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 217 records · Page 12Linked to original sources
PubMed1986

Developmental stage specificity and dose response of secalonic acid D-induced cleft palate and the absence of cytotoxicity in developing mouse palate.

Incidence of cleft palate (CP) in full-term mouse fetuses was evaluated following administration of 25 mg/kg of the mycotoxin, secalonic acid D (SAD), to groups of female mice on each of Days 10, 11, 12, 13, 14, or 15 of pregnancy. Although the highest numerical incidence (45.3%) of cleft palate resulted following SAD exposure on Day 12 of pregnancy, and the response tapered off to 16.9% on Day 10 and 0% on Day 15 of pregnancy, similar responses were produced also following exposures on Days 11 (38.4%) and 13 (39.9%) of pregnancy. Maternal exposure to doses of 0, 15, 20, 25, or 30 mg/kg of SAD, given on Day 12 of pregnancy indicated that although fetuses in the 30-mg/kg group had the highest incidence (51.9%) of CP, the effect was associated with increased resorptions and decreased fetal weights. The 25-mg/kg dose was optimally teratogenic (45.3% cleft palate) and maximally tolerable with neither an increase in resorptions nor a decrease in fetal body weights. Cytotoxicity of the optimally teratogenic dose of SAD (25 mg/kg given ip) on Day 12 of pregnancy was evaluated as a possible mechanism of SAD teratogenicity using indices such as mesenchymal cell density, mitotic index, and the uptake of [3H]thymidine in the developing palatal shelves. No evidence of SAD cytotoxicity was obtained in palatal shelves indicating a possible role for nonlethal cellular effects of SAD in the pathogenesis of CP. These studies also suggest the suitability of the maternal 25-mg/kg dose of SAD to study cellular biochemical effects in the developing embryo without the complicating influence of cytotoxic effects.

Animals↗
PubMedDate not supplied

Abnormal patterns of tongue-palate contact in the speech of individuals with cleft palate.

Individuals with cleft palate, even those with adequate velopharyngeal function, are at high risk for disordered lingual articulation. This article attempts to summarize current knowledge of abnormal tongue-palate contact patterns derived from electropalatographic (EPG) data in speakers with cleft palate. These data, which have been reported in 23 articles published over the past 20 years, have added significantly to our knowledge about cleft palate speech. Eight abnormal patterns of tongue-palate contact are described and illustrated with data from children and adults with repaired cleft palate. The paper also discusses some of the problems in interpreting EPG data from speakers with abnormal craniofacial anatomy and emphasizes the importance of quantifying relevant aspects of tongue-palate contact data. Areas of research requiring further investigation are outlined.

Adolescent↗
PubMed1986

Craniofacial growth during human secondary palate formation and potential relevance of experimental cleft palate observations.

Although formation of the secondary palate is known to involve a complex sequence of developmental events, current concepts of palatal clefting emphasize alterations in the palatal shelves. The objective of this study was to identify similarities in facial growth and palatal formation in man and in rodent experimental models and to examine mechanisms of experimentally induced cleft palate that might be relevant to human clefting. Morphometric analyses of facial growth changes reveal similar patterns of mandibular prominence, head extension, and increased oronasal cavity vertical dimension during secondary palate development, with more pronounced changes in the human. Experimental studies of induced cleft palate in rats and mice show that interference with growth changes can contribute to cleft palate. Failure of palatal shelves to make contact, often associated with delayed horizontal movement, has been observed with increased tongue obstruction secondarily to mandibular retrognathia after either growth inhibition in Meckel's cartilage or morphologic deformation of Meckel's cartilage. In other experiments, failure of adequate shelf contact has been observed with reduced shelf growth or with altered craniofacial relations associated with abnormally flexed head posture resulting from fetal growth abnormalities or oligohydramnios. The results of these studies show that the etiology of cleft palate malformation can be related to interference with a number of different development events not immediately in the palatal shelves. Similar alterations of craniofacial growth that affect the palate secondarily appear to be associated with etiology of cleft palate in human syndromes such as Pierre Robin syndrome and the oligohydramnios syndrome.

Animals↗
PubMed1980

Oral language characteristics of adult cleft-palate speakers compared on the basis of cleft type and sex.

