[Closure of hard and especially soft palate clefts with pedunculated tube grafts].
Explore the source record for details and available documents.
Cleft Palate↗
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.
[Cleft palate and dysfunction of the eustachian tube].
Secretory otitis media (SOM) is a frequent complication in infants with cleft palate. In cleft palate the muscles that open the Eustachian tube (tensor palatini and levator palatini) have abnormal connections thereby making the tube opening either difficult or impossible. This will lead to secretory otitis media in 95% of cases, since the middle ear will not be aerated. In this paper, 14 patients operated on for cleft palate during the first year of life were examined. SOM was treated only by medical therapy without the insertion of tympanostomy tubes. Post-operative follow-up ranged from 2 months to 5 years. In all patient SOM was still present at last follow-up with poor efficacy of medical therapy. Therefore, our therapeutic protocol includes myringotomy and insertion of tympanostomy tubes during the first general anesthesia for cleft palate treatment.
Adolescent↗
[Spontaneous cleft palate in CF#1/Ohu mice].
We found a spontaneous cleft palate in a mouse of CF#1/Ohu (Ohu University, Japan). Further, the frequency of the spontaneous cleft palate in strains of CF#1/Jms (Institute of Medical Science, University of Tokyo, Japan) and CF#1/Jah (National Institute of Animal Health, Japan) were about 3%, respectively. The frequency and the types of spontaneous cleft palate in CF#1 were clearly different from those in A/J and CL/Fr strains which were used as model animals of lip and cleft palate. We think that CF#1 is the new animal models to analyze a cleft palate genetically and biochemically.
Animals↗
[Clinical study on fistula incidence of early cleft palate repair].
OBJECTIVE: To study the regularity of fistula incidence after early cleft palate repair METHODS: 531 patients aged 2-12 months at the operation were included in the retrospective study, who underwent cleft palate repair during July 1995 to September 2001. RESULTS: The overall frequency of fistulas was 4.9%. The fistula incidence of bilateral complete cleft palate was obviously higher (7.8%) than that of incomplete cleft palate (4.4%) and the unilateral complete group (4.3%) (P < 0.005). There was no significant difference between the latter two. Fistula incidence was irrelevant to the patient age and the operation method. Seventy percent of fistulas in complete cleft palate occurred on the hard palate, which was significantly higher than that on the other parts. CONCLUSION: Infant cleft palate repair did not increase fistula incidence. We recommend preoperative orthodontics for bilateral cleft palate infants.
Cleft Palate↗
Genetic studies of a cleft palate clinic population.
The genetic program at the Lancaster Cleft Palate Clinic is briefly described. The aim of the study is to obtain quantitative estimates of various components which contribute to genetic heterogeneity. Of 260 families interviewed, 26.1% of cleft lip, 42.5% of cleft lip and palate and 30.0% of isolated cleft palate propositi had one or more affected relatives. That isolated cleft palate is etiologically distinct from cleft lip with or without cleft palate is once again demonstrated. Eight of the cleft palate propositi are from mixed pedigrees with Van der Woude syndrome. While a majority of the familial cleft cases are compatible with the multifactorial hypothesis, five pedigrees of cleft lip and cleft palate propositi and one of a cleft palate propositus are in apparent agreement with the hypothesis of single autosomal dominant gene in each pedigree. No case of sex-linked inheritance was found.
Cleft Lip↗
Genetics of cleft palate in chickens and the relationship between the occurrence of the trait and maternal riboflavin deficiency.
Reciprocal crosses were made between a New Hampshire line of chickens free of cleft palate and affected individuals of a highly inbred S.C.W. Leghorn line having 30 to 50% incidence of cleft palate. The frequency of cleft palate was observed under normal and riboflavin deficient maternal nutrition for the reciprocals of the F1, F2, and backcross to the cleft palate line. Two cases of cleft palate were found in dead embryos of 1368 F1 observations. These may not have represented the genetic trait under study. The response of egg hatchability to riboflavin deficiency was shown to be earlier for cleft palate line hens than for F1 hens, but no maternal effects were found for cleft palate incidence. The frequency of cleft palate in the F2 increased from 0.7% during normal maternal nutrition, to 4.4% during maternal riboflavin deficiency. A similar increase from 8.0% to 12.4% was seen in the backcross progeny. The cleft palate trait was found to be semi-lethal, with mortality associated with severe expression of the trait. No significant sex differences in cleft palate incidence was found in the F2 or backcross generations. The F2 and backcross cleft palate data fit models of genetic control by 3 recessive loci during normal maternal nutrition, and 2 recessive loci during maternal riboflavin deficiency. Penetrance was indicated to be under additive genetic control, and the average was calculated to be between 50 and 75% for all cases. The loss of relevance of one locus during maternal riboflavin deficiency was interpreted to indicate that the homozygous recessive condition at that locus gave disturbed riboflavin metabolism. It was further interpreted to explain the increased occurrence of some traits during teratogenic circumstances as due to the increased probability of obtaining recessive homozygosity at (n - 1) loci compared to (n) loci, and that the role of teratogens in some traits may be in mimicking specific genetic components of the traits.
