PURPOSE:

The palate is assembled from at least six neuroembryological developmental fields. Abnormalities or deficiencies in any of these fields during development may lead to clefting of the palate. There are multiple clinical manifestations of cleft palate (submucous, isolated cleft palate versus cleft-lip associated cleft palate, unilateral, bilateral, primary and secondary), which may be understood by analyzing the interrelationships between the different developmental fields.

METHODS:

The concept of the neuromeric field theory of embryological development may be applied to the formation of the palate by outlining the growth of the individual anatomical components of the palate (bony, muscular, and surrounding maxillary structures).  With knowlege of the interplay between separate developmental fields, it is possible to explain the neuroembryological basis of both the physical and functional manifestations of anomalous developmental field assembly in cleft palate formation.

RESULTS:

Palatogenesis occurs at 18-20 days gestation, and involves six fields derived from the embryological neuromeres.  The ethmoid field is derived from r1 mesenchyme; absence of this field as seen in holoprosencephaly causes cleft palate when the defective perpendicular plate of the ethmoid prevents subsequent migration of the premaxilla and vomer.  Attenuation of the perpendicular plate may be seen in the case of high arched palate.  Deficiency in the r2′ fields (vomer, premaxilla) may lead to clefting when midline closure cannot be achieved due to a critically large distance between these structures and the maxillary shelves.  Similarly, defects in the r2-derived maxillary shelves can lead to clefting as these are unable to contact the vomer and premaxilla at the midline.

Deficiency in the mandible (r3 field) as seen in Pierre-Robin sequence may indirectly lead to cleft palate by tongue malposition and interference with normal palatal closure.  Deficiency in the r6-derived fields containing the levator veli palatini and superior constrictor muscles can cause speech abnormalities in the absence of significant clinical manifestation of cleft palate, as seen in submucous clefts.

CONCLUSION:

Deficiency states in a number of developmental fields can lead to cleft palate; neuromeric terminology provides an embryologic anatomic basis for differentiating different types of cleft palate.  Cleft palate pathophysiology may be categorized by the field(s) involved in their formation.  Stratification of cleft palate by embryologic mechanism may lead to more complete understanding and treatment of associated developmental and functional defects.