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PubMed1992

NaOH cell maceration/scanning electron microscopic studies on the architecture of the lamina propria of the mouse palate.

NaOH cell-maceration/SEM method was applied to the oral surface of the mouse palate to demonstrate the three-dimensional architecture of the lamina propria. In the caudal part of the hard palate, the lamina propria was characterized by the conspicuous parallel ridges which ran side by side in sagittal direction. In the boundary between the hard palate and the soft palate the parallel ridges interrupted abruptly, in the soft palate the ridges were extremely undeveloped to show the shrunken cloth-like appearance. Furthermore, the conical connective tissue papillae were lined up along the boundary. These findings suggest that the boundary between the hard plate and the soft palate is clear not only in the bony structure but in the lamina propria, and that the parallel ridges in the hard palate play an important role in ensuring from the excessive extending force during mastication.

Animals↗

PubMed1991

Sucking efficiency of early orthopaedic plate and teats in infants with cleft lip and palate.

Intraoral negative pressure during bottle feeding with two kinds of teats (a regular Nuk and a cleft Nuk) was measured in 7 infants with cleft lip and palate, 8 infants with cleft palate, 2 infants with cleft lip, 4 infants with operated cleft lip and palate and 7 normal infants. Infants with cleft lip and palate or cleft palate were unable to generate negative pressure before cleft lip and palate closure. The presence or absence of an early orthopaedic plate did not make any difference. In infants with unoperated cleft lip and with operated cleft lip and palate, peak negative pressure during feeding differed little from that of normal infants.

Bottle Feeding↗

PubMed2003

Nicotine inhibits palatal fusion and modulates nicotinic receptors and the PI-3 kinase pathway in medial edge epithelia.

OBJECTIVES: To analyze the effects of nicotine on palatal fusion inhibition in vitro and determine if nicotine modulated transforming growth factor beta3 or phosphatidylinositol-3 kinase signaling. A second objective was to determine the localization and regulation of nicotinic receptors in the medial edge epithelia (MEE) during palatal fusion. DESIGN: Palatal shelves from embryonic day (E) 13.5 mice were cultured in serum free media and treated with 0, 0.06, 0.6, or 6 mM nicotine, nicotinic receptor antagonist alpha-bungarotoxin, or the combination of nicotine and alpha-bungarotoxin. Tissues harvested at 72 h were analyzed for epithelial-mesenchymal transformation (EMT) and fusion. MEE samples collected at 20 h were analyzed for phosphorylated Akt-Ser473, phosphorylated Smad2, and nicotinic receptors. RESULTS: Nicotine inhibited palatal fusion in vitro in a dose dependent manner. Activated Akt-Ser473 was greater in control MEE than in nicotine treated tissues; while there was no difference in activated Smad2 between groups. The alpha7 subunit of nicotinic receptor was expressed in MEE during palate fusion and increased in nicotine treated tissues. Alpha-bungarotoxin did not rescue the nicotine treated palates. CONCLUSION: Nicotine treatment had no effect on Smad2, but caused a down regulation of the PI-3 kinase pathway that may have contributed to inhibiting palatal fusion in vitro.

Animals↗

PubMed1999

Epidermal growth factor receptor function is necessary for normal craniofacial development and palate closure.

