Search Results (86)

Background: Asthma is a heterogeneous chronic airway disease characterized by inflammation, airflow obstruction, hyperresponsiveness, and remodeling. Severe eosinophilic asthma is driven by eosinophilic inflammation, which contributes to tissue damage, recurrent exacerbations, and progressive impairment of airway structure and function. Eosinophils play a central role through the release of cytokines, cytotoxic granule proteins, and extracellular traps, and their persistence in the airways is sustained by type 2 inflammatory pathways, particularly interleukin-5-mediated signaling. A better understanding of eosinophil biology has promoted the development of targeted therapies, including anti-interleukin-5/interleukin-5 receptor agents and biologics that indirectly modulate eosinophilic inflammation, such as anti-interleukin-4 receptor alpha and anti-thymic stromal lymphopoietin antibodies. Aim: This narrative review summarizes the immunopathology of eosinophilic asthma and links eosinophil biology to current and emerging pharmacological strategies. We discuss biologics that directly target the IL-5/IL-5 receptor axis, as well as agents that indirectly modulate eosinophilic inflammation, including IL-4 receptor alpha and TSLP blockade. We also review the clinical positioning of available biologics, focusing on blood eosinophils, FeNO, exacerbation history, oral corticosteroid exposure, lung function, type 2 comorbidities, treatment response, remission and switching. Conclusions: Overall, eosinophilic inflammation remains a central therapeutic target and a key component of precision medicine in severe asthma, but biologic selection should be individualized and reassessed through multidomain clinical outcomes. Full article

The lower airways are a dynamic environment where physical, microbial, and molecular factors intersect to regulate respiratory health and disease. The muco-microbiotic (MuMi) layer, composed of mucus, resident microbes, and extracellular vesicles (EVs), is not just a passive barrier but also an active site for host–microbe communication. This layer integrates epithelial cell biology, microbial activity, and immune responses within the bronchial environment. New transcriptomic and metatranscriptomic technologies show that it is not only which microbes are present but also their gene activity that closely links to airway inflammation and disease. EV-associated RNAs from both host and microbial cells act as key messengers, influencing epithelial responses, immune activity, mucus properties, and microbial behaviour. This review highlights evidence that positions the MuMi layer as central to understanding lower airway disease, particularly asthma and chronic obstructive pulmonary disease (COPD). Distinct gene expression programs and biomarker profiles, such as exhaled nitric oxide, may reflect different disease mechanisms even in cases with similar clinical features, such as eosinophilia. Multi-omic approaches focused on the MuMi layer enable better disease classification, biomarker discovery, and therapy selection. By putting the MuMi interface at the core of precision pulmonology, we provide a framework for advancing personalised care in chronic respiratory diseases. Full article

Background: Central compartment atopic disease (CCAD) is a recently developed terminology used to describe a specific phenotype of chronic rhinosinusitis (CRS). The aim of this study is to provide a thorough analysis of the clinical and radiological characteristics by assessing the prevalence of symptoms, asthma, allergy, aeroallergen sensitization and radiological sinus involvement. Methods: The authors searched for articles on PubMed, Cochrane, and Embase databases. A review of the articles was carried out following PRISMA guidelines; all articles were assessed for quality according to NICE criteria. Afterwards, the meta-analysis was performed with STATA 18SE software. Studies were also assessed for heterogeneity and risk of publication bias. Mean Lund-Mackay (LMK) score of patients with and without CCAD was compared. Results: A total of 16 studies were included, including 1254 patients with CRS; 537 of these were diagnosed with CCAD. The most prevalent symptoms were obstruction at 78% and congestion at 70%, followed by rhinorrhea at 66%, hyposmia at 54%, and facial pain at 24%. Dust mite at 71% was the most prevalent sensitization. Overall, the prevalence of asthma in patients with CCAD was 26%, prevalence of allergy was 67%. The mean difference in LMK scores was −3.38 in CCAD. Conclusions: Patients frequently present with nasal obstruction and congestion; the most common allergen sensitization is to dust mites. Findings on allergy and asthma prevalence support the “Unified Airway Disease” concept and emphasize the importance of a multidisciplinary approach to managing this phenotype. CCAD patients usually do not develop very high LMK scores; high scores may rule out this diagnosis. PROSPERO registration number: CRD420261361696. Full article

