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At least 937 records · Page 52Linked to original sources
PubMed1999

[A longitudinal research on palate growth in the normal mixed dentition by three-dimensional image analysis].

OBJECTIVE: To investigate the trait of the palate growth and to provide a method of three-dimensional image analysis on revealing the entire variation of palate. METHODS: A longitudinal study on the palate growth of 30 subjects (male 8, female 22) with normal occlusion during mixed dentition was carried out by three-dimensional image analysis. The observation period was from 7 to 10 years of age. RESULTS: During growth, the palate vaults in 16 cases (53%) descend for 1-5 mm, whereas, the palate vaults in 14 cases (47%) ascend for 2.6 mm at most. CONCLUSION: The variations of palate growth can be investigated by three-dimensional image analysis. During growth, the palate vault may descend or ascend, which shows the individual differences of oronasal function.

Adolescent↗
PubMed2002

[Osteo-distractive technique for bony repair of cleft palate in a dog model].

OBJECTIVE: To investigate the possibility of closing bony palatal cleft and lengthening hard palate. METHODS: Ten 6-month mongrel dogs were divided into three groups: the control(n = 2), sham control (n = 2) and the experimental group(n = 6). An 8 mm x 25 mm posterior hard palatal cleft was made surgically by bilateral and anterior osteotomies of the palate in six experimental dogs. After a 5-day latency period, a distraction device made of NiTi-shape memory alloy was placed in position for continuous extension of the hard palate. Each distractor was kept in place for 8 weeks after the cleft was closed. RESULTS: The posterior cleft was closed in 2-3 weeks period of the distraction, while the anterior cleft was narrowed to 1-2 mm in width. The hard palate was lengthened backward obviously. The new bone was observed in the area after the distraction. CONCLUSION: The above-mentioned technique may be an effective technique for bony repair of the cleft palate.

Animals↗
PubMed1992

The gene responsible for X-linked cleft palate (CPX) in a British Columbia native kindred is localized between PGK1 and DXYS1.

Human craniofacial malformations are a class of common congenital anomalies in which the etiology is heterogeneous and often poorly understood. To better delineate the molecular basis of craniofacial development, we have undertaken a series of experiments directed toward the isolation of a gene involved in human secondary palate formation. DNA marker linkage studies have been performed in a large British Columbia (B.C.) Native family in which cleft palate segregates as an X-linked trait. We have examined 62 family members, including 15 affected males and 8 obligate carrier females. A previous clinical description of the clefting defect in this kindred included submucous cleft palate and bifid or absent uvula. Our recent reevaluation of the family has indicated that ankyloglossia (tongue-tie) is also a feature of X-linked cleft palate in some of the affected males and carrier females. Ankyloglossia has previously been associated with X-linked cleft palate in an Icelandic kindred in which a gene responsible for cleft palate (CPX) was assigned to the Xq21.3-q22 region between DXYS12 and DXS17. For the B.C. kindred reported here, we have mapped the gene responsible for cleft palate and/or ankyloglossia to a more proximal position on the X chromosome. No recombination was observed between B.C. CPX and the DNA marker DXS72 (peak lod score [Zmax] = 7.44 at recombination fraction [theta] = .0) localized to Xq21.1. Recombination was observed between CPX and PGK1 (Zmax = 7.35 at theta = .03) and between CPX and DXYS1 (Zmax = 5.59 at theta = .04). These recombination events localize B.C. CPX between PGK1 and DXYS1 in the Xq13-q21.31 region.

Blotting, Southern↗
PubMedDate not supplied

Nasal cavity perforation by palatal implants: false-positive records on the lateral cephalogram.