Craniofacial malformations are among the most frequent congenital birth defects in humans; cleft palate, that is inadequate fusion of the palatal shelves, occurs with an annual incidence of 1 in 700 to 1 in 1,000 live births among individuals of European descent. The secondary palate arises as bilateral outgrowths from the maxillary processes, and its formation depends on the coordinated development of craniofacial structures including the Meckel's cartilage and the mandible. Cleft lip and palate syndromes in humans are associated with polymorphisms in the gene (TGFA) encoding transforming growth factor-alpha (TGF-alpha), an epidermal growth factor receptor (EGFR) ligand made by most epithelia. Here we have characterized craniofacial development in Egfr-deficient (Egfr-/-) mice. Newborn Egfr-/- mice have facial mediolateral defects including narrow, elongated snouts, underdeveloped lower jaw and a high incidence of cleft palate. Palatal shelf explants from Egfr-/- mice fused, but frequently had residual epithelium in the midline. In addition, morphogenesis of Meckel's cartilage was deficient in cultured mandibular processes from Egfr-/- embryos. The secretion of matrix metalloproteinases (MMPs) was diminished in Egfr-/- explants, consistent with the ability of EGF to increase MMP secretion and with the decreased MMP expression caused by inhibition of Egfr signalling in wild-type explants. Accordingly, inactivation of MMPs in wild-type explants phenocopied the defective morphology of Meckel's cartilage seen in Egfr-/- explants. Our results indicate that EGFR signalling is necessary for normal craniofacial development and that its role is mediated in part by its downstream targets, the MMPs, and may explain the genetic correlation of human cleft palate with polymorphisms in TGFA.

Animals↗

PubMed2006

Identification and characterization of a novel gene, Mcpr1, and its possible function in the proliferation of embryonic palatal mesenchymal cells.

We cloned a novel mouse cDNA, Mcpr1 (mouse cleft palate-related gene 1), between retinoic acid (RA)-treated murine embryonic palatal and control shelves by improved subtractive hybridization. Its transcript was identified by Northern blotting. The open reading frame encodes 132 amino acids and shows almost no identity to other genetic products. Mcpr1 expression could be detected extensively in adult mouse tissues and during murine embryonic development. It was identified to be significantly stimulated by RA in murine palatal shelves at embryonic day 12 and in palatal mesenchymal cells in vitro. We demonstrate that MCPR1 protein was localized primarily in the cytoplasm and could be synthesized and secreted by transfected COS-7 cells. Both the secretory and recombinant proteins of Mcpr1 inhibited proliferation of murine embryonic palatal mesenchymal cells and impeded the progression from the G1 to S phase in the cell cycle. The cells were prone to apoptosis after exposure to glutathione S-transferase-MCPR1. Furthermore, knockdown of MCPR1 protein levels by antisense oligodeoxynucleotides promoted progression of cells from the G1 to S phase and completely abolished the RA-induced block of the cell cycle from the G1 to S phase. These findings suggest that Mcpr1 might function as one of the RA-up-regulated genes involved in inhibiting cell proliferation during palatogenesis and RA-induced cleft palate by regulating proliferation and apoptosis of embryonic palatal mesenchymal cells and might even play a role in the development of many other organs.

Adaptor Proteins, Signal Transducing↗

PubMed2002

Comparative study of the extent of palatal lengthening by different methods.

Palatal lengthening is often emphasized in performing palatoplasty. However, definitive data regarding the method of measuring palatal length and the extent of palatal lengthening expressed quantitatively have not been reported. The authors have devised an easy method of measuring palatal length that can be expressed quantitatively, and they examined the characteristics of various methods of palatoplasty that are presently used commonly. A paper ruler was used to measure both a straight-line and a curved distance while the patient was under general anesthesia before and immediately after the palatoplasty. According to this study, the straight-line distance was lengthened to a significantly greater degree than the curved distance was after pushback palatoplasty for incomplete types of cleft palate and two-flap palatoplasty for complete types. Furlow double-opposing Z-palatoplasty and two-flap palatoplasty appeared to allow for greater palatal lengthening than the pushback palatoplasty. Further investigations will be undertaken to determine the correlation between the extent of palatal lengthening and speech development.

Cleft Palate↗

PubMed2001

The transforming growth factor-beta 3 knock-out mouse: an animal model for cleft palate.