Chronic rhinosinusitis (CRS) is a persistent inflammatory disorder of the nasal and paranasal mucosa, typically attributed to local infection or anatomical obstruction. However, recent evidence suggests that CRS may also reflect systemic inflammatory dysregulation influenced by the gut microbiome, establishing a potential ‘gut–sinus axis’. This systematic review aims to synthesise current evidence linking gut microbiome alterations to the pathogenesis and clinical course of CRS and to explore emerging therapeutic strategies targeting this axis. Five databases were comprehensively searched for studies published between January 2000 and October 2025. Data were extracted and evaluated for quality using the JBI and SYRCLE tools. A total of 441 records were retrieved, of which 20 studies met the inclusion criteria. Human studies consistently showed gut dysbiosis in CRS, characterised by reductions in Roseburia, Bifidobacterium, Faecalibacterium and Akkermansia species. These microbial shifts correlated with increased levels of systemic cytokines, such as interleukin-6, interleukin-17 and tumour necrosis factor-α, and disease severity. Animal and interventional studies confirmed that high-fibre diets and short-chain fatty acid (SCFA) supplementation modified airway inflammation, whereas antibiotic-induced dysbiosis exacerbated it. Current evidence substantiates a gut–sinus axis mediated by immune, metabolic and neuroendocrine pathways. Dysbiosis-driven reductions in SCFA-producing bacteria appear central to systemic pro-inflammatory signalling implicated in CRS. Full article

Background: Obstructive sleep apnea (OSA) is a major modifiable risk factor for atrial fibrillation (AF), promoting arrhythmogenesis through intermittent hypoxia, autonomic activation, and atrial remodeling. Although continuous positive airway pressure (CPAP) effectively treats OSA, real-world evidence linking objectively measured CPAP exposure to clinically relevant AF recurrence remains limited. Aims: We aimed to evaluate the association between CPAP adherence and risk of recurrent paroxysmal AF, and to compare time to first recurrence between patients with mean nightly CPAP use ≥4 h/night versus <4 h/night. Materials and Methods: In this prospective observational cohort (2017–2024), consecutive hospitalized and outpatient adults with severe obstructive sleep apnea (OSA; apnea–hypopnea index > 30 events/h) and documented paroxysmal atrial fibrillation (AF) were enrolled. Persistent and long-standing persistent AF were excluded to ensure a homogeneous population with respect to atrial substrate. OSA was assessed using home sleep apnea testing (ResMed ApneaLink), and all patients initiated continuous positive airway pressure (CPAP) therapy (ResMed AirSense 10). Objective adherence data were obtained via the ResMed AirView telemonitoring platform. Exclusion criteria included permanent AF, prior pulmonary vein isolation, central sleep apnea, left ventricular ejection fraction < 50%, end-stage chronic kidney disease (eGFR < 15 mL/min/1.73 m² or dialysis), or inability to initiate or maintain CPAP therapy. Patients were followed for 12 months. The primary endpoint was time to first documented recurrence of paroxysmal AF (≥30 s on 12-lead electrocardiography or 24-h Holter monitoring). Progression to permanent AF, defined after unsuccessful rhythm control attempts and subsequent transition to a rate control strategy, was assessed as a secondary endpoint. Time-to-event analyses used Kaplan–Meier estimates with log-rank testing, and Cox proportional hazards regression adjusted for age, body mass index, apnea–hypopnea index, heart failure, left atrial volume index, and antiarrhythmic drug therapy. Results: The final analysis included 91 patients (mean age 62.15 ± 8.29 years; 68.13% men). Mean nightly CPAP use was ≥4 h/night in 49 patients and <4 h/night in 42 patients. During follow-up, paroxysmal AF recurrence occurred in 12/49 (24.5%) patients in the ≥4 h/night group and 16/42 (38.1%) in the <4 h/night group. Mean arrhythmia-free survival at 12 months was numerically higher in the ≥4 h/night group (11.25 vs. 10.51 months), without a statistically significant difference in Kaplan–Meier curves (log-rank p = 0.11). In multivariable Cox regression, binary adherence (≥4 h/night) was not independently associated with recurrence (HR 0.52, p = 0.13), whereas mean nightly CPAP use analyzed as a continuous variable remained independently associated with delayed recurrence (per 1-h increase: HR 0.66, 95% CI 0.48–0.91, p = 0.01). Progression to permanent AF occurred in 4/49 (10.0%) versus 9/42 (17.6%) patients, respectively (p = 0.29). Conclusions: In this real-world cohort of patients with severe OSA and paroxysmal AF, higher objectively measured CPAP exposure was independently associated with delayed AF recurrence when analyzed as a continuous variable, suggesting a graded association between objectively measured CPAP exposure and AF recurrence. Larger studies with extended follow-up and continuous rhythm monitoring are warranted to confirm long-term rhythm benefits and effects on AF progression. Full article

