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At least 631 records · Page 35Linked to original sources
PubMed1994

A comparative study on the effects of 5-fluorouracil on glycosaminoglycan synthesis during palate development in quail and hamster.

A comparative study was undertaken to investigate the effects of 5-fluorouracil (FU) on glycosaminoglycans (GAG) synthesis during morphogenesis of the secondary palate in birds (where, unlike mammals, palate morphogenesis begins in a horizontal direction ad initium and lacks mammalian-type shelf reorientation) and mammal. Previous studies have shown that FU induces cleft palate in both birds and mammals. Air sacs of quail eggs were injected with 100 micrograms FU in 0.1 ml saline or 0.1 ml saline only. Hamsters were given intramuscular injection of 81 mg/kg FU in 1 ml saline or 1 ml saline only. Total GAG synthesis was measured by incorporation of 3H-glucosamine. Sulfated and non-sulfated GAGs were identified by Alcian Blue histochemistry combined with the use of GAG-degrading enzymes. The results indicated that a continuous synthesis of GAG at a steady rate was associated with normal palate morphogenesis in both quail and hamster. The amount of GAG synthesized in hamster palate was four-fold higher than in quail palate. In contrast to the developing hamster palate where the predominant GAG was hyaluronate, the major GAGs present during quail palate development were sulfated and were concentrated on the nasal side. FU treatment did not affect the rate of GAG synthesis in the developing palate of quail. In contrast, FU administration altered the rates of GAG synthesis, and affected hyaluronate accumulation, during palate morphogenesis in hamster.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcian Blue↗
PubMed2000

Palatability and intake relationships in free-living humans: measurement and characterization in the French.

To investigate palatability influences on the ad lib eating behavior of free-living humans, 54 French participants were paid to maintain food intake diaries for four 7-day periods. They recorded their intake along with palatability ratings, on a seven-point scale, of each individual item eaten and also a global rating of the palatability of the entire meal. Higher levels of palatability were found to be related to larger meal sizes, durations, and deprivation ratios, smaller satiety ratios, greater hunger, and lower depression and anxiety. The global palatability rating was found to be superior to individual item palatability ratings as a measure of the palatability of the meal. Although palatability was found to have fairly large effects on intake, it accounted for less than 2% of the variance. It was concluded that, in the natural environment, there are a large number of other powerful variables present that add variance. In addition, people tend to self-select only a restricted range of highly palatable foods. As a result, in the natural environment, the influence of palatability on intake is limited.

Adolescent↗
PubMed1997

A possible role for palatability of the food in diet-induced thermogenesis.

OBJECTIVE: A regulatory increase in energy expenditure, induced by excess intake of palatable food (cafeteria diet), is well documented. It has also been shown that excess feeding by gastric intubation, fails to enhance thermogenesis, suggesting that the palatability of the food could have a role in producing this regulatory response. A study was planned to find out if a palatable diet pair-fed with standard laboratory chow would produce diet-induced thermogenesis (DIT) and if the brown adipose tissue (BAT) was involved in this process. DESIGN: Body weight gain, BAT activity and body temperature response to norepinephrine were measured in rats fed for 40 d either the standard laboratory pellets (control), a palatable high carbohydrate diet fed ad libitum and the same palatable diet but fed in restricted amounts to match the intake of the control group. RESULTS: It was found that palatable food either fed ad libitum or pair-fed, increased DIT and reduced food efficiency (which is the body weight gain per 100 kj of food consumed). These responses were paralleled by increased BAT activity and enhanced response to noradrenaline. Since the DIT with pair-feeding was proportionally as large as with excess intake of the same food in the group fed ad libitum, it is concluded that the palatability of the food, rather than the excess intake per se, is responsible for the increased thermogenesis. CONCLUSIONS: DIT was observed when palatable food was fed either ad libitum or in restricted amounts. It is suggested that the palatability of the diet rather than the quantity or composition of the ingested food is responsible for the DIT. It is also proposed that the excess energy expenditure due to sensory stimulation induced by palatable food, is directly related to an enhanced sympathetic activity which stimulates the BAT thermogenic capacity.

Adipose Tissue, Brown↗
PubMed2004

Effects of manipulated palatability on appetite depend on restraint and disinhibition scores from the Three-Factor Eating Questionnaire.

