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 73 records · Page 4Linked to original sources
PubMed1988

Articulation proficiency and error pattern of cleft palate children with delayed hard palate closure.

Prior to 1982, children with cleft palate received delayed hard palate closure at Chang Gung Memorial Hospital. In this treatment, soft palate is usually repaired with Widmaier palatoplasty at about 18 months with surgery; hard palate is not closed until the age of 6 or 7. Our previous study indicated that the articulation skill of the cleft palate children before delayed hard palate closure is generally far inferior to the non-cleft children of the same age. Further investigation was carried out to look into the articulation proficiency and error patterns of the cleft palate children undergoing delayed hard palate closure. Data of 47 children (32 boys, 15 girls) were analyzed. Articulation proficiency was compared in four phoneme categories: nasals, plosives, fricatives and affricates. The results indicated that affricates are most difficult for Chinese cleft palate children to pronounce. At age 5, just before the hard palate closure, none of the phonemes is produced correctly except nasals.

Age Factors↗
PubMed2005

Palate morphology after unilateral and bilateral cleft lip and palate closure.

The aim of the present study was to compare the morphology of the hard palate of patients with uni- and bilateral cleft lip and palate after palatoplasty using vomer and palatal pedicled flaps with the palatal morphology of non-cleft individuals. Eighty patients were enrolled into this retrospective study: 40 patients with cleft lip and palate (30 unilateral, 10 bilateral) and 40 non-cleft patients with class I occlusion, who served as controls. Analysis of the development of the maxillary arch and evaluation of palatal morphology were accomplished from reformatted CT scans from plaster casts of the maxilla at the age of 4, 10 and 15 years (cleft patients) and 10 years (controls). Width and symmetry of the maxillary arch and morphology of the hard palate were assessed in the canine and molar region and compared both among the cleft groups and the controls. Maxillary arch width as assessed from plaster casts did not differ significantly between uni- and bilateral cleft patients and was not significantly different from controls at the age of 10. Deviation from symmetry was present in both types of cleft and significant in unilateral clefts when compared to bilateral clefts and non-cleft patients. Palatal morphology did not differ significantly between uni- and bilateral clefts until the age of 15, but was significantly different from control patients in the molar area at the age of 10 presumably due to the medial shift of soft tissue flaps used for palatoplasty. It is concluded that palatoplasty significantly alters hard palate morphology particularly in the posterior area. The relevance of this alteration for speech and articulation remains to be explored.

Adolescent↗
PubMed1991

Misarticulation caused by abnormal lingual-palatal contact in patients with cleft palate with adequate velopharyngeal function.

Misarticulations produced by three patients with cleft palate (2 isolated cleft palate; 1 unilateral cleft lip, alveolus, and palate) who attained adequate velopharyngeal function and normal palatal vault by early surgical repairs were examined using electropalatography (EPG) and sound spectrography (SG). Common characteristics of lingual-palatal contact in which the contact area was broader and/or was more posterior than normal were observed. These misarticulations can be divided into three types based on the direction of the breath emission: palatalized misarticulation (in which air passes along the midline of the palate), lateral misarticulation (in which air flows laterally through the occluded dental arch), and nasopharyngeal misarticulation (in which air flows out the nose). These three are considered to be similar to intractable posterior pattern of articulation in cleft palate patients previously reported. However, these types of misarticulations can be produced by cleft patients who have achieved adequate velopharyngeal function and normal palatal vault.

Articulation Disorders↗
PubMed1996

Prediction of early palatal growth and development in children with cleft lip and palate.

With the use of multilevel modeling of longitudinal data, the relationship between the developmental status of the palate at 4 years of age and early palatal growth and development from birth to 1.5 years of age was studied. A model to predict palatal depths and widths at 4 years of age was developed and tested. The sample consisted of 130 children with cleft lip and/or palate. They were divided into three groups according to surgical treatment; (1) no palatal surgery, (2) soft palatal surgery, and (3) soft and hard palatal surgery. Results showed that in groups 1 and 2, the total arch depth at 4 years of age is strongly related to the initial arch depth at birth. No or low correlations were found between palatal depth at 4 years of age and the growth velocity at birth. The anterior arch width in groups 2 and 3 at 4 years of age appeared to be strongly related to the early growth velocity. In group 1, a moderate correlation with the palatal width and growth velocity at birth was observed. The results of the individual predictions of arch depths and arch widths were reasonable to fair. It was concluded that prediction of individual arch variables at 4 years of age is possible, although within limits. Clinically this means that extreme development can be discriminated from more average development.

