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Results for “CLEFT PALATE”

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At least 73 records · Page 4Linked to original sources
PubMed2001

The mechanism of palatal clefting in the Col11a1 mutant mouse.

The occurrence of cleft palate in mutant mice offers an opportunity to understand the possible role of specific genes in palatogenesis. Here, cleft palate in mice carrying the chondrodysplasia (cho) defect, which consists of an autosomal-recessive mutation in the collagen gene Col11a1, was investigated. The proposed cause of cleft palate in cho homozygous mice is failure of the palatal shelves to adhere and make contact due to mandibular growth abnormalities. Another cause of cleft palate that has recently been demonstrated in other animal models is failure of the midline epithelial seam forming between the shelves to undergo epithelial-mesenchymal transformation (EMT). The present strategy to test the likelihood of this second possibility was to culture the unfused cho/cho palatal shelves at different stages of development to see if they were capable of adhering and undergoing EMT in vitro. By using carboxydichlorofluorescein succinimidyl ester to trace the fate of the medial-edge epithelium (MEE), it was shown that cho/cho palates have full potential for MEE adherence and EMT up to embryonic day 17.5/18.5, when epithelia keratinize before birth, preventing the adherence of both the normal and homozygous palatal shelves. Thus, the major effect of the mutant collagen gene on the palate is likely to be via mandibular growth disruption. The possibility that unfused palatal shelves in other clinical syndromes can adhere and undergo EMT if brought into contact at appropriate times before birth has important therapeutic implications.

Animals↗
PubMed2004

The development of symbolic play and language in toddlers with cleft palate.

This study compared the longitudinal performance of two groups of toddlers with palatal clefts and an age-matched group of children without palatal clefts on measures of elicited symbolic play at 18, 24, and 30 months. The results indicated that the group with isolated cleft palate differed significantly from both the cleft lip and palate group and the noncleft group on all but 1 play measure. Correlational analyses for each group indicated significant positive correlations between a number of the play variables at 18 months and productive vocabulary and MLU at 24 and 30 months of age. The findings suggest that assessment of early play gestures may assist clinicians in identifying children with clefts who are at risk for later language impairment.

Case-Control Studies↗
PubMedDate not supplied

Distraction osteogenesis for cleft palate closure in a canine model.

OBJECTIVE: To assess the utility of distraction osteogenesis (DO) when applied to closure of a hard palate cleft in dogs. METHODS: A midline hard palate cleft was created in 10 mature dogs. Two were controls and had no distraction; the other 8 dogs underwent osteotomies with installation of customized DO devices to the hard palate. After a 10-day latency, distraction commenced at 1 mm/d. After a 14-day consolidation period, the device was removed and the mucosa closed. Each dog was injected with fluorochrome labels and serially killed at 2-week intervals. Bone healing was analyzed further with traditional histologic analysis and fluorochrome labeling. RESULTS: No serious complications occurred. Bone resorption and cleft widening occurred in both control dogs. Complete bone closure of the hard palate cleft was achieved with DO in 5 of 8 experimental dogs. Three experimental dogs had bone resorption and incomplete palatal closure. CONCLUSIONS: The application of DO techniques in closure of a hard palate cleft in a canine model is safe and well tolerated. Furthermore, in some cases, it proved effective in achieving bony closure of the cleft. Further investigation is warranted into innovative use of DO in treating children born with cleft palate.

Animals↗
PubMed2004

Genetic analysis of TTF-2 gene in children with congenital hypothyroidism and cleft palate, congenital hypothyroidism, or isolated cleft palate.

Homozygous null mice for thyroid transcription factor (TTF)-2 gene exhibit cleft palate and thyroid malformation. We performed a genetic analysis of the TTF-2 gene in 2 children with congenital hypothyroidism (CH) and cleft palate, 45 children with thyroid dysgenesis, 19 children with isolated cleft palate or cleft lip, 4 patients with thyroid hemiagenesis. The entire coding-region of the TTF-2 gene was analyzed by direct sequencing. Direct sequencing of the TTF-2 gene revealed polymorphisms in the length of the polyalanine tract. The most frequent stretch length was 14 residues and it was found in 50 of 70 (71%) and in 45 of 53 (85%) normal healthy controls. A polyalanine tract of 16 residues in the heterozygous state was seen in 18 of 70 (26%) cases and in 4 of 53 (7%) normal subjects. In 1 of 4 (25%) case of hemiagenesis a polyalanine tract of 16 residues in the homozygous state was observed. In 1 of 26 agenesis the polyalanine tract consisted of 12 residues in the heterozygous state. Direct sequencing also revealed the presence of two silent polymorphisms. No mutations were identified in the TTF-2 gene. In conclusion, our results show that no genetic alteration was present in the TTF-2 gene of these patients, suggesting that defects in the TTF-2 gene are a rare event.

Adolescent↗
PubMed1998

Classification, recording, and cleft palate surgery at the Uppsala Cleft Palate Centre.

