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Differences in the size of the palatal processes in mouse embryos with cleft palate induced in two critical periods

The Cleft Palate Journal
|January 1, 1978
PubMed

Insights

Cortisone acetate given to pregnant mice reduced the size of palatal processes in embryos, hindering their ability to fuse. 6-amino-nicotinamide had no significant effect on palatal process development.

Area of Science:

  • Developmental biology
  • Teratology
  • Pharmacology

Background:

  • Cleft palate is a common birth defect.
  • Understanding the molecular and developmental mechanisms is crucial for prevention and treatment.
  • Exogenous factors during gestation can significantly impact embryonic development.

Purpose of the Study:

  • To investigate the effects of cortisone acetate and 6-amino-nicotinamide on palatal process development in ICR-Velaz mouse embryos.
  • To determine if these agents cause or contribute to cleft palate formation.

Main Methods:

  • Planimetric measurements of palatal process projections in ICR-Velaz mouse embryos.
  • Intramuscular administration of cortisone acetate (7.5 mg) on day 12 of gestation.
  • Intramuscular administration of 6-amino-nicotinamide (0.5 mg) on day 14 of gestation.
  • Comparison of treated embryos with control groups.

Main Results:

  • Cortisone acetate administration resulted in smaller pre-horizontalization palatal processes compared to controls.
  • Following horizontalization, palatal processes in cortisone-treated embryos were inadequate to meet in the midline.
  • 6-amino-nicotinamide administration did not significantly alter palatal process size.

Conclusions:

  • Cortisone acetate exposure during a critical period of palatogenesis can lead to impaired palatal fusion in mice.
  • The findings suggest cortisone acetate is a teratogen that interferes with normal palate development.
  • 6-amino-nicotinamide does not appear to affect palatal process size at the tested dosage and administration timing.

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