Olfactory dysfunction (OD) is a prevalent condition affecting 10%–20% of the population, with 60%–80% of chronic rhinosinusitis (CRS) patients experiencing smell impairment. The olfactory cleft (OC) serves as the critical conduit for odorant delivery to the olfactory epithelium, and abnormalities in this narrow anatomical region represent a major cause of peripheral OD. This review proposes an anatomy-based framework that positions OC obstruction as the initiating event in a self-amplifying cascade involving type 2 inflammation and microbiota dysbiosis. We synthesize current evidence on three etiological domains: anatomical obstruction, type 2 inflammatory damage, and microbiota dysbiosis. Diagnostic approaches are reviewed, including subjective assessment, psychophysical testing, endoscopic scoring, imaging, and olfactory cleft mucus biomarkers. For treatment, we evaluate pharmacological therapies, local drug delivery innovations, biologics targeting type 2 inflammation, and emerging surgical and regenerative options. Novel contributions include discussion of OC dilatation and blocking techniques as complementary surgical approaches based on symptom mechanism, and platelet-rich plasma injection as a regenerative therapy. Evidence quality is graded using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) system. This anatomy-based approach provides clinicians with a mechanistic framework for understanding why OC-related OD is often refractory to single-modal therapy and supports endotype-driven, multi-node intervention strategies.

Background: Large defects after endoscopic transoral skull base surgery remain difficult to reconstruct, particularly in previously irradiated fields. The submental flap is widely used in head and neck reconstruction, but its application in endoscopic skull base surgery has rarely been described.

Methods: Eight fresh cadaveric heads underwent endoscopic transoral skull base dissection to evaluate harvesting, arc of rotation, and transparapharyngeal transposition of the submental flap. Clinical feasibility was then assessed in 30 consecutive patients who underwent submental flap reconstruction for nasopharyngeal skull base defects after endoscopic transoral surgery, with or without a combined transnasal approach.

Results: When dissected to the origin of the facial artery, the flap measured 11.3 ± 1.0 cm in length and 4.1 ± 0.8 cm in width. Anatomically, the flap adequately covered the ipsilateral inferior petrous apex, nasopharynx, lower clivus, parapharyngeal space, and Eustachian tube region. Clinically, all flaps reached the target defect. Total flap necrosis occurred in 5 of 30 patients (16.7%), and all were salvaged with temporalis muscle flap reconstruction; no carotid blowout occurred during follow-up.

Discussion: The submental flap provides vascularized tissue with a favorable arc of rotation and can address selected lateral and inferior skull base defects beyond the reach of standard intranasal flaps.

Conclusion: The submental flap is a feasible complementary reconstructive option after endoscopic transoral skull base surgery in carefully selected patients, especially when carotid coverage is required. Meticulous patient selection, flap handling, and postoperative surveillance remain essential.

Background: Ketogenic enzymes are downregulated and act as tumor suppressors in nasopharyngeal carcinoma (NPC), yet the antitumor mechanisms of the ketone body β-hydroxybutyrate (β-HB) in NPC remain unclear.

Methods: Network pharmacology, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment, and molecular docking were used to identify candidate β-HB–NPC targets. In vitro, the effects of β-HB on cell viability, colony formation, caspase-3 enzymatic activity, and apoptosis were assessed in NPC cells. Dose- and time-response cell viability analyses were also performed using NP69 cells. Caspase-3 involvement was evaluated using Z-DEVD-FMK and CASP3 siRNA. Two independent NPC C17 patient-derived xenograft (PDX) experiments used alternate-day fasting or a ketogenic diet to induce ketosis. Epstein–Barr virus (EBV) lytic-gene expression, EBV DNA copy number, and tumor EBV-encoded RNAs (EBER) status were also assessed.

Results: We identified 177 overlapping β-HB–NPC targets and five hub targets, with caspase-3 prioritized as an apoptosis-associated functional node. Molecular docking predicted a compatible binding pose for β-HB within caspase-3, but did not establish direct binding. In vitro, β-HB suppressed cell viability and clonogenic growth without reducing NP69 viability under the tested conditions. It increased caspase-3 activity, cleaved caspase-3, PARP-1, and promoted apoptosis. Both Z-DEVD-FMK and CASP3 silencing attenuated β-HB-induced apoptosis. In vivo, both independent PDX experiments demonstrated tumor suppression accompanied by elevated ketone-related measures. Tumors from both intervention groups exhibited reduced Ki-67 expression, and increased terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) positivity. β-HB also upregulated the EBV immediate-early lytic gene expression (BZLF1 and BRLF1), while a nonsignificant trend toward increased EBER positivity was observed in fasting-treated tumors.

