However, the primary structural abnormality present in obese children with OSAS is the lymphoid tissue, rather than other soft tissue components [9]. Obesity features, long face syndrome, elevated systemic blood pressure and craniofacial alterations characterize the clinical presentation of children with OSAS. During the physical examination it is possible to find adenotonsillar hypertrophy [5; 9; 13], inflammation of the nasal mucosa, deviation of the nasal septum, pseudo-macroglossia, narrow upper airway, maxillary constriction and/or some degree of mandibular retrusion [5; 13; 14]. The dento-facial orthopedic treatment procedure of rapid maxillary expansion (RME) is routinely used in young patients to treat constricted maxillary arches [15; 16] and it is also considered a potential additional treatment in children with OSAS. Through methods of facial analysis, it is common to find an increase of the craniomandibular and intermaxillary angles (high angle face) and a posterior rotation of the mandible in children with OSAS [17; 18]. The obstructive sleep apnea symptoms in children are divided into nocturnal and diurnal, with important neurobehavioral effects [1; 5; 19]. Among the diurnal, the most prevalent symptoms are daytime sleepiness, frequent headaches, hyperactivity, nasal speech [5], rebelliousness, inattentive behavior [1; 20; 21], depression [1; 5; 22], mood instability, irritability, and aggressiveness [1; 4; 6; 20; 23]. Nocturnal symptoms include snoring, excessive sweating, observed apnea, intermittent hypoxemia, hypercapnia, sleep fragmentation [5; 6; 24], gasping, oral breathing, sleepwalking and nightmares, paradoxical thoracic movements, and nocturnal enuresis [6; 25]. One of the main reasons why this diagnosis is relevant especially in teenagers is because of the association between a poor academic performance and sleep disordered breathing and daytime sleepiness [4; 23]. Furthermore, children affected by severe OSAS may develop early metabolic syndromes: obesity, dyslipidemia, insulin resistance as well as systemic hypertension [5]. Particular attention should be given to the presence of a short lingual fronulum, which is also associated with difficulties in sucking, swallowing and speech. The presence of this anatomical anomaly induces oral dysfunctions that can lead to oro-facial dysmorphism that decreases the size of the upper airway increasing the risk of upper airway collapsibility during sleep [26; 27]. The precise role that genetics plays in the pathogenesis of pediatric OSAS is still a matter of debate, but there are some clinical syndromes such as Down syndrome, midface hypoplasia and neuromuscular disorders [5, 28] that increase the chances of developing OSAS. This underlines the fact that any acquired or congenital condition involving a respiratory control center may potentially lead to the development of OSAS [5]. Some inflammatory factors and biomarkers like inflammatory cytokines are related to pediatric OSAS [28, 29]. Furthermore, it has been shown that allergic rhinitis can affect sleep because nasal congestion secondary to a nasal mucosa inflammatory process induces an increase in the airway resistance that could result in oral breathing and sleep disruption [5]. Childhood OSAS is difficult to diagnose because, in contrast to adults, children do not usually complain of daytime sleepiness, which is considered to be one of the most significant neurological consequences [1]. The gold standard test to diagnose childhood OSAS is an in-laboratory polysomnography (PSG) [30]. This diagnostic procedure gives various quantitative parameters to assess the respiratory function such as the lowest oxygen saturation (LSAT) and apnea-hypopnea index (AHI) [30, 31]. Patients that present a narrow and/or high arched hard palate are more prone to the development of OSAS and often present dental malocclusions that can be treated with RME [32].