PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Cleft Palate”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1996

Long-term results of segmental repositioning of the maxilla in cleft palate patients without previously grafted alveolo-palatal clefts.

Eleven patients (9 UCLP, 2 BCLP) were treated with segmental osteotomies with or without osteotomies at the Le Fort I level and simultaneous bone grafting of the alveolo-palatal clefts at adult age. These patients were clinically and radiographically evaluated after a mean follow-up period of 59 months (range 39-110 months). One patient showed complete dentoalveolar relapse, whereas the skeletal stability after miniplate fixation proved to be adequate in all cases. Only one patient presented with a persisting oro-nasal fistula. In six cases, the alar base asymmetry had improved to such an extent that further nasal corrections were not necessary. The procedure described is a reliable technique to graft the alveolo-palatal cleft and reposition the dentoalveolar segments simultaneously in those adult cleft palate patients who had no previous alveolar bone grafting.

Adolescent↗
PubMed2001

An in vitro mouse model of cleft palate: defining a critical intershelf distance necessary for palatal clefting.

It is unclear whether cleft palate formation is attributable to intrinsic biomolecular defects in the embryonic elevating palatal shelves or to an inability of the shelves to overcome a mechanical obstruction (such as the tongue in Pierre Robin sequence) to normal fusion. Regardless of the specific mechanism, presumably embryonic palatal shelves are ultimately unable to bridge a critical distance and remain unapproximated, resulting in a clefting defect at birth. We propose to use a palate organ culture system to determine the critical distance beyond which embryonic palatal shelves fail to fuse (i.e., the minimal critical intershelf distance). In doing so, we hope to establish an in vitro cleft palate model that could then be used to investigate the contributions of various signaling pathways to cleft formation and to study novel in utero treatment strategies. Palatal shelves from CD-1 mouse embryos were microdissected on day 13.5 of gestation (E13.5; term = 19.5 days), before fusion. Using a standardized microscope ocular grid, paired palatal shelves were placed on a filter insert at precisely graded distances ranging from 0 (in contact) to 1.9 mm (0, 0.095, 0.19, 0.26, 0.38, 0.48, 0.57, 0.76, 0.95, and 1.9 mm). A total of 68 paired palatal shelves were placed in serum-free organ culture for 96 hours (n = 68). Sample sizes of 10 were used for each intershelf distance up to and including 0.48 mm (n = 60). For intershelf distances of 0.57 mm and greater, two-paired palatal shelves were cultured (n = 8). All specimens were assessed grossly and histologically for palatal fusion. Palatal fusion occurred in our model only when intershelf distances were 0.38 mm or less. At 0.38 mm, eight of 10 palates appeared grossly adherent, whereas six of 10 demonstrated clear fusion histologically with resolution of the medial epithelial seam and continuity of the palatal mesenchyme. None of the 18 palates fused when placed at intershelf distances of 0.48 mm or greater. Using our selected intershelf distances as a guideline, we have established an approximate minimal critical intershelf distance (0.48 mm) at which we can reliably expect no palatal fusion. Culturing palatal shelves at intershelf distances of 0.48 mm or greater results in nonfusion or clefting in vitro. This model will allow us to study biomolecular characteristics of unfused or cleft palatal shelves in comparison with fused shelves. Furthermore, we plan to study the efficacy of grafting with exogenous embryonic mesenchyme or candidate factors to overcome clefting in vitro as a first step toward future in utero treatment strategies.

Animals↗
PubMed1999

Relationship between genetic anomalies of different levels and deviations in dermatoglyphic traits. Part 6: Dermatoglyphic peculiarities of males and females with cleft lip (with or without cleft palate) and cleft palate--family study.

The present study was carried out to evaluate the effect of polygenic morbidity with respect to Cleft Palate and Cleft Lip with or without Cleft Palate (CL) in males and females based on dermatoglyphic traits (DT) and indices of intraindividual diversity (Div), fluctuating (FA) and directional (DA) asymmetry. The main objectives of the present study were as follows: a) to find DT and FA indices, which could be "marker" traits and could indicate the degree of developmental instability of the organism; b) to explore the possibility of using DT, FA, Div and DA indices of CL patients and their parents and to predict the likelihood of the disease appearing in the offsprings of apparently healthy individuals. The samples were of 106 CL patients (59 males and 47 females) and 156 of their parents (67 fathers and 89 mothers), all Israeli Jews. The prints were collected in the Beilinson (Petah-Tikva) and Rambam (Haifa) and Hadassah (Mount Scopus, Jerusalem) Hospitals, or in the abodes of the CL patients. The results were compared with the control group of healthy women and men whose data are detailed in our previous publication. Interpretation of the prints were done according to the methods and included identification of patterns, ridge counts and the measurements of distances and angles in the palms, 79 DT for every individual, 28 continuous traits, 9 discrete traits, 11 indices of Div, 15 DA indices and 16 FA indices. In CL groups increased FA indices values were found and a decreased sexual dimorphism in DT of the CL and parental groups as compared to the control--this both in terms of the number of significant differences, as well as in values of the traits (e.g. smaller differences between the male and female values). The above mentioned findings were partly confirmed also by the discriminant analysis. The values of DT parents were generally similar to those of the control. The best discrimination was obtained between the CL and control groups (70.44% between CL males and control males and 83.47% between CL females and control females). Over 50% of the DT variables were found to be suitable for including into the discriminant function.