Animals↗
Some acoustic evidence for vocal abuse in adult speakers with repaired cleft palate.
Acoustic evidence for vocal abuse in adult speakers with cleft palate and hypernasality has not been reported. This study was undertaken to determine if there was acoustic evidence of inappropriate vocal fold adduction during stop consonant production in this population. The results indicated that spectrograms of speakers without cleft palate and severe hypernasality exhibited acoustic characteristics different from spectrograms of speakers without cleft palate and speakers with cleft palate and mild hypernasality. Specifically, voiceless stop productions of severe hypernasal speakers resembled voiced stop productions. Their vocal folds were inappropriately adducted to provide a constriction inferior to the inadequately functioning velopharyngeal port to minimize the nasal air leak. The acoustic evidence supports the hypothesis that a cause of vocal abuse in the cleft palate population is due to compensatory laryngeal valving activities secondary to severe hypernasality.
Adolescent↗
[Molecular mechanism of cleft palate induced by retinoic acid].
OBJECTIVE: To explore the molecular mechanism of cleft palate induced by chemicals. METHODS: Retinoic acid was used as a known teratogen to induce cleft palate in ICR mice and a suppression subtractive hybridization (SSH) technique was applied to identify differentially expressed genes that related to cleft palate of ICR mice. RESULTS: 14 reverse differently and 9 forward differentially expressed clones were obtained. Some clones were selected to be sequenced and aligned to GenBank. CONCLUSION: In this study, suppressed Gpc3 and Insulin-Induced protein 1 could affect growth of palate shelves and resulted in cleft palate by reducing the size of the palate shelves. Down-regulation of Ptprs interfered with a cell signal pathway and down-regulation of Tn C inhibited the cell de-adhesion and expression of Egfr, then suppressed Egfr prevented the normal expression of MMPs that influenced the medial edge epithelium disruption and caused cleft palate. Tn C could bind to Ptprs and Gpcs, and HSPGs were ligands for Ptrps. Up-regulate of Rps25 might play a role in cleft palate by excessively apoptosis.
Animals↗
Diazepam-induced cleft palate in the mouse and lack of correlation with the H-2 locus.
Cleft palate frequencies were studied in AJ and SW mice following either 1- or 2-day dosing schedules with the anxiolytic drug diazepam (DAZ). In all cases, mice were food and water deprived for 24 and 48 hours in the 1- and 2-day dosing schedules, respectively. High cleft palate frequencies in control mice of both strains resulting from 48-hour food and water deprivation (on days 13.5 and 14.5 of gestation) were reduced in mice deprived for 24 hours, indicating a stress related effect. Two-day dosing with DAZ (400 mg/kg) produced a net increase in cleft palate frequency in SW (33%) and AJ (18%) mice. Mice treated only on day 13.5 had reduced control and DAZ cleft palate frequencies, neither of which were significant. Clefting was significant but reduced following 1-day dosing on day 13/20 of gestation (13 days 20 hours) in SW mice (18%), whereas no clefting was seen in the AJ strain. This strain difference was shown not to be related to differences in developmental timing. Production of cleft palate seen in AJ mice after 2 days of dosing may be indicative of an interaction of DAZ with the stresses resulting from food and water deprivation. Genes of the major histocompatibility locus, H-2, have been shown to regulate cleft palate formation following glucocorticoid and phenytoin administration to mice. Despite pharmacological similarities between DAZ and phenytoin, comparison of cleft palate frequencies following administration of DAZ to various strains of mice of different H-2 haplotypes indicated that genes associated with the H-2 locus do not regulate DAZ-induced cleft palate in these strains.
Animals↗
Recovery of eustachian tube function and hearing outcome in patients with cleft palate.
