Abstract â–¡ 145

The cranio-facial features that are risk factors for sleep-disordered breathing derive from the first three bronchial arcs. Unfortunately, genes involved in cranio-facial development are still poorly understood. Homeobox genes are found from Drosophilia to man. Recently, knock-out models have been developed but bringing only limited information. Agreement on a genetic participation in cranio-facial development, however, is strong. Hypoxic and hypercapnic responses also involve genetic factors. Finally, obesity may be under genetic control.

Environmental factors may also lead to mild dysmorphia. Experimentally induced increased nasal resistance in rhesus monkeys and the subsequent mouth breathing leads to significant changes in the firing patterns of genioglossus and geniohyoid muscles and the arrest of maxillo-mandibular growth. Mouth breathing during sleep related to allergy and upper airway infections have the same consequences in infants, i.e. abnormal mandibular growth, nasal disease, high and narrow hard palate. Head posture, ultradian rhythm of nasal engorgement and even prone position may also lead to mouth breathing and secondary cranio-facial changes. Sleep fragmentation, which can be a consequence of abnormal upper airway resistance, leads to blunting of hypoxic and hypercapnic responses during wake and sleep. When combined, genetic and environmental factors create an even greater risk of abnormal breathing during sleep. Dolichocephalic children are more likely to be found in families with a history of sleep-disordered breathing.