cleft palate - Medical Dictionary

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cleft palate		Congenital fissure of the soft and/or hard palate, due to faulty fusion. [ Articles \| Books \| Images \| Discussion groups ]

Additional comments : Cleft palate is one of the most common birth defects in humans, in which both genetic and environmental factors are involved. Hagiwara N, Katarova Z, Siracusa LD, Brilliant MH. Dev Biol. 2003 Feb 1;254(1):93-101. Isolated cleft palate is a common congenital craniofacial birth defect, occurring once in every 1,000 births. Cleft palate as an isolated malformation is distinct from cleft lip with or without cleft palate, which has a higher incidence (1:700). Cleft palate associated with other abnormalities as part of a syndrome account for 55% of cases. R Rice, B Spencer-Dene, EC Connor, A Gritli-Linde, … - J. Clin. Invest, 2004 Cleft lip and/or cleft palate is among the most frequent birth defect seen in humans, with a reported prevalence of 1 in 700 births worldwide. ACB Marcano, K Doudney, C Braybrook, R Squires, MA … - Journal of Medical Genetics, 2004 Cleft palate is a gap in the hard or soft palate, which forms from the fifth through twelfth weeks of development. Orofacial clefts (cleft lip, cleft palate) are among the most common of all major birth defects, but very little is known about their causation. Genetic factors are thought to play a major role, and there has been considerable recent effort to map and identify genes that constitute risk factors for clefts. RA Spritz - Curr Opin Pediatr, 2001 - co-pediatrics.com Free Full Text Cholesterol precursors and facial clefting J Clin Invest. 2006 Sep;116(9):2322-5. Inborn errors of cholesterol synthesis cause human malformation syndromes, including Smith-Lemli-Opitz syndrome, lathosterolosis, desmosterolosis, X-linked dominant chondrodysplasia punctata type 2, and congenital hemidysplasia with ichthyosiform erythroderma and limb defects. Because adequate cholesterol is not transported across the placenta, low cholesterol and elevated sterol precursor levels are present during embryogenesis. It has been debated whether the malformations result from low cholesterol or the buildup of sterol precursors. In this issue of the JCI, Engelking et al. provide evidence that sterol precursor accumulation plays a pivotal role in the genesis of facial malformations. Surgical repair of hard palate cleft with absorbable membrane: the new surgical technique and its clinical application Swiss Med Wkly. 2006 Feb 4;136(5-6):86-8. This study evaluated a new surgical technique with absorbable membrane to repair hard palate cleft without extensive mobilisation of the mucoperiosteum. From 2001 to 2002, 32 selected patients with complete unilateral clefts underwent this surgical operation. The traditional flap surgical operation was performed at the soft palate, uvula and anterior alveolar cleft. The absorbable membrane was implanted to the hard palate cleft gap to guide the regeneration of the mucoperiosteum. The patients were followed up for 1-6 months after the operation. The speech assessment was carried out 12 months after the operation. Of 32 patients, 30 were successfully operated by this method and no obvious complications occurred. Primary healing on tissue defect of hard palate was obtained in 27 patients and secondary healing in 3 patients. Eighty percent of the 30 patients had good or excellent speech 12 months after the operation. The operation failed in 2 patients. The surgical technique with absorbable membrane to repair hard palate appears to have several valuable advantages including the decreased area of the hard palate involved and favourable outcome for speech in the majority of cases. Cleft lip and palate versus cleft lip only: are they distinct defects? Am J Epidemiol. 2005 Sep 1;162(5):448-53. Epub 2005 Aug 2. Cleft lip defects are usually regarded as a single entity, with the assumption that an accompanying cleft palate represents the more severe form. The authors linked data from the Medical Birth Registry of Norway with medical records from two centralized centers to provide a population-based data set. They assessed the distribution of cleft lip only and cleft lip with cleft palate by covariate. Among 1.8 million Norwegian livebirths between 1967 and 1998, there were 1,572 cases of cleft lip with cleft palate and 1,122 cases with cleft lip only. Seventeen percent of those with cleft lip and palate had another defect compared with 9% of those with cleft lip only. For boys, the risk was greater for cleft lip and palate than for cleft lip only (odds ratio=2.4 vs. 1.8, p<0.001 for difference). The risk of cleft lip only, but not of