Oxidant stress and inflammation in the snoring child: Confluent pathways to upper airway pathogenesis and end-organ morbidity - 11/08/11

Doi : 10.1016/j.smrv.2005.07.005

David Gozal ^a,^b,^c,^⁎ , Leila Kheirandish ^a,^{^{1
Division of Pediatric Sleep Medicine, University of Louisville, 571 S. Floyd Street, Suite 409, Louisville, KY 40202, USA. Tel.: +1 502 852 5391; fax: +1 502 852 2215.}}
^a Division of Pediatric Sleep Medicine, Department of Pediatrics, Kosair Children’s Hospital Research Institute, University of Louisville, 570 S. Preston Street, Suite 321, Louisville, KY 40202, USA
^b Department of Pharmacology and Toxicology, University of Louisville, 570 S. Preston Street, Suite 321, Louisville, KY 40202, USA
^c Department of Psychology and Brain Sciences, University of Louisville, 570 S. Preston Street, Suite 321, Louisville, KY 40202, USA

Corresponding author. Tel.: +1 502 852 2323; fax: +1 502 852 2215.

Summary

Snoring in children is increasingly being recognized as a highly prevalent condition, and indicates the presence of heightened upper airway resistance during sleep. In this paper, we present evidence to support the hypothesis that local inflammatory processes within the upper airway contribute to the pathophysiology of adenotonsillar hypertrophy and altered reflexes potentially leading to increased propensity for upper airway obstruction during sleep. Furthermore, the cumulative evidence supporting multiorgan morbidity for sleep-disordered breathing (SDB) is reviewed, and a unified hypothesis of a triple risk model proposing oxidative-inflammatory mechanisms as mediating the morbid consequences of SDB is presented. This hypothetical working model incorporates both dose-dependent disease severity components, as well as environmental and genetic elements of susceptibility.

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Keywords : Sleep, Children, Polysomnography, Oxidant stress, Learning, Memory, ADHD, Inflammation, Adenotonsillar hypertrophy, Obstructive sleep apnea