PURPOSE: Lateral cephalometric films were examined for their validity as a tool for the postoperative evaluation of palatal implant placement. MATERIALS AND METHODS: Cephalometric and histometric data of 20 partially edentulous human cadaveric maxillae were compared. Lateral cephalograms of the specimens were made, and the palatal complex was pencil traced. In addition, low-dose dental computerized tomography (CT) scans were obtained from every specimen. Based on the CT data, palatal implants (Orthosystem; Institut Straumann, Waldenburg, Switzerland) were placed. Postimplantation, another lateral cephalometric film was recorded. The specimens were prepared for histologic examination. The preoperative tracings were superimposed on the postoperative cephalometric films. RESULTS: Of 20 implants placed, 12 were 4 mm long and 8 were 6 mm long. The distance between the cranial end of the implants and the nasal floor on microscopy ranged from 0.3 to 9.3 mm. Perforation of the nasal floor was absent throughout on intraoperative probing, while 2 implants projected beyond the nasal floor on histologic analysis of the specimens. An analysis of the superimposed pre- and postoperative cephalograms showed 5 implants projecting beyond the nasal floor. Histologically, only 1 of these projecting implants had actually caused perforation of the palatal complex. A comparison between the histometric and the cephalometric data showed that cephalometry, on average, imaged the palatal complex 0.8 mm below the actual anatomic site. DISCUSSION AND CONCLUSIONS: Twenty percent of palatal implants projecting beyond the nasal floor were false-positive records on the postoperative lateral cephalograms. Despite CT scans, 10% of the implants placed caused fenestration of the nasal cavity by histologic evidence. If the palatal complex was perforated, intraoperative probing with a periodontal probe did not confirm the perforation. Bone perforations up to 1.3 mm did not necessarily result in frank perforation of the nasal mucosa. Two-dimensional images could not be related to actual penetrations into the nasal cavity.

Adult↗
PubMed2005

[A clinical study of presurgical nasoalveolar molding in infants with complete cleft lip and palate].

OBJECTIVE: To observe the clinical effect of presurgical nasoalveolar molding in infants with complete cleft lip and palate. METHODS: Presurgical nasoalveolar molding was performed in 38 infants with cleft lip and palate (26 patients with unilateral cleft lip and palate, 12 patients with bilateral cleft lip and palate), aged between 5 and 30 days. The width of alveolar cleft was measured before and after the operation and the effect of treatment was assessed. RESULTS: After 108 - 152 days of therapy, the average width of alveolar cleft decreased by 5.3 mm in 26 patients with unilateral cleft lip and palate. Nasal profile was improved in 76 percent of cases. In 12 patients with bilateral cleft lip and palate, the average width of left cleft decreased by 4.7 mm and that of the right decreased by 4.2 mm. The distance between right and left cleft increased by 5.1 mm. Nasal profile was improved in 66 percent of cases. CONCLUSION: Presurgical nasoalveolar molding in complete cleft lip and palate can improve nasal profile and decrease the width of alveolar cleft.

Alveolar Process↗
PubMed1975

Glandular tumors of the palate.

Salivary gland tumors of the palate originate in the minor salivary glands located in the glandular zone of the palate. Approximately 7 per cent of all tumors of the salivary gland occur in the palate, and approximately one-half of such tumors are cancers. The salivary gland tumor is more often found in the hard palate. Of the 90 salivary gland tumors of the palate reported herein, 49 per cent were benign, and all were pleomorphic adenomas. Of the cancers, 70 per cent were cylindromas, 15 per cent mucoepidermoid cancers, and the remaining 15 per cent included acinic cell carcinomas, undifferentiated carcinomas, and papillary adenocarcinomas. There is a 50 per cent likelihood of a lump in the palate in the glandular zone being a cancer. The simplistic diagnosis of a cyst should be considered only after other lesions have been excluded. The recommended form of treatment is surgical excision. Fenestration of the palate is a potential consequence of excision in 30 to 60 per cent of patients, depending upon whether or not the lesion is benign or malignant. The results of surgical treatment are good, but fenestration shoud be accepted as a necessary result of adequate treatment. Surgical treatment of cylindromas continues to be most difficult and demands the utmost of that intangible essence known as surgical judgment. Radiotherapy has been considered as a palliative agent for the treatment of inoperable and recurring cancers, especially cylindromas.

Adenocarcinoma↗
PubMed1991

Hypodontia in patients with isolated cleft palate, its relationship to etiopathogenesis.

The authors studied the incidence of hypodontia in 200 patients with isolated cleft palate. These patients were divided into 3 groups according to the degree of malformation (complete cleft palate, incomplete cleft palate, soft palate cleft). In the 3 groups, hypodontia was studied on permanent teeth, with the exception of the 3rd molars. Compared with the healthy population, hypodontia in patients with cleft palate appeared at a significantly higher rate (25.5%). No difference was found between boys and girls. Hypodontia in the mandible appeared in 18%, in the maxilla in 10%. The upper jaw showed maximum incidence in complete cleft palate (21%), while in the mandible hypodontia was observed most frequently in soft palate clefts (37% patients). In most cases the dental germs of the 2nd lower premolar failed to develop. Our results correlate with hypotheses based on experimental studies on the etiopathogenesis of facial clefts.