OBJECTIVES: The present study evaluated the effects of dietary restraint on short-term appetite in response to manipulated palatability. DESIGN: The effects of palatability on appetite during a lunchtime meal were assessed by contrasting intake of a bland and palatable version of a simple food (within subject). To test how responses to palatability varied with restraint, these meals consumed by women were classified according to restraint (R) and disinhibition (D) scores from the Three-Factor Eating Questionnaire (TFEQ) as high R/high D (HR-HD), high R/low D (HR-LD), low R/high D (LR-HD) and low R/low D (LR-LD). SUBJECTS: A total of 40 normal-weight women subdivided into four groups based on TFEQ scores. MEASUREMENTS: The overall intake, appetite and hedonic ratings before, during and after the meal. RESULTS: All groups ate similar amounts of the bland food, but the LR-HD group ate significantly more of the palatable version than the other groups, whereas HR-LD did not increase intake in response to palatability. Hunger increased on tasting the palatable food in all but the HR-LD group, and this group ended both meals more hungry/less full than the others. CONCLUSION: Women classified as HR-LD were unresponsive to manipulated palatability, whereas those classified as LR-HD were over-responsive. These findings imply that some individuals are prone to over-respond to palatability and so are at greater risk of developing obesity, whereas others are able to resist the effects of palatability and so successfully self-restrict their food intake. Implications for obesity are discussed.

Adult↗
PubMed1989

[Basic experiments on denture rigidity at various types of palatal bars].

UNLABELLED: The purpose of this study was to investigate the rigidity of removable partial denture with a palatal bar. A metal model with a Kennedy Class II-modification 1, was fabricated as a simulated dental arch. The model palate was adjustable to three different radii (17.5 mm, 20.0 mm and 22.5 mm) on the frontal section. MATERIALS: These were bending palatal bars and preformed plastic patterns. One of the bending palatal bars was 3.4 mm wide 1.4 mm thick, the other was 3.1 mm wide and 1.1 mm thick. Two other bars, 5.0 mm wide, 1.7 mm thick and 5.0 mm wide, 1.5 mm thick, were cast in Ticonium p-100 alloy from the plastic pattern. METHOD: The materials were fitted to the model and rigidity was measured by loading at various parts equivalent to the distal extension base. The experiments were performed with a 1 mm space between the frames and the model and again with a 1 mm thick sheet of mercaptan rubber-base impression material between them. RESULTS: 1. Cast palatal bars showed a smaller deflection than the bending palatal bars. 2. The bending palatal bars showed a large deflection of the distal extension base. So, care should be exercised when fitting a bending palatalbar in a distal extension case because of the incompressibility of the mucous membrane. 3. Bar deflection was only slightly different for the three types of palate. 4. Deflection of the palatal bar and distal extension base was smaller when the bar was thicker and wider. 5. The amounts of palatal bar and base deflection with the 1.0 mm space was in proportion to the load. 6. With the rubber-base sheet between, the amounts of deflection was not proportional to the load, and the amount of deflection under a 30 kg load was almost twice that of a 5 kg load.

Denture Design↗
PubMed1998

Insulin-like growth factor II receptor, transforming growth factor-beta, and Cdk4 expression and the developmental epigenetics of mouse palate morphogenesis and dysmorphogenesis.

The B10/B10.A congenic mouse pair serves as a model for identifying specific genes related to morphogenesis and dysmorphogenesis of the embryonic palate and other organs. The present report describes our initial investigation of the Fraser-Juriloff paradigm, which proposes that susceptibility to malformation results from genetically determined differences in normal developmental patterns. Specifically, we evaluated the relationship between Igf2r gene expression, transforming growth factor-beta (TGF-beta) activation, and cdk4 gene expression. By using in situ hybridization, RNase protection assays, indirect immunofluorescence, Western blots, and bioassays, we show 1) the presence of insulin-like growth factor II (IGF-II), IGF-II receptor (IGF-IIR), IGF-IR, TGF-beta, plasminogen, plasminogen activators [urokinase plasminogen activator (uPA) and tissue plasminogen activator (tPA)], and Cdk4 in developing palates; 2) on embryonic day 14 (E14), which is a critical day for palatal growth, B10.A embryos have 82% greater IGF-IIR mRNA than B10; 3) on E14, B10.A embryonic palates have a 57% greater level of active TGF-beta2 than B10, although the total TGF-beta2 is nearly identical; and 4) on E14, B10 embryonic palates have a 52% greater level of Cdk4 mRNA than B10.A palates, a measure of cell cycle progression. Because cellular activation of latent TGF-beta appears to require binding to the mannose-6-phosphate (M6P) binding site of the IGF-IIR and is plasmin and plasminogen activator dependent, the positive correlation of IGF-IIR levels and active TGF-beta2 levels seems to be key. Thus, the strain variation of TGF-beta2/IGF-IIR-mediated growth inhibition in late G1 phase would appear to account for the slower growth and development of B10.A palates relative to B10. Elevated corticosteroid (CORT) exposure in E14 B10.A embryos significantly increases TGF-beta levels, 87% of which is TGF-beta2, as well as the levels of active TGF-beta, 64% of which is TGF-beta2. Without exogenous CORT, B10.A embryos do not have clefts; hence, we present an outline of pathogenesis: slower growing B10.A embryos have an up-regulation of IGF-IIR, which serves to sequester IGF-II from the growth-promoting IGF-IR and to bind more CORT-up-regulated, latent TGF-beta2 for subsequent plasmin-dependent activation; higher levels of TGF-beta2 signaling down-regulate Cdk4 and result in greater palatal growth inhibition at a critical stage of palatogenesis and, thus, cleft palate. We present an epigenetic model of information processing related to cell proliferation. The model is a dynamical network that uses continuous logic to learn its rules from changing conditions.