Eustachian tube dysfunction is a nearly universal complication of cleft palate, resulting in chronic ear disease and conductive hearing loss. Cleft palate repair is thought to result in recovery of eustachian tube function, but the length of time between repair and recovery of eustachian tube function is not known. Furthermore, the efficacy of tympanostomy tubes in the treatment of eustachian tube dysfunction and hearing sequelae has not been examined in a systematic way. To answer these questions, we performed a retrospective study that used serial audiometric data and tympanometry on 81 patients with cleft palates (162 ears), with follow-up ranging from 1 to 17.3 years. Average time to recovery of eustachian tube function was 6.0 years (range, 1.0 to 10.3 years) after cleft palate surgery. For children followed up for at least 6 years (longest follow-up, 17.3 years), 70% (67 of 85) had normal eustachian tube function at their last follow-up visit. Ears treated with Armstrong tympanostomy tubes required an average of 3.1 tubes per ear until recovery of eustachian tube function, whereas ears treated with Goode T tubes required only 1.1 tubes per ear (p < 0.05). Hearing evaluation revealed that 67% of ears had abnormal hearing thresholds (> 20 dB) before tympanostomy tube placement, whereas only 7.5% of ears demonstrated this loss after tube placement. Furthermore, more than 90% of ears maintained normal thresholds after recovery of eustachian tube function. These data indicate that most children with cleft palates eventually recover normal eustachian tube function after palatoplasty, but for the majority of children, this does not occur for many years.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Toward pathogenesis of Apert cleft palate: FGF, FGFR, and TGF beta genes are differentially expressed in sequential stages of human palatal shelf fusion.
OBJECTIVE: Critical cellular events at the palatal medial edge epithelium (MEE) occur in unperturbed mammalian palatogenesis, the molecular control of which involves a number of growth factors including transforming growth factor beta 3 (TGF beta 3). Apert syndrome is a monogenic human disorder in which cleft palate has been significantly correlated to the fibroblast growth factor receptor (FGFR) 2-Ser252Trp mutation. We report the relative expression of these genes in human palatogenesis. METHODS: The expression of the IgIIIa/b and IgIIIa/c transcript isoforms of FGFR2 and the proteins FGFR1, FGFR2, and FGFR3 was studied in situ throughout the temporospatial sequence of human palatal shelf fusion and correlated with the expression of TGF beta 3. In addition, the immunolocalization of the ligand FGFs 2, 4, and 7 was undertaken together with the intracellular transcription factor STAT1, which is activated by FGFR signaling. RESULTS: FGFRs are differentially expressed in the mesenchyme and epithelia of fusing palatal shelves, in domains overlapping those of their ligands FGF4 and FGF2 but not FGF7. Coexpression is seen with TGF beta 3, which is implicated in MEE dynamics and FGF and FGFR upregulation, and STAT1, an intracellular transcription factor that mediates apoptosis. CONCLUSIONS: The coregulation of molecules of the FGFR signaling pathway with TGF beta 3 throughout the stages of human palatal fusion suggests their controlling influence on apoptosis and epitheliomesenchymal transdifferentiation at the MEE. Experimental evidence links FGFR2-IgIIIa/b loss of function with palatal clefting, and these correlated data suggest a unique pathological mechanism for Apert cleft palate.
Acrocephalosyndactylia↗
Application of hydroxyapatite-coated implants as support for palatal lift prostheses in edentulous patients with cleft palate: a clinical report.
A palatal lift prosthesis (PLP) is a prosthetic speech aid used to compensate for palatopharyngeal incompetence. However, it requires dental abutments to facilitate its function. In two edentulous patients with cleft palate, hydroxyapatite-coated dental implants were used to increase PLP retention. In both cases, palatopharyngeal closure was obtained and PLP function was deemed effective, as determined by speech evaluation and nasal air flow measurements, for more than 3 years. This treatment is useful for enhancing the retention of a PLP in patients who have few or no remaining natural tooth abutments.
Adult↗
Comparison of the hearing histories of children with and without cleft palate.
Aggressive otologic management has been recommended for children with cleft palate because of the almost universal occurrence of otitis media with effusion (OME) in these children and the association of OME with hearing loss and possible language, cognitive, and academic delays. In this study, 28 children with cleft palate and 29 noncleft children were seen at 3-month intervals from 9 to 30 months to compare otologic treatment and management. Hearing and middle ear function were tested at each session; information on ventilation tube placement was obtained from medical records. Ventilation tubes were placed earlier and more often in children with cleft palate, but children with cleft palates failed the hearing screening more often. The correlation between age at first tube placement and frequency of hearing screening failures was significant for the children with cleft palate, indicating that the later tubes were first placed, the poorer the child's hearing.
Acoustic Impedance Tests↗
[Simultaneous primary palate repair and alveolar bone grafting in unoperated cleft palate patients over 8 years old].
