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Journal ArticleDOI

Cleft lip and palate

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TLDR
Prevention is the ultimate objective for clefts of the lip and palate, and a prerequisite of this aim is to elucidate causes of the disorders.
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This article is published in The Lancet.The article was published on 2009-11-21. It has received 1344 citations till now. The article focuses on the topics: Oral cleft & IRF6.

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Citations
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Journal ArticleDOI

Sociodemographic Predictors of Missed Appointments Among Patients With Cleft Lip and Palate.

TL;DR: Disparities exist in attendance rates among patients with CL/P, and at-risk patient populations have been identified, and the allocation of cleft care resources must be efficiently planned in order to enhance the quality of care for at- risk individuals.
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Modulation of lipid metabolic defects rescues cleft palate in Tgfbr2 mutant mice

TL;DR: It is shown that Tgfbr2 mutant palatal mesenchymal cells spontaneously accumulate lipid droplets, resulting from reduced lipolysis activity, which highlights the influence of alternative TGFβ signaling on lipid metabolic activities, as well as how lipid metabolic defects can affect cell proliferation and adversely impact palatogenesis.
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Prevalence of orofacial clefts in Saudi Arabia and neighboring countries: A systematic review.

TL;DR: The eightfold variation in the prevalence of orofacial clefts between highest and lowest prevalence is likely to be due, at least in part, to problems with ascertainment, but there may also be underlying genetic or environmental factors that require further investigation.
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Palatal and oral manifestations of Muenke syndrome (FGFR3-related craniosynostosis).

TL;DR: High-arched palate in Muenke syndrome is common and may warrant clinical attention, as these individuals are more susceptible to recurrent chronic otitis media with effusion, dental malocclusion, and hearing loss.
References
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Journal ArticleDOI

Retinoic Acid Embryopathy

TL;DR: It is possible that a major mechanism of isotretinoin teratogenesis is a deleterious effect on cephalic neural-crest cell activity that results in the observed craniofacial, cardiac, and thymic malformations.
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Apaf1 (CED-4 homolog) regulates programmed cell death in mammalian development.

TL;DR: It is suggested that Apaf1 is essential for Casp3 activation in embryonic brain and is a key regulator of developmental programmed cell death in mammals.
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Clinical manifestations in 105 persons with nevoid basal cell carcinoma syndrome.

TL;DR: The frequency of the clinical and radiological anomalies in Nevoid basal cell carcinoma syndrome in a large population of US patients is delineated and guidelines for diagnosis and management are discussed.
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Transforming growth factor-β3 is required for secondary palate fusion

TL;DR: This result demonstrates that TGF–β3 affects palatal shelf fusion by an intrinsic, primary mechanism rather than by effects secondary to craniofacial defects.
Related Papers (5)

A genome-wide association study of cleft lip with and without cleft palate identifies risk variants near MAFB and ABCA4