Obstructive sleep apnea (OSA) is the most common type of sleep-disordered breathing, affecting 9% to 15% of middle-aged adults.¹ Obstructive sleep apnea is clinically important because it has a potential risk of causing a wide range of comorbidities. Among those possible associated comorbidities, cardiovascular diseases, including myocardial infarction, ischemic heart disease, and stroke, can result in high levels of morbidity and mortality, which require clinical intervention.^2-5 Nevertheless, it is unclear how OSA can cause these diseases, and numerous studies have attempted to determine the underlying pathogenic mechanism of this undesirable association.

Objectives: Pediatric obstructive sleep apnea syndrome (OSAS), like adult OSAS, is characterized by intermittent upper airway collapse during sleep and is associated with anatomic and neuromuscular factors. However, the clinical manifestations, diagnostic criteria, and Polysomnographic findings of OSAS in children are likely to be different from those in adults. The purpose of this study was to identify the characteristics that distinguish the clinical manifestations and Polysomnographic findings of OSAS in children from those in adults. Methods: The study population consisted of 34 children (mean age, 7.6 years; range, 4 to 16 years) with OSAS and 33 adults (mean age, 40.1 years; range, 18 to 58 years) with OSAS. We compared various clinical manifestations, such as body mass index, tonsil size, severity of symptoms and signs, and Polysomnographic data, between these groups. Results: Obesity was more common among the adults, whereas tonsillar hypertrophy was more common among the children. There were significant differences between the groups in the severity of symptoms and signs, including witnessed apnea, daytime sleepiness, morning headache, memory reduction, and daytime fatigue. In the children with OSAS, slow-wave sleep was relatively well preserved, and respiratory events such as apnea and hypopnea occurred mainly during rapid eye movement sleep. Conclusions: The clinical manifestations and Polysomnographic findings in children with OSAS differ from those in adults with OSAS.

The aim of this study was to develop a predictive model of objective oropharyngeal obstructive sleep apnea (OSA) surgery outcomes including success rate and apnea-hypopnea index (AHI) reduction ratio in adult OSA patients. Retrospective outcome research. All subjects with OSA who underwent oropharyngeal and/or nasal surgery and were followed for at least 3 months were enrolled in this study. Demographic, anatomical [tonsil size (TS) and palate-tongue position (PTP) grade (Gr)], and polysomnographic parameters were analyzed. The AHI reduction ratio (%) was defined as [(postoperative AHI—preoperative AHI) x 100 / postoperative AHI], and surgical success was defined as a ≥ 50% reduction in preoperative AHI with a postoperative AHI < 20. A total of 156 consecutive OSAS adult patients (mean age ± SD = 38.9 ± 9.6, M / F = 149 / 7) were included in this study. The best predictive equation by Forward Selection likelihood ratio (LR) logistic regression analysis was: The best predictive equation according to stepwise multiple linear regression analysis was: (TS/PTP Gr = 1 if TS/PTP Gr 3 or 4, TS/PTP Gr = 0 if TS/PTP Gr 1 or 2) The predictive models for oropharyngeal surgery described in this study may be useful for planning surgical treatments and improving objective outcomes in adult OSA patients.

Cigarette smoke exposure has been shown to be associated with chronic rhinosinusitis and tissue remodeling. The present study aimed to investigate the effects of cigarette smoke extract (CSE) on matrix metalloproteinase (MMP) and tissue inhibitor of metalloproteinase (TIMP) production in nasal fibroblasts and to determine the underlying molecular mechanisms. Primary nasal fibroblasts from six patients were isolated and cultured. After the exposure of fibroblasts to CSE, the expression levels of MMP-2, MMP-9, TIMP-1, and TIMP-2 were measured by real-time PCR, ELISA, and immunofluorescence staining. The enzymatic activities of MMP-2 and MMP-9 were measured by gelatin zymography. Reactive oxygen species (ROS) production was analyzed using dichloro-dihydro-fluorescein diacetate and Amplex Red assays. PI3K/Akt phosphorylation and NF-κB activation were determined by Western blotting and luciferase assay. CSE significantly increased MMP-2 expression and inhibited TIMP-2 expression but did not affect MMP-9 and TIMP-1 expression. Furthermore, CSE significantly induced ROS production. However, treatment with ROS scavengers, specific PI3K/Akt inhibitors, NF-κB inhibitor, and glucocorticosteroids significantly decreased MMP-2 expression and increased TIMP-2 expression. Our results suggest that steroids inhibit CSE-regulated MMP-2 and TIMP-2 production and activation through the ROS/ PI3K, Akt, and NF-κB signaling pathways in nasal fibroblasts. CSE may contribute to the pathogenesis of chronic rhinosinusitis by regulating MMP-2 and TIMP-2 expression.