Pulmonary hypertension (PH) is a progressive disorder characterized by elevated pulmonary arterial pressure and the extensive remodeling of pulmonary vasculature. Chronic intermittent hypoxia (CIH), a hallmark of obstructive sleep apnea (OSA), is a well-established contributor to the pathogenesis of PH. OSA is defined by repetitive episodes of upper airway obstruction during sleep, leading to cycles of hypoxia and reoxygenation that trigger a cascade of deleterious events including oxidative stress, inflammation, endothelial dysfunction, and vascular remodeling. Growing evidence underscores the critical role of transient receptor potential canonical (TRPC) channels in mediating hypoxia-induced vascular alterations that contribute to the development of PH. TRPC channels are non-selective cation channels that regulate calcium influx in response to mechanical stimuli, pro-inflammatory cytokines, oxidative stress, and hypoxia. These channels are expressed in both pulmonary arterial smooth muscle cells (PASMCs) and pulmonary artery endothelial cells (PAECs), where they modulate key processes such as proliferation, migration, apoptosis, endothelial permeability, and vasoconstriction. Under hypoxic conditions, the upregulation of TRPC1, TRPC3, TRPC4, and TRPC6 has been implicated in dysregulation of calcium homeostasis and activation of pathological signaling pathways that contribute to increased pulmonary arterial pressure. In this review, we propose that upregulation and functional modulation of TRPC channels under CIH represents a central pathogenic mechanism linking OSA to PH. We hypothesize that TRPC1, TRPC3, TRPC4, and TRPC6 act as critical molecular effectors mediating hypoxia-driven calcium influx and downstream signaling pathways that lead to pulmonary vascular remodeling, endothelial dysfunction, and increased pulmonary arterial pressure. This framework allows us to integrate mechanistic insights from molecular, cellular, and translational studies, and to evaluate the therapeutic potential of targeting TRPC channels in OSA-associated PH. Full article

We report a thirty-six-year-old woman with intellectual disability who was referred for evaluation of suspected obstructive sleep apnea. The initial clinical impression suggested a syndromic case, so comprehensive genetic testing was undertaken. Overnight polysomnography revealed a severe rapid eye movement–predominant obstructive sleep apnea syndrome with an apnea–hypopnea index of 31.9 events per hour, rapid eye movement apnea–hypopnea index of 113.8 events per hour, and lowest oxygen saturation of 66%. Treatment with continuous positive airway pressure improved respiratory and sleep quality indices and was well tolerated. Whole-exome sequencing identified a de novo splice site variant in the pleckstrin homology domain interacting protein gene (c.41-1G > A), confirming a molecular diagnosis of Chung–Jansen Syndrome. Chung–Jansen syndrome is a rare neurodevelopmental disorder caused by heterozygous pathogenic variants in the pleckstrin homology domain interacting protein gene, marked by developmental delay, intellectual disability, behavioral abnormalities, dysmorphism, and progressive obesity. PHIP influences central and peripheral pathways controlling satiety, pancreatic function, and body weight. Despite frequent reports of sleep problems, systematic evaluation of sleep-disordered breathing has been limited. This adult case provides the first polysomnographic confirmation in the syndrome, supporting proactive screening for obstructive sleep apnea—especially in those with obesity. Integrating genetic assessment into sleep care can reduce diagnostic delays and better guide therapy and prognosis. Full article

