The prevalence and severity of overweight and obesity in children and adolescents has witnessed dramatic increases in the last few decades worldwide.19,20 For example, the prevalence of childhood overweight doubled among children 6 to 11 years of age and tripled among children 12 to 17 years of age in the United States between 1980 and 2000.21,22 It has become apparent that obese children may be at increased risk for OSA.23–29 Indeed, the proportion of respiratory disturbances during sleep was found markedly increased among obese children.25,26 In a case-control study design, Redline and colleagues23 examined the risk factors for sleep-disordered breathing (SDB) in children age 2 to 18 years, and they found that the risk among obese children was increased fourfold to fivefold. In fact, for every increment in body mass index (BMI) of 1 kg/m2 beyond the mean BMI for age and gender, the risk of OSA increased by 12%. Similar trends demonstrating an increased risk of OSA among obese and overweight children have been reported from all over the world. In this context, we have reported30,31 that the presence of obesity appears to modify the end-organ susceptibility to OSA and prescribes some of the differences in phenotypic manifestations and clinical presentations. Thus, similar to adults, obese children appear to be at increased risk for the development of SDB, and the severity of OSA seems to be proportional to the degree of obesity.23,27,29 Conversely, hypertrophic adenotonsillar tissues may not always be the main contributing factor to the development of OSA in obese children, and even among nonobese children, tonsil size correlated with the severity of OSA only among younger children (ie, < 7 years of age).13,32,33 However, the respective contributions of adenotonsillar size and BMI on pediatric OSA have not been critically examined. Therefore, we conducted the present study to test several related hypotheses, as follows: (1) that obese children with OSA will have less adenotonsillar hypertrophy compared to nonobese children with OSA of matched severity; (2) that this effect will not differ among children below or above the age of 7 years after controlling for gender and ethnicity; and (3) obese children with OSA will have a higher Mallampati classification score34 when compared to nonobese children with OSA of matched severity. To examine these issues, we conducted a retrospective examination of polysomnographic findings in a large cohort of age-, gender- and ethnicity-matched obese and nonobese children with OSA of similar severity who received a diagnosis in our pediatric sleep center.