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PubMed2006

Successful engraftment of cultured autologous mesenchymal stem cells in a surgically repaired soft palate defect in an adult horse.

The objective of this study was to graft autologous mesenchymal stem cells (MSCs) at the site of surgical repair of a soft palate defect in an adult horse in an attempt to improve wound healing and to investigate whether the transplanted MSCs would integrate into the soft palate structure and participate in regeneration. Bone marrow was collected from an adult horse with a full-thickness soft palate defect. The MSCs were isolated, cultured in monolayers, and labeled with 5-bromo-2-desoxymidine (BrdU) and chloromethylbenzamido-DiI-derived (cm-DiI) before transplantation. The soft palate defect was repaired by mandibular symphysiotomy, and the labeled MSCs were injected into the repaired soft palate. Postmortem examination revealed that 90% of the soft palate defect had been sutured. Staining by BrdU and cm-DiI was intense in the soft palate tissue. Labeled MSCs were detected in tissue slices from the injection sites. The cells were organized in a manner similar to that in native soft palate tissue, indicating successful engraftment.

Animals↗
PubMed1991

Immunodetection of the transforming growth factors beta 1 and beta 2 in the developing murine palate.

The expression of some members of the TGF beta family of genes in embryonic craniofacial tissue suggests a functional role for these molecules in orofacial development. In other systems, TGF beta 1 and TGF beta 2 have been shown to regulate cell proliferation and extracellular matrix metabolism, processes critical to normal development of the secondary palate. We have thus determined the amount and tissue distribution of both TGF beta 1 and TGF beta 2 in embryonic palatal tissue. Cellular extracts of murine embryonic palatal tissue from days 12, 13 and 14 of gestation were assayed for the presence of TGF beta 1 and TGF beta 2 by immunoprecipitation. Physiological levels, ranging from 0.05-20 ng/micrograms protein, of both growth factors were detected in all tissues examined. Immunostaining with antibodies directed against either TGF beta 1 or TGF beta 2 demonstrated the presence of these growth factors in palatal epithelium and mesenchyme early during palatal development (gestational day [GD] 12) a period characterized by tissue growth. On GDs 13 and 14, characterized by palate epithelial differentiation, immunostaining for both growth factors predominated in epithelial tissue. Immunostaining for TGF beta 1 and TGF beta 2 was also intense in mesenchyme surrounding tooth germs and in perichondrium. Chondrocytes and cartilage extracellular matrix did not stain for either TGF beta 1 or beta 2. Combined with existing evidence for the presence of functional receptors for the transforming growth factor-beta s in the developing palate, these results provide rationale for studies designed to clarify a specific role for these signalling molecules in palate epithelial differentiation and/or epithelial-mesenchymal interactions.

Animals↗
PubMed1990

[Morphological studies on the dental arch and palate of the Chinese in Fukien Province, Taiwan, using Moiré patterns].

Using Moiré topography, the forms of the dental arch and palate of males and females were compared. This was carried out in Fukien province, Taiwan. The materials used consisted of plaster casts of the upper dentitions of 65 males and 69 females with normal occlusion, aged from 20 to 22 years. The results are as follows: 1. The standard form of the upper dental arch represented by a pentagon is shown in Table 1 and in Fig. 3. 2. The dental arch of the male was larger than that of the female, the difference being significant for the anterior and posterior widths of the arch. 3. The correlation coefficients were generally lower in the female than in the male. This was especially true with regard to the size of the anterior portion of the female dental arch. In the posterior portion, there was no correlation between the dental arch length and dental arch width of either sex. 4. The distance from the origin (F) to the papilla incisiva was 23.47 mm in the male and 23.67 mm in the female. The number of moiré band in the bottom of the palate at the origin from the basal plane was 12.89 in the male and 12.73 in the female. There were no significant differences in these two measurements between sexes. 5. On the vertical section of the palate, the anterior portion of the palate of the female was deeper than the male. However, in the posterior portion the male was deeper and wider in the palate morphology than the female. The vertical section in the palate of the male was similar in form to that of the female at the midpoint between the anterior and posterior portions, the canine and/or first premolar. 6. The horizontal section of the palate showed that the distance from the origin to the canine and/or to the first premolar were similar in both sexes at any palate depth.

Adult↗
PubMed1989

Palatal shelf reorientation in hamster embryos following treatment with 5-fluorouracil.