Age Factors↗
PubMed1984

2,3,7,8-Tetrachlorodibenzo-p-dioxin-induced cleft palate in the mouse: evidence for alterations in palatal shelf fusion.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) causes a high percentage of cleft palate in fetuses when administered during organogenesis in certain strains of mice including the C57BL/6J, but not in certain other strains (AKR/J). The purpose of the present study was to examine various biochemical and morphological aspects of TCDD-induced changes in the developing palatal shelves. Our results indicate that when TCDD (100 micrograms/kg) was given on individual days between days 8 and 10 of gestation, a high percentage of cleft palate was observed. Receptors specific for TCDD were detected in the C57BL/6J but not AKR/J palatal shelves. The amount of TCDD receptors is highest in the palatal shelves on day 13 as compared to other embryonic tissues including the liver. Examination of cryostat sections taken from embryos during the time of palatal elevation and fusion demonstrated that TCDD does not interfere with growth, elevation, or initial contact of the palatal shelves, but does interfere with firm adhesion and/or degeneration of the medial epithelial cells. Our results suggest that TCDD exerts a direct effect on the embryonic palatal shelves which results in formation of cleft palate.

Animals↗
PubMed2001

Incidence of cleft palate fistula: an institutional experience with two-stage palatal repair.

The purpose of this study was to determine the incidence of cleft palatal fistula in a series of nonsyndromic children treated at the authors' institution. This retrospective analysis of 103 patients with cleft palate treated by five surgeons between 1982 and 1995 includes 60 boys and 33 girls, whose median age was 18.4 months at the time of surgery. The median length of follow-up was 4.9 years after primary palatoplasty. Cleft palatal fistula was defined as a failure of healing or a breakdown in the primary surgical repair of the palate. Intentionally unrepaired fistulas of the primary and secondary palate were excluded. Extent of clefting was described according to the Veau classification. Statistical examination of multiple variables was performed using contingency table analysis, multivariate logistic regression, and the Wilcoxon rank sum test. The incidence of cleft palatal fistula in this series was 8.7 percent. All of these fistulas were clinically significant. The rate of fistula recurrence was 33 percent. The incidence of cleft palatal fistula when compared by Veau classification was statistically significant, with nine fistulas occurring in patients with Veau 3 and 4 clefts and no fistulas occurring in patients with Veau 1 and 2 clefts (p = 0.0441). No significant differences between patients with and without fistulas were identified with respect to operating surgeon, patient sex, patient age at palatoplasty, type of palatoplasty, and use of presurgical orthopedics or palatal expansion. All three recurrent fistulas occurred in the anterior palate, two in patients with Veau class 3 clefts and one in a patient with a Veau class 4 cleft. The low rate of clinically significant fistula was attributed to early delayed primary closure, with smaller secondary clefts allowing repair with a minimum of dissection and disruption of vascularity.

Cleft Palate↗
PubMed2006

Hard palate repair timing and facial morphology in unilateral cleft lip and palate: Before versus after pubertal peak velocity age.

OBJECTIVE: To investigate whether timing of hard palate repair, before versus after pubertal peak velocity age, had a significant effect on facial growth in patients with unilateral cleft lip and palate. DESIGN: Retrospective cross-sectional study. SETTING: Sri Lankan Cleft Lip and Palate Project. PATIENTS: A total of 125 adult patients with nonsyndromic unilateral cleft lip and palate were recruited and their last cephalometric radiographs were used. MAIN OUTCOME MEASURES: Clinical notes were used to record surgical treatment histories. Cephalometry was used to determine facial morphology. RESULTS: The patients who had hard palate repair after pubertal peak velocity age had a deeper bony pharynx (Ba-PMP), a longer alveolar maxilla (PMP-A), a longer effective length of the maxilla (Ar-ANS, Ar-A), and as a result had a more favorable anteroposterior jaw relation (ANS-N-Pog, ANB, NAPog) and larger overjet, compared with those who had hard palate repair before pubertal peak velocity age. CONCLUSION: Timing of hard palate repair significantly affects the growth of the maxilla in patients with unilateral cleft lip and palate. Hard palate repair after (versus before) pubertal peak velocity age has a smaller adverse effect on the forward growth of the maxilla. This timing affects the forward displacement of the basal maxilla and the anteroposterior development of the maxillary dentoalveolus.