The recent report of a transforming growth factor-beta 3 (TGF-beta 3) knock-out mouse in which 100 percent of the homozygous pups have cleft palate raised the question as to the potential usefulness of these animals as a model for cleft palate research. The specific aim in this study was to carefully document the anatomy of the cleft palate in the TGF-beta 3 knock-out mice as compared with wild type controls. Special attention was paid to the levator veli palatini muscle, the tensor veli palatini muscle, and their respective innervation. Because the TGF-beta 3 knock-out is lethal in the early perinatal period and because the heterozygotes are phenotypically normal, polymerase chain reaction was required to genotype the animals before mating. Time-mated pregnancies between proven heterozygotes were then delivered by cesarean section at gestational day 18.5 to prevent maternal cannibalism of homozygote pups. All delivered pups were killed and their tails processed by polymerase chain reaction to verify genotype. The heads were then fixed and sectioned in axial, coronal, or sagittal planes. Sections were stained with hematoxylin and eosin or processed for immunohistochemistry with nerve specific protein gene product 9.5 and calcitonin gene-related peptide antibodies. Sections were analyzed in a serial fashion. Nine wild type control animals were analyzed along with nine TGF-beta 3 knock-out homozygotes. Time matings between proven heterozygotes yielded wild type pups, heterozygote pups, and homozygote knock-out pups in the expected mendelian ratios (28 percent to 46 percent to 26 percent; n = 43). The results demonstrated 100 percent clefting in the homozygous TGF-beta 3 knock-out pups. Complete clefting of the secondary palate was seen in four of nine and incomplete clefting was seen in five of nine. The levator veli palatini and tensor veli palatini muscles were demonstrated coursing parallel to the cleft margin in all cleft mice. The orientation of these muscles differs from the normal transverse sling of the levator veli palatini muscle and the normal palatine aponeurosis of the tensor veli palatini muscle at the soft palate in control animals. Innervation of the levator veli palatini muscle by cranial nerve IX and the tensor veli palatini muscle by cranial nerve V were demonstrated in both cleft and control animals by use of immunohistochemistry with nerve-specific antibodies. Demonstration of a teratogen-free, reproducible animal model of clefting of the palate with a known, single-gene etiology is an important step in the systematic understanding of a congenital defect whose multifactorial etiology has hampered previous research efforts. This study presents a detailed anatomic description of such a model, including a description of the muscular anatomy and the innervation of the muscles of the palate. Because of early perinatal mortality, this model has limited applications for postnatal studies.

Animals↗

PubMed1996

Palatal changes associated with reverse smoking in Filipino women.

OBJECTIVE: To determine baseline data for the presence or absence of reverse-smoking and conventional smoking associated oral palatal mucosal changes in women. DESIGN: A cross-sectional evaluation of the clinical and cytological changes associated with the condition. SETTING: Nine rural barangays in Cabanatuan City, Philippines. SUBJECTS AND METHODS: Nine-one volunteer women smokers (61 reverse and 30 conventional) were examined clinically and photographically. Smears were also taken from three areas and the palate to investigate the cytology of palatal mucosal epithelium. MAIN OUTCOME MEASURES: Variations in colour, texture and topography of the palatal mucosa; determination of epithelial cell characteristics and inflammatory cell populations present in the lesions. RESULTS: Clinical findings showed that subjects could be grouped into three categories: Group A subjects showed pigmentation and some erythema only; Group B subjects included those with ulceration, marked erythema and non-descript mucosal roughening; Group C subjects (comprising the majority of reverse smokers) exhibited various combination of leukoplakia, fissuring, thickening and pigmentation of the palatal mucosa. Additional features, including nodularity, erythema, prominence and reddening of minor salivary gland duct openings were also occasionally observed in this group. Cytologic analysis revealed that, within each smoking group, there was a significant site-dependent difference in the predominant epithelial cell type present. CONCLUSIONS: This study reports the first systematic description of reverse smoking associated palatal mucosal changes in Filipino women. It also provides a basis for classification of the palatal mucosal changes among reverse smokers.

Adult↗

PubMedDate not supplied

Homocysteine oxidation and apoptosis: a potential cause of cleft palate.