Animals↗
PubMed1991

Pathogenesis of bromodeoxyuridine-induced cleft palate in hamster.

In the present study, the morphological, histochemical, biochemical, and cellular aspects of the pathogenesis of bromodeoxyuridine (BrdU)-induced cleft palate in hamster fetuses were analyzed. Morphological observations indicated that BrdU interferes with the growth of the vertical shelves and thus induces cleft palate. At an ultrastructural level, BrdU-induced changes were first seen in the mesenchymal cells. Eighteen hours after drug administration, the initial alterations were characterized by swelling of the nuclear membrane and the appearance of lysosomes in the mesenchymal cells of the roof of the oronasal cavity. During the next 6 hr, as the palatal primordia developed, lysosomes were also seen in the overlying epithelial cells. The appearance of lysosomal activity, which was verified by acid phosphatase histochemistry, was temporally abnormal and was interpreted as a sublethal response to BrdU treatment. Later the cellular alterations subsided; 48 hr after BrdU treatment, they were absent in both the epithelial and mesenchymal cells of the vertically developing palatal shelves. Subsequently, unlike controls (in which the palatal shelves undergo reorientation and fusion), the BrdU-treated shelves remained vertical until term. Biochemical determination of DNA synthesis indicated that although there was an inhibition of DNA synthesis at the time of appearance of palatal primordia, a catch-up growth during the ensuing 12 hr may have restored the number of cells available for the formation of a vertical palatal shelf. It was suggested that BrdU affected cytodifferentiation in the palatal tissues during the critical phase of early vertical development to induce a cleft palate.

Acid Phosphatase↗
PubMed1979

Correlation between mandibular retrognathia and induction of cleft palate with 6-aminonicotinamide in the rat.

A single injection of the niacin antimetabolite 6-aminonicotinamide (6-AN) late in gestation produces cleft palate in the rat. In order to achieve an understanding of the mechanism of induction of cleft palate, craniofacial growth and palate development were studied in Sprague-Dawley rats after treatment with 6-AN on day 15 of gestation. The rats were maintained on a high niacin diet (95 ppm) and subjected to three different teratogenic levels of 6-AN. The first group was injected with 8 mg/kg, the second was fasted and injected with 8 mg/kg and the third was treated with 16 mg/kg. The lowest teratogenic dose, 8 mg/kg, produced mild mandibular retrognathia on day 16, delayed shelf elevation a few hours and resulted in small rostral and small caudal clefts of the secondary palate. The moderate dose, 8 mg/kg with fasting, produced more severe mandibular retrognathia, delayed shelf elevation about 24 hours and resulted in 37% full clefts and 63% partial clefts of the palate. The highest teratogenic dose, 16 mg/kg, produced severe mandibular retrognathia, delayed shelf elevation by more than 24 hours and resulted in 100% full clefts of the palate. In each 6-AN group, the most severe mandibular retrognathia was present between days 16 and 17, the critical time for palate closure in the rat. Treatment with 6-AN also produced abnormality of the epithelial cells of the palate, the toothbuds and the nasal septum. Molar and incisor toothbuds were small and malformed, and the epithelial surfaces of the palate and the soft tissue nasal septum did not fuse.

6-Aminonicotinamide↗
PubMed2001

[Wavy incision of the soft palate. Modification of intravelar veloplasty].