Adolescent↗
PubMed1994

Alterations in vascular pattern of the developing palate in normal and spontaneous cleft palate mouse embryos.

The alterations in the vascularization of the developing palate were studied through the use of resin cast images of vascular networks in normal and spontaneous cleft lip and palate (CL/Fr) mouse embryos (crown rump [CR] Length 9-18 mm, body wt. 0.11-0.65 g). A more dense vascular plexus was observed in the oral side than in the nasal side before the reorientation of the palatal shelves. Prominent terminal dilatations of the vascular plexus were observed in the extreme medial edge of the elevating palatal shelves which may exert significant force for palatal shelf elevation. The vascular plexus showed a lateral extension. Many small spherical masses of resin were observed in the medial edge of the palatal shelves at the time of medial extension and during fusion, indicating some changes occurring in the capillary wall leading to the resin leakage. In the spontaneous cleft group, a similar vascular pattern was observed, but the greater palatine artery showed discontinuity in the premaxillary region at an early stage. At the same time, terminal dilatations were delayed and frequently absent in the contralateral shelf. After the reorientation of the palatal shelves, the vascular plexus formed an irregular lattice pattern. Dilated vasculature was apparent in the anterior nasopalatine region, indicating the persistence of a more primitive vascular structure in the spontaneous cleft embryos. However, the area where capillary dilatation occurred was different between unilateral and bilateral cleft embryos. In conclusion, blood vessels in the palatal shelves are underdeveloped and remained immature in cleft lip and palate embryos and showed different patterns in the anterior nasopalatine region between unilateral and bilateral cleft embryos. These variant vascular patterns may be due to the inadequate blood supply to the nasopalatine region from the early embryonic stages possibly resulting from the discontinuity of the greater palatine artery.

Animals↗
PubMed1998

Pathology of the palatal aponeurosis in cleft palate.

OBJECTIVE: The palatal aponeurosis is a controversial structure, both in terms of its anatomy and its function. This article points out a pathologic finding in the cleft palate condition that has not been previously described. DESIGN AND METHOD: By means of surgical dissections, this study demonstrates in detail that the palatal aponeurosis exists even in cleft palates, but it is disrupted, malpositioned, and folded in two layers. PATIENTS: This dissection method has been performed on more than 150 patients with cleft of the hard and soft palate, with or without cleft of the lip and alveolus. At the time of operation, the children were between 6 and 8 months of age. RESULTS: It is possible to dissect the two layers of the palatal aponeurosis, to unfold the aponeurosis, and to form a tough tendinous plane. CONCLUSION: For a functional physiologic reconstruction of the cleft palate, it is necessary not only to reconstruct the levator veli palatini and palatopharyngeus muscle slings, but also to approximate and suture the fibers of the palatal aponeurosis to the corresponding fibers of the opposite side after unfolding them in a medio-dorso-cranial direction. In this manner, a continuous palatal aponeurosis can be created, which subsequently can serve as a transmitter of the muscle forces.

Cleft Palate↗
PubMed2002

[A histological study on healing process of palatal wound with denuded bone restored with transplanted buccal or palatal mucosa].