Cleft palate is the most common craniofacial anomaly. Affected individuals require extensive medical and psychosocial support. Although cleft palate has a complex and poorly understood etiology, low maternal folate is known to be a risk factor for craniofacial anomalies. Folate deficiency results in elevated homocysteine levels, which may disturb palatogenesis by several mechanisms, including oxidative stress and perturbation of matrix metabolism. We examined the effect of homocysteine-induced oxidative stress on human embryonic palatal mesenchyme (HEPM) cells and demonstrated that biologically relevant levels of homocysteine (20-100 microM) with copper (10 microM) resulted in dose-dependent apoptosis, which was prevented by addition of catalase but not superoxide dismutase. Incubation of murine palates in organ culture with homocysteine (100 micro) and CuSO(4) (10 microM) resulted in a decrease in palate fusion, which was not significant. Gelatin gel zymograms of HEPM cell-conditioned media and extracts of cultured murine palates, however, showed no change in the expression or activation of pro-matrix metalloproteinase-2 with homocysteine (20 microM-1 mM) with or without CuSO(4) (10 microM). We have demonstrated that biologically relevant levels of homocysteine in combination with copper can result in apoptosis as a result of oxidative stress; therefore, homocysteine has the potential to disrupt normal palate development.

Apoptosis↗

PubMed1995

Treatment of cleft palate associated with Robin sequence: appraisal of risk factors.

Mandibular hypoplasia, airway obstruction, and a typical wide U-shaped cleft palate comprise the Robin sequence. Although much has been written regarding the treatment of these patients in the neonatal period, the literature reveals little information regarding later care of the cleft palate in these patients. The purpose of this study is to examine patients with the Robin sequence and evaluate the risk of postsurgical problems and outcome related to the neonatal period. Thirty-six patients with the Robin sequence presenting from 1972 through 1990 were reviewed. A majority of patients had feeding and respiratory difficulties, to varying degrees, following birth. These problems were treated successfully by maneuvers ranging from positioning to two infants who eventually required tracheostomy. Thirty-four patients had palate repair. Age at repair averaged 16.2 months, and one third of patients had associated anomalies. Infants who experienced problems following palatoplasty were those who had histories of severe difficulties and complications in the early months of life. In addition, patients with associated congenital anomalies has significantly more problems at the time of palate repair than those without anomalies. Those patients with the Robin sequence, who historically had minimal difficulty following birth, experienced few complications at the time of palate repair. Of the 34 patients with repaired palates, 23 demonstrated sufficient follow-up to allow for evaluation of speech outcome. Satisfactory or normal speech production was noted in 65.4%. This is not significantly different from that observed in all patients undergoing cleft palate repair during this same time period (74.9%). Secondary pharyngoplasty procedures were required in 17.4%.(ABSTRACT TRUNCATED AT 250 WORDS)

Cleft Palate↗

PubMed2000

A method of "unilateral operation" for early repair of unilateral complete cleft palate. Preliminary report.

OBJECTIVE: This article describes a method of "unilateral operation" and the preliminary results of a group of patients with unilateral complete cleft palate undergoing the operation at early age. DESIGN: The "unilateral operation" consists of four relaxation maneuvers. After all of the four maneuvers have been performed on the deformed side of an unilateral complete cleft palate, the deformed side can be moved posteriorly and medially to contact with the normal side. Then the cleft can be closed without tension. RESULTS: From 1995 to 1998, 19 cases of unilateral complete cleft palate were repaired with this method at 5-12 months of age. Postoperatively, there were no deaths nor dehiscences. Under the care and guidance of an experienced speech pathologist, 15 of 17 of these children have normal vocal quality at 1-2 years of age. CONCLUSIONS: The "unilateral operation" is a rational, adequate, and safe method for early repair of unilateral complete cleft palate. It's design addresses four principles. First, operating only on the deformed side of a unilateral complete cleft palate leaves the normal side unperturbed. Second, complete relaxation of the deformed side is achieved before closing the cleft. Third, in comparison with conventional procedures, which operate on both sides of the palate, this method has the advantage of less surgical trauma, less blood loss, and shorter time of operation. Fourth, all of these advantages are beneficial to early cleft palate repair, which is an important factor in achieving good speech.