Conclusion: β-HB suppresses NPC cell growth and promotes apoptosis, with caspase-3 serving as a functional mediator. In vivo, both dietary interventions suppressed tumor growth and were accompanied by increases in ketone-related measures. β-HB also induces EBV immediate-early lytic gene expression, supporting further investigation of ketone metabolism as a potential therapeutic strategy for NPC.

Background: Laryngomalacia (LM) is a life-threatening condition in infants characterized by stridor. In this study, we aim to identify potential genetic variants associated with LM.

Methods: We conducted a retrospective analysis of whole-exome sequencing (WES) results from 55 LM patients who underwent supraglottoplasty at Shanghai Children’s Hospital between January 2021 and December 2023, and performed a systematic review of published literature on LM, screening for studies involving genetic abnormalities.

Results: We identified 15 likely pathogenic variants from 36 out of the 55 patients (65.45%). Among these 15 likely pathogenic variants, 10 variants were found in 2 or more patients, including 22q11.2 deletion (3 cases), CHD7 (2 cases), COL2A1 (2 cases), COL6A2 (6 cases), COL6A3 (2 cases), FLNB (4 cases), RYR1 (6 cases), KMT2D (2 cases), PLP1 (2 cases), and COLQ (2 cases).

Conclusion: We are the first to report COL6A2, COL6A3, COL2A1, RYR1, PLP1, and COLQ as likely candidate genetic variants for LM. In addition, CHD7-related disorders represent one of the most frequently reported genetic conditions associated with laryngomalacia.

Background: This study aimed to explore the pterygopalatine fossa (PPF) from a novel bone-preserving perspective and to evaluate the educational value of this approach for otolaryngology trainees in mastering complex PPF anatomy.

Methods: Rigid endoscopes were used on three dry skulls (5 sides) to illustrate the bony corridors of the nasal cavity, inferior orbital fissure (IOF), and pterygomaxillary fissure (PMF) to demonstrate the anatomy of the PPF. In addition, three fresh frozen cadaveric heads (5 sides) were dissected to demonstrate the PPF neurovascular contents and bony anatomy and replicate the approach in clinical scenarios via the conventional endoscopic transmaxillary approach (ETMA). The educational outcome was assessed via a trainee questionnaire.

Results: The advantage of the endoscopic IOF and the PMF approach is that a complete exposure of the intact bony architecture of the PPF can be performed in dry skulls. Dry skull specimens were rated significantly higher than fresh cadaveric specimens in terms of exposure quality scores, three-dimensional (3D) comprehension, structure identification, learner confidence, reusability, and convenience for clinical teaching.

Conclusion: This anatomical study suggests the feasibility of using the IOF and PMF approaches to access the PPF and help surgeons to master the osseous anatomy of the PPF. This method allows for a visual examination of the bony structures within the PPF without destructive dissection. Subjective trainee feedback suggests this method serves as a valuable tool for anatomical education.

Introduction: Unilateral vestibular hypofunction (UVH) is an important cause of dizziness, postural instability, impaired gaze stability, and activity limitation, substantially affecting functional capacity, social participation, and quality of life. Vestibular rehabilitation therapy (VRT), based on mechanisms of vestibular compensation and neuroplasticity, is a non-pharmacological intervention that can improve dizziness, imbalance, gaze instability, and gait dysfunction in patients with UVH.

Methods: To standardize the clinical practice of vestibular rehabilitation for UVH in China, the guideline working group systematically reviewed relevant domestic and international clinical guidelines, expert consensuses, and evidence-based studies. Recommendations were developed through evidence synthesis and expert consultation.

Recommendations: The guideline addresses the diagnosis and etiological identification of UVH, disease staging, indications for VRT, rehabilitation assessment, development and implementation of individualized training programs, outcome evaluation, discontinuation criteria, and the application of emerging adjunctive technologies. A total of 19 recommendations were formulated to guide the standardized and individualized management of patients with UVH.