Several language measures were administered to 103 cleft-palate adults and analyses were carried out with the subjects classified according to type of cleft (cleft palate only, unilateral cleft lip and palate, bilateral cleft lip and palate) and sex. Between-group differences according to cleft type and sex indicate that patients with cleft lip and palate have better speech and language skills than the cleft-palate-only groups. The results of this study also suggest that females have more complete sentence structure than male cleft-lip and palate subjects. Appropriate habilitative measures should continue through later ages until the cleft-palate individuals gain acceptable levels of communication.

Adult↗
PubMedDate not supplied

Ultrastructural observations on the development of triamcinolone-induced cleft palate in hamsters.

Cleft palate was induced in fetuses by administration of triamcinolone to pregnant hamsters. Twenty hours after treatment, alterations were seen at the epithelial-mesenchymal interface in the prospective fusion epithelium of the vertical shelf. The alterations included contacts between the epithelial and mesenchymal cells, and disruptions in the continuity of the basal lamina. Thirty-two hours after triamcinolone treatment, the basal epithelial cells in some of the reorienting palatal shelves were necrotic. When compared with normal cells, the drug treated necrotic cells were lighter in appearance due to reduced polyribosomes; they also lacked lysosomes. In other reorienting shelves, the basal cells were lost and the epithelial continutity was maintained by the superficial cells. The alterations at the epithelial-mesenchymal interface, and the necrotic changes in the basal cells, became more severe with delayed horizontal reorientation of the palatal shelves. The necrotic debris was cleared by macrophages. At a later stage, the opposing epithelia of the horizontal shelves did not fuse but underwent stratification. It appears that triamcinolone induces alterations at the epithelial-mesenchymal interface, and inhibits the normal process of protein synthesis in the epithelial cells during palatogenesis. This, along with delayed differentiation of mesenchymal cells, distrupts the timing of coordinated development of the palatal tissues. These changes are associated with a delay in the reorientation of the palatine shelves, and cleft palate results.

Animals↗
PubMed2001

Tympanometric findings in cleft palate patients: influence of age and cleft type.

Tympanometry was analysed according to cleft type with respect to age in 239 cleft palate patients (57 with bilateral cleft lip and palate (BCLP)), 122 with unilateral cleft lip and palate (UCLP) and 60 with isolated cleft palate (ICP). The frequency of type B tympanograms was 46.5 per cent in the BCLP group, 50.6 per cent in the UCLP group and 58.3 per cent in the ICP group. Type A tympanograms were more frequently observed in older patients (median age 11 years) in comparison to type B (median age five years; p < 0.001) and type C (median age six years; p < 0.001). The total sample showed an age-related decrease in the frequency of type B tympanograms (rs = -0.3942; p < 0.001). The frequency of type A tympanograms increased significantly with age (rs = 0.4263; p < 0.001), whereas type C was not correlated with age. In the UCLP group, the frequency of type B tympanograms decreased with age (rs = -0.4430; p < 0.001), the decrease being faster than in the BCLP group (rs = -0.3186; p = 0.001) and the ICP group (rs = -0.3378; p < 0.0001)). Type B tympanograms had the highest correlation with a hearing loss of 21-40 dB at mean hearing level at speech frequencies (MHLSF) (rs = 0.4574; p < 0.001), a lower correlation with a hearing loss of 11-20 dB (rs = 0.2184; p = 0.02) and the lowest correlation with hearing loss above 40 dB. At the ages of one to three, the frequency of type B is higher in UCLP patients than in the BCLP and ICP groups, decreasing at seven to 12, increasing again at 13 to 15, and thereafter showing a continuous decrease. In the BCLP group, the frequency of type B increased significantly at the ages of four to six and then decreased continuously from seven to 18. In ICP patients, the changes in the frequency of type B with age are not significant until the age of 15; at the age of seven, it is higher than in the BCLP and ICP groups. The type C tympanogram is not typically found in cleft palate patients and its frequency is not correlated with age. It can be presumed that each type of cleft lip and palate, due to its characteristic conditions in the epipharynx, will favour a different mode of pathophysiological development of middle-ear disease.

Acoustic Impedance Tests↗
PubMed1991

Palate morphology in children with cleft palate with palatalized articulation.

This study was designed to examine postoperatively morphological characteristics of the palate of children with cleft palate with palatalized articulation. Palate morphology was measured in children with good velopharyngeal closure function after surgery, who were classified in Hellman's Dental Age II A group with unilateral cleft lip and palate, and the groups of children with palatalized articulation (CP-P) and normal articulation (CP-N) were compared. The results showed that the group of children with palatalized articulation was characterized by small palatal volume. In particular, there was narrowing and shortening of the anterior palate, and the palate was shallow. It was surmised that morphology may be one cause of palatalized articulation. Accordingly, it is important that early tongue-clicking movements are encouraged in patients exhibiting narrow palate morphology.