Anesthesia, General↗

PubMed2000

Effect of X irradiation on secondary palate development in mice.

The mechanisms whereby X irradiation induces palatal clefting were investigated in vivo and in an in vitro organ culture system. When pregnant mice at day 12.5 of gestation were exposed to a 4-Gy dose of whole-body X radiation, the incidence of palatal clefting in their offspring was 91%. The volume of the irradiated palatal shelves was too low for them to make contact with each other. On gestational day 13.5 after labeling, bromodeoxyuridine-positive cells were sparse and apoptotic cells were abundant in the irradiated shelves. To prevent secondary effects of irradiation from the injured maternal body, fetal palatal explants were immediately transferred to an organ culture system after X irradiation in utero. The incidence of palatal clefting was 24%, much lower than the incidence in vivo. The addition of 10(-4) M of dexamethasone to the culture medium increased the incidence of palatal clefting to 56%. These findings indicated that X irradiation inhibited cell proliferation and induced apoptosis, resulting in small-volume palatal shelves that could not fuse with each other. The organ culture data also indicated that 4 Gy of irradiation appears to produce its effects both by a direct action on the fetus and indirectly by affecting the metabolism of the pregnant dam.

Animals↗

PubMed1979

The occurrence of taste buds in the palate of human adults as evidenced by light microscopy.

There is some uncertainty in the literature as to the existence of taste buds in the palate of the human adult. In those histologic studies in which the ages of the individuals have been reported, taste buds have not been found in the palates of adults, but have been found in fetuses or newborn. However, clinical studies have demonstrated taste perception in the palate of the human adult. Thus, the aim of the present study was to attempt to find taste buds in the human palate in subjects of different ages. In serial sections of selected areas of the palatal mucosa from autopsy material from individuals 0--80 years of age no taste buds could be demonstrated. However, in four of seven subjects aged 25--44 years, one or two taste buds were found in biopsies from areas of the soft palate where taste perception had been demonstrated clinically just prior to excision. Thus the present study indicates that scattered taste buds exist also in the soft palate of human adults.

Adolescent↗

PubMed1996

Characteristics of cleft palate speech.

In recent years, interest in the nature of cleft palate speech and the influences on speech quality has increased. This overview of contemporary research reveals new perspectives on cleft palate speech development and the phonological consequences of early articulatory constraints. Cleft palate speech is perceived as the result of the synthesis between physical, physiological, cognitive and linguistic development. Developmental influences on cleft palate speech are considered in the context of early vocalisations of cleft and non-cleft children, followed by an examination of the literature on the development of babble, the emergence of early words and consonant development in children born with cleft palate. Speech development is then discussed from a phonological perspective interpreting reported characteristics as 'cleft-type developmental processes', for example, lack of target stabilisation; compensatory articulations; active/passive strategies; and systematic sound preference. Given these influences on speech development the extent to which cleft palate speech should be regarded as an 'articulatory disorder' has been reconsidered. Descriptions and interpretations of nasal resonance, nasal emission, and nasal turbulence are followed by discussion of articulatory errors in place and manner and patterns of change in cleft palate speech. Finally, some of the available evidence on speech in relation to structural imperfections, such as unrepaired clefts, velopharyngeal insufficiency, oro-nasal fistulae, dental and occlusal deviations, and open-mouth posture is summarised briefly. These new perspectives aim to facilitate more effective clinical management and to provide indications for future research.

Child, Preschool↗

PubMed1976

Developmental aspects of secondary palate formation.

