## 4 Discussion  
Although some authors consider the relationship between nasal obstruction and craniofacial growth unclear [16], others have reported that the presence of obstacles in the nose and pharyngeal areas can cause an increase in nasal airway resistance, even in a pediatric population [17], and affect lower facial height and maxillary length [18] producing malocclusion [11,12] and ogival palate [19]. It has been reported that an anatomically narrow airway is a predisposing factor, particularly in a child, for mouth breathing [20]. Hypertrophy of the adenoids and tonsils [17] and unilateral choana atresia or sinonasal tumors (even in children) such as lymphomas or sarcomas [21,22] are some of the conditions most commonly associated with an increase in nasal airway resistance in children. As it causes upper airway obstruction, AR has also been found to be a risk factor for malocclusion [11,12]. A study comparing sibling pairs with and without AR uncovered that mouth breathing was associated with an increased palatal height [23]. These results confirm earlier reports that allergic rhinitis may be associated with altered facial growth. Interestingly, some have noted that even when these factors are removed, many continue to breathe through the mouth out of habit [24]. It has been shown that the adaptation from nasal to mouth breathing can affect facial growth. The typical facial characteristics of the mouth-breathing subject have, in fact, been described as the \"adenoid face\" or \"long face syndrome\". It is typically associated with a number of classical features including a longer lower third of the face, under-developed nose, narrow nostrils, lip incompetence at rest, and short hypertrophic upper lip [7,25]. The prevalence of malocclusion in mouth-breathing children is highly variable, reaching its highest point of 81.4% [26]. The variability could be due to the type of malocclusion [27], but also to the presence of AR and increased nasal resistance. Furthermore, malocclusion can have an impact on nasal obstruction due to reduced maxillary expansion [28], thus promoting inflammation of the nasal mucosa and nasal obstruction even in absence of AR. Previous studies have shown that the transverse dimension of the upper arch is significantly smaller in children affected by mouth breathing due to AR [11,12]. While it is true  
\begin{table}
\begin{tabular}{c c c c c c} \hline \hline
**Coefficients** & & & & & \\ \hline  & **Estimate** & **Exp (Estimate)** & **Std. Error** & **z Value** & **Pr (\textgreater{}z)** \\ \hline (Intercept) & 1.81334 & & 0.49636 & 3.653 & 0.000259 *** \\ \hline \begin{tabular}{c} Allergic \\ rhinitis \\ \end{tabular}  & 0.64921 & 1.9403 & 0.29896 & 2.172 & 0.029890 * \\ \hline \ \begin{tabular}{c} Age \\ \end{tabular}  & \(-\)0.11330 & 0.8929 & 0.03121 & \(-\)3.631 & 0.000283 *** \\ \hline
\begin{tabular}{c} Signif. codes: 0 ***\(\!\! that some studies performed until now have demonstrated contrasting results [11; 12; 13; 19; 27], most were conducted on small groups of patients or were not controlled studies. Although retrospective, the current study is a controlled one conducted on a large group of homogeneous children (all treated by the same group of orthodontists) with the aim to evaluate the influence of AR and asthma on maxillary transverse contraction/expansion. The posterior arch width was smaller in the study than in the control group. This supports the fact that posterior arch width is a good support for the diagnosis of posterior crossbite The presence of AR was found to be marginally significant (not quite at the 5% level) meaning that AR has only a slight effect on the presence of posterior crossbite/ogival palate. Since some studies have demonstrated that upper and lower airway functions are strictly correlated [29; 30] even in pediatric populations [31], the presence of asthma was also considered in order to evaluate its possible influence on malocclusion in children.