Articulation Disorders↗
PubMed1999

Periodontal disease in patients with cleft palate and patients with unilateral and bilateral clefts of lip, palate, and alveolus.

BACKGROUND: Long-term health of the stomatognathic system, as well as esthetics, is the therapeutic goal in patients with facial clefts. The aim of this study was to analyze the periodontal situation of patients with cleft palate (CP) and cleft lip, palate, and alveolus (CLPA) to elicit the differing degrees and localization of periodontal disease. METHODS: In 30 patients with unilateral cleft lip, palate, and alveolus (UCLPA), 30 patients with cleft palate (CP), and 20 patients with bilateral cleft lip, palate, and alveolus (BCLPA), the gingival situation was identified and classified according to the sulcus bleeding index (SBI). Periodontal attachment loss and pathological loosening of teeth were noted for identification of periodontal lesions. The state of oral hygiene was recorded by the approximal plaque index (API). RESULTS: In general, poor oral hygiene was found in all patients. The SBI showed a high incidence of gingivitis in patients with cleft lip, palate, and alveolus. Patients with cleft palate had a minor extent of sulcus bleeding. Periodontal disease was found to a similar extent to that in the general population in patients with cleft palate, whereas patients with cleft lip, palate, and alveolus had a predisposition to deep periodontal destruction of teeth adjacent to the cleft. The registration of pathological loosening of teeth, a result of attachment loss, corresponded to the degree of periodontal disease shown by the attachment loss. CONCLUSIONS: A critical periodontal situation was found in patients with unilateral and bilateral cleft lip, palate, and alveolus, ultimately leading to tooth loss in the front tooth region. In contrast, patients with cleft palate exhibited periodontal situations similar to that found in the general population with additional damage, which may be attributed to orthodontic treatment.

Adolescent↗
PubMed1989

[Prosthetic treatment by pushing back part of the hard palate in third-degree cleft palate].

In the third degree of cleft palate, the palate bones are short, the cleft is wide, the degree of palatal tissue atrophy and the anterior displacement of the muscles are great. It is difficult to repair satisfactorily. We carried out a treatment plan by pushing the soft palate and posterior part of the palatal bone fully back to the physiological closure position by surgical means without cutting through the palatal aponeurosis. By using a palatal plate with pharyngeal prong immediately after operation to fix the composite flap posteriorly and restore the defect of the hard palate. The palatal palate is changed with a silicon obturator or performed secondary operation to repair the perforation of the hard palate after the primary wound is well healed. 24 cases have been performed by this means since 1984. The outcomes are good. It is well conditioned for surgical orthodontics of severe crossbite which results from undeveloped maxilla also.

Adolescent↗
PubMed1982

Prevention of experimentally induced cleft palate in mice.

Cleft palate was induced by giving cyclophosphamide (CPA) to pregnant mice on different days of pregnancy. Application of Solcoseryl, an oxygen stimulating, protein-free extract of the blood of calves, modified the teratogenic and embryolethal effect of CPA and significantly decreased the frequency of cleft palate (from over 70% to about 20% in some groups). This study supports the clinical findings of a reduction in the incidence of facial clefting in man following application of Solcoseryl and vitamins (Gabka, 1975).

Actihaemyl↗
PubMed2003

Collagen XI sequence variations in nonsyndromic cleft palate, Robin sequence and micrognathia.

Cleft palate is a common birth defect, but its etiopathogenesis is mostly unknown. Several studies have shown that cleft palate has a strong genetic component. Robin sequence consists of three of the following four findings: micrognathia, glossoptosis, obstructive apnea, and cleft palate. While cleft palate is mainly nonsyndromic, about 80 percent of Robin sequence cases are associated with syndromes. Mutations in genes coding for cartilage collagens II and XI, COL2A1, COL11A1 and COL11A2, have been shown to cause chondrodysplasias that are commonly associated with Robin sequence, micrognathia or cleft palate. We therefore analyzed a cohort of 24 patients with nonsyndromic Robin sequence, 17 with nonsyndromic cleft palate and 21 with nonsyndromic micrognathia for mutations in COL11A2. A total of 23 Robin sequence patients were also analyzed for mutations in COL2A1 and COL11A1. We detected two disease-associated mutations in patients with Robin sequence, an Arg to stop codon mutation in COL11A2 and a splicing mutation in COL11A1. Two putatively disease-associated sequence variations were found in COL11A1 in Robin sequence patients, one in COL11A2 in a patient with micrognathia and one in COL2A1 in two patients with Robin sequence. The results showed that sequence variations in these genes can play a role in the etiology of Robin sequence, cleft palate and micrognathia but are not common causes of these phenotypes.

