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PubMed1979

Taste acuity of the human palate. III. Studies with taste solutions on subjects in different age groups.

The taste acuity at the midline of the hard and soft palate near their junction and, for comparison, on representative areas of the tongue was determined in 80 subjects aged 11-79 years by applying test solutions of the four basic tastes. Twenty-one subjects (26%) could identify at least one taste on the hard palate but none could recognize all four tastes. Seventy subjects (87%) could identify at least one taste on the soft palate and 37 subjects (46%) could recognize all four tastes. Taste thresholds were much higher on the hard palate than on the tongue and were in most cases higher on the soft palate than on the tongue. The ability to recognize all four tastes was less frequent in older than in younger subjects and the difference was greatest on the soft palate and least at the foliate papillae. The differences were greatest for citric acid and least for sucrose. There was a tendency to lower thresholds for women compared to men for all four tastes on all areas examined which was most pronounced on the soft palate. No differences in taste thresholds were found between denture wearers and subjects with natural dentition. Smokers had higher thresholds than non-smokers only for salt on the soft palate and the base of the tongue.

Adolescent↗
PubMed2003

[Clinical study on fistula incidence of early cleft palate repair].

OBJECTIVE: To study the regularity of fistula incidence after early cleft palate repair METHODS: 531 patients aged 2-12 months at the operation were included in the retrospective study, who underwent cleft palate repair during July 1995 to September 2001. RESULTS: The overall frequency of fistulas was 4.9%. The fistula incidence of bilateral complete cleft palate was obviously higher (7.8%) than that of incomplete cleft palate (4.4%) and the unilateral complete group (4.3%) (P < 0.005). There was no significant difference between the latter two. Fistula incidence was irrelevant to the patient age and the operation method. Seventy percent of fistulas in complete cleft palate occurred on the hard palate, which was significantly higher than that on the other parts. CONCLUSION: Infant cleft palate repair did not increase fistula incidence. We recommend preoperative orthodontics for bilateral cleft palate infants.

Cleft Palate↗
PubMed2006

[Establishment and application of fetal rolling palate organ culture model of mouse].

OBJECTIVE: To investigate the effect of all-trans retinoic acid (atRA) on the development of mouse palates and its possible mechanism, a model of fetal mouse rolling plate organ culture was establishted. METHODS: Mouse embryonic palates were explanted on GD12 and cultured in a roller device for 72h induced by atRA in different concentrations from 10(-5) micromol/L to 10(-1) micromol/L. RESULTS: Similar to development in vivo, palates in control normal fused. Compared with the control, palates development and fusion were promoted in group of 10(-15) micromol/L, while were inhibited in groups of 10(-4) micromol/L or greater, resulting in cleft palate. The proportion of fusion was reduced in a significant dose-response pattern. CONCLUSION: In the model, the cultured palates continued developing and fusing. Palatal fusion was promoted by normally atRA in 10(-5) micromol/L level and were inhibited by atRA in 10(-4) micromol/L level or greater, which resulting in cleft palate. These mentioned confirm the validity and reliability of this model.

Animals↗
PubMed1977

Longitudinal analysis of growth of the soft palate and nasopharynx from six months to six years.

Between the ages of six months and six years, longitudinal lateral headfilms were taken on 54 patients with palatal clefts or with unilateral and bilateral clefts of the lip and palate. They were measured and were compared to data on both normals and subjects with clefts of the lip only. The objectives of the study were: 1. To sutdy the effects of palatal surgery on the growth of the soft palate. 2. To compare the growth of the soft palate and nasopharynx among the patients with various types of clefts and normals. 3. To study the growth acceleration or so-called catch-up growth after palatal surgery at various ages. (Anterior palatal surgery at 14 months +/- 2 months. Posterior palatal surgery at 16 months +/- 2 months.) 4. To evaluate the relationship between velopharyngeal growth in cleft groups and voice quality.

Child↗
PubMed1977

Post-fusion cleft of the fetal rat palate.

