Comment on “Near-Normalized Maxillomandibular Relationship and Upper Airway in Infants With Robin Sequence Treated With Stanford Orthodontic Airway Plate”

Abstract

It's interesting to note that despite clinical improvements in upper airway dimensions, the maxillary, mandibular, and mandibular body lengths remained smaller than those of controls. This finding may represent an underlying neurocristopathy, which represents a deficiency in the population of neural crest cells available in the embryonic maxillary and mandibular processes de novo. Indeed, it is known that craniofacial dimensions in infants with malformations, such as cleft palate, are often smaller when compared to non-cleft counterparts. The post-treatment decrease in the SNA angle and increase in angle SNB, which resulted in a decreased ANB angle may be associated with a “headgear effect” whereby the maxilla is dragged postero-inferiorly by the mandible, aided by gravity. To avoid this effect, proactive maxillary development might be beneficial. In fact, the concept of “catch-up growth” is also noteworthy since a developmental mechanism would need to be invoked. The authors referred to the old Functional matrix hypothesis, but the treatment effect was primarily a change in jaw position, which evoked a positive functional outcome. Thus, according to the Spatial matrix hypothesis, clinical decompensation of a dysfunctional spatial matrix leads to a cascade of events since a change in mandibular position is associated with changes in gene expression. Recently, genetic expression of Sdf1 and Foxc1 associated with histologic changes following mandibular advancement in rats has been reported as well as the effects of the PINK1/Parkin pathway on the genioglossus muscle through mandibular advancement device use in rabbits with obstructive sleep apnea. Clinically, therapeutic epigenetic changes using an orthodontic mandibular advancement device have also been reported in children.