Developmental malformations of human tongue and associated syndromes (review)

The development of the tongue begins as known, in the floor of the primitive oral cavity, when the human embryo is four weeks old.More specifically, the tongue develops from the region of the first three or four branchial arches during the period that the external face develops. Malformations of the tongue, are structural defects, present at birth and happening during embryogenesis. The most common malformations are:1. Aglossia2. Microglossia, which is always combined with other defects and syndromes, like Moëbius syndrome3. Macroglossia, which is commonly associated with cretinism, Down’s syndrome, Hunter’s syndrome, Sanfilippo syndrome and other types of mental retardation4. Accesory tongue5. Long tongue6. Cleft or Bifid tongue, condition very usual in patients with the orodigitofacial syndrome7. Glossitis Rhombica Mediana, a developmental malformation?8. Lingual thyroid.Malformations are extensively analysed and discussed.Le développement de la langue commence au niveau du plancher de la cavité orale primitive lorsque l’embryon humain est âgé de 4 semaines.Plus précisément, la langue se développe dans la région des trois ou quatre premiers arcs branchiaux durant la période du développement de la face externe. Les malformations de la langue correspondent à des défauts de structure présents à la naissance et survenant au cours de l’embryogenèse. Les malformations les plus communes sont:1. Aglossie2. Microglossie, qui est souvent combinée à d’autres anomalies ou syndromes, tel le syndrome de Moebius3. Macroglossie, qui est communément associée au crétinisme, au syndrome de Down, au syndrome de Hunter, au syndrome de Sanfilippo et à d’autres types de retard mental4. Langue accessoire5. Langue longue6. Langue bifide, condition très usuelle chez des patients présentant le syndrome orodigitofacial7. Glossite rhomboïde médiane (?)8. Thyroïde linguale.Les malformations sont analysées et discutées

Histological observations of palatal malformations in rat embryos induced by retinoic acid treatment

Malformations of the palate were induced in white rat embryos following maternal exposure to retinoic acid (tretinoin). Five experimental groups and the controls were treated by the following protocol: Group 1: pregnant rats received 100 mg retinoic acid (RA)/kg b.w. suspended in corn oil on gestational day (GD) 11.5; Group 2: 20 mg RA/kg b.w. from GD 8-12; Group 3. 20 mg RA/kg b.w. from GD 7.5-11.5; Group 4. 100 mg RA/kg b.w. on GD 10-11; Group 5: 100 mg RA/kg b.w. on GD 10 and 12; Group 6 received corn oil vehicle from GD 7-14.5; and Group 6: served as non-injected controls. In all retinoic acid treated groups, varying degrees of clefts with occasional attempts of fusion were noted. The severity and frequency of the malformations were dependent on dosage or gestational day of drug treatment. Our results indicate that RA, even at the lowest dose tested (20 mg/kg b.w.) severely affects the various tissues constituting the embryonic palatal shelves by altering cell interaction and possibly programmed cell death. These events would then result in lack of or inadequate differentiation with subsequent formation of aberrant craniofacial architecture