Several hypotheses of post-fusion rupture of the previously intact palate as a cause of cleft palate have been advanced but with minimal supportive experimental evidence. In this investigation an animal model was evolved in which the intact palates of 19 1/2 day Sprague Dawley rat fetuses were surgically ruptured. Fetuses were grossly and histologically examined at 0.24, 48, and 72 hours after surgery. The operation resulted in a range of clefts including complete cleft of the hard and soft palate, isolated cleft of the hard palate and submucous cleft palate. There were no associated defects, and the fetal mortality was low. The various hypotheses of post-fusion rupture were reviewed, and it was concluded that this model supports the hypothesis that isolated clefts of the hard palate may result from post-fusion rupture and submucous cleft from late disturbances in palatal mesenchyme.

Animals↗
PubMed1988

Effect of diazepam on the embryonic development of the palate in the rat.

The results of previous studies on the effect of diazepam on palate formation in animals have been inconclusive. Teratogen-induced cleft palate is usually caused by a delay in palatal shelf elevation. The present study investigated the effect of diazepam on palate formation in the Sprague-Dawley rat. Five groups of dams received subcutaneous doses of either 10, 20, 30, 40, or 50 mg/kg body weight of diazepam. Control dams received propylene glycol (vehicle). Dams in each dosage group were killed at 16.9 (16 d 9 h); 16.16, and 17.9 days of gestation, respectively, to assess delay in palatal shelf elevation. Crown rump length (CRL) of 1,283 fetuses collected from 105 dams was measured. Fetuses in each time/dosage group showed a reduction in CRL (P less than .01). With increasing dosage the number of fetuses showing delayed palatal shelf elevation was significantly increased (P less than .01). These results demonstrate that with an increase in dose there is an increased delay in palatal shelf elevation and a decrease in CRL. However, in this strain there seems to be a rapid prenatal recovery, resulting in a marked reduction in the incidence of delayed palatal shelf elevation.

Animals↗
PubMed1985

Experimental fusion of the naturally cleft, embryonic chick palate.

The palatal shelf medial edges of day 8 (Hamburger-Hamilton [HH] stages 32-33) and day 9 (HH stage 35) embryonic chicks were surgically disrupted in ovo and in vitro in an attempt to discover if the naturally cleft chick palate could be induced to fuse experimentally. At HH stages 32-33 (day 8) the chick palatal shelves were apart at the time of in ovo operation. Consequently, their medial edges did not fuse but rather underwent embryonic would healing with re-epithelialisation (which often formed needle track invaginations), but no signs of inflammation or scar or scab tissue formation. Conversely, at HH stage 35 (day 9) the palatal shelves are in contact at the time of in ovo operation and so underwent fusion. The extent of palatal fusion depended upon the extent of initial medial edge epithelial disruption. Fusion did not spread from the operated sites to adjacent unoperated areas, where the palatal shelves were in contact with each other. Occasional epithelial seams were formed, but these persisted and did not undergo cell death. There was no evidence of inflammation or scar or scab tissue at the operated sites. Abnormal bony and muscular blastemae appeared in the continuity zones of these experimentally intact chick palates. Mortality was high for embryos operated upon in ovo. Palatal shelves explanted from HH stages 32, 33, and 35 chick embryos and cultured in vitro with their medial edges in contact did not fuse unless their medial edge epithelia were surgically disrupted, in which cases fusion always occurred regardless of the stage of the explanted shelves.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Fistula formation and repair after palatal closure: an institutional perspective.

