Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PALATE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 37 records · Page 2Linked to original sources
PubMed1996

Developmental expression and CORT-regulation of TGF-beta and EGF receptor mRNA during mouse palatal morphogenesis: correlation between CORT-induced cleft palate and TGF-beta 2 mRNA expression.

Glucocorticoids (CORT) have been shown to induce cleft palate in mice. Although the pathogenetic pathway of CORT-induced cleft palate has been investigated for several decades, the molecular details remain to be elucidated. Since growth factors have been shown to regulate palate morphogenesis, and the expression of several growth factors or their receptors, e.g. TGF-beta, EGF receptor (EGF-R), are known to be modulated by CORT, we postulate that CORT modulation of growth factor (or receptor) gene expression is a key mechanism involved in CORT-induced cleft palate. To test this hypothesis, we analyzed the steady-state levels (Northern and RNase protection) and developmental expression (in situ hybridization) of four CORT-responsive genes--TGF-Beta 1, TGF- beta 2, TGF-beta 3, and EGF receptor (EGF-R)--in developing mouse palates in the presence or absence of exogenous CORT. Pregnant B10.A dams were injected on day 12 of gestation with CORT or sham-injected and embryonic palates were collected at 1, 2, and 3 days postinjection (E13-E15). During mouse palate development, significant increases in TGF-beta 1 and TGF-beta 3 mRNA levels, as well as significant decrease in TGF-beta 2 mRNA levels, are detected; no significant difference in EGF-R transcript level is observed with progressive development. In CORT-exposed palates, we demonstrate no significant differences in the direction or magnitude of change with time in TGF-beta 1, TGF-beta 3, and EGF-R mRNA levels compared to controls. However, CORT delays by 1 day the down-regulation of palatal TGF-beta 2 transcript normally seen on day 14 of gestation. TGF-beta 2 is known to inhibit cell proliferation. The level of TGF-beta 2 mRNA, the only isoform primarily expressed in the palatal mesenchyme, significantly decreases with progressive palatal development; this down-regulation of TGF-beta 2 expression is associated with increased mesenchymal cell proliferation and palatal shelf growth. CORT, at a critical stage of palatogenesis, induces a delay in the normal down-regulation of TGF-beta 2 gene expression. Given that CORT is known to inhibit mesenchymal cell proliferation and palatal shelf growth, we conclude that the CORT-induced delay in the normal down-regulation of TGF-beta 2 gene expression is probably key event in the pathogenesis of CORT-induced cleft palate.

Animals↗
PubMed1981

Cortisone-induced cleft palate in A/J mice: failure of palatal shelf contact.

Although cortisone treatment for induction of cleft palate in mice has been shown to delay the time of palatal shelf elevation, the effects of delayed elevation of shelf contact have not been critically evaluated in a cortisone-sensitive mouse strain. The objective of this study was to evaluated palatal development in cortisone-treated A/J mice in order to determine whether the shelves make contact upon elevation. Morphometric analysis of frozen sections revealed that cortisone-treated shelves were smaller than control shelves with apparent reductions in both the content of extracellular matrix and the number of cells. At a light microscopic level, thinning of medial epithelium in cortisone-treated palates appeared similar to that in untreated palates with spontaneous cleft lip and palate. Shelf elevation was delayed by approximately 12 hours and only half of the cortisone-treated palates achieved complete horizontal positioning of the shelves in all regions of the palate. Immediately after elevation, all control palates had extensive vertical contact along the complete length of the palate. In contrast, approximately 20% of the cortisone-treated fetuses had contact between the shelves in the middle palate region only, with the mean area of contact only 20% as large as in control fetuses. As result, the net shelf contact in all the cortisone-treated fetuses was only 4% of the potential contact shown in control fetuses. Therefore, failure of the palatal shelves to elevate and make extensive contact appeared to be the major factor contributing to cortisone-induced cleft palate in A/J mice.

Animals↗
PubMed2006

Temporal and spatial expression of Pax9 and Sonic hedgehog during development of normal mouse palates and cleft palates in TGF-beta3 null embryos.

Transforming growth factor-beta (TGF-beta3) gene disruption causes cleft secondary palate. Pax9 and Sonic hedgehog (Shh) genes are involved in the patterning of vertebrate embryonic tissues, including the facial skeleton. We investigated the expression of Pax9 and Shh genes during normal mouse palate development and in the developing cleft palates of TGF-beta3 null embryos. Whole mount in situ hybridization was conducted with use of Pax9 and Shh riboprobes for TGF-beta3 null, heterozygous and wild type mice at E12.5-E16.5. Histological analysis was processed by section in situ hybridization. In the wild type, Pax9 and Shh were expressed in the palate between E12.5-E15.5. Shh expression in the secondary palate was restricted to the rugae and the soft palate. Pax9 expression was predominantly in the palatal medial edge between E14.5 and E15.5. These patterns suggest that Shh and Pax9 may have different functions during palate development. In TGF-beta3 null mice, both genes expression patterns in the palate were different to those in wild type mice. In TGF-beta3 null mice, Pax9 expression was much reduced in the palatal medial edge at the critical time of palatal fusion (E14.5-E15.5). Shh expression in the palates of TGF-beta3 null mice was reduced throughout E12.5-E15.5, whilst Shh expression in heterozygous did not appear down regulated compared with the wild type. These results indicate that Pax9 and Shh expression are altered when the TGF-beta3 gene is deleted and suggest that Pax9 and Shh may be involved in the TGF-beta3 regulation of normal palatal fusion.