Discussion: The guideline integrates current evidence with clinical expertise and focuses on key issues throughout the rehabilitation process. It emphasizes individualized assessment, appropriate selection and progression of rehabilitation interventions, regular outcome evaluation, and timely adjustment or discontinuation of treatment according to patient response and functional recovery.

Conclusion: This guideline provides evidence-informed recommendations for vestibular rehabilitation in patients with UVH and is intended to support standardized clinical decision-making, optimize rehabilitation practice, and improve patient-centered outcomes in China.

Introduction: Bilateral vestibulopathy (BVP), often termed bilateral vestibular hypofunction (BVH) in rehabilitation literature, is a chronic vestibular disorder characterized by bilateral impairment of the vestibulo-ocular reflex, resulting in oscillopsia, postural instability, gait dysfunction, increased fall risk, and reduced quality of life. This clinical practice guideline provides evidence-based recommendations for the diagnosis, etiological evaluation, rehabilitation assessment, and management of adults with BVH.

Methods: Clinical questions were formulated using the population, intervention, comparator, and outcomes (PICO) framework. Recommendations were developed through systematic evidence synthesis and assessment of evidence certainty.

Recommendations: Vestibular rehabilitation therapy (VRT) is recommended as a safe and effective first-line intervention for adults with BVH-related impairments and functional limitations. Rehabilitation should be individualized according to residual vestibular function, symptom severity, fall risk, comorbidities, functional limitations, and patient-centered goals. Task-specific, progressive, and multimodal programs incorporating gaze-stabilization, balance, gait, sensory substitution, functional, and endurance exercises are recommended. Treatment should be regularly reassessed and adjusted, paused, or discontinued according to clinical response, safety, goal attainment, and therapeutic plateau.

Discussion: Current evidence supports improvements in gaze stability, postural control, functional mobility, dizziness-related disability, and quality of life following VRT. However, evidence supporting vestibular implants, non-invasive neuromodulation, and other emerging technologies remains insufficient for routine clinical use.

Conclusion: VRT should be considered a core component of management for adults with BVH. Further research is needed to establish optimal training dosage, long-term effectiveness, clinically meaningful outcome measures, and the role of emerging rehabilitation technologies.

Introduction: Chronic invasive fungal rhinosinusitis (CIFRS) is a rare, potentially lethal opportunistic infection that typically affects mildly immunocompromised hosts and pursues an insidious course over months. It predominantly affects patients with mild immunocompromise, such as diabetes mellitus, renal insufficiency, or low-dose glucocorticoid exposure, and, unlike acute invasive disease, pursues an indolent course over months to years.

Case presentation: A 77-year-old man with type 2 diabetes mellitus and renal insufficiency presented with a six-month history of left facial numbness followed by hoarseness and dysphagia for 12 days. Progressive, multilevel cranial neuropathies evolved in a cranial-nerve-specific sequence (II, V, VII/VIII, IX/X), culminating in left vocal fold fixation and nasogastric feeding. Cross-sectional imaging demonstrated extensive skull base osteomyelitis with marrow signal loss and a clival necrotic focus, and right internal carotid artery (C3–C6) involvement with mild foramen lacerum stenosis.

Results: Histopathology from the right sphenoid sinus, nasopharynx, and left parapharyngeal space showed fungal hyphae within necrotic and granulation tissue (Grocott’s methenamine silver- and periodic acid-Schiff-positive); the morphology was compatible with an Aspergillus-like hyaline septate mould, without definitive species identification. Maximal safe debridement was performed, intentionally retaining right-sided disease in the deep nasopharynx and right greater sphenoid wing, adjacent to the cavernous sinus, orbital apex, and internal carotid artery. The early postoperative course was favorable within a 29-day observation window.

Discussion: This case illustrates that, in the mildly immunocompromised elderly, CIFRS may declare itself through sequentially accruing multiple cranial neuropathies, and that a non-diagnostic initial biopsy can compound diagnostic delay. The distinction between sinonasal CIFRS and central skull base osteomyelitis warrants explicit consideration, as it shapes surveillance strategy.

Conclusion: A high index of suspicion, histopathological confirmation with fungal stains, maximal safe debridement that honestly acknowledges intentionally retained disease, and individualized antifungal therapy guided by therapeutic drug monitoring constitute the cornerstones of management. Early postoperative imaging documents surgical extent and short-term course but cannot establish durable disease control.