We retrospectively reviewed 119 consecutive patients who underwent cleft palate repair at the Mayo Clinic to determine the incidence of postoperative fistula formation, to assess possible contributing factors, and to review the methods of surgical management. Fistulas of the secondary palate were included, but nasal-alveolar fistulas and intentionally unrepaired anterior palatal fistulas were excluded. Six patients whose repairs were performed after 2.5 years of age were excluded to ensure a more uniform patient population. Cleft palate fistulas occurred in 13 of the 113 patients (11.5 percent). The median age at repair was 8.2 months, and the median follow-up period was 5.2 years. Several variables were analyzed by means of the log-rank test to determine their significance in postoperative fistula formation. Sex, extent of clefting (as estimated by the Veau classification), and type of palatal closure did not significantly affect the rate of fistula formation. However, patients who had palatal closure at an age younger than 12 months had a lower incidence of fistula formation (7.8 percent) than children whose closures were performed between the ages of 12 and 25 months (19.4 percent) (p = 0.058). The strongest predictor of the occurrence of a cleft palate fistula was the surgeon performing the procedure (p = 0.008). Fistula repair was deemed necessary in 11 of 13 patients, and 91 percent of these fistulas were healed with a single operation. Most of these fistulas were closed by using local flaps and two-layered closures. Cleft palate repair carries a significant but acceptable risk of fistula formation, which can be managed with local flaps. Fistula occurrence is related most to the experience level of the operating surgeon.

Child, Preschool↗
PubMed2006

Cleft palate repair using a marginal musculo-mucosal flap.

OBJECTIVE: To describe a modified procedure consisting of a mucoso-periosteal flap palatoplasty with a marginal musculo-mucosal flap (3M flap). This is also the first report of a primary repair for complete cleft palate using the 3M flap. We describe the lengthening effect of the nasal mucous layer of the soft palate and evaluate the fistula formation rate associated with this method. METHODS: This procedure has been performed on 21 patients with unilateral complete clefts and on 27 patients with incomplete clefts. A mucoso-periosteal flap raised from the hard palate was used mainly for closure of the cleft and not for the push-back. The 3M flap repaired the deficit of the nasal mucosa, making sure that the soft palate was lengthened. Intravelar veloplasty was performed also. RESULTS: The dimension of the nasal mucosal defect that can be filled with the 3M flap is 10 to 12 mm in length, oriented anterior-posterior, and 15 to 20 mm wide. Oronasal fistula formation was recognized in only 3 of 48 cases (2 of 21 complete clefts, 1 of 27 incomplete clefts) and were located at the hard-soft palate junction at the anterior portion of the 3M flap. CONCLUSIONS: This method has the theoretical advantages of (1) preventing fistula formation by filling the tissue deficiency with the 3M flap; (2) achieving better velopharyngeal function due to elongation of the soft palate and retropulsion of the muscular bundle, utilizing the 3M flap; and (3) minimizing maxillary growth retardation by adopting a non-push-back method of hard palate repair.

Biological Dressings↗
PubMed2002

Palate re-repair revisited.

OBJECTIVE: To analyze the results of a consecutive series of palate re-repairs performed using the operating microscope and identify predictive factors for outcome. DESIGN: Prospective data collection, with blind assessment of randomized recordings of speech and velar function on lateral videofluoroscopy and nasendoscopy. PATIENTS: One hundred twenty-nine consecutive patients with previously repaired cleft palates and symptomatic velopharyngeal incompetence (VPI) and evidence of anterior insertion of the levator veli palatini underwent palate re-repairs by a single surgeon from 1992 to 1998. Syndromic patients, those who had significant additional surgical procedures at the time of re-repair (23 patients), and all patients with inadequate pre- or postoperative speech recordings were excluded, leaving a total of 85 patients in the study. INTERVENTIONS: Palate re-repairs, with radical dissection and retropositioning of the velar muscles, were performed using the operating microscope with intraoperative grading of anatomical and surgical findings. MAIN OUTCOME MEASURES: Pre- and postoperative perceptual speech assessments using the Cleft Audit Protocol for Speech (CAPS) score, measurement of velar function on lateral videofluoroscopy, and assessment of nasendoscopy recordings. RESULTS: There were significant improvements in hypernasality, nasal emission, and nasal turbulence and measures of velar function on lateral videofluoroscopy, with improvement in the closure ratio, velopharyngeal gap at closure, velar excursion, velar movement angle, and velar velocity. CONCLUSIONS: Palate re-repair has been shown to be effective in treating VPI following cleft palate repair, both in patients who have not had an intravelar veloplasty and those who have had a previous attempt at muscle dissection and retropositioning. Palate re-repair has a lower morbidity and is more physiological than a pharyngoplasty or pharyngeal flap.