OBJECTIVE: The purpose of this study was to observe the healing process of palate wound with denuded bone restored with transplanted buccal or palatal mucosa and to elucidate the mechanism of maxillary growth inhibition following palate repair. METHODS: 32 Japan white rabbits, 5 weeks old, were selected as the subjects for this study. They were divided into 4 groups at random. The rabbits in group I was the control without receiving any treatment. The rabbits in group II, III, IV was surgically denuded the bone of palate, and afterwards, the rabbits in group II were not received further restoration, but rabbits in group III and IV were restored with transplanted buccal and palatal mucosa respectively. From 2 to 14 weeks after surgery, at regular intervals, palatal wounds were observed by using a light microscope. Histological changes were also compared among different groups. RESULTS: It was found in group II that dense connective tissue was formed 2 weeks after the surgery, and Sharpey's fibers was formed between the scar and bone tissue 4 weeks after the surgery. However, no Sharpey's fiber was found in group III and group IV, and in the latter two groups, the histological character of tissue was similar to that of the control. CONCLUSION: Prevention of the attachment of Sharpey's fibers to the palatal bone could be effectively accomplished by covering the denuded palatal bone with the transplanted buccal or palatal mucosa.

Animals↗
PubMed2005

[Influence of dexamethasone on fusion of embryonic palatal medial edge epithelium in mouse palatal shelves in vitro].

OBJECTIVE: To study the effect of dexamethasone on the differentiation and proliferation of type A mouse palatal medial edge epithelial cells when there is type A mouse embryonic palatal mesenchymal cells. METHODS: The mouse palatal shelves were harvested from a female mouse of gestation day 14 by microsurgical dissection and cultured in vitro. The differentiation was investigated through microscope and transmission electron microscope under condition of the palatal shelves fusion. RESULTS: Dexamethasone promoted the palatal medial edge epithelium differentiated into squamause epithelium and affected normal development and obstructed the fusion of mouse palatal shelves. CONCLUSION: The results of histological observation indicate that dexamethasone promotes the proliferation of palatal meseuchymal cells and inhibits the normal differentiation of palatal medial edge epithelial cells, which results in cleft palate.

Animals↗
PubMed1975

In vitro development of palatal tissues from embryonic mice. I. Differentiation of the secondary palate from 12-day mouse embryos.

Single palatal processes or homotypic paired palatal processes from 12-day mouse embryos (strain C57Bl) were grown in organ culture on Millipore filters. The epithelium along the medial edge of each palatal process became disrupted, and, by 72 hours of culture, paired palatal processes achieved mesenchymal fusion at the site of disruption. The nasal epithelium of paired palatal processes became a recognizable pseudostratified ciliated columnar epithelium by 96 hours of culture, and the oral epithelium became a recognizable stratified squamous epithelium by 120 hours of culture. These events correspond temporally to the differentiation of palatal tissue in vivo. Differentiative changes of single palatal processes followed the same schedule as double processes. Observations also suggest that the epithelium at the tip of the vertically oriented young palatal process corresponds to the medial epithelium of the more advanced horizontal process-these observations have bearing on the mechanism of palatal movement. In addition, the results suggest that a re-evaluation of the terminology "potential for fusion" is necessary.

Animals↗
PubMed1980

Palate morphogenesis: II. Contraction of cytoplasmic processes in ATP-induced palate rotation in glycerinated mouse heads.

It has been previously shown that non-muscle contractile system(s) exist in mouse palate mesenchyme underlying the palatal epithelium before shelf rotation. In order to obtain evidence that the non-muscle contractile system(s) function to elevate the palate, glycerinated heads have been incubated with ATP. It was shown that 5 mM ATP and a 30 min incubation at 25 degrees C stimulated palate rotation optimally. Elevation of the anterior end of the palate was nearly complete (PSI = 3.90, p less than 10(-6)). Although rotation of the posterior end was significant (p less than 0.02), movement was limited (PSI = 1.70). Light microscopy of the palate revealed that ATP caused a marked condensation of the cytoplasmic processes of the mesenchymal cells. The contraction of the processes of the mesenchymal cells induced by ATP increased roughly with increased palate shelf rotation and was greater at the peripheral than at the internal mesenchyme. Cytochalasin B pretreatment at 40 microM completely blocked the ATP-induced rotation at the anterior end. The effect of other nucleotides on palate rotation was tested. GTP caused a significant stimulation of anterior shelf rotation (p less than 0.005), which was less than ATP, while ADP and CTP were ineffective. Low temperature (6 degrees C) prevented the ATP-induced shelf rotation. These results suggest that the non-muscle contractile cells in the mesenchyme play a role in palate elevation and that contraction of the actomyosin containing microfilaments supplies the motive force.