PURPOSE: The problem with primary soft palate repair is shortness of the soft palate and a soft tissue deficit in this region. The authors introduce a modification of the intravelar veloplasty allowing lengthening of the soft palate at the time of primary closure. METHODS: The "soft palate wavy incision procedure" combines a wavy or undulating type of incision at the velar cleft margins with intravelar veloplasty. In 12 patients with complete clefts of the palate, postoperative breathing and speech was analyzed 3 years later. The investigator did not know whether a modification of the common procedure had been performed in these patients or not. RESULTS: It was found that the soft palate wavy line procedure is easy to perform and closure in three layers is possible even in wide clefts of the soft palate. No postoperative fistula was observed. An average lengthening of the soft palate of about 56% (24-83%) was achieved, measured immediately at the end of surgery. Three years later the patients have good speech results following this technique. CONCLUSIONS: Experience has shown that the soft palate wavy incision procedure is straightforward, safe, and easy. It seems that this technique leads to better results than classic intravelar veloplasty. This paper is only a first report, and further investigations are necessary.

Child, Preschool↗
PubMedDate not supplied

MSX-1 gene expression and regulation in embryonic palatal tissue.

The palatal cleft seen in Msx-1 knock-out mice suggests a role for this gene in normal palate development. The cleft is presumed secondary to tooth and jaw malformations, since in situ hybridization suggests that Msx-1 mRNA is not highly expressed in developing palatal tissue. In this study we demonstrate, by Northern blot analysis, the expression of Msx-1, but not Msx-2, in the developing palate and in primary cultures of murine embryonic palate mesenchymal cells. Furthermore, we propose a role for Msx-1 in retinoic acid-induced cleft palate, since retinoic acid inhibits Msx-1 mRNA expression in palate mesenchymal cells. We also demonstrate that transforming growth factor beta inhibits Msx-1 mRNA expression in palate mesenchymal cells, with retinoic acid and transforming growth factor beta acting synergistically when added simultaneously to these cells. These data suggest a mechanistic interaction between retinoic acid, transforming growth factor beta, and Msx-1 in the etiology of retinoic acid-induced cleft palate.

Animals↗
PubMed2005

Overexpression of Smad2 in Tgf-beta3-null mutant mice rescues cleft palate.

Transforming growth factor (TGF)-beta3 is an important contributor to the regulation of medial edge epithelium (MEE) disappearance during palatal fusion. SMAD2 phosphorylation in the MEE has been shown to be directly regulated by TGF-beta3. No phospho-SMAD2 was identified in the MEE in Tgf-beta3-null mutant mice (Tgf-beta3-/-), which was correlated with the persistence of the MEE and failure of palatal fusion. In the present study, the cleft palate phenotype in Tgf-beta3-/- mice was rescued by overexpression of a Smad2 transgene in Keratin 14-synthesizing MEE cells following mating Tgf-beta3 heterozygous mice with Keratin 14 promoter directed Smad2 transgenic mice (K14-Smad2). Success of the rescue could be attributed to the elevated phospho-SMAD2 level in the MEE, demonstrated by two indirect evidences. The rescued palatal fusion in Tgf-beta3-/-/K14-Smad2 mice, however, never proceeded to the junction of primary and secondary palates and the most posterior border of the soft palate, despite phospho-SMAD2 expression in these regions at the same level as in the middle portion of the secondary palate. The K14-Smad2 transgene was unable to restore all the functional outcomes of TGF-beta3. This may indicate an anterior-posterior patterning in the palatal shelves with respect to TGF-beta3 signaling and the mechanism of secondary palatal fusion.

Animals↗
PubMed2003

Role of ERK1/2 signaling during EGF-induced inhibition of palatal fusion.

During mammalian palatal fusion, the medial edge epithelial (MEE) cells must stop DNA synthesis prior to the initial contact of opposing palatal shelves and thereafter selectively disappear from the midline. Exogenous EGF has been shown to inhibit the cessation of DNA synthesis and induce cleft palate; however, the precise intracellular mechanism has not been determined. We hypothesized that EGF signaling acting via ERK1/2 would maintain MEE DNA synthesis and cell proliferation and consequently inhibit the process of palatal fusion. Palatal shelves from E13 mouse embryos were maintained in organ cultures and stimulated with EGF. EGF-treated palates failed to fuse with intact MEE and had significant ERK1/2 phosphorylation. Both EGF-induced ERK1/2 phosphorylation and BrdU-incorporation were localized in the nucleus of MEE cells. Subsequent inhibition assays using U0126, a specific inhibitor of ERK1/2 phosphorylation, were conducted. U0126 inhibited EGF-induced ERK1/2 phosphorylation in a dose-dependent manner and consequently MEE cells stopped proliferation. The threshold of ERK1/2 inactivation to stop MEE DNA synthesis coincides with the level required to rescue the EGF-induced cleft palate phenotype. These results indicate that EGF-induced inhibition of palatal fusion is dependent on nuclear ERK1/2 activation and that this mechanism must be tightly regulated during normal palatal fusion.

