PubMed · 3044501
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A L Moss, R W Piggott, K J Jones. 1988-07-09. Submucous cleft palate.. https://doi.org/10.1136/bmj.297.6641.85
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Recent studies have unveiled disrupted metabolism in the progression of cleft palate (CP), a congenital anomaly characterized by defective fusion of facial structures. Nonetheless, the precise composition of this disrupted metabolism remains elusive, prompting us to identify these components and elucidate primary metabolic irregularities contributing to CP pathogenesis. We established a murine CP model by retinoic acid (RA) treatment and analyzed control and RA-treated embryonic palatal tissues by LC-MS-based proteomic approach. We identified 220 significantly upregulated and 224 significantly downregulated proteins. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis revealed that these differentially expressed proteins (DEPs) were involved in translation, ribosome assembly, mitochondrial function, mRNA binding, as well as key metabolic pathways like oxidative phosphorylation (OXPHOS), glycolysis/gluconeogenesis, and amino acid biosynthesis. These findings suggest that dysregulated ribosome-related pathways and disrupted metabolism play a critical role in CP development. Protein-protein interaction analysis using the STRING database revealed a tightly connected network of DEPs. Furthermore, we identified the top 10 hub proteins in CP using the Cytohubba plugin in Cytoscape. These hub proteins, including RPL8, RPS11, ALB, PA2G4, RPL23, RPS6, CCT7, EGFR, HSPD1, and RPS28, are potentially key regulators of CP pathogenesis. In conclusion, our comprehensive proteomic analysis provides insights into the molecular alterations associated with RA-induced CP in Kun Ming mice. These findings suggest potential therapeutic targets and pathways to understand and prevent congenital craniofacial anomalies.
A number of modifications of the tongue blade of the Dott mouth gag for cleft palate surgery are described and illustrated. These modifications facilitate cleft palate surgery, especially on small infants and patients with micrognathia, as well as surgery under the microscope and also reduce the risk of compression of the endotracheal tube.
It is the aim of presurgical infant orthopedics (PSIO) to reduce the width of the cleft and to achieve optimal alignment of the cleft palate segments within the first few months of infancy prior to any surgical cleft closure. The question about the amount that PSIO can stimulate and steer the growth of the maxilla using a Hotz and Gnoinski passive appliance has not yet been satisfactorily answered. In this study, a 3-dimensional digital computer-aided procedure was developed to analyze metrically and to visualize the growth of the edentulous maxilla of cleft lip and palate in infants. In a pilot study, a series of digital scans of consecutive plaster casts was carried out. 5 infants with complete unilateral cleft lip and palate (UCLP), who had been treated with passive appliances were evaluated. Impressions were taken at the age of one week and after 3, 6 and 12 months. Following digitizing, the casts were computer-reconstructed and segmented perpendicular to the alveolar crest, the reference points being C1, C1', C2, C2' and I. The volume of the resulting segments was ascertained. Computer superimposition of reconstructed consecutive casts was employed to facilitate a visualization of the extent and direction of morphological changes. Our first results have shown that with our method it is possible to quantify the growth rate of defined segments of the maxilla. The 3-dimensional analysis presented here will be the basis for further studies to objectify PSIO.