A study was undertaken to examine the issue of whether achieving a critical mass of cells and/or palatal shelf volume during vertical development of shelf is essential for reorientation to occur. In control and 5-fluorouracil (5FU)-treated hamster embryos' palatal shelves, at different times during gestation, the numbers of both epithelial and mesenchymal cells were counted and cross-sectional area was measured. DNA synthesis was measured by 3H-thymidine incorporation and was used as an index of growth by cell proliferation. The control data indicated that, unlike development during initial 24 hours, the later period of vertical palatal development was characterized by a steady level of mesenchymal and epithelial cell numbers and palatal shelf area. Following 5FU treatment all the measurements were reduced, and until they reached the equivalent of control values, the palatal shelves did not reorient. The density of mesenchymal cells in the developing palate did not seem to affect cell number. On the basis of the analysis of results of the present study, along with those reported in the literature, it is suggested that, in hamsters, acquisition and maintenance of both a specified number of mesenchymal cells and shelf area, at least 24 hours prior to reorientation, may be critical for ensuing mesenchymal differentiation to enforce palatal shelf reorientation on schedule. 5FU affected these features to delay reorientation of the palatal shelf.

Abnormalities, Drug-Induced↗
PubMed1989

Characterization of soluble cyclic adenosine monophosphate-dependent protein kinase isozymes in murine embryonic palatal tissue.

Certain hormonal primary messengers identified in the mammalian palate during its ontogeny transmit information to the interior of the cell via transmembrane signaling systems that control the production of the secondary messenger cyclic adenosine monophosphate. The singular role of intracellular cyclic AMP is to activate cAMP-dependent protein kinases (cAMP-dPK). cAMP-dPK were thus identified and characterized in the developing murine embryonic palate. Incubation of cytosolic fractions of embryonic palatal tissue with cAMP resulted in a dose-dependent increase in the cAMP-dPK activity ratio. A transient elevation of basal cAMP-dPK was seen during the period of palatal ontogeny that corresponded temporally with a previously demonstrated transient elevation of palatal basal cAMP levels. Fractions of embryonic palatal tissue cytosols derived by diethylaminoethyl (DEAE)-Sephacel chromatography were analyzed for phosphotransferase activity and for [3H]-cAMP binding to the regulatory (R) subunits of cAMP-dPK. Such analyses revealed two peaks of activity on day 13 of gestation. Based on the salt concentration at which the material in these peaks eluted from DEAE, its ability to cochromatograph with authentic cAMP-dPK isozymes, its molecular weight as determined by sodium dodecyl sulfate-polycrylamide gel electrophoresis, and the ability of the material to be photoaffinity labeled with [3H]-8-azidoadenosine 3',5' cyclic phosphate, types I and II cAMP-dPK were identified. Regulatory subunits of cAMP-dPK were characterized by the binding of [3H]-cAMP to cytosolic fractions of embryonic palatal tissue. Such binding was saturable (Bmax = 1,096 fmol/mg protein) and of high affinity (Kd = 7 nM). Only cAMP and cyclic guanosine monophosphate competed in a dose-related manner with [3H]-cAMP for binding to R subunits of cAMP-dPK. Adenosine, cTMP, and adenosine triphosphate, at doses up to 10(-4) M, did not compete for binding. Temporal analysis of binding data indicated that the number of binding sites transiently decreased during day 13 of gestation. Characterization of cAMP-dPK in tissue derived from the developing mammalian palate allows consideration of cAMP-dPK as a key regulatory enzyme capable of transducing hormonally elevated intracellular levels of cAMP into metabolic responses during orofacial ontogenesis.

Animals↗
PubMed1988

Cleft palate: more genetic lessons from mice.

Cleft palate occurred in high frequency (14%) in the F2 generation of the cross between two stocks of mice, LGG and SELH, neither of which produces more than 2% cleft palate. The cleft palate trait results from a new combination of alleles that is not present in either parental stock. The lack of cleft palate in the F2 generation after outcrosses of both parental stocks to other strains shows that this new combination of alleles has specific contributions from both parental strains, and also that there must be at least two loci involved. A deficiency of Mod-1 homozygotes in the SELH/LGG F2 adults suggests that one of the loci involved may be linked to Mod-1 and that the number of loci involved is few. Significantly more F2 males (19%) than females (9%) were affected with cleft palate. The data can be explained by a two-locus epistatic model with a dominant mutation (P) at one locus that causes cleft palate when not suppressed by or compensated for by a dominant allele (S) at a second locus. The parental stocks would be PPSS and ppss. In the F2 generation, the new combinations PPss and Ppss would express cleft palate, a total expected of 19%. Similar new combinations of alleles at two loci may explain some instances of high occurrence of cleft palate or other developmental threshold traits in previously unaffected human families.