Animals↗
PubMed2001

A comparison of dental and dentoalveolar changes between rapid palatal expansion and nickel-titanium palatal expansion appliances.

A tandem-loop nickel titanium temperature-activated palatal expansion appliance was developed that produces light, continuous pressure on the midpalatal suture and requires little patient cooperation or laboratory work. The purpose of this study was to compare the effectiveness of the nickel titanium palatal expansion appliance with that of a rapid palatal expansion appliance. The study sample comprised 25 patients who required palatal expansion as part of their orthodontic treatment. The sample was divided into 2 groups, with 13 patients in the nickel titanium group and 12 patients in the rapid palatal expansion group. Study models were taken before treatment and at the end of the retention period after expansion. Intermolar width, palatal width, palatal depth, alveolar tipping, molar tipping, and molar rotation were analyzed. In addition, occlusal radiographs were obtained before and 2 weeks after expansion to evaluate for sutural separation by the appliances. Results showed significant increases in midpalatal sutural separation, tipping of the alveolus, and tipping of the molars after expansion in both groups. However, greater midpalatal sutural separation was found in the rapid palatal expansion group and greater molar rotation was found in the nickel titanium group. Stepwise multiple regression analysis showed that alveolar tipping, palatal width change, and molar tipping are the best predictors of intermolar width change in the rapid palatal expansion group. Radiographic evidence of midpalatal sutural separation was less obvious in the nickel titanium group. These results suggest that both the nickel titanium and the rapid palatal expansion appliances are capable of expanding the maxillary dentition and alveolar process and are equally capable of correcting posterior crossbites. In the current study, the rapid palatal expander widened the palate more reliably, whereas the nickel titanium expander tipped the molars buccally to a greater extent and caused more distal molar rotation. The clinician's choice of expander will depend on his or her initial diagnosis and treatment goals.

Alveolar Process↗
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↗
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↗
PubMed2002

The fetal cleft palate: III. Ultrastructural and functional analysis of palatal development following in utero repair of the congenital model.

The role of fetal surgery in the management of congenital anomalies and intrauterine abnormalities is appropriately restricted on the basis of feasibility and risk-to-benefit analyses of intrauterine intervention. Recently, the authors demonstrated that in utero cleft palate repair of the congenital caprine model is technically feasible and results in scarless healing of the mucoperiosteum and velum, with subsequent development of a potentially functional bilaminar palate with distinct oral and nasal mucosal layers, following single-layer repair of the fetal mucoperiosteal flaps. A slight indentation at the site of repair was the only remaining evidence of a cleft. At 6 months of age, normal palatal architecture, including that of mucosal, muscular, and glandular elements, was seen grossly and histologically. The present work investigated the ultrastructural and functional aspects of the palate following in utero cleft repair to determine what benefits might be derived from fetal intervention. Six goats pregnant with twins were gavaged twice daily for 10 days (gestational days 32 to 41; term, 145 days) with dry, ground Nicotiana glauca plant delivering between 2.4 and 14 mg/kg per day of anabasine, doses that were adjusted in response to mater-nal toxicity. At 85 days' gestation, six fetuses underwent in utero palatoplasty using a modified von Langenbeck technique with elevation of bilateral mucoperiosteal flaps and lateral relaxing incisions. A single-layer repair of the mucoperiosteal flaps was performed using interrupted 6-0 Vicryl sutures. Six fetuses remained as unrepaired clefted controls. Six months after in utero palatoplasty, each group of goats underwent nasoendoscopy to evaluate palatal function; two unclefted 6-month-old goats served as controls. Subsequently, soft palate muscle was harvested from each of the goats and was evaluated by light and electron microscopy. Velar muscle was also harvested from the unclefted control goats and was similarly studied. Nasoendoscopy demonstrated functional palates capable of dynamic velopharyngeal closure following in utero cleft repair; this motion was similar to that observed in unclefted animals. Unrepaired clefted goats did not demonstrate any evidence of velar motion or velopharyngeal closure. Soft palate muscle from this group demonstrated evidence of myofibril degeneration, atrophy, and loss compared with unclefted control velar muscle. Ultrastructural changes included sarcomere "scalloping, " partial Z-line degeneration and loss, and progressive I-band degeneration and loss. Repaired clefted soft palate muscle was remarkably similar to unclefted control muscle. Significantly less myofibril, Z-line, and I-band degeneration and loss were observed with minimal evidence of sarcomere scalloping. In utero cleft palate repair results in a functional soft palate with restoration of ultrastructural architecture of the velum. These findings were attributed to reconstitution of the velar muscular sling, which is disrupted during the clefting process and remains abnormally inserted into the posterior edge of the palatal bone and along the bony cleft. Although repaired velar muscle does demonstrate some evidence of ultrastructural change compared with control muscle, these findings are significantly less pronounced than those observed in the unrepaired clefted muscle.