Adolescent↗
PubMed1991

Molecular and morphologic changes during the epithelial-mesenchymal transformation of palatal shelf medial edge epithelium in vitro.

The fate of the medial edge epithelial (MEE) cells during palatal fusion has been proposed to be either programmed cell death or epithelial-mesenchymal transformation. Vital cell labeling techniques were used to mark the MEE and observe their fate during palatal fusion in vitro. Fetal mouse palatal shelves were labeled with Dil and allowed to proceed through fusion while maintained in an organ culture system. The tissues were examined at several stages of palatal fusion for the distribution of Dil, presence of specific antigens and ultrastructural appearance of the cells. The MEE labeled with Dil occupied a midline position at all stages of palatal fusion. Initially the cells had keratin intermediate filaments and were separated from the underlying mesenchyme by an intact basement membrane. During the process of fusion the basement membrane was degraded and the Dil-labeled MEE were in contact with the mesenchymal-derived extracellular matrix. In the late stages of fusion the Dil-labeled MEE altered their cellular morphology, had vimentin intermediate filaments, and were not associated with an identifiable basement membrane. Dil-labeled cells, without an epithelial phenotype, remained present in the midline of the completely fused palate. The data indicate that the MEE did not die but underwent a phenotypic transformation to viable mesenchymal cell types, which were retained in the palatal mesenchyme.

Animals↗
PubMed1991

[Comparison of different types of cleft lip and palate in regards to dental anomalies and sexual incidence].

The present study addresses two questions. Does the incidence of dental anomalies differ among the four following types of cleft lip and palate: the isolated cleft palate, the unilateral cleft lip and palate, (right or left), and the bilateral cleft lip and palate. Furthermore is the sexual incidence comparable among the four above mentioned types? Radiographic records and complete family history of clefting of 156 patients with a complete cleft lip and palate were obtained from the Cleft Lip and Palate Teams of Ste-Justine Hospital. Patients in which the cleft was part of a syndrome were excluded from the study. According to the analysis of the data, the incidence of dental anomalies was relatively high, specifically as high as 92% for the bilateral cleft lip and palate. The sexual incidence differed among the four types.

Anodontia↗
PubMed1990

Variability of palatal dimensions in South Australian twins.

Estimates of genetic contributions to variability in three palatal dimensions were obtained from a sample of 70 pairs of South Australian twins aged between 11 and 26 years. Palatal width and length were measured directly from dental models, while palatal height was assessed indirectly from moiré contourographs. For each of the three palatal variables there was evidence of significant genetic variance, with heritability estimates for palatal width and height generally exceeding those for palatal length. Furthermore, palatal height measurements displayed greatest relative variability and strongest correlation between monozygous twins (r = 0.95), suggesting that this dimension could be useful as an additional comparative feature in forensic odontological investigations.

Adolescent↗
PubMed1989

[Hearing disorders in patients with cleft lip and palate].

Hearing threshold in cleft lip/or palate was assessed in 316 ears by pure tone audiometry. Normal hearing threshold was found in almost a half (164/51,9%) of the ears examined. Hearing defects were most frequently observed in cases of complete unilateral cleft palate (48/60%), whereas they were least frequently recorded in cases of cleft lip (15/19,2%). Complete bilateral cleft lip and palate was associated with conduction deafness in 29 (42,9%) ears examined, thus occupying the last but one place according to the frequency of association between deafness and cleft defects. A hearing conduction gap or more than 40 dB was most frequently present in complete cleft lip and palate (7/5,6%), followed by cleft palate (4/5%). Submucous cleft palate was observed to be less frequently accompanied by conduction deafness (9/56,2%) as compared to complete cleft palate, despite a common feature of bone and muscle support discontinuity. Cleft lip was least frequently accompanied by conduction deafness, but it was still present to a relatively high percentage when compared to the cleft-free population.

Adolescent↗
PubMed1989

[Morphological changes in the dental arch and the palate during orthodontic treatment].