Actomyosin↗
PubMed1999

AhR, ARNT, and CYP1A1 mRNA quantitation in cultured human embryonic palates exposed to TCDD and comparison with mouse palate in vivo and in culture.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is developmentally toxic in many species and induces cleft palate in the C57BL/6N mouse embryo. Palatogenesis in mouse and human embryos involves homologous processes at the morphological, cellular, and molecular levels. In organ culture, mouse and human palates respond similarly to TCDD. The present study quantitates the expression of AhR, ARNT, and CYP1A1 mRNA in human embryonic palates in organ culture. Palatal tissues were exposed to 1 x 10(-10), 1 x 10(-9), or 1 x 10(-8) M TCDD or control medium and sampled at 0, 2, 4, and 6 hours for quantitative RT-PCR using a synthetic RNA internal standard. Similar measurements of CYP1A1 gene expression were collected for mouse palates cultured in this model. In human palates, AhR expression correlated with ARNT and CYP1A1 mRNA expression. TCDD induction of CYP1A1 was time- and concentration-dependent. The expression of these genes presented a uniform and continuous distribution across the group of embryos, with no subset of either high or low expressors/responders. The ratio of AhR to ARNT was approximately 4:1. AhR mRNA increased during the culture period in both treated and control subjects; however, ARNT expression was relatively constant. TCDD did not alter either AhR or ARNT expression in a consistent dose- or time-related manner. Comparison of human and mouse data showed a high correlation across species for the induction of CYP1A1. Human embryos expressed approximately 350 times less AhR mRNA than the mouse, and in earlier studies it was shown that human palates required 200 times more TCDD to produce the same effects. When the morphological, cellular, and molecular responses to TCDD between mouse and human are compared, it seems highly unlikely that human embryos could be exposed to sufficient TCDD to achieve changes in palatal differentiation that would lead to cleft palate.

Animals↗
PubMed1998

Cleft palate and craniofacial teams in the United States and Canada: a national survey of team organization and standards of care. The American Cleft Palate-Craniofacial Association (ACPA) Team Standards Committee.

OBJECTIVE: This study is the first comprehensive national survey of the organization, function, and composition of cleft palate and craniofacial teams in the U.S. and Canada. Complete descriptions of cleft and craniofacial teams are not currently provided in the literature, and this study will provide an overview for health services research and policy use. Conducted by a national organization, this study examines teams in detail using a pretested and standardized methodology. DESIGN: All known (n = 296) North American cleft palate and craniofacial teams were contacted for team listing purposes using a self-assessment method developed by an interdisciplinary committee of national stature. Team clinical leaders classified their teams into several possible categories and provided data on team care. The response rate was 83.4% (n = 247). RESULTS: The distribution of listed teams was: 105 (42.5%) cleft palate teams, 102 (41.3%) craniofacial teams (including craniofacial teams that are both cleft palate and craniofacial teams), 12 (4.9%) geographically listed teams, and 28 (11.3%) other teams (including interim cleft palate teams, low-density cleft palate teams, and evaluation and treatment review cleft palate teams). Eighty-five percent of all teams systematically collected and stored clinical data on their team's patient population in the past year. Furthermore, 50% of all teams had a quality assurance program in place to measure treatment outcomes. Other findings presented include the annual number of face-to-face team meetings; new and follow-up patient censuses; and surgical rates for initial repair of cleft lip/palate, orthognathic/osteotomy procedures, and intracranial/craniofacial procedures. CONCLUSIONS: Two of five North American teams classify themselves as having the capacity to provide both cleft palate and craniofacial care. An additional two of five teams limit their primary role to cleft palate care. Issues are raised regarding the distribution of teams, the regionalization of craniofacial services, health policy, and resource allocation.

Canada↗
PubMed1999

Comparison of periodontal disease in patients with clefts of palate and patients with unilateral clefts of lip, palate, and alveolus.