Animals↗
PubMed2005

Long-term effects of palate repair on craniofacial morphology in patients with unilateral cleft lip and palate.

OBJECTIVE: To identify the long-term effects of palate repair on craniofacial growth in patients with unilateral cleft lip and palate (UCLP). DESIGN: Retrospective cross-sectional study. SETTING: Sri Lankan Cleft Lip and Palate Project. SUBJECTS: Forty-eight adults with nonsyndromic unilateral cleft lip and palate, 29 men and 19 women, had lip repair only (LRO group). Fifty-eight adults with nonsyndromic unilateral cleft lip and palate, 35 men and 23 women, had lip and palate repairs by the age of 9 (LPR group). MAIN OUTCOME MEASURES: Clinical notes were used to record surgical treatment histories. Cephalometry was used to determine craniofacial morphology. RESULTS: In the lip and palate repair group, the depth of the bony pharynx (Ba-PMP), the maxillary length at the alveolar level (PMP-A), the effective length of the maxilla (Ar-IZ, Ar-ANS, Ar-A), the maxillary protrusion (S-N-ANS, SNA), the anteroposterior jaw relation (ANS-N-Pog, ANB), and the overjet were smaller than in the lip repair only group. There were no significant differences in the maxillary length at the basal level (PMP-IZ, PMP-ANS) and the anterior and posterior maxillary heights (N-ANS and R-PMP, respectively) in the two groups. CONCLUSION: Palate repair inhibits the forward displacement of the basal maxilla and anteroposterior development of the maxillary dentoalveolus in patients with unilateral cleft lip and palate. Palate repair has no detrimental effects on the downward displacement of the basal maxilla or on palatal remodeling in patients with unilateral cleft lip and palate.

Adolescent↗
PubMed1996

Palatal asymmetry in cleft palate subjects.

In subjects with different types of cleft palate, palatal shape and symmetry were evaluated utilizing the moiré contourography technique. The sample consisted of 95 subjects with cleft palate and 68 controls. The differences between cleft and control subjects in the transverse and anteroposterior location of the highest point of the palate, palatal axis angle, and the palatal index were assessed by analysis of variance. Effects of cleft type, gender, developmental stage of the dentition, missing teeth, and eight skeletal and pharyngeal cephalometric variables on palatal shape and symmetry were assessed using multiple-regression analyses. In comparison with the noncleft individuals, the cleft palate subjects showed parallel but clearly more remarkable asymmetry in palatal shape and position of the first maxillary molars. The anteroposterior location of the deepest point in the palate was more posterior, and the palate was relatively shallower. The severity of the cleft type affected both the anteroposterior and transverse position of the highest point in palatal morphology.

Adolescent↗
PubMed2001

[Palatal aponeurosis and the insertion of the tensor muscle of the soft palate. An anatomic study and clinical applications].

INTRODUCTION: Knowledge of the anatomy of soft palate muscles is of great interest in cleft palate surgery, in surgical correction of obstructive sleep apnea syndrome and in excision of maxillo-facial carcinomas. Some authors described the palatal aponeurosis as the expansion of the tendon of the two tensor veli palatini muscles, others stated that the palatal aponeurosis is a distinct anatomic entity. METHOD: Ten dissections of the soft palate have been performed to improve our knowledge of its anatomy. RESULTS: The palatal aponeurosis is a distinct anatomic entity continuous with the periosteum of the nasal cavity. The tendon of the tensor veli palatini terminated on the inferior side of the aponeurosis. One fifth of the tensor's tendinous fibers terminated on the posterior border of the palatine bone and the others are spreading on the anterior and inferior side of the palatal aponeurosis. DISCUSSION: In cleft palate patients, this aponeurosis is absent, the palatal muscles are attached to the posterior border of the palatine bones. So it seems to be logical to recommend a soft-palate "pushback" to create a new space between the posterior border of the palatine bones and the soft-palate muscles.

Cleft Palate↗
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↗
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↗
PubMed2005

Palatal development of preterm and low birthweight infants compared to term infants - What do we know? Part 1: The palate of the term newborn.

