not been previously addressed. We aimed to elucidate whether fibroblasts could have a role in the inflammatory response in chronic rhinosinusitis with nasal polyps (CRSwNP)., Methodology: We performed whole-transcriptome microarray in fibroblast cultured from CRSwNP samples and confirmed our results by qRT-PCR. We selected patients without other associated diseases in upper airway. To investigate shifts in transcriptional profile we used fibroblasts from nasal polyps and uncinate mucosae from patient with CRSwNP, and fibroblasts from uncinate mucosae from healthy subjects as controls., Results: This study exposes activation of a pro-inflammatory and pro-fibrotic transcriptional program in nasal polyps and CRSwNP fibroblasts when compared to controls. Our Gene-set Enrichment Analysis (GSEA) pointed to common up-regulation of several pro-inflammatory pathways in patients-derived fibroblasts, along with higher mRNA expression levels of cytokines, growth factors and extracellular matrix components., Conclusions: Our work reveals a potential new source of inflammatory signaling in CRSwNP. Furthermore, our results suggest that deregulated inflammatory signaling in tissue-resident fibroblasts could support a Type-2 inflammatory response. Further investigations will be necessary to demonstrate the functionality of these novel results.

<b>Introduction:</b> Stapedotomy is currently the surgical technique of choice for treating otosclerosis. Despite this, there is no agreement about the best technique to perform a small fenestra footplate, therefore multiple procedures have been proposed. The aim of this study was to investigate the hearing outcomes of microdrill and manual perforator. <br><b>Material and Methods:</b> An observational prospective study was carried out on patients who underwent stapedotomy. We analyzed the hearing threshold in two groups of patients according to the way the fenestra footplate was realized by microdrill or manual perforator. <br><b>Results:</b> A total of 113 patients were evaluated. Postoperative hearing gain of the microdrill group was 23.29 (18.58) dB HL 95% CI (18.40-28.18), while in the manual perforator group, it was 22.67 (12.91) dB HL 95% CI (19.07-26.26). Both groups were statistically significant. Postoperative bone conductive hearing threshold at the frequencies of 0.5, 1 and 2 KHz and postoperative air conductive hearing threshold at the frequencies of 2 and 4 KHz showed statistically significant differences in the manual perforator group. The closure of air-bone gap was higher in the microdrill group with statistically significant differences. <br><b>Conclusion:</b> Both manual perforator and microdrill have good hearing outcomes at six months after surgery. The manual perforator has better audiological outcomes than microdrill. Hence, the manual perforator is a safe technique and can be used in centers that do not have other methods to make the small fenestra.

The rising incidence of human papillomavirus (HPV)-associated malignancies, especially for oropharyngeal cancers, has highlighted the urgent need to understand how the interplay between high-risk HPV oncogenes and carcinogenic exposure results in squamous cell carcinoma (SCC) development. Here, we describe an inducible mouse model expressing high risk HPV-16 E6/E7 oncoproteins in adults, bypassing the impact of these viral genes during development. HPV-16 E6/E7 genes were targeted to the basal squamous epithelia in transgenic mice using a doxycycline inducible cytokeratin 5 promoter (cK5-rtTA) system. After doxycycline induction, both E6 and E7 were highly expressed, resulting in rapid epidermal hyperplasia with a remarkable expansion of the proliferative cell compartment to the suprabasal layers. Surprisingly, in spite of the massive growth of epithelial cells and their stem cell progenitors, HPV-E6/E7 expression was not sufficient to trigger mTOR activation, a key oncogenic driver in HPV-associated malignancies, and malignant progression to SCC. However, these mice develop SCC rapidly after a single exposure to a skin carcinogen, DMBA, which was increased by the prolonged exposure to a tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA). Thus, only few oncogenic hits may be sufficient to induce cancer in E6/E7 expressing cells. All HPV-E6/E7 expressing SCC lesions exhibited increased mTOR activation. Remarkably, rapamycin, an mTOR inhibitor, abolished tumor development when administered to HPV-E6/E7 mice prior to DMBA exposure. Our findings revealed that mTOR inhibition protects HPV-E6/E7 expressing tissues form SCC development upon carcinogen exposure, thus supporting the potential clinical use of mTOR inhibitors as a molecular targeted approach for prevention of HPV-associated malignancies., (© The Author 2016. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)