OBJECTIVE: To analyze the applicability and results of simultaneous primary palate repair and alveolar bone grafting in unoperated cleft lip and palate patients over 8 years old. METHODS: A retrospective study was performed in a group of unoperated cleft palate patients who received simultaneous primary palate repair and alveolar bone grafting. Between December 1990 and March 1998, a consecutive of 38 complete unilateral cleft lip and palate patients were treated by the procedures of simultaneous primary cleft palate repair and alveolar bone grafting at the Peking University of Cleft Lip and Palate Treatment Center. All the patients had their lip repaired before they were admitted. The age range was 8 to 24 years, with the average of 14.7 years old. The duration of operation as well as the blood loss during the operation was recorded, and compared with those patients who only received alveolar bone grafting. All the patients have been followed up for at least twelve months, and the results of bone grafting were evaluated according to radiographs. RESULTS: All the operations were successful, and the wound healed well. Compared with simple alveolar bone grafting, simultaneous primary palate repair and alveolar bone grafting prolonged the operation time to an average of 37 minutes. The procedure of simultaneous primary palate repair and alveolar bone grafting did not prolong the operating time compared with simple alveolar bone grafting and no blood transfusion due to bone grafting was needed. All the wounds both in the grafted area and donor site healed uneventfully. No major complications occurred during or shortly after the operation. The overall clinical successful rate of alveolar bone grafting in this group of patients was 89.5%. CONCLUSION: Simultaneous primary palate repair and alveolar bone grafting are safe and applicable procedure for unoperated cleft palate patients, and this procedure should be performed in those unoperated cleft palate patients above 8 years old.
Adolescent↗
Malformation of the vomer in submucous cleft palate.
Background: Several criteria are described in the literature to diagnose a submucous cleft palate. Commonly the differences in the extent of the submucous cleft will not be as overt as in open clefts. Nevertheless, complete submucous cleft palate may cause imperfect palato-pharyngeal closure so that the affected person needs to undergo speech training and surgical treatment. Patients: We investigated 30 patients who underwent palatal repair to correct this disorder. They were evaluated according to the Koch's documentation system. Results: In all patients an additional malformation of the inner nose was found: The vomer was not fused with the palatal shelves. There were with different degrees of severity of this malformation and they were not necessarily correlated with the extent of the palatal cleft. Conclusion: In our opinion, this malformation of the vomer should be seen as a typical symptom of classical submucous cleft palate. Discussion is needed on how the vomerine malformation should be incorporated into the surgical procedure. Since we know from septal surgery that a basal septal perforation will lead to disturbances of nasal breathing. Copyright 2001 European Association for Cranio-Maxillofacial Surgery.
Journal Article↗
Application of a temporary palatal prosthesis in a puppy suffering from cleft palate.
A 3-month-old Schnauzer was presented with congenital defects of the secondary palate. On the clinical examination, coughing, sneezing, drainage of nasal discharge from the external nares and poor growth were found. Vital signs and results of blood examination were within normal ranges. Thoracic radiography revealed mild pneumonia in the right lung lobes. In a puppy suffering from cleft palates, a palatal prosthesis was applied to the hard palate in order to protect the surgical wound, because a routine surgery was not successful. A palatal prosthesis was applied and held in place using the instant glue and plastic bands to protect the surgical wound following the third repeated surgery. Although a small oronasal fistula still remained, there was no functional defect. This prosthesis was easy to apply and helpful to protect the surgical wound. In addition, this implant could be placed or adjusted without or sedation/anesthesia.
Animals↗
Mendelian inheritance of isolated nonsyndromic cleft palate.
Isolated, apparently nonsyndromic cleft palate (CP) is thought to be etiologically heterogeneous. The multifactorial threshold explanation for CP is postulated in most cases. Mendelian inheritance has been documented in 3 families. We report on three unrelated white families with 17 relatives in several generations affected with CP, including submucous CP and bifid/absent uvula. We could find no evidence of a cleft syndrome. In one family, the pattern is consistent with autosomal dominant inheritance. In 2 families, the pattern is consistent with X-linked recessive inheritance. The specific findings and their implications for family evaluation and genetic counseling are discussed.
Adolescent↗
Induction of cleft palate in newborn pigs by maternal ingestion of poison hemlock (Conium maculatum).
Cleft palates were induced in newborn pigs of gilts fed Conium maculatum seed or plant during gestation days 30 through 45. Twelve of 23 newborn pigs born to 3 gilts given Utah-grown C maculatum seed and 9 of 12 newborn pigs born to a single gilt given the fresh Utah spring-growth C maculatum plant had cleft palates. The cleft palates ranged from a unilateral cleft, involving only 1 side of the palate, to a full bilateral cleft. Brachygnathia was also observed in some of these newborn pigs with cleft palate. Other malformations were not observed. Chemical analysis of seed and plant samples indicated that gamma-coniceine was the responsible teratogenic alkaloid. A daily dose of plant or seed that provided greater than or equal to 1.07 mg of gamma-coniceine/kg of body weight fed to gilts during the 30th through the 45th day of pregnancy resulted in teratogenic effects.
Alkaloids↗