Cleft Palate↗
PubMed1984

Biochemical mechanism of glucocorticoid-and phenytoin-induced cleft palate.

The production of cleft palate by glucocorticoids and phenytoin is a complicated interference in a complex developmental program involving many genetic and biochemical processes. The H-2 histocompatibility region includes genes which affect (1) susceptibility to glucocorticoid- and phenytoin-induced cleft palate; (2) glucocorticoid receptor level in a variety of tissues including maternal and embryonic palates, adult thymuses, and lungs; and (3) the degree of inhibition of prostaglandin and thromboxane production by glucocorticoids and phenytoin in thymocytes. A gene linked to a minor histocompatibility locus (H-3) on the second chromosome also influences susceptibility to glucocorticoid- and phenytoin-induced cleft palate. Phenytoin is an alternate ligand for the glucocorticoid receptor affecting prostaglandin and/or thromboxane production. The capacity of glucocorticoids to induce cleft palate is correlated with their anti-inflammatory potency. At least some of the anti-inflammatory effects of glucocorticoids can be explained by the inhibition of prostaglandin and/or thromboxane release, which in turn could be caused by inhibition of arachidonic acid release from phospholipids. Similar mechanisms may be involved in cleft palate induction, as exogenous arachidonic acid injected into pregnant rats and mice at the same time as glucocorticoids reduces the teratogenic potency of the steroids, and indomethacin, an inhibitor of cyclooxygenase, blocks the corrective action of arachidonic acid. Glucocorticoids and phenytoin cause a delay in shelf elevation, and this delay is promoted by fetal membranes and the tongue. However, the cells of the medial edge epithelium are programmed to die whether contact is made with the apposing shelf or not. Glucocorticoids and phenytoin interfere with this programmed cell death, and this interference by both drugs seems to be glucocorticoid receptor mediated, to require protein synthesis, and to be related to arachidonic acid release.

Animals↗
PubMed2006

Cytokeratin expression in palatal and marginal mucosa of cleft palate patients.

OBJECTIVE: The margin of a palatal cleft is a unique anatomical site since the palatal mucosa is continuous with the nasal or nasopharyngeal mucosa. The aim of this study was to compare the expression patterns of cytokeratins and basal membrane components of the mucosa in the area of the cleft. DESIGN: Biopsies from the mucosa of the hard palate and from the cleft margin in the soft palate were obtained from five patients during the primary surgical closure of the cleft. The tissues were processed for haematoxylin-eosin staining and for immunohistochemistry. Antibodies against the cytokeratins (CK) 4, 7, 8, 10, 13, 16 and 18, and the basal membrane components heparan sulphate (HS) and collagen type IV (CIV) were used for immunostaining. RESULTS: The nasopharyngeal epithelium was thinner than the epithelium of the soft palatal mucosa, and showed less interpapillary ridges. The nasopharyngeal epithelium was stratified but expressed the keratins of a simple epithelium (CK 7, 8 and 18). The expression pattern abruptly changed into that of a typical non-keratinized stratified epithelium (CK 4, 13) at the transition to the soft palatal epithelium. The epithelium of the hard palate was a fully differentiated, keratinized and stratified epithelium (CK 10, 16). The basal membrane was thinner in the nasopharyngeal epithelium, which might be related to the presence of abundant inflammatory cells. CONCLUSION: The area around the palatal cleft showed three different types of epithelium. There was an abrupt transition in phenotype of the epithelium from the oral side to the nasopharyngeal side.

Child, Preschool↗
PubMed1977

The mechanism of palatal shelf elevation and the pathogenesis of cleft palate.

Both normal Wistar rat fetuses and those with cleft palate induced by 5-Fluoro-2-Desoxyuridine were studied with a view to elucidating the mechanism of palatal shelf elevation and the pathogenesis of cleft palate. It was postulated that normal shelf elevation is brought about rapidly by an intrinsic turgor shelf force generated by binding of water to mucopolysaccharides. Interference with mucopolysaccharide synthesis would seem to be an important factor in the pathogenesis of some types of cleft palate.

Animals↗