Chronic Obstructive Pulmonary Disease (COPD) is a complex inflammatory lung condition characterized by oxidative stress, changes in airway structure, and gradually worsening airflow blockage. Existing treatments offer only symptomatic management, emphasizing the need for multi-target therapeutic interventions. This study employed a combined approach of network pharmacology and molecular docking to investigate the therapeutic effects of bioactive compounds derived from Cladophora glomerata on COPD. Disease-associated genes were collected from GeneCards, Online Mendelian Inheritance in Man (OMIM), and National Center for Biotechnology Information (NCBI), while compounds from C. glomerata and their predicted molecular targets were obtained from SwissTargetPrediction. A cross-comparison of targets related to compounds and diseases revealed nine common genes, among which three central genes TP53, CASP8, and EGFR were identified using protein–protein interaction (PPI) network analysis. Analysis of gene–disease interactions highlighted Tumor Protein p53 (TP53) and Epidermal Growth Factor Receptor (EGFR) as major regulatory targets. GeneMANIA-based functional and co-expression analysis revealed predominant physical interactions (77.64%) and co-expression relationships (8.01%), highlighting strong functional connectivity among the identified genes. Molecular docking further confirmed that C. glomerata derived compounds, particularly Quinoline, 1,2,3,4-tetrahydro-1-((2-phenylcyclopropyl)sulfonyl)-, trans- (Pubchem ID: 91709903) (−7.5 kcal/mol) and1,2,4-Oxadiazole, 3-(1,3-benzodioxol-5-yl)-5-[(4-iodo-1H-pyrazol-1-yl)methyl]- (Pubchem ID: 5301194) (−7.3 kcal/mol), exhibit favorable predicted binding affinities toward EGFR and TP53 in molecular docking analysis. Overall, these insights suggest that Cladophora glomerata compounds may modulate key COPD-related pathways through multi-target interactions, providing a scientific basis for future experimental studies and the development of marine-derived therapeutic agents for COPD management. Full article

Objectives: Central airway obstruction (CAO) caused by malignant tumors may necessitate combined and prompt treatment. The aim is to recanalize and stabilize the airways as palliation. We present our multicentric experience managing malignant CAO through the placement of Y-shaped self-expanding covered metallic or silicone trachea-bronchial stents. Methods: This retrospective study includes patients who underwent placement of Y-shaped stents from 2002 to 2024 across six different centers in Italy and Great Britain. We evaluated outcomes related to the feasibility and safety of the procedure, as well as the palliation of dyspnoea on the Modified Borg Scale of Dyspnoea. Results: Eighty patients (56.2% female) with a mean age of 64.8 ± 9.6 years were included in the study. Successful placement was achieved in 76 (95%) cases, with no cases of intraoperative mortality. The mean procedure time was 36.64 ± 15.7 min. The complications noted included: 7 (8.7%) cases of periprocedural clinical complications and 7 (8.7%) patients requiring intensive care unit admittance after the procedure. Fifty patients (78.1%) received cancer treatment following the procedure. The mean dyspnoea score on the Borg scale decreased from 7.78 ± 0.98 to 4.02 ± 2.2 (p < 0.05). Conclusions: The placement of metal or silicone Y-shaped stents is a feasible and safe procedure for the palliative treatment of dyspnoea in patients with malignant stenosis of the trachea and main bronchi. Stabilizing the airway also enables these patients to access cancer treatments. Full article

Background/Objectives: Maxillary transverse deficiency is linked to impaired nasal breathing and pediatric sleep-disordered breathing. This systematic review evaluated the effects of maxillary expansion (ME) on upper-airway morphology and breathing function in growing patients. Methods: The search was conducted on PubMed/MEDLINE, Scopus, ScienceDirect, Cochrane CENTRAL, and gray literature (January 2015–April 2025). Eligible RCTs, controlled trials, and cohort/observational studies assessed airway morphology and/or respiratory outcomes after ME in pediatric/adolescent patients. Risk of bias was evaluated with RoB 2 (RCTs) and ROBINS-I (non-randomized studies). The findings were synthesized qualitatively and certainty graded with GRADE. Results: Forty-one studies were included. Imaging consistently showed enlargement of the nasal cavity and nasopharynx after expansion, whereas the effects in the oropharynx and hypopharynx, as well as in the maxillary sinuses, were smaller or variable. Objective patency improved in several studies (higher peak nasal inspiratory flow, reduced nasopharyngeal obstruction, and nasal resistance), whereas computational fluid dynamics generally showed non-significant trends toward lower resistance. Spirometry improved, particularly in oral breathers (gains in FEV₁, FVC, FEF25–75%). Polysomnography indicated reductions in AHI and improved oxygenation in some pediatric OSA cohorts, although other RCTs reported null PSG effects. Caregiver-reported sleep and quality-of-life outcomes were consistently enhanced. Device design modestly influenced regional widening, but overall respiratory effects were similar across expanders. By GRADE, certainty was low for airway morphology and very low for breathing function. Conclusions: In growing patients, ME reliably enlarges upper-airway compartments, especially the nasal cavity and nasopharynx, yet functional improvements are heterogeneous. Standardized outcomes and integrated morphological–functional assessments are needed to strengthen the evidence base. Full article