Adolescent↗
PubMed2000

Evaluation of prenatal diagnosis of cleft lip with or without cleft palate and cleft palate by ultrasound: experience from 20 European registries. EUROSCAN study group.

Ultrasound scans in the mid-trimester of pregnancy are now a routine part of antenatal care in most European countries. Using data from registries of congenital anomalies a study was undertaken in Europe. The objective of the study was to evaluate prenatal detection of cleft lip with or without cleft palate (CL(P)) and cleft palate (CP). All CL(P) and CPs suspected prenatally and identified at birth in the period 1996-98 were registered from 20 Congenital Malformation Registers from the following European countries: Austria, Croatia, Denmark, France, Germany, Italy, Lithuania, Spain, Switzerland, The Netherlands, UK, Ukraine. These registries followed the same methodology. A total of 709,027 births were covered; 7758 cases with congenital malformations were registered. Included in the study were 751 cases reported with facial clefts: 553 CL(P) and 198 CP. The prenatal diagnosis by transabdominal ultrasound of CL(P) was made in 65/366 cases with an isolated malformation, in 32/62 cases with chromosomal anomaly, in 30/89 cases with multiple malformations and in 21/36 syndromic cases. The prenatal diagnosis of CP was made in 13/198 cases. One hundred pregnancies were terminated (13%); in 97 of these the cleft was associated with other malformations.

Cleft Lip↗
PubMed2005

[Expression of sHsps of normal palate and cleft palate during mouse embryogenesis].

OBJECTIVE: To study the expression of sHsps in normal palate and cleft palate during mouse embryogenesis. METHODS: At GD10, gestational mice of the treatment and the control were administered with 80 mg/kg retinoic acid and the same volume vegetable oil separately, and the normal palate and cleft palate of embryos were harvested in GD15-GD17. The relative abundance of sHsps of all samples was measured by reverse transcript polymerase chain reaction (RT-PCR). RESULTS: In the normal limbs, except that there is no expression of Hspb10 at GD17, all the other Hsps expressed obviously in GD15-GD17. To the normal palates, the expressional abundance of Hsp20, Hsp25, Hsp27, Hsp32, Hspb2, Hspb3, Hspb7 was stable, that of Hsp30, Hspb5 was increased following the embryos aging, and the expressional peak of Hsp10, Hsp22, Hspb4 occurred at GD16. In GD15-GD17, the expressional abundance of Hsp30, Hsp32, Hspb4, Hspb10 of the cleft palates was higher than that of the normal palates, but the expressional abundance of Hsp60, Hspb5, Hspb9 of the cleft palates was lower than that of the normal palates. The expressional models of Hspb9, Hspb 10 of the normal palates were different from those of the cleft palates obviously. CONCLUSION: Except that there is no expression of HspblO at GD17, all the other Hsps expressed obviously in GD15-GD17 during normal clefts' development. To different Hsps, there is different expressional characteristic. Hsp30, Hsp32, Hspb4, Hspb10 maybe play a protective role in the stress action of cleft palate, and Hsp10, Hsp60, Hspb5, Hspb9, Hspb10 were maybe relative to cleft palate.

Animals↗
PubMed2006

Analysis of Meox-2 mutant mice reveals a novel postfusion-based cleft palate.

Cleft palate represents a common human congential disease involving defects in the development of the secondary palate. Major steps in mammalian palatogenesis include vertical growth, elevation, and fusion of the palate shelves. Our current study with the homeobox gene Meox-2 during mouse secondary palate development reveals a novel postfusion-based mechanism for cleft palate. Meox-1 and Meox-2 are two functionally related homeobox genes playing important roles in somitogenesis and limb muscle differentiation. We found that the expression of Meox-2, not Meox-1, marks the specification of early mouse palatal mesenchymal cells in the maxillary processes at embryonic day 11.5 (E11.5). From E12.5 to E15.5, the expression of Meox-2 occupies only the posterior part of the palate, providing an early molecular marker for the anterior-posterior polarity in mouse secondary palate formation. A total of 35.3% of Meox-2-/- (n = 17) and 25.5% of Meox-2+/- (n = 55) mouse embryos display a cleft palate phenotype at E15.5, indicating that the reduction of Meox-2 function is associated with susceptibility to cleft palate. Unlike previously reported clefts, none of the clefts found in Meox-2 mutants contain any epithelial sheets in the medial edge areas, and detailed examination revealed that the clefts resulted from the breakdown of newly fused palates. This article is the first report of a gene required to maintain adherence of the palatal shelves after fusion.