Animals↗
PubMed1988

Olfactory deficits in boys with cleft palate.

An odor identification task was used to determine whether individuals with cleft palate (with or without cleft lip) also have an increased prevalence of olfactory deficits. Olfactory responses of 35 affected subjects (7 to 22 years of age) were compared with those of 68 subjects of comparable age without cleft palates. Subjects were requested to identify the smell of ten common household odors. They selected their responses from an alphabetized list of the test odorants. After a practice trial, the set of odorants was presented five times in randomized sequences. The percentage of correct responses increased with age for prepubertal and pubertal subjects without cleft palates. Although the olfactory scores of girls without cleft palates continued to increase after puberty, this trend was absent in boys. On the average, the girls with cleft palates, compared with only three of 34 boys without cleft palates, had olfactory scores less than 60% correct. There was no evidence of heterogeneity in the magnitude or direction of the relationship between any of the subtypes of cleft palate and olfactory dysfunction. In this study, cleft palate is more strongly associated with olfactory deficits in boys than in girls, suggesting the possibility that the deficit may be a sex-influenced trait.

Age Factors↗
PubMed1988

Tooth maturation in cleft lip, cleft palate, or both.

The relation between chronologic age and the development of permanent teeth in patients with cleft lip, cleft palate, or both was investigated according to the method described by Demirjian et al (1973). The patients were divided into three groups: (1) those with bilateral cleft lip and palate (BCLP), (2) those with unilateral cleft lip and palate (UCLP), and (3) those with cleft palate only (CP). Panoramic radiographs of 107 Caucasian children (66 boys and 41 girls) aged 4 to 12 years were evaluated. The degree of maturation of each of the permanent teeth on the left side of the mandible was determined, and a dental maturation score was computed for each child. The scores were compared with those obtained in a previous study of dental maturation in Caucasian children without cleft from the Chicago area (Loevy, 1983). Evaluation of the data demonstrated that there was no significant difference in dental maturity between girls with cleft lip, cleft palate, or both and with the sample of those free from cleft. There was a significant difference in dental maturity in boys when all cleft groups were evaluated together. There was no significant difference from the normal sample in boys with bilateral cleft lip and cleft palate or with cleft palate alone, but there was a highly significant difference from the normal sample in the group of boys with unilateral cleft lip and palate.

Age Determination by Teeth↗
PubMed1986

Epigenetically regulated genomic expressions for shortened stature and cleft palate are regionally specific in the 11-day mouse embryo.

Chronokinetic synergism, a holistic and extremely sensitive experimental design, has shown in the mouse embryo that site-specific epigenetic forces differentially regulate genesis of the palate (cleft palate) and limb bud organogenesis (shortened stature). Acute exposures of 11-day pregnant mice to minimally effective doses of thymidine or ethanol followed 5 or 8 hr later by minimal exposure to retinoic acid have enabled quantitative and qualitative assay for genomic-epigenetic interactions. These site-specific morphogenetic regulations occurred during palatal genesis from the maxillary prominence of the first pharyngeal arch and during limb bud prechondrogenesis. Thymidine is presumed to induce its response by inhibition of DNA polymerase and hence by transitory cytostatic block. (Embryo size was not detectably changed). Ethanol is interpreted, guilt by associated response, indirectly to interfere with histone regulation of transcription. Two central findings have demonstrated the coordinated regulation of genomic and epigenetic positional information. First, thymidine or ethanol as epigenetic probes for limb prechondrogenesis and palatal precursor cells have activated distinctive site-specific responses. Second, responses to chronokinetic synergisms have indicated that epigenetic regulators for limb and palate dysmorphogenesis may affect distinctly different phases of the cell division cycle and hence induce differential DNA expressions. Although each of palate and limb is concurrently susceptible to epigenetic regulation, their differential intrinsic genomic capabilities appear to have been uncoupled. The putative homeostatic balance of genomic expressions in the palate precursor and the prechondrogenic limb bud cells of the 11-day mouse embryo has been characterized as epigenetically regulated, alternatively expressed, and positionally restricted. We propose that the chronokinetic synergisms have disclosed the existence of distinctive palate-determining genes and stature-determining genes.