Active Transport, Cell Nucleus↗
PubMedDate not supplied

Palatal ruga anomaly induced by all-trans-retinoic acid in the Crj:SD rat: possible warning sign of teratogenicity.

We have reported that the critical period for cleft palate formation by all-trans-retinoic acid (RA) is on gestation day 14 in rats, and classified abnormal patterns of palatal rugae into minor variations and anomalous patterns. In this study, we examined the dose-response relationship for cleft palate and an anomalous pattern of palatal rugae formation and discussed the toxicologic significance of the palatal ruga anomaly as an indicator of teratogenicity. The ED(50) values for cleft palate and anomalous pattern were calculated to be 43.6 and 4.95 mg/kg, respectively. The results clearly show that anomalous rugal patterns occur in the fetuses from litters receiving RA at a lower dose than cleft palate induction; the anomalous ruga pattern is thus more sensitive than cleft palate induction. The anomalies of palatal rugae could be taken as a warning sign or an indicator of teratogenicity of a drug.

Abnormalities, Drug-Induced↗
PubMed1999

Isolated cleft palate in mice with a targeted mutation of the LIM homeobox gene lhx8.

Formation of the mammalian secondary palate is a highly regulated and complex process whose impairment often results in cleft palate, a common birth defect in both humans and animals. Loss-of-function analysis has linked a growing number of genes to this process. Here we report that Lhx8, a recently identified LIM homeobox gene, is expressed in the mesenchyme of the mouse palatal structures throughout their development. To test the function of Lhx8 in vivo, we generated a mutant mouse with a targeted deletion of the Lhx8 gene. Our analysis of the mutant animals revealed a crucial role for Lhx8 in palatogenesis. In Lhx8 homozygous mutant embryos, the bilateral primordial palatal shelves formed and elevated normally, but they often failed to make contact and to fuse properly, resulting in a cleft secondary palate. Because development of other craniofacial structures appeared normal, the impaired palatal formation in Lhx8-mutant mice was most likely caused by an intrinsic primary defect in the mesenchyme of the palatal shelves. The cleft palate phenotype observed in Lhx8-mutant mice suggests that Lhx8 is a candidate gene for the isolated nonsyndromic form of cleft palate in humans.

Animals↗
PubMed1994

Symptomatic and essential palatal tremor. 1. Clinical, physiological and MRI analysis.

Palatal tremor (brief, rhythmic involuntary movements of the soft palate) apparently comprises two different nosological entities: essential palatal tremor (EPT) and symptomatic palatal tremor (SPT). The site of the abnormality in EPT is unknown, whereas SPT is believed to arise from a lesion of the brainstem or cerebellum (within the Guillain-Mollaret triangle). The clinical and physiological properties of these conditions were studied in four patients with EPT and six patients with SPT. Patients with EPT had normal cerebellar function, but those with SPT had clinical signs of cerebellar dysfunction. The palatal movements were consistent with activation of the tensor veli palatini muscle in EPT and of the levator veli palatini muscle in SPT. During sleep, EPT stopped, whereas SPT continued with only slight variations in the tremor rate. The cycle of palatal tremor could not be reset by stimulation of trigeminal afferents in either EPT or SPT patients, and Valsalva's manoeuvre did not consistently affect the rhythm of the tremor in either group. The palatal tremor cycle exerted remote effects on the tonic electromyographic activity of the upper and lower extremities only in patients with SPT. These effects were present only on the side of the cerebellar signs (opposite the side with the enlarged inferior olive) in patients with a unilateral syndrome. Essential palatal tremor patients had only polysynaptic brainstem reflex abnormalities, whereas SPT patients had abnormalities of monosynaptic, oligosynaptic and polysynaptic brainstem reflexes. Magnetic resonance imaging showed no evidence of structural abnormalities in EPT patients, but SPT patients had a hyperdense signal of the ventral upper medulla (the region of the inferior olive) on T2-weighted images. These observations support the hypothesis that EPT and SPT are two different diseases. In SPT, cerebellar dysfunction ipsilateral to the palatal tremor may be due, in part, to abnormal function of the contralateral hypertrophic inferior olive. The proposed basis of SPT is a disturbance of electrotonic coupling between the cells of the inferior olive induced by a lesion of the dentato-olivary pathway. Similar mechanisms could be responsible for postural tremors in general. The pathophysiological basis of EPT remains unknown.

