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[Comparative histomorphological study on the craniomaxillary development of the trisomy-18 with cleft palate and
Z Cai1, H von Domarus, E Engel
1Department of Oral and Maxillofacial Surgery, School of Stomatology, Bejing Medical University.
Insights
Trisomy 18 with cleft palate (Ts + CP) mouse models exhibit significant developmental hypoplasia in craniomaxillary hard tissues. These findings suggest a strong link between autosomal trisomy and craniofacial malformations.
Area of Science:
- Developmental Biology
- Genetics
- Craniofacial Biology
Background:
- Cleft palate is a common congenital anomaly.
- Trisomy 18 (Edwards syndrome) is a genetic disorder associated with multiple birth defects, including craniofacial abnormalities.
Purpose of the Study:
- To compare the histological morphology of the craniomaxillary complex in Trisomy 18 with cleft palate (Ts + CP) mouse fetuses and euploid controls.
- To investigate whether cleft palate in Ts + CP is linked to craniomaxillary complex maldevelopment or adjacent tissue hypoplasia.
Main Methods:
- Histomorphological analysis of serially sectioned craniomaxillary complexes from 30 pairs of Ts + CP and euploid mouse fetuses.
- Comparative study focused on primary palate, hard palate, and soft palate structures.
Main Results:
- Ts + CP fetuses showed significant developmental hypoplasia of primary palatal shelves.
- Hypoplasia was observed in palatal shelves, vomer, palatal bone, and nasal septal cartilage.
- Wider nasal septum, nasal capsule, and increased airway/nasopharyngeal volume were noted in Ts + CP samples.
Conclusions:
- Hard tissues of the craniomaxillary complex in Ts + CP mouse fetuses demonstrate severe maldevelopment and hypoplasia.
- These craniofacial changes are likely associated with the underlying autosomal trisomic condition.
Objective:
The aim of this study is to compare histological morphology of craniomaxillary complex of Trisomy 18 with cleft palate (Ts + CP) and euploid mouse foetuses to understand whether cleft palate is associated with maldevelopment of the craniomaxillary complex or with hypoplasia of the adjacent tissues.
Methods:
Thirty pairs of Ts + CP and euploid mouse foetuses with about equal body weight were selected, and sixty craniomaxillary complex were precisely orientated in the coronal plane, then serially sectioned with 7 microns thickness through the primary palate, the whole hard palate and the soft palate. Finally six sections were selected for comparative histomorphological study based on anatomical landmarks.
Results:
The trisomy with cleft palate mouse foetuses had significantly developmental hypoplasia in the primary palatal shelves. The palatal shelves, vomer, palatal bone and nasal septal cartilage in cleft samples showed significantly developmental hypoplasia with a relatively wider nasal septum, nasal capsule and a bigger nasal airway volume, nasopharyngeal cavity.
Conclusion:
The hard tissues of the craniomaxillary complex in Ts + CP mouse foetuses, including bone and cartilage show serious maldevelopment or developmental hypoplasia, and these may be closely related to the autosomal trisomic condition.