This paper describes the classification system, method of recording, and surgical techniques used in Uppsala for children with isolated cleft palate. The classification is based on the system described by Kernahan and Stark and the more detailed system described by the American Cleft Palate Association. Separation of the hard palate into thirds, and into right and left sides, assures a detailed description of the cleft, and separates small morphological differences. The longitudinal registration system was introduced into the Uppsala Cleft Palate Centre in 1967. After the initial recording at the time of primary surgery, it is repeated at 5, 8, 11, 14, 17, and 20 years. By emphasising the therapeutic aspects of various stages of growth, it has been possible to limit the recording to once every third year. This has resulted in an important reduction in the dose of radiation without compromising the reliability of the results. Children born before 1975 had clefts of both the soft and hard palate closed at 18-24 months in a one-stage procedure. For children born in 1975 and later a two stage technique has been used, while clefts limited to the soft palate only have been closed entirely in the first operation. At first, the soft palate cleft was closed at 18 months of age and the hard palate at 4 to 5 years. The timing was changed in several steps to the present soft palate closure at 6 months and hard palate closure at 2 years of age.

Adolescent↗
PubMed1995

Aspirin-alcohol interaction in the production of cleft palate and limb malformations in the TO mouse.

Our objective in the present study was to determine the effects of alcohol on stages when the limb buds and renal primordia develop in the TO mouse and to see if aspirin pretreatment would prevent these organ systems from being malformed as was shown by Randall et al. ('91) in the C57 mice. On one of days 9-12 of gestation, groups of TO mice were injected intraperitoneally (IP) with a single dose of 200 mg/kg of aspirin, or a proportionate volume of physiological saline. An hour later, half of the aspirin-treated animals received a single dose of 0.03 ml/g of freshly prepared 25% (v/v) solution of absolute alcohol and the other half received a proportionate volume of saline. Half of the saline-treated animals received a single dose of 0.03 ml/g of saline or a proportionate volume of alcohol solution. All animals were killed on day 18 of gestation. Alcohol significantly increased embryonic resorption and caused remarkable intrauterine growth retardation (IUGR). It also induced arched palate, cleft palate and deformities of the digits with haematomas in a modest number of embryos. Aspirin alone did not have any teratogenic effects. Pretreatment with aspirin significantly augmented alcohol-induced resorption, IUGR, cleft palate and digital malformations associated with haematomas. Chronological observations on the development of the treated limbs showed the occurrence of vascular stasis, haematomas, edema and cell death at early stages. Subsequently, digital rays were either destroyed (ectrodactyly) or remained hypoplastic (brachydactyly). It appears that limb development in the aspirin- and alcohol-treated TO mouse embryos is largely affected by vascular disruption. These data provide further evidence to our earlier observation that alcohol and aspirin interact in the production of malformations and that the teratogenic effects of alcohol in the TO mouse are possibly not mediated via treatment related prostaglandin elevation.

Abnormalities, Drug-Induced↗
PubMed2002

[Osteo-distractive technique for bony repair of cleft palate in a dog model].

OBJECTIVE: To investigate the possibility of closing bony palatal cleft and lengthening hard palate. METHODS: Ten 6-month mongrel dogs were divided into three groups: the control(n = 2), sham control (n = 2) and the experimental group(n = 6). An 8 mm x 25 mm posterior hard palatal cleft was made surgically by bilateral and anterior osteotomies of the palate in six experimental dogs. After a 5-day latency period, a distraction device made of NiTi-shape memory alloy was placed in position for continuous extension of the hard palate. Each distractor was kept in place for 8 weeks after the cleft was closed. RESULTS: The posterior cleft was closed in 2-3 weeks period of the distraction, while the anterior cleft was narrowed to 1-2 mm in width. The hard palate was lengthened backward obviously. The new bone was observed in the area after the distraction. CONCLUSION: The above-mentioned technique may be an effective technique for bony repair of the cleft palate.

Animals↗
PubMed1993

Relationship between cleft severity and dentocraniofacial morphology in Japanese subjects with isolated cleft palate and complete unilateral cleft lip and palate.

Relationships between the width of the palatal cleft measured at palatoplasty and the craniofacial morphology or the occlusal conditions present at approximately 4 years of age were studied in 25 cleft palate (CP) and 39 complete unilateral cleft lip and palate (UCLP) subjects treated at the Dental Clinic of Kyushu University. Posteroanterior cephalograms and dental casts showed that the width of the palatal cleft was significantly correlated with wider upper facial width and posterior dental arch width in UCLP, but not in CP subjects. Cleft width was not significantly correlated with the buccolingual occlusal relationship in either subject type. The anterior occlusal relationship in UCLP was not as good as in CP subjects. On lateral cephalograms, the width of the palatal cleft was significantly correlated with vertical hypoplasia of the upper face in UCLP, but not in CP subjects. The cleft palate width appears to be related to the lateral displacement and the retardation of the downward and forward growth of the nasomaxillary complex in UCLP subjects.

Cephalometry↗