BACKGROUND: The evidence on prematurity as 'a priori' a risk for palatal disturbances that increase the need for orthodontic or orthognathic treatment is still weak. Further well-designed clinical studies are needed. The objective of this review is to provide a fundamental analysis of methodologies, confounding factors, and outcomes of studies on palatal development. One focus of this review is the analysis of studies on the palate of the term newborn, since knowing what is 'normal' is a precondition of being able to assess abnormalities. METHODS: A search profile based on Cochrane search strategies applied to 10 medical databases was used to identify existing studies. Articles, mainly those published before 1960, were identified from hand searches in textbooks, encyclopedias, reference lists and bibliographies. Sources in English, German, and French of more than a century were included. Data for term infants were recalculated if particular information about weight, length, or maturity was given. The extracted values, especially those from non-English paper sources, were provided unfiltered for comparison. RESULTS: The search strategy yielded 182 articles, of which 155 articles remained for final analysis. Morphology of the term newborn's palate was of great interest in the first half of the last century. Two general methodologies were used to assess palatal morphology: visual and metrical descriptions. Most of the studies on term infants suffer from lack of reliability tests. The groove system was recognized as the distinctive feature of the infant palate. The shape of the palate of the term infant may vary considerably, both visually and metrically. Gender, race, mode of delivery, and nasal deformities were identified as causes contributing to altered palatal morphology. Until today, anatomical features of the newborn's palate are subject to a non-uniform nomenclature. CONCLUSION: Today's knowledge of a newborn's 'normal' palatal morphology is based on non-standardized and limited methodologies for measuring a three-dimensional shape. This shortcoming increases bias and is the reason for contradictory research results, especially if pathologic conditions like syndromes or prematurity are involved. Adequate measurement techniques are needed and the 'normal palatal morphology' should be defined prior to new clinical studies on palatal development.

Humans↗
PubMed2000

[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↗
PubMed2004

Three-dimensional morphology of the palate in subjects with unilateral complete cleft lip and palate at the stage of permanent dentition.

OBJECTIVE: Three-dimensional analysis of palate size and shape in patients with complete unilateral cleft lip and palate (UCLP) at the stage of permanent dentition. SUBJECTS: Thirty randomly selected dental casts of boys approximately 15 years old with complete UCLP and 28 dental casts of normal boys of the same age. INTERVENTIONS: All patients underwent lip repair according to Tennison with primary periosteoplasty (mean age 8.5 months) and palate repair by pushback and pharyngeal flap surgery (mean age 4.9 years). MAIN OUTCOME MEASURES: Data on the palate height in 210 defined locations. RESULTS: The palate in patients with UCLP was narrower throughout its whole extent, more anteriorly than posteriorly. From the canines posteriorly, it was also lower, and the difference as compared with controls increased in a posterior direction up to the level of second premolars (up to 30%) and then slightly diminished (to 21% between the first molars). The reduction of area of transverse sections reached 45% between premolars and 39% between first molars. The palate in the anterior portion was highest on the cleft side and in a posterior direction the maximum height of the palate shifted toward the midline and even beyond that line toward the noncleft side. Palatal height did not depend on dentoalveolar arch width. CONCLUSION: The smaller width and height of the palate confirm the substantially reduced space for the tongue in patients with UCLP. The reduction is only slightly larger than in previously examined patients with isolated cleft palate. Palatal vault is asymmetrical, highest anteriorly on the cleft side and posteriorly on the noncleft side.

Adolescent↗
PubMed2003

Three-dimensional morphology of the palate in subjects with isolated cleft palate at the stage of permanent dentition.

OBJECTIVE: Three-dimensional analysis of palate size and shape in patients with isolated cleft palate at the stage of permanent dentition. DESIGN: Cross-sectional study using Fourier transform profilometry. SUBJECTS: Twenty-nine randomly selected dental casts of approximately 15-year-old boys with isolated cleft palate and 28 dental casts of normal boys of the same age. INTERVENTIONS: All patients were operated on by the same method (pushback and pharyngeal flap surgery) at a mean age of 4.5 years. MAIN OUTCOME MEASURES: Data on the palate height in 210 defined locations (pixels). RESULTS: The palate in isolated clefts is narrower throughout its whole extent and lower from the level of the first premolars. The difference, as compared with controls, increases in a posterior direction. At the level of the first molars, palatal height is reduced by one-quarter, the area of the transversal section by more than one-third. The shaping of the palate vault is, on average, symmetrical with a marked interindividual variability. Palatal height does not depend on the width of the dentoalveolar arch, and the height of the primary palate is not reduced. CONCLUSION: The smaller width and reduced height from the level of the first premolars posteriorly confirm the substantially reduced space available for the tongue in patients with isolated cleft palate. Deviations are on the average symmetrical, and the anterior part of the palate is not shallower.

Adolescent↗