LETTERS FROM OUR READERS:

RE: The Angle Orthodontist, 1999; 69:523–528

To: Editor, The Angle Orthodontist

RE: Epithelial-mesenchymal transformation, palatogenesis and cleft palate

We write with regard to the article by Shapira et al1 entitled “The distribution of clefts of the primary and secondary palates by sex, type, and location.” While we find great merit in the objectives of the study, we would like to clarify some points of discussion concerning palatogenesis and the etiology of cleft palate. The authors comment that clefts form when palatogenesis is disrupted including when ‘the mesenchyme… penetrate(s) through the epithelial membranes.’ Using the references of Loevy2 and Kitamura3 perpetuates the notion that palatogenesis is an example of programmed cell death in which apoptosis of medial edge epithelial cells occurs.

It has been shown by electron microscopy4 and Tunel staining5 that in vivo cell death is rare and is restricted to the periderm with basal cells remaining healthy. When 2 palatal shelves are placed together in vitro, peridermal cells slough off and are trapped in the fusing epithelial seam, inciting the appearance of lysosomes and leading to the erroneous conclusion that all cells in the seam are dying. In fact, the mechanism in palatogenesis following adherence of the 2 palatal shelves is epithelial-mesenchymal transformation.4,6,7 This has been confirmed by Carboxyfluorescein staining at light and electron microscopic levels8,9 and by DiI staining.10,11 Epithelial-mesenchymal transformation of medial edge epithelium to form mesodermal confluence of the palate is now a well-recognized mechanism in palatogenesis.12,13

While this is not the focus of the Shapira et al1 paper, we feel it is important to correct this point. We congratulate the authors on their epidemiologic study of the distribution of cleft palate.