Animals↗
PubMed1993

Issues and controversies in the management of cleft palate.

Cleft palate management is complex. There is no current agreement on the appropriate treatment strategy. Extensive disagreement on the pathophysiology, timing of intervention, and techniques of surgical repair have added to the confusion. To provide a comprehensive guide to the management of cleft palate is difficult. However, several main points should be emphasized. Normal speech should be the most important consideration in the therapeutic plan. Growth disturbance should be minimized, but not at the expense of speech impairment, because the facial distortion can be satisfactorily managed with further surgery, whereas speech impairment can often be irreversible. We believe repair of cleft palate to establish a competent velopharyngeal sphincter should be completed from 6 to 12 months of age. This is done early enough to minimize the development of an often irreversible pathologic compensatory speech pattern, but late enough not to increase significantly the surgical risk to the infant. Surgical interventions should be designed to cause minimal disruption of the palate, to decrease the severity of subsequent growth problems. There is a need for well-controlled, prospective studies to establish the validity of the widely different claims of superior results from various techniques. We believe strongly that cleft patients should be managed in a center with a multidisciplinary team. The benefits of these teams have been elaborated. Cleft palate embodies one of the major tenets of plastic surgery, the achievement of an aesthetic result with minimal interference with function. Cleft palate remains a significant and interesting challenge for current and future plastic surgeons.

Cleft Palate↗
PubMed1971

X-linked cleft palate.

Cleft lip with or without cleft palate is twice as frequent among Indians of British Columbia as among non-Indians, although the reverse is the case whenever we consider isolated cleft palate. A family is described with 12 affected males. Close examination of this family revealed that the most likely explanation for the cleft palate was an X-linked recessive gene. It is concluded that isolated cleft palate among the Indians of British Columbia is an extremely rare anomaly.

Chromosome Aberrations↗
PubMed1976

[Risk of recurrence of several congenital malformations: anencephaly, spina bifida, cleft palate and cleft lip].

Recurrence risks were estimated for some congenital malformation from a multifactorial model according to the method given by Smith (1971). Risks were estimated for cleft lip with or without cleft palate, cleft palate alone, anencephaly and spina bifida from data on frequency and heritability collected in France. Results are given in tables representing risks for some 180 specific family histories.

Anencephaly↗
PubMed2004

[Cleft palate and cleft lip. Clinical review].

UNLABELLED: The aim of this study is to do an analytical study of cleft palate and cleft lip in our hospital. PATIENTS AND METHODS: 85 clinical charts of patients attended in our hospital born between 1976 and 2001 in Aragon and Rioja were reviewed. We studied the incidence of oral cleft, associated malformations and morbidity, familial antecedents and perinatal data, phonatory disfunctions, serose otitis, growth failure and psychiatry problems. RESULTS: The mean incidence was 0.5/1000 newborns. 41.5% presented associated malformations and 19.3% were associated with a specific syndrome, being more frequent in patients affected of cleft palate and cleft lip (50%) than patients with only cleft palate (41.2%) or only cleft lip (8.8%). The most frequent malformations were: facial defects (50%), skeletal (33%), congenital cardiopathies (33%). 19% were born prematurely. The percentage of serose otitis that required control at hospital was 37.3%. 34.2% presented phonatory problems. There was a high incidence of growth failure and psychiatry problems. CONCLUSION: Oral clefts represent a complex clinical condition with a high percentage of medical complications that require a multidisciplinary treatment. The high incidence of congenital defects associated with this condition demand an exhaustive screening in the newborns affected.

Abnormalities, Multiple↗
PubMed2004

Feeding interventions for growth and development in infants with cleft lip, cleft palate or cleft lip and palate.