Abnormalities, Drug-Induced↗
PubMed1986

The effect of reducing ATP levels on reorientation of the secondary palate.

The force for directing palate shelf reorientation appears to be associated with elements of the presumptive hard palate (Brinkley & Vickerman, 1979; Bulleit & Zimmerman, 1985). The palatal elements that mediate this process do not require palate cells to be metabolically active for expression of the force. This contention was demonstrated using an in vitro system that allows substantial reorientation of the hard palate to occur. ATP levels were reduced by treatment with metabolic inhibitors and the degree of reorientation was measured 1 h following pretreatment with inhibitors. Treatment of cultured embryonic heads under anoxic conditions with 2,4-dinitrophenol or KCN had no effect on the degree of reorientation occurring in vitro. These agents reduced ATP levels by 71% and 62%, respectively. Treatment of cultured heads with 2-deoxy-D-glucose under anoxia also had no effect on reorientation. This treatment reduced ATP levels in embryonic heads by 92-94%. A similar reduction was observed if ATP levels were measured in palate tissue alone. The treatment of cultured heads with 2-deoxy-D-glucose and anoxia not only reduced levels of ATP but also reduced CTP, GTP and UTP. These results indicate that palate shelf reorientation is independent of cellular metabolic activity and supports the hypothesis that reorientation is dependent on a pre-existing infrastructure within the palate shelves.

Adenosine Triphosphate↗
PubMed1985

Palatal anteversion as part of the iniencephaly malformation sequence.

We describe a fetus with hydrocephalus and the cranial and cervical findings of iniencephaly (enlarged foramen magnum, fusion of the upper cervical vertebrae, and a retroflexed, webbed neck) who had an unusual palatal abnormality ("palatal anteversion"). The posterio-lateral border of the secondary palate arose at the oral commissures, giving the palate an appearance of being folded so that the uvula was directed anteriorly. There were no clefts. Histologic sections of the junction of the secondary palate with the inner aspect of the oral commissures revealed continuity of the epithelial basement membranes and no unusual disarray of collagen fibers. This indicates that the unusual palatal orientation occurred during palatal formation and was not due to adhesion formation later in development. Failure of rotation of the palatal shelves prior to fusion and merging could account for the observed findings.

Abnormalities, Multiple↗
PubMed1971

Genetic studies of a cleft palate clinic population.

The genetic program at the Lancaster Cleft Palate Clinic is briefly described. The aim of the study is to obtain quantitative estimates of various components which contribute to genetic heterogeneity. Of 260 families interviewed, 26.1% of cleft lip, 42.5% of cleft lip and palate and 30.0% of isolated cleft palate propositi had one or more affected relatives. That isolated cleft palate is etiologically distinct from cleft lip with or without cleft palate is once again demonstrated. Eight of the cleft palate propositi are from mixed pedigrees with Van der Woude syndrome. While a majority of the familial cleft cases are compatible with the multifactorial hypothesis, five pedigrees of cleft lip and cleft palate propositi and one of a cleft palate propositus are in apparent agreement with the hypothesis of single autosomal dominant gene in each pedigree. No case of sex-linked inheritance was found.

Cleft Lip↗
PubMed1979

Palate morphogenesis. IV. Effects of serotonin and its antagonists on rotation in embryo culture.

Previous studies have localized non-muscle contractile systems in the posterior (region 2) and the anterior (region 3) ends of mouse palates at the time of shelf movement. In order to determine whether these contractile systems function in shelf rotation, effects of pharmacologic agents have been analyzed in embryo culture. First, it was shown that the posterior end of the palate rotates before the anterior end, and its rotation in culture was proportionally greater as development of the embryo progressed. Generally, the posterior end of the palate was more easily inhibited in embryo culture than the anterior end. Serotonin at 10(-8) M to 10(-5) M was shown to significantly stimulate rotation at the anterior end of the palate after 2 h in embryo culture. The effect on the posterior palate was less pronounced. To investigate further the role of this neurotransmitter on palate shelf rotation, serotonin antagonists were employed. Methysergide (10(-4) M) inhibited anterior shelf rotation to 12% of control values (P less than 0.005), while not significantly affecting the posterior end. Ergotamine (10(-6) M) significantly inhibited the stimulation induced by 10(-5) M serotonin (P less than 0.025). Cyproheptadine (10(-9) M) partially inhibited anterior and posterior shelf rotation in embryo culture. When injected into the pregnant dam, cyproheptadine partially inhibited shelf rotation and fusion. The palate was examined histologically after embryo culture. In the presence of 10(-4) M methysergide, the elongated contractile cells in region 3 at the anterior and midpalatal mesenchyme were prevented from rounding. Thus, serotonin may be regulating rotation of the anterior end of the palate by an effect on cell-mediated process.

