Introduction: Evidence from the adult population suggests that sleep-disordered breathing (SDB) (i.e., obstructive sleep apnea [OSA]) is negatively associated with bone mineral density. Whether a similar association exists in children with SDB has not been investigated. Using the mandibular cortical width (MCW) as a proxy for skeletal bone density, we investigated if children at risk of SDB or diagnosed with OSA have a reduced mandibular cortical width compared to children without SDB.
Methods: Two retrospective cross-sectional studies were performed. The first study included comparison of MCW between 24 children with polysomnographically (PSG) diagnosed OSA and 72 age- and sex-matched control children. The second study included a cohort of children in which SDB was suggested by the Pediatric Sleep Questionnaire (PSQ) ( n = 101). MCW was measured from panoramic radiographs.
Results: Multiple-predictors regression analysis from the first study indicated that in children with a severe form of SDB, as induced by OSA severity, there was a negative association with MCW (β = -0.290, P = 0.049). Moreover, PSG-diagnosed OSA children had thinner MCW (2.9. ± 0.6mm) compared to healthy children (3.5 ± 0.6 mm; P = 0.002). These findings were further supported by the second study illustrating that PSQ total scores were negatively associated with MCW (β = -0.391, P < 0.001).
Conclusions: Findings suggest that children at risk for or diagnosed with SDB exhibit reduced mandibular cortical width that purportedly may reflect alterations in bone homeostasis.
Knowledge Transfer Statement: We report that sleep-disordered breathing (including its severe form, obstructive sleep apnea) in children is associated with reduced mandibular cortical width. This association might be a direct consequence of reduced bone health to sleep-disordered breathing or a reflection that reduced bone formation underlies the development of sleep-disordered breathing. Our findings suggest that mandibular cortical width can be used as an adjunct diagnostic parameter for the diagnosis of sleep-disordered breathing.
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http://dx.doi.org/10.1177/2380084418776906 | DOI Listing |
Sleep Breath
January 2025
Department of Cardiac and Vascular Diseases, Jagiellonian University Medical College, John Paul II Hospital, Prądnicka 80, Kraków, 31-202, Poland.
Background: Obstructive sleep apnoea (OSA) may lead to heart rhythm abnormalities including bradycardia. Our aim was to ascertain clinical and echocardiographic parameters in patients with OSA in whom severe bradycardia was detected in an outpatient setting, as well as to evaluate the efficacy of CPAP therapy on heart rate normalization at the early stages of treatment.
Methods: Fifteen patients mild, moderate or severe OSA and concomitant bradycardia were enrolled.
BMC Med
January 2025
Sleep Medicine Center, State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, National Center for Respiratory Medicine, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, NO.28 Qiaozhong Mid Road, Guangzhou, Guangdong, 510160, China.
Background: Obstructive sleep apnea (OSA) is linked to brain alterations, but the specific regions affected and the causal associations between these changes remain unclear.
Methods: We studied 20 pairs of age-, sex-, BMI-, and education- matched OSA patients and healthy controls using multimodal magnetic resonance imaging (MRI) from August 2019 to February 2020. Additionally, large-scale Mendelian randomization analyses were performed using genome-wide association study (GWAS) data on OSA and 3935 brain imaging-derived phenotypes (IDPs), assessed in up to 33,224 individuals between December 2023 and March 2024, to explore potential genetic causality between OSA and alterations in whole brain structure and function.
Handb Clin Neurol
January 2025
Department of Neurology and Clinical Research Center of Neurological Disease, Second Affiliated Hospital of Soochow University, Suzhou, China.
Sleep and circadian dysfunction are common nonmotor symptoms in patients with Parkinson disease (PD). Sleep and circadian dysfunction usually have a significant negative impact on quality of life and may also serve as markers to identify patients in the preclinical stage of PD. Sleep disturbances have different types in PD such as insomnia, excessive daytime sleepiness, rapid eye movement sleep behavior disorders, restless legs syndrome, and sleep-disordered breathing.
View Article and Find Full Text PDFHandb Clin Neurol
January 2025
Department of Systems Medicine, University of Rome Tor Vergata, Rome, Italy; Sleep Medicine Centre, Neurology Unit, University Hospital of Rome Tor Vergata, Rome, Italy.
Obstructive sleep apnea syndrome (OSAS) significantly affects the sleep-wake circadian rhythm through intermittent hypoxia and chronic sleep fragmentation. OSAS patients often experience excessive daytime sleepiness, frequent awakenings, and sleep fragmentation, leading to a disrupted circadian rhythm and altered sleep-wake cycle. These disruptions may exacerbate OSAS symptoms and contribute to neurodegenerative processes, particularly through the modulation of clock gene expression such as CLOCK, BMAL1, and PER.
View Article and Find Full Text PDFBMC Endocr Disord
January 2025
Department of Respiratory and Critical Care Medicine, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Background: Menopause is a significant phase in women's health, in which the incidence of obstructive sleep apnea (OSA) is significantly increased. Body fat distribution changes with age and hormone levels in postmenopausal women, but the extent to which changes in body fat distribution affect the occurrence of OSA is unclear.
Methods: This research performed a cross-sectional analysis utilizing data from the 2015-2016 National Health and Nutrition Examination Survey (NHANES).
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