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Experimental fusion of the naturally cleft, embryonic chick palate
Insights
Experimentally disrupting embryonic chick palatal shelves at specific stages induced fusion. Surgical disruption of medial edge epithelia was key for fusion, regardless of developmental stage or culture conditions.
Area of Science:
- Developmental biology
- Embryology
- Craniofacial development
Background:
- Palatal fusion is a critical developmental process.
- Failure of palatal fusion results in cleft palate, a common birth defect.
- Understanding the mechanisms of palatal fusion can inform strategies to prevent or treat cleft palate.
Purpose of the Study:
- To investigate the potential for experimentally inducing palatal fusion in chick embryos.
- To determine the role of medial edge epithelial integrity in palatal fusion.
- To explore the effects of surgical disruption on palatal shelf healing and fusion.
Main Methods:
- Surgical disruption of medial edges of chick palatal shelves in ovo and in vitro at Hamburger-Hamilton (HH) stages 32-33 and 35.
- Culturing explanted palatal shelves in vitro.
- Histological examination for signs of fusion, healing, inflammation, and tissue abnormalities.
Main Results:
- Palatal shelves disrupted at HH stages 32-33 (day 8) healed without fusion, showing embryonic wound healing.
- Palatal shelves disrupted at HH stage 35 (day 9) fused, with fusion extent dependent on disruption.
- In vitro cultures fused only after medial edge epithelial disruption, irrespective of stage.
- Abnormal blastemae formed in experimentally intact palates; in ovo mortality was high.
Conclusions:
- Experimental induction of palatal fusion is possible through surgical disruption of medial edge epithelia.
- Medial edge epithelial integrity is crucial for natural palatal fusion.
- Chick embryo palatal fusion is sensitive to developmental stage and surgical intervention.
Abstract:
The palatal shelf medial edges of day 8 (Hamburger-Hamilton [HH] stages 32-33) and day 9 (HH stage 35) embryonic chicks were surgically disrupted in ovo and in vitro in an attempt to discover if the naturally cleft chick palate could be induced to fuse experimentally. At HH stages 32-33 (day 8) the chick palatal shelves were apart at the time of in ovo operation. Consequently, their medial edges did not fuse but rather underwent embryonic would healing with re-epithelialisation (which often formed needle track invaginations), but no signs of inflammation or scar or scab tissue formation. Conversely, at HH stage 35 (day 9) the palatal shelves are in contact at the time of in ovo operation and so underwent fusion. The extent of palatal fusion depended upon the extent of initial medial edge epithelial disruption. Fusion did not spread from the operated sites to adjacent unoperated areas, where the palatal shelves were in contact with each other. Occasional epithelial seams were formed, but these persisted and did not undergo cell death. There was no evidence of inflammation or scar or scab tissue at the operated sites. Abnormal bony and muscular blastemae appeared in the continuity zones of these experimentally intact chick palates. Mortality was high for embryos operated upon in ovo. Palatal shelves explanted from HH stages 32, 33, and 35 chick embryos and cultured in vitro with their medial edges in contact did not fuse unless their medial edge epithelia were surgically disrupted, in which cases fusion always occurred regardless of the stage of the explanted shelves.(ABSTRACT TRUNCATED AT 250 WORDS)