OBJECTIVE: Long-term health of the stomatognathic system as well as esthetic aspects are the therapeutic goals in patients with orofacial clefts. The aim of this study was to analyze the periodontal condition of patients with cleft palate (CP) and cleft lip, palate, and alveolus (CLP) and to determine the differing degrees and localization of periodontal disease. DESIGN: In 30 patients with unilateral cleft lip, palate, and alveolus and 30 patients with cleft palate (CP), periodontal lesions were identified and classified according to the Community Periodontal Index of Treatment Needs (CPITN) and pathological mobility of teeth was noted. The state of oral hygiene was recorded by the Approximal Plaque Index. RESULTS: In general, poor oral hygiene was found in all patients. Patients with CLP were classified as CPITN code 0 in 0%, codes 1 and 2 in 7%, code 3 in 43%, and code 4 in 50% of cases. Patients with cleft palate showed code 0 in 0%, codes 1 and 2 in 30%, code 3 in 45%, and code 4 in 25% of cases. In this study, periodontal disease was found in patients with cleft palate to a similar extent to that in the general population, 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 mobility of teeth and resulting loss of attachment corresponded to the periodontal disease classification according to the CPITN. CONCLUSION: A critical periodontal situation was found in patients with unilateral cleft lip, palate, and alveolus. In contrast, patients with cleft palate exhibited a similar periodontal situation to that found in the general population, with additional damage that may be attributed to orthodontic treatment.

Adolescent↗
PubMed1999

[Hard palate lengthening by palatal suture expansion: an experimental study in dogs].

OBJECTIVE: Scar contraction and lack of bony support for soft palate in traditional surgery of cleft palate are main causes of a shortening soft palate and its developmental deficiency. The wound and scar also lead to aberration of facial growth. In order to resolve these problems, lengthening of hard palate by transverse palatal suture expansion was studied. METHODS: Six mongrel dogs of 8-week age were used in the study. Amalgam markers were implanted in the hard palate of the animal. A NiTi-shaped memory alloy (NiTi-SMA) arch wire with a force level of 600 g was used to expand the palato-maxillary suture with a retention period of 8 weeks. The dogs were killed at the age of 36 weeks. Serial X-ray and cephalometry were used to investigate the changes. RESULTS: The suture expansion was generally completed in 4 weeks. The distance of separation of the palatine bone and maxilla was 1.0 to 1.5 cm. Premaxilla became protrusive significantly at the beginning of the suture expansion, then restored gradually to its original position. The length of hard palate increased 4.6 to 5.9 mm by dry skull measurement. CONCLUSION: Hard palate could be permanently lengthened anterior-posteriorly by transverse palatal suture expansion.

Animals↗
PubMed1990

[Comparative study of the palatal rugae and shape of the hard palatal in Japanese and Indian children].

The materials for study were serial upper jaw plaster casts of 58 Japanese (29 boys and 29 girls) aged 3 to 7 years, and 93 Indians (46 boys and 47 girls) aged 5 to 8 years. I observed and measured the palatal rugae, the papilla incisiva and the shape of the hard palate using the method of Yamazaki, following Lysell's and Hauser's. The differences according to population (1-5), palatal findings (6) and sex (7) are summarized as follows. 1. The number of primary rugae of Japanese children were more than those of Indian children, but the number of transverse palatal rugae were the same. 2. There were differences between Japanese and Indian children in the primary rugae shapes, the posterior limit of the rugae zone, the number and position of the secondary rugae and fragmentary rugae. 3. The papilla incisiva of the Japanese children were a little larger than those of the Indians. Generally the papilla incisiva of the two populations were pear-shaped, but the Indians showed more variability. 4. The palatal raphe of the Japanese were wider than those of the Indians. The number of children with no palatal raphe branch was large for Indian children, but small for Japanese. 5. The frontal view of the hard palate of Japanese children was broad and that of Indian children was narrower than the Japanese. The palatal shape of the two populations was almost trapezoid. The occlusal view of the two populations was broad and U-shaped. 6. There were many transverse palatal rugae in the two populations at the left side. The posterior limit of the ruga zone of the left side was shifted further back than the right side. 7. There were no significant differences between sexes for most of the above points.

Child↗