The changes of the dental arch form after the tooth movement and the sequential changes occurred on the palate during orthodontic treatment were examined in the coordinate system based on the standard point at the palatal vault. The subjects selected for this study were 20 patients of Angle Class II div. 1. Both left and right maxillary premolars were extracted and an edgewise appliance had been treated. The plaster models prepared before and after treatment were used for materials. Only suitable materials were measured as a result of an examination of the reproducibility of the palatal core at the palatal vault. Results obtained were as follows: 1. It was suggested that the dental arch and the palate was mutually effected on each other in the arch length and the arch width. 2. The morphological changes in the dental arch and the palate due to orthodontic treatment was discussed on the basis of the results of Fourier analysis. The dental arch and the area from F division to J division were significantly smaller after orthodontic treatment than before it. The shape became closer to a semicircle. 3. Values representing morphological changes in the dental arch and J division were similar and values representing morphological changes in the other division were getting smaller as the area being close to the palatal vault.

Dental Arch↗
PubMed1988

[The role of the soft palate in respiration].

The soft palate is a muscular fold suspended from the posterior border of the bony palate and extending downwards and backwards into the oropharynx. Usually, the soft palate and tongue are in tight apposition, closing the oropharyngeal isthmus; the soft palate can however rise and touch the posterior pharyngeal wall, closing the nasopharynx: thus the soft palate regulates the flow of air through nose and/or mouth. During oronasal breathing (as during exercise, speech or smoking) the impedance of naso and oropharynx respectively is determined by the position of the soft palate. Hence partitioning of the airflow through nose and mouth will depend on the latter. This is true in both adults and babies. Babies are not obligatory nasal breathers (as was previously thought). This applies as well as to near miss for sudden infant death syndrome babies. The soft palate is also involved in the genesis of snoring and the sleep apnea syndrome.

Adult↗
PubMed1979

Palatal process movement in the rat as demonstrated in frozen sections.

During mammalian secondary palate development, movement of the lateral palatine processes from the vertical plane to the horizontal plane involves a complex interaction of the palatine processes and the tongue within a dynamic growing oronasal cavity environment. This study of pre-fixation facial profile photographs and frozen sections was undertaken to evaluate external and internal changes in the oronasal complex during secondary palate elevation without the shrinkage known to be present with routinhistological preparation of embryonic tissues. Frozen sections of Sprague-Dawley rat embryos between 15 and 17 days of (conceptual) age were prepared by hexane quenching and cryostat cutting. The results showed that, during the stages of palate development prior to shelf elevation, the tongue and mandible became positioned beneath the primary palate, and the vertical dimension of the oronasal cavity increased by the lifting of the nasomaxillary complex. The tongue and mandible maintained contact with the primary palate, whereas a space developed above the tongue in the middle and posterior palate regions. As the vertical dimension increased the volume of the palatomaxillary processes increased rapidly, the tongue became squeezed, and the palatine processes bulged medially above the level of the tongue. After shelf elevation extensive contact between the palatine processes was present, and the tongue became flattened. The results of this study support the observations of Lazzaro (1940) that rapid increase in shelf volume owing to increased intercellular volume contributes to movement of the processes above the tongue. But, rapid increase in shelf volume occurred contemporaneously with the time when the tongue and mandible outgrew the oronasal cavity and became positioned beneath the primary palate. Therefore, it would appear that the simultaneous occurrence of a lower and more forward tongue position, and an increased palatomaxillary process volume without change in maxillary width, contributed to the medial movement of the processes above the tongue.

Animals↗
PubMed1983

Serotonin regulation of palatal cell motility and metabolism.