Adult↗
PubMed2005

Treatment outcome in unilateral cleft lip and palate evaluated with the GOSLON yardstick: a meta-analysis of 1236 patients.

BACKGROUND: The goal of this study was to assess determinants for treatment outcome in unilateral cleft lip and palate, evaluated according to the Great Ormond Street London and Oslo (GOSLON) Yardstick and 5-year-index ratings by means of a meta-analysis. METHODS: Multiple databases were searched for publications in which patient groups were evaluated by GOSLON ranking or the GOSLON-like 5-year index. From the 15 selected publications, the following background variables could be extracted and were evaluated as determinants for treatment outcome in unilateral cleft lip and palate: year of birth, average age of the patient at the time of GOSLON classification, racial background, presence of Simonart's band, infant orthopedics, palatal closure before the age of 3 versus palatal closure at a later age, bone graft, and number of surgeons. RESULTS: The total number of patients included in the meta-analysis was 1236. Patients whose soft and hard palate were closed before the age of 3 presented significantly poorer (p = 0.003) GOSLON scores (mean score, 2.9; SD 0.4) than patients whose palate was closed at a later age (mean GOSLON score, 2.3; SD 0.2). CONCLUSIONS: Delayed palatal closure generally results in better dental arch relationships than early palatal closure. Well-designed, randomized clinical trials are required for further investigation of the optimal timing for palatal closure.

Age Factors↗
PubMed2005

Shox2-deficient mice exhibit a rare type of incomplete clefting of the secondary palate.

The short stature homeobox gene SHOX is associated with idiopathic short stature in humans, as seen in Turner syndrome and Leri-Weill dyschondrosteosis, while little is known about its close relative SHOX2. We report the restricted expression of Shox2 in the anterior domain of the secondary palate in mice and humans. Shox2-/- mice develop an incomplete cleft that is confined to the anterior region of the palate, an extremely rare type of clefting in humans. The Shox2-/- palatal shelves initiate, grow and elevate normally, but the anterior region fails to contact and fuse at the midline, owing to altered cell proliferation and apoptosis, leading to incomplete clefting within the presumptive hard palate. Accompanied with these cellular alterations is an ectopic expression of Fgf10 and Fgfr2c in the anterior palatal mesenchyme of the mutants. Tissue recombination and bead implantation experiments revealed that signals from the anterior palatal epithelium are responsible for the restricted mesenchymal Shox2 expression. BMP activity is necessary but not sufficient for the induction of palatal Shox2 expression. Our results demonstrate an intrinsic requirement for Shox2 in palatogenesis, and support the idea that palatogenesis is differentially regulated along the anteroposterior axis. Furthermore, our results demonstrate that fusion of the posterior palate can occur independently of fusion in the anterior palate.

Animals↗
PubMed2004

Histopathological findings of cleft palate in rat embryos induced by triamcinolone acetonide.

Triamcinolone acetonide (TAC), a synthetic glucocorticoid, induces cleft palate resulting from poor development of palatal shelves in mice. However, TAC has no effect on medial edge epithelial cells (MEE cells) in secondary palatal shelves. In the present study, we examined the relationship between the pathogenesis of cleft palate and the effects on MEE cells and palatal mesenchymal cells in rat embryos/fetuses exposed to TAC. Pregnant Wistar Hannover rats were given TAC intramuscularly at 0.5 mg/kg at gestation days (Day) 12, 13, and 14, then embryos/fetuses were harvested on Days 14.5, 15, 16 and 20. The effects of TAC were as follows; an inhibition of palatal mesenchymal cell proliferation on Day 14.5, a decrease in the density of palatal mesenchymal cells and MEE cells, and expression of epidermal growth factor (EGF) receptors in MEE cells on Day 15, and stratified squamous differentiation of MEE cells with expression of cytokeratin and EGF receptors on Day 16. These findings indicated that TAC inhibited the proliferation of mesenchymal cells and affected the differentiation of MEE cells into stratified squamous epithelia in the palatal shelves of rat embryos. However, these stratified squamous MEE cells partially fused with each other. Thus, we suspected that a major contributing factor to the formation of TAC-induced cleft palate might not be the altered differentiation of MEE cells, but the inhibition of mesenchymal cell proliferation.

Animals↗