Background and Clinical Significance: Endobronchial leiomyoma is a rare benign tumor of the respiratory tract, accounting for less than 2% of all benign pulmonary neoplasms. Most cases have been treated surgically or with endoscopic modalities such as laser or rigid bronchoscopy-assisted cryotherapy. Flexible bronchoscopic cryoextraction has been rarely reported, typically with 2.2-mm probes. Small-caliber cryoprobes (1.1- and 1.7-mm) have been validated for diagnostic transbronchial cryobiopsy but not for therapeutic removal of leiomyoma. We report a case of complete removal of endobronchial leiomyoma using a 1.7-mm cryoprobe via flexible bronchoscopy, demonstrating full airway and physiologic recovery. Case Presentation: A 25-year-old never-smoking man was referred after an abnormal health-screening chest radiograph demonstrated right middle and lower lobe atelectasis. Chest CT revealed a mass obstructing the proximal bronchus intermedius. Spirometry showed reduced FEV₁ and FVC with preserved FEV₁/FVC ratio, consistent with central airway obstruction. Therapeutic flexible bronchoscopy (Olympus BF-1TQ290) was performed under endotracheal intubation. Initial forceps biopsies were followed by transbronchial cryobiopsy with a 1.7-mm cryoprobe, applied for five freeze–adhesion cycles. The mass detached en bloc and was retrieved without complications, resulting in complete airway recanalization and visualization of the right middle and lower lobe bronchi. Histopathology showed interlacing fascicles of bland spindle cells with cigar-shaped nuclei, positive for SMA and desmin and negative for S-100 and CD34, confirming leiomyoma. The patient was discharged the next day. At one-year follow-up, bronchoscopy and CT demonstrated no recurrence, and spirometry normalized. Conclusions: Reports combining flexible bronchoscopy with a 1.7-mm small-caliber cryoprobe for en bloc removal of endobronchial leiomyoma are rare. This technique may represent a minimally invasive option for selected cases, provided careful hemostatic planning and appropriate case selection. Full article

Matrix metalloproteinase-9 (MMP-9) is a zinc-dependent endopeptidase that plays a central role in extracellular matrix (ECM) remodeling, angiogenesis, immune cell trafficking, and cytokine activation. Dysregulated MMP-9 activity has been implicated in the pathogenesis of diverse conditions, including atherosclerosis, aneurysm formation, chronic obstructive pulmonary disease (COPD), asthma, neurodegeneration, and malignancy. Although broad-spectrum synthetic MMP inhibitors were initially developed as therapeutic agents, clinical trials failed due to lack of selectivity, poor tolerability, and impairment with physiological tissue repair. This outcome has shifted attention toward indirect pharmacological modulation of MMP-9 using drugs that are already approved for other indications. In this paper, we review the evidence supporting MMP-9 modulation by established therapeutics and adjunctive strategies. Cardiometabolic agents such as statins, angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), metformin, and pioglitazone reduce MMP-9 expression and enzymatic activity, contributing to vascular protection, improved insulin sensitivity, and attenuation of aneurysm progression. Anti-inflammatory and respiratory drugs, including glucocorticoids, phosphodiesterase-4 (PDE4) inhibitors, macrolide antibiotics, montelukast, and nonsteroidal anti-inflammatory drugs (NSAIDs), suppress MMP-9-driven airway inflammation and pathological tissue remodeling in asthma, COPD, and acute lung injury. Tetracycline derivatives, particularly sub-antimicrobial dose doxycycline, directly inhibit MMP-9 activity and are clinically validated in the treatment of periodontal disease and vascular remodeling. Hormone-related therapies such as rapamycin, estradiol, and tamoxifen exert tissue- and disease-specific effects on MMP-9 within endocrine and oncologic pathways. In parallel, nutritional interventions—most notably omega-3 polyunsaturated fatty acids and antioxidant vitamins—provide adjunctive strategies for mitigating MMP-9 activity in chronic inflammatory states. Taken together, these findings position MMP-9 as a modifiable and clinically relevant therapeutic target. The systematic integration of approved pharmacologic agents with lifestyle and nutritional interventions into disease-specific treatment paradigms may facilitate safer, context-specific modulation of MMP-9 activity and unveil novel opportunities for therapeutic repurposing. Full article