Adolescent↗
PubMed1976

Catecholamine-sensitive adenylate cyclase in the developing golden hamster palate.

The present study was initiated to determine whether specific hormones would influence adenylate cyclase activity within the maxillary-palatal complex during formation of the hamster secondary palate. Stages from initial appearance of the palatal processes to shortly after birth were studied. Highest basal adenylate cyclase activities occurred during the earliest periods of palate development. This basal enzyme activity began to diminish as palatal fusion occurred and remained lowered until birth. Activation of adenylate cyclase by fluoride was maximal at concentrations of 5-10 mM, and was observed throughout the span of palatal development. Fluoride activation of adenylate cyclase was greatest prior to fusion of the palatal processes, then decreased until birth when a slightly increased enzymatic stimulation was seen. Norepinephrine and epinphrine were the catecholamines most capable of inducing increased activation of adenylate cyclase at most periods of palatal growth. Increased enzyme activity in the presence of norepinephrine was more susceptible to antagonism by the beta adrenergic agent, propranolol, than to the alpha adrenergic agent, phentolamine. The remaining catecholamines, namely isoproterenol and dopamine, displayed a lesser ability to activate the enzyme, and adenylate cyclase was not equally responsive to these catecholamines at identical developmental stages. Other hormones, i.e. histamine, serotonin, thyrotropin, growth hormone, thyroxine and glucagon were generally ineffective in activating the enzyme. Phosphodiesterase activity was not detected until shortly before birth.

Adenylyl Cyclases↗
PubMed1984

Differentiation of cultured palatal shelves from alligator, chick, and mouse embryos.

Palatal shelves from embryonic alligators, chicks, and mice were explanted at various stages of development and organ cultured in either chemically defined, serumless media or the same media supplemented with 10% fetal calf serum. Shelves from each vertebrate were either cultured singly or in contact, and heterologous combinations of palatal shelves from different animals were made: chick/mouse, chick/alligator, and mouse/alligator. Epithelial differentiation (particularly that of the medial shelf edge) was assayed by vital staining, histology, and scanning electron microscopy. In vitro medial edge epithelial differentiation, and consequently the mechanisms of palatal closure, were identical to those normally seen in vivo for each species, i.e., cobble-stoned migrating epithelia in the alligator, cell death and fusion in the mouse, and keratinisation and cleft palate in the chick. Differentiation was optimal in the chemically defined, serumless media and was independent of shelf contact in all three species. No heterologous combinations of palatal shelves closed with each other: Evidently, the modes of palatal closure in mice and alligators are sufficiently different to prevent them forming a chimeric palate, whilst neither is capable of inducing closure in a cocultured chick palatal shelf. These unified defined culture conditions make possible a large number of epithelial-mesenchymal recombination studies as well as specific inhibitor, teratogenic, and hormonal investigations.

Alligators and Crocodiles↗
PubMed1992

An extracellular matrix infrastructure provides support for murine secondary palatal shelf remodelling.

A crucial part of secondary palate morphogenesis is the movement of the palatal shelves from an initial vertical position on either side of the tongue to a final horizontal one above it to achieve palate closure. The immunocytochemical localization of extracellular matrix (ECM) molecules in the palatal shelf during this remodelling and reorientation revealed the existence of an ECM infrastructure within the mesenchyme. The major components of this infrastructure were collagen III, fibronectin, and hyaluronate (HA). With remodelling, HA's domain within the mesenchyme was expanded, whereas those of fibronectin and collagen III became more circumscribed. The expansion of an HA-rich matrix within the mesenchyme is thought to be crucial for palatal reorientation. The results of this study suggest that, as this expansion occurs, it is modulated by collagen and fibronectin components of the ECM infrastructure. Prior to shelf remodelling, this infrastructure may be anchored by a specialized region of the midoral epithelial-mesenchymal interface and the subjacent mesenchyme which is characterized by the unique distribution of collagen III, fibronectin, and tenascin. The midoral palatal epithelium also may play a role in directing shelf expansion. This epithelial region undergoes changes in cell packing and epithelial cell layering that correlate with shelf remodelling. These changes occur concomitantly with changes in the expression of collagen III, collagen IV, and laminin within the underlying basement membrane. The localization and patterning of tenascin within the developing palate suggests that it not only contributes to the postulated anchoring structure of the midoral epithelial-mesenchymal region, but also plays a role in the determining the fate of the medial edge epithelial cells during the final stage of palate closure.

