Morphofunctional aspects of clefts and their repercussions on growth

Over the last 50 years, the dominant conception of the etiology of facial clefts postulated that they resulted from a mesodermal deficit that accounted for the primary hypoplasia and the unpredictable nature of subsequent oro-facial growth. Because of this notion, rigid dogmatic interdictions, with no allowance for nuanced treatment adjustments were issued banning sub-periosteal and sub-perichondrial dissections as well as the undertaking of any nasal surgery during the growth period. These prohibitions have had a grave braking effect on the development of treatment for cleft lip and palate patients. With a new comprehension of the important role that the dynamics of fetal ventilation plays in the development of the airways and its influence on maxillary growth researchers no longer have any doubt that normal growth mechanisms operating under abnormal anatomic conditions created by the cleft are the actual causes of the malformations and the facial growth deficit suffered by children born with clefts. It now seems likely that the nasal septum plays only a passive role in growth, as Moss believed, rather than the active one that Scott as well as Delaire defined, calling it the driving force of maxillary development. They advocated re-inserting the lateral muscles on the anterior nasal spine. But practitioners who limit their functional approach to this procedure risk being deceived. In addition this focusing on muscles distracts us from what is essential, nasal ventilation, whose rehabilitation beginning with the first operation and preservation throughout treatment are absolutely necessary to ensure the normal unfolding of a cleft palate patient’s facial growth.