Research on development of the secondary palate has, in the past, dealt primarily with morphological aspects of shelf elevation and fusion. The many factors thought to be involved in palatal elevation, such as fetal neuromuscular activity and growth of the cranial base and mandible, as well as production of extracellular matrix and contractile elements in the palate, are mostly based on gross, light microscopic, morphometric or histochemical observations. Recently, more biochemical procedures have been utilized to described palatal shelf elevation. Although these studies strongly suggest that palatal extracellular matrix plays a major role in shelf movement, interpretation of these data remains difficult owing to the complexity of tissue interactions involved in craniofacial development. Shelf elevation does not appear to involve a single motive factor, but rather a coordinated interaction of all of the abovementioned developmental events. Further analysis of mechanisms of shelf elevation requires development of new, and refinement of existing, in vitro procedures. A system that enables one to examine shelf elevation in vitro would allow more meaningful analysis of the relative importance of the various components in shelf movement. Much more is known about fusion of the palatal shelves, owing in large part to in vitro studies. Fusion of the apposing shelves, both in vivo and in vitro, is dependent upon adhesion and cell dealth of the midline epithelial cells. Adhesion betweeen apposing epithelial surfaces appears to involve epithelial cell surface macromolecules. Further analysis of palatal epithelial adhesion should be directed towards characterization of those cell surface components responsible for this adhesive interaction. Midline epithelial cells cease DNA synthesis 24-36 h before shelf elevation and contact, become active in the synthesis of cell surface glycoproteins, and subsequently manifest morphological signs of necrosis. Death of the midline epithelial cells is thought to involve a programmed, lysosomal-mediated autolysis...

Animals↗

PubMed1976

Distribution of glands in the mucosa of the hard palate and its relation to carcinoma.

Carcinoma of the hard palate in women who practice reverse smoking is very common in Visakhapatnam. This carcinoma usually occurs in the middle of the posterior half of the hard palate and not in the soft palate or in the anterior half of hard palate. The volume of the glandular tissue in the mucosa of the hard palate is maximum to the right or left half of the midline in the posterior half in both fetuses and adults. The localization of the carcinoma of the hard palate in reverse smokers corresponds to the glandular area of the mucosa of the hard palate.

Adult↗

PubMed1997

[Significance of glycosaminoglycans content in developing mechanism of cleft palate].

To explore significance of Glycosaminoglycans content in the development of embryo and forming mechanism of cleft palate, Dexamethason acetate was injected into the abdomen of NIH mouse on the 12th day of gestation to induce cleft palate mouse embryo model. Then by taking cranio-maxillary coronary sections, stained with Alcian blue/PAS and quantitatively analysing the area of the palatal process covered by glycosaminoglycans using a TDS-90 photodigital system with computer. Results indicate that on 13(12) day(hour) of gestation the colour of Alcian blue starts to show in the palatal process. By then, the area covered by glycosaminoglycans in the normal group is 4.69 mm whereas for the experimental group is 2.40 mm, showing a significant statistical difference (P < 0.05). The area of the palatal process covered by glycosaminoglycans gradually increases as the embryo developes, but is distinctly smaller in experimental than in the normal group (P > 0.05). This proves that there's a relationship between the level of glycosaminoglycans in the palatal process and development of cleft palates.

Animals↗

PubMed1997

[An experimental study of the influence and mechanism of surgically induced cleft palate and palatoplasty on teeth and dental arch in dogs].

The dogs were selected as the experimental subjects in this study. The authors continuously observed the maxillary teeth and dental arch form in preoperation and 2, 4, 6, 10, 14, 18, 22, 26, 30, 34 weeks of post operation to all the animals. 40 puppies were divided into four groups, which were unoperated control group, surgically induced cleft palate group, cleft palate repaired group and cleft palate implanted bone group. The experimental result showed: there were remarkable differences at rate of itself growth between deciduous dentition and permanent dentition in the four groups. The result suggested that the cleft palate was a reason for disturbances of dental arch development, an exposed bone wound in hard palate of maxillary after palatoplasty was an important reason that it made maxillary dental arch growth problem heavier, authors could prevent the disturbs the transverse development of the maxillary dental arch from cleft palate who had or had not repaired by implanted bone in total cleft palate.

Animals↗