Serotonin has been previously shown to stimulate palate reorientation. To elucidate the mechanism by which the neurotransmitter may be regulating palate morphogenesis, the effects of serotonin on cell motility and various metabolic reactions have been measured in vitro. To monitor cell motility, a chemotactic system was employed in which cultured palate mesenchymal cells in a modified Boyden chamber migrate toward the chemoattractant(s) in N-18 neuroblastoma conditioned medium. Serotonin stimulated cell motility and 10(-5) M was optimal with nearly 100% stimulation achieved. With N-18 conditioned medium diluted 1:100, serotonin stimulated cell motility 4.9-fold. Serotonin itself was not chemotactic but modulated cell movement in the presence of the chemoattractant. Protein carboxyl methylation was stimulated by serotonin about 100% at concentrations ranging from 3 X 10(-7) M to 3 X 10(-6) M in different experiments. The net stimulation may have been elicited by an indirect effect since serotonin also inhibited demethylation of protein methyl esters. Serotonin was shown to inhibit cyclic AMP in cultured palate cells: 10(-5) M agonist depressed levels to 19% of control in 3 h. Further, prostaglandin E1, which stimulated cyclic AMP levels, markedly inhibited cell motility in the chemotactic assay. Thus there is an inverse relationship between cyclic AMP levels and cell motility in fetal palate cells. Finally it was observed that serotonin stimulated cyclic GMP levels; 10(-5) M serotonin optimally stimulated cyclic GMP with a spike of stimulation (6.1-fold) within 30 sec. In summary, serotonin in palate cells stimulates both protein carboxyl methylation and cyclic GMP. Modulation of these reactions could be regulating cell motility and/or protein secretion, which in turn could function in palate reorientation.

Animals↗
PubMed1984

Variations in craniofacial morphology with severity of isolated cleft palate.

Cephalometric X-ray studies were carried out in 90 adult males with isolated cleft palate operated upon by the same method. The results were evaluated according to the extent of the clefts (complete, incomplete, or soft palate alone). But for a few exceptions the neurocranium and the cranial base showed no substantial deviations. Similarly, as in cleft lip and palate, a shortening of maxillary depth and a deficient mandibular growth were recorded, with no reduction of the vertical growth of the upper face, retroclination of the dentoalveolar maxillary component or increase of the interocular distance noted. No posterior displacement of the maxilla was found. The two observed deviations resulted in the retrusion of the upper and lower jaws, the flattening of the skeletal profile, impaired maxillomandibular relations and limitation of anterior growth rotation. Soft palate clefts were associated with less retrusion of the maxilla, while the growth deficiency of the mandible was even more marked. The least shortening of the mandible occurred in complete clefts. In general, incomplete clefts were associated with the most marked changes. The flattening of the skeletal profile in complete and incomplete clefts was masked by an increased thickness of the upper lip. Soft palate clefts were associated frequently with a shorter and hard palate. Our results were in agreement with experimental knowledge of the role played by the mandible in the development of isolated cleft palate.

Adult↗
PubMed1981

The prevalence of congenital heart disease among the population of a metropolitan cleft lip and palate clinic.

The entire infant population of the Tufts-New England Medical Center Cleft Palate Clinic was reviewed, and the prevalence rates of congenital cardiac anomalies were calculated. The overall prevalence rate of congenital heart disease among the facial cleft clinic population was 6.7%, with a prevalence rate of 9.1% among patients with submucous cleft palate, 7.7% with congenital palato-pharyngeal incompetence, 0% with cleft lip only, 5.3% with unilateral cleft lip and palate, 12.5% with bilateral cleft lip and palate, 4.3% with cleft palate only, 13.6% with Pierre-Robin anomaly, 7.1% with cleft lip and palate and a syndrome diagnosis, 16.7% with cleft palate and a syndrome diagnosis.

Child↗
PubMed1993

Monoclonal antibodies recognising stage and region specific epitopes in embryonic mouse palatal epithelial cells.

Four monoclonal antibodies raised against murine embryonic palatal epithelium were used to stain frontal cryosections of embryonic mouse heads (d 11-15). One antibody (6A11) recognised the nasal epithelium at the angle of the palate prior to shelf elevation (embryonic d 11-d 13) and the epithelia at the tips of the approximated shelves (embryonic d 14.5). Two further antibodies (2H6 and 3H2) recognised epitopes on the entire palatal epithelium until shelf elevation (embryonic d 14.5) when their expression ceased. The epitope recognised by antibody 6D3 was absent from the palatal epithelium until embryonic d 13 when it displayed region specific expression, being present on the nasal aspect in the midpalate and the tip of the palate posteriorly. On embryonic d 14.5 staining of the medial edge epithelia was present in all regions. Whilst the nasal palatal epithelium stained in the anterior and mid regions, only patchy staining of the oral epithelium was detected. By embryonic d 15 staining was present throughout the palatal epithelia. These antibodies are directed against intracellular epitopes, possibly keratins. Indeed, immunoblotting assays revealed that antibody 2H6 recognised keratin 18. The developmental regulation of the epitopes recognised by the antibodies corresponds with differentiative events occurring during murine palatogenesis.

Animals↗