cleft lip and palate, was increased for twins (odds ratio=1.6 vs. 1.1, p=0.11) and infants whose parents were first cousins (odds ratio=2.7 vs. 0.7, p=0.07). Although cleft lip with cleft palate may simply represent a more severe form of the defect, epidemiologic assessments of cleft lip should, when possible, include separate analyses of these two groups. Primary dentition status and treatment needs of children with cleft lip and/or palate J Indian Soc Pedod Prev Dent. 2005 Jun;23(2):80-82. The aim of this study was to assess the primary dentition status and treatment needs in children with cleft lip, cleft palate and or both. A descriptive, cross-sectional study was done through oral examination on a sample of 83, 2-5 years old cleft lip/palate children (46 boys and 37 girls). A self-designed questionnaire to obtain pertinent data related to level of education of parents and infant-feeding practices was used for recording the data while examining the children. Majority of cleft affected children had dental caries experience and required different types of treatment. The result of this study shows that: (1) all age groups of cleft affected children had dental caries experience, (2) children with primary type of cleft had less dental caries prevalence than children with cleft of secondary or combination type ( P <0.05), (3) treatment needs due to caries were more in combination type of cleft compared to primary and secondary. Cancer risk in persons with oral cleft--a population-based study of 8,093 cases Am J Epidemiol. 2005 Jun 1;161(11):1047-55. The authors conducted a nationwide study of the occurrence of cancer among 8,093 Danish oral cleft cases born in 1936 through 1998 and followed in the Danish Cancer Registry from 1968 through 1998, a total of 175,863 person-years, to assess a possible association between cancer and oral clefts. Observed and expected numbers of cancers among oral cleft cases were summarized as the overall and as 52 site-specific standardized incidence ratios. The expected overall number of all cancers was 131, but 140 incident cancers were found, corresponding to a standardized incidence ratio of 1.07 (95% confidence interval (CI): 0.90, 1.26). Analyses of the 52 sites for all oral cleft cases and analyses stratified for three cleft subgroups and the two sexes revealed only a few significant associations: an increased occurrence of breast cancer among females born with cleft lip and/or cleft palate (standardized incidence ratio (SIR) = 1.52, 95% CI: 1.05, 2.14), primary brain cancer among females born with cleft palate (SIR = 3.11, 95% CI: 1.14, 6.78), and primary lung cancer among males born with both cleft lip and cleft palate (SIR = 2.49, 95% CI: 1.00, 5.14). The results do not provide evidence for an increased overall cancer risk for individuals born with oral clefts. An update on the aetiology of orofacial clefts Hong Kong Med J. 2004 Oct;10(5):331-6. OBJECTIVE: To review recent data on the aetiology of cleft lip and palate. DATA SOURCES: MEDLINE literature search (1986-2003). STUDY SELECTION: Literature and data on aetiology of cleft lip and palate using the following key words: 'cleft lip', 'cleft palate', 'aetiology', and 'genetics'. DATA EXTRACTION: Relevant information and data were reviewed by the authors. DATA SYNTHESIS: Cleft lip and palate is one of the most common types of congenital malformation. The aetiology seems complex, but genetics plays a major role. Recently several genes causing syndromic cleft lip and palate have been discovered. Three of them--namely T-box transcription factor-22 (TBX22), poliovirus receptor like-1 (PVRL1), and interferon regulatory factor-6 (IRF6)--are responsible for causing X-linked cleft palate, cleft lip/palate-ectodermal dysplasia syndrome, and Van der Woude's and popliteal pterygium syndromes, respectively; they are also implied in non-syndromic cleft lip and palate. The nature and function of these genes vary widely, illustrating high vulnerability within the craniofacial developmental pathways. The aetiological complexity of non-syndromic cleft lip and palate is also exemplified by the large number of candidate genes and loci. CONCLUSIONS: The aetiology of non-syndromic cleft lip and palate is still largely unknown, but mutations in candidate genes have already been identified in a small proportion of cases of non-syndromic cleft lip and palate. Determining the relative risk of cleft lip and palate, on the basis of genetic background and environmental influence, including smoking, alcohol use, and dietary factors, will aid in genetic counselling and the development of future preventive measures.

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