Background: Sleep disorders are a group of disorders characterized by abnormalities of respiration during sleep. OSA (Obstructive Sleep Apnea) is characterized by the repetitive episodes of complete or partial collapse of the upper airway during sleep, causing a cessation or a significant reduction of airflow.
Method: The study population consisted of 30 control patients (AHI ≤ 5) events per hour, 74 patients with OSAS, including 34 Obese (BMI ≥ 27) and 40 non-obese (BMI ≤ 27). Polysomnography and measurements of 21 cephalometric variables were carried out for all patients with OSAS.
Results: Obese patient with OSAS showed significant difference in following cephalometric parameters: (1) PAS (2) MPT (3) MPH (4) PNS-P (5) SAS. In addition, obese patient had longer tongue (TGL), more anteriorly displaced hyoid bones (H-VL) and more anterior displacement of mandible (G-VL) when compared with control groups. The findings of non-obese patients when compared to controls showed all the findings of obese patients and in addition to that narrow bony oropharynx were significant. Step wise regression analysis showed the significant predictors for all patients were MPH, PNS-P, bony nasopharynx (PNSBa), MPT, and palatal length (ANS-PNS) for AHI. The significant predictors for obese OSA (obstructive sleep apnea) group were MAS while for non-obese OSA group ANS-PNS was significant predictor for AHI (apnea-hypopnea index).
Conclusion: Craniofacial landmarks such as increase in hyoid distance, longer tongue and soft palate with increased thickness and narrowing of superior pharyngeal, oropharyngeal and hypopharyngeal airway space may be important risk factors for development of OSAS.
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http://dx.doi.org/10.1016/j.mjafi.2014.07.001 | DOI Listing |
J Int Med Res
January 2025
Quanjiao County People's Hospital, Quanjiao County, Chuzhou, Anhui, China.
Objective: We aimed to examine the relationship between the weight-adjusted waist index (WWI) and obstructive sleep apnea (OSA), a condition often caused by obesity, which remains unclear.
Methods: In this cross-sectional study, we analyzed data from the National Health and Nutrition Examination Survey among adults in the United States (US) aged 20 to 65 years, covering the periods 2005 to 2008 and 2015 to 2018. The study included 8278 participants; we used multivariate logistic regression, restricted cubic splines, and subgroup analyses to explore the relationship between WWI and OSA.
Otolaryngol Head Neck Surg
January 2025
Department of Otolaryngology, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania, USA.
Objective: To compare the incidence of motor vehicle accidents (MVAs) among patients with obstructive sleep apnea (OSA) undergoing continuous positive airway pressure (CPAP) therapy and sleep surgery.
Study Design: Retrospective cohort study using the TriNetX national clinical database.
Setting: Analysis of a nationwide patient cohort.
Hu Li Za Zhi
February 2025
Department of Internal Medicine, Chang Gung Memorial Hospital, Taiwan, ROC.
Background: Obstructive sleep apnea (OSA) is a common sleep disorder shown to be significantly correlated with metabolic syndrome (MS). Healthcare professionals affected by both MS and OSA may suffer from poor sleep quality, raising potential concerns about patient safety. Currently, there remains a gap in research specifically addressing the relationship between MS and OSA in healthcare professionals.
View Article and Find Full Text PDFExpert Rev Respir Med
January 2025
Department of Pulmonology and Sleep Disorders Centre, University Hospital Zurich, Zurich, Switzerland.
Mol Ther
January 2025
Immune Health, Hunter Medical Research Institute and The University of Newcastle, Newcastle, New South Wales, Australia; Centre for Inflammation, Centenary Institute and University of Technology Sydney, School of Life Sciences, Faculty of Science, Sydney, New South Wales, Australia. Electronic address:
Vitronectin (VTN) is an important extracellular matrix protein in tissue remodeling, but its role in COPD is unknown. We show that VTN regulates tissue remodeling through urokinase plasminogen activator (uPA) signaling pathway in COPD. In human COPD airways and bronchoepithelial cells and the airways of mice with cigarette smoke (CS)-induced experimental COPD, VTN protein was not changed, but downstream uPA signaling was altered (increased plasminogen activator inhibitor-1, uPAR) that induced collagen and airway remodeling.
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