BACKGROUND: Cleft lip and cleft palate are common birth defects, affecting about one baby of every 700 born. Feeding these babies is an immediate concern and there is evidence of delay in growth of children with a cleft as compared to those without clefting. In an effort to combat reduced weight for height, a variety of advice and devices are recommended to aid feeding of babies with clefts. OBJECTIVES: This review aims to assess the effects of these feeding interventions in babies with cleft lip and/or palate on growth, development and parental satisfaction. SEARCH STRATEGY: We searched the Cochrane Oral Health Group's Trials register (June 2001), the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library, Issue 2, 2004), MEDLINE (1966 to May 24th 2004), EMBASE (1980 to August 7th 2002), CINAHL (1982 to August 7th 2002), PsychINFO (1967 to August 13th 2002), AMED (1985 to August 13th 2002). Attempts were made to identify both unpublished and ongoing studies. There was no restriction with regard to language of publication. SELECTION CRITERIA: Studies were included if they were randomised controlled trials (RCTs) of feeding interventions for babies born with cleft lip, cleft palate or cleft lip and palate up to the age of 6 months (from term). DATA COLLECTION AND ANALYSIS: Studies were assessed for relevance independently and in duplicate. All studies meeting the inclusion criteria were data extracted and assessed for validity independently by each member of the review team. Authors were contacted for clarification or missing information whenever possible. MAIN RESULTS: Four RCTs with a total of 232 babies, were included in the review. Comparisons made within the RCTs were squeezable versus rigid feeding bottles (two studies), breastfeeding versus spoon-feeding (one study) and maxillary plate versus no plate (one study). No statistically significant differences were shown for any of the primary outcomes when comparing bottle types, although squeezable bottles were less likely to require modification. No statistically significant difference was shown for infants fitted with a maxillary plate compared to no plate. A statistically significant difference in weight (kg) at 6 weeks post-surgery was shown in favour of breastfeeding when compared to spoon-feeding (mean difference 0.47; 95% CI: 0.20, 0.74). REVIEWERS' CONCLUSIONS: Squeezable bottles appear easier to use than rigid feeding bottles for babies born with clefts of the lip and/or palate, however, there is no evidence of a difference in growth outcomes between the bottle types. There is weak evidence that babies should be breastfed rather than spoon-fed following surgery for cleft lip. No evidence was found to assess the use of any types of maternal advice and/or support for these babies.

Cleft Lip↗
PubMed1983

Dose-response relations of palatal slit, cleft palate, and fetal mortality in mice treated with a glucocorticoid.

C57BL/6 (C57BL) and SWV mice were treated subcutaneously with triamcinolone acetonide in a single dose of 1.0-7.0 mg/kg on day 12 of pregnancy, and the palate of their fetuses was examined at term. In C57BL mice palatal slit occurred spontaneously and its frequency increased with increasing doses of triamcinolone. However, this defect was not seen in SWV fetuses, even when dams were treated with the doses that induced cleft palate. The frequency of cleft palate increased in both C57BL and SWV as the dose of triamcinolone increased. Fetal mortality increased in SWV, but not in C57BL, with increasing doses of triamcinolone. Dose-response relations were analyzed by the log-probit transformation method. In C57BL mice, the slope of the dose-response curve of palatal slit was significantly different from that of cleft palate. In contrast, the dose-response curves of cleft palate were similar in both C57BL and SWV; the median effective dose was significantly greater in C57BL than in SWV. The mechanism of induced palatal slit appears to be different from that of induced cleft palate; the mechanism of cleft palate induction may be the same in both C57BL and SWV. The slope of the dose-response curve of fetal mortality in SWV mice was different from that of cleft palate; the mechanisms underlying the resorption and cleft palate responses must be different.

Animals↗
PubMedDate not supplied

Homocysteine oxidation and apoptosis: a potential cause of cleft palate.

Cleft palate is the most common craniofacial anomaly. Affected individuals require extensive medical and psychosocial support. Although cleft palate has a complex and poorly understood etiology, low maternal folate is known to be a risk factor for craniofacial anomalies. Folate deficiency results in elevated homocysteine levels, which may disturb palatogenesis by several mechanisms, including oxidative stress and perturbation of matrix metabolism. We examined the effect of homocysteine-induced oxidative stress on human embryonic palatal mesenchyme (HEPM) cells and demonstrated that biologically relevant levels of homocysteine (20-100 microM) with copper (10 microM) resulted in dose-dependent apoptosis, which was prevented by addition of catalase but not superoxide dismutase. Incubation of murine palates in organ culture with homocysteine (100 micro) and CuSO(4) (10 microM) resulted in a decrease in palate fusion, which was not significant. Gelatin gel zymograms of HEPM cell-conditioned media and extracts of cultured murine palates, however, showed no change in the expression or activation of pro-matrix metalloproteinase-2 with homocysteine (20 microM-1 mM) with or without CuSO(4) (10 microM). We have demonstrated that biologically relevant levels of homocysteine in combination with copper can result in apoptosis as a result of oxidative stress; therefore, homocysteine has the potential to disrupt normal palate development.

Apoptosis↗