Animals↗
PubMed2001

Variations of the prominences of the bony palate and their relationship to complete dentures in Korean skulls.

The osteological and morphological variations of the prominences in the bony palate of 160 Korean skulls were studied. The frequency of the occurrence of the posterior palatine crest, located on the posterior border of the greater palatine foramen, was 13.8%. Palatal ridges were observed commonly in the skulls; however, the smooth type, which has no palatal ridges in the palate, was shown in 14.7% of cases, and palatal spines were observed in 33.8%. The prevalence of palatal tubercles was 11.6%, and all were found in the molar region. The palatine torus was found in 18.8% of cases and the most common type was along the median palatine suture from the incisive foramen to the posterior border of the palatine bone (63.3%). No significant differences between sexes or sides were found in the posterior palatine crest, palatal ridges, and palatal tubercle. However, the sex distribution of the palatine torus was significantly different (P < 0.05). These results would be helpful clinically in fabricating maxillary complete dentures for edentulous patients.

Adult↗
PubMed2005

PDGFR-alpha signaling is critical for tooth cusp and palate morphogenesis.

Platelet-derived growth factor receptor alpha (PDGFR-alpha) and PDGF ligands are key regulators for embryonic development. Although Pdgfralpha is spatially expressed in the cranial neural crest (CNC)-derived odontogenic mesenchyme, mice deficient for Pdgfralpha are embryonic lethal, making it impossible to investigate the functional significance of PDGF signaling in regulating the fate of CNC cells during tooth morphogenesis. Taking advantage of the kidney capsule assay, we investigated the biological function of PDGF signaling in regulating tooth morphogenesis. Pdgfralpha and Pdgfa are specifically and consistently expressed in the CNC-derived odontogenic mesenchyme and the dental epithelium, respectively, throughout all stages of tooth development, suggesting a paracrine function of PDGF signaling in regulating tooth morphogenesis. Highly concentrated expression patterns of Pdgfralpha and Pdgfa are associated with the developing dental cusp, suggesting possible functional importance of PDGF signaling in regulating cusp formation. Loss of the Pdgfralpha gene does not affect proper odontoblasts proliferation and differentiation in the CNC-derived odontogenic mesenchyme but perturbs the formation of extracellular matrix and the organization of odontoblast cells at the forming cusp area, resulting in dental cusp growth defect. Pdgfralpha-/- mice have complete cleft palate. We show that the cleft palate in Pdgfralpha mutant mice results from an extracellular matrix defect within the CNC-derived palatal mesenchyme. The midline epithelium of the mutant palatal shelf remains functionally competent to mediate palatal fusion once the palatal shelves are placed in close contact in vitro. Collectively, our data suggests that PDGFRalpha and PDGFA are critical regulators for the continued epithelial-mesenchymal interaction during tooth and palate morphogenesis. Disruption of PDGFRalpha signaling disturbs the growth of dental cusp and interferes with the critical extension of palatal shelf during craniofacial development.

Animals↗
PubMed1984

D-penicillamine-induced cleft palate in mice.

The teratogenic potential of the lathyrogen, D-penicillamine (DP), was assessed in pregnant mice, especially with respect to its ability to produce cleft palate. The dosage and the duration of treatment as they relate to the induction of cleft palate were also studied. Two different doses of DP were administered orally for either 5 or 4 consecutive days during the critical period of palatal closure. D-penicillamine (DP) at a dose level which does not have any apparent maternal toxic effects produced cleft palate in the offspring, and this teratogenic effect depended more upon the duration of treatment than the dosage administered. Inhibitory effects on the formation of bone matrix were observed at the base of the palatal shelf. It is suggested that DP is potentially an osteolathyrogenic agent. The mechanism of induction of cleft palate in DP-treated mice was explored by histological studies using light microscopy. Delayed elevation of the palatal shelves was observed and is considered to be the cause of the induction of cleft palate. No other external malformations could be detected in DP-treated fetuses.