Obstructive sleep apnea is a common but underdiagnosed sleep-related breathing disorder characterized by recurrent episodes of upper airway obstruction during sleep, leading to intermittent episodes of hypoxia and systemic consequences. Anatomical and ventilatory control factors are well-established contributors, but less is known about how mitochondria influence upper airway muscle function in this condition. As central regulators of muscle performance and cellular adaptation to hypoxia, mitochondria are particularly vulnerable to dysfunction under chronic intermittent hypoxia. Mitochondrial dysfunction increases production of reactive oxygen species, predisposing to oxidative stress, that further impairs mitochondrial function. This review focuses on the mitochondrial involvement in obstructive sleep apnea, specifically synthesizing findings on the impact on upper airway muscles. The role of mitochondrial alterations in muscle dysfunction in this context is not well understood. A better understanding of oxidative damage in these muscles may also contribute to the development of therapeutic approaches, including antioxidant strategies, to mitigate the effects of chronic intermittent hypoxia in the upper airway muscles. Full article

Background/Objectives: Congenital laryngomalacia (LM) is the most common cause of stridor in infants, presenting with a clinical spectrum that ranges from benign, self-limiting symptoms to severe airway obstruction. This study aimed to objectively characterize the type and severity of sleep-disordered breathing in infants with LM using polysomnography (PSG) and to correlate findings with LM subtypes, clinical presentation, and type of surgical intervention. Methods: A cohort of 42 infants diagnosed with LM (Type I: n = 14, Type II: n = 18, Type III: n = 10) underwent overnight PSG before surgical treatment. The Apnea–Hypopnea Index (AHI), Oxygen Desaturation Index (ODI), minimum and mean SpO₂, and heart rate were recorded. Clinical features (stridor, feeding difficulties, respiratory effort) and type of surgery (supraglottoplasty [S] or supraglottoplasty with epiglottopexy [S + E]) were analyzed across LM subtypes. Results: Baseline AHI was significantly higher in LM Type III (25.41 ± 6.95 events/h) compared with Type II (12.50 ± 5.05) and Type I (2.84 ± 1.96; p < 0.001). After surgery, AHI decreased to 1.76 ± 1.56 in Type III and 0.97 ± 0.70 in Type II. ODI showed a similar trend (Type III: 9.87 ± 5.99 before vs. 0.78 ± 0.69 after surgery; p < 0.001). Minimum SpO₂ increased from 69.50 ± 7.76% to 93.60 ± 1.82% in Type III (p < 0.001). Feeding difficulties were observed in 100% of Type III patients, compared with 83.3% of Type II and 42.9% of Type I patients. The distribution of apnea type differed significantly across groups (p < 0.001), with mixed obstructive–central apnea predominating in Type III. Conclusions: Polysomnography is an effective and objective tool for assessing LM severity and guiding surgical qualification. Increasing LM severity is associated with more pronounced PSG abnormalities, greater clinical burden, and a higher likelihood of requiring advanced surgical correction. Full article

Background: Obstructive Sleep Apnea Syndrome (OSAS) is a prevalent and underdiagnosed condition with significant systemic and quality-of-life impacts. While polysomnography remains the gold standard for diagnosis, cone-beam computed tomography (CBCT) presents a potential adjunctive imaging tool for anatomical airway evaluation. Objective: We aimed to assess the effectiveness of three-dimensional airway evaluation via CBCT as a complementary diagnostic tool for OSAS. Methods: A diagnostic test study (experimental pilot study) was conducted using CBCT scans of 30 patients, divided into two groups: 15 scans from patients with a confirmed OSAS diagnosis through polysomnography and 15 scans from healthy controls. Five tomographic variables were analyzed: anteroposterior distance, lateral distance, minimum cross-sectional area, airway volume, and airway shape. Statistical analysis was performed comparing both groups. Results: The minimum cross-sectional area and airway volume showed statistically significant differences between the OSAS and control groups (p = 0.038 and p = 0.0055, respectively). Anteroposterior and lateral distances showed trends toward significance but were not statistically significant. Conclusions: CBCT-based airway analysis, particularly focusing on volumetric and cross-sectional area parameters, demonstrates strong potential as a complementary tool in the diagnosis of peripheral-type OSAS. However, it cannot replace polysomnography, especially for central OSAS diagnosis. Full article