Abnormalities, Drug-Induced↗
PubMed1987

Diazepam-induced cleft palate in the mouse and lack of correlation with the H-2 locus.

Cleft palate frequencies were studied in AJ and SW mice following either 1- or 2-day dosing schedules with the anxiolytic drug diazepam (DAZ). In all cases, mice were food and water deprived for 24 and 48 hours in the 1- and 2-day dosing schedules, respectively. High cleft palate frequencies in control mice of both strains resulting from 48-hour food and water deprivation (on days 13.5 and 14.5 of gestation) were reduced in mice deprived for 24 hours, indicating a stress related effect. Two-day dosing with DAZ (400 mg/kg) produced a net increase in cleft palate frequency in SW (33%) and AJ (18%) mice. Mice treated only on day 13.5 had reduced control and DAZ cleft palate frequencies, neither of which were significant. Clefting was significant but reduced following 1-day dosing on day 13/20 of gestation (13 days 20 hours) in SW mice (18%), whereas no clefting was seen in the AJ strain. This strain difference was shown not to be related to differences in developmental timing. Production of cleft palate seen in AJ mice after 2 days of dosing may be indicative of an interaction of DAZ with the stresses resulting from food and water deprivation. Genes of the major histocompatibility locus, H-2, have been shown to regulate cleft palate formation following glucocorticoid and phenytoin administration to mice. Despite pharmacological similarities between DAZ and phenytoin, comparison of cleft palate frequencies following administration of DAZ to various strains of mice of different H-2 haplotypes indicated that genes associated with the H-2 locus do not regulate DAZ-induced cleft palate in these strains.

Animals↗
PubMed1990

Study of the mechanisms of BUdR-induced cleft palate in the mouse.

This study was designed to examine the pathogenesis of bromodeoxyuridine (BUdR)-induced clefts of the secondary palate in the LACA mouse. Intraperitoneal injections of BUdR (500 mg/kg body weight) were given at various days and combinations of days between E11 and E15 (plug day = E1). Treatment on E11 alone resulted in approximately 22% of fetuses with cleft palate when the latter were examined either on E16 or E19. Treatment on E11 and E12 approximately doubled the above incidence, and treatment on E11, 12 and 13 raised it to 100%. However, no treatment, either single or multiple, caused cleft palate when given later than E11. This suggests that the cellular changes caused by BUdR that lead to cleft palate must be inflicted during E11 and that such damage can be repaired in about 80% of embryos. All fetuses with cleft palate had severe micrognathia on E16 and E19, which skeletal staining showed to be the result of a bilateral sigmoid buckling of Meckel's cartilage. Studies with the scanning electron microscope (SEM) on E15, 16, and 19 suggested strongly that the micrognathia caused a relative macroglossia and hence mechanical interference with palatal shelf reorientation. Histological studies with the light microscope showed that BUdR caused cellular necrosis in many embryonic tissues during the 24 hours after its administration. This necrosis was strikingly more severe in the mandibular rudiment of the first branchial arch than in the maxillary. The latter observation accords well with findings by other workers that cell proliferation is more rapid in the mandibular blastema than in the maxillary. Transmission electron microscope (TEM) studies of the buckled region of Meckel's cartilage failed to reveal any ultrastructural differences from control Meckel's cartilage. Hence BUdR had only interfered with the shape of the cartilage but not with its histiogenesis. We conclude that BUdR, by its cytotoxicity or antidifferentiative effects, interfered with the formation of the anterior end of Meckel's cartilage, initiating a chain of events leading through micrognathia and relative macroglossia to failure of palatal shelf reorientation and cleft palate.

Animals↗