Animals↗
PubMed1980

Immunohistochemical localization of cyclic AMP in the developing rodent secondary palate.

During development of the mammalian secondary palate, medial-edge epithelia (MEE) from apposing palatal shelves adhere and undergo autolysis allowing palatal mesenchymal regions to unite. In a prior study (Greene & Pratt, 1979), we reported a transient increase in levels of cyclic AMP (cAMP) in the mouse and rat palate during epithelial adhesion and cell death. The objective of this study was to examine the distribution of cyclic AMP in the developing rodent secondary palate using immunohistochemistry to localize cyclic AMP. Staining for cAMP was observed in the epithelium just prior to and during epithelial fusion (day 16 in the rat; day 14 in the mouse). Cyclic AMP was distributed throughout the epithelial cytoplasm whereas no staining was seen in nuclei. Epithelial staining for cAMP was faint or absent 24 and 48 h prior to epithelial contact. Mesenchymal staining for cAMP was minimal and associated with the plasma membrane at all stages studied. These results demonstrate that elevated levels of cAMP in the rat and mouse palate during epithelial adhesion and cell death are mainly due to increases of the nucleotide in palatal epithelium. This observation suggests that a transient increase in epithelial cAMP may play a role in palatal epithelial differentiation.

Animals↗
PubMed1995

Inhibition of TGF-beta 3 (but not TGF-beta 1 or TGF-beta 2) activity prevents normal mouse embryonic palate fusion.

The critical stage of palatal development is the fusion of apposing individual palatal shelves. Palatal shelves, from the day 13 murine embryo, cultured in vitro fuse normally in the absence of exogenous factors. Therefore, some endogenous factor(s) is responsible for the normal fusion process. Prevention of mature TGF-beta 3 activity during a specific time window of development in palate organ cultures, either by antisense oligodeoxynucleotides or neutralizing antibody, resulted in failure of palate fusion. Northern analysis was used to demonstrate that the antisense treatment down-regulated TGF-beta 3 mRNA. Inhibition of TGF-beta 1 or -beta 2 activity (by either antibodies or antisense oligodeoxynucleotides) had no such effect on palate development and palate fusion was normal. These data indicate an isoform specific role for TGF-beta 3 in palatal fusion.

Animals↗
PubMed1994

Evidence in infants with cleft palate that breast milk protects against otitis media.

OBJECTIVE: Most infants with cleft palate suckle unproductively and require feeding by artificial means. Most also have unremitting otitis media accompanied by (usually) nonpurulent middle-ear effusion, a complication generally attributed to impaired eustachian tube ventilatory function. We observed two infants with cleft palate in whom one or both ears appeared effusion-free on more than one occasion, and who also were receiving or previously had received breast milk feedings. This prompted us to analyze the relation between middle-ear status and feeding mode in a large series of infants with cleft palate. Our objective was to determine whether in these infants the receipt of breast milk mitigated the otherwise virtually invariable development and continued presence of otitis media. METHODS: We reviewed and analyzed data concerning both feeding mode and the presence or absence of middle-ear effusion in 315 infants with cleft palate, as recorded systematically in the course of prospective studies at our Cleft Palate-Craniofacial Center. Analysis was limited to periods preceding the infants' receipt of tympanostomy-tube placement or palate repair, or their second birthday, whichever occurred first. RESULTS: Freedom from effusion in one or both ears was found at one or more visits in only seven (2.7%) of 261 infants fed cow's milk or soy formula exclusively, but in 17 (32%) of 54 infants fed breast milk exclusively or in part for varying periods (P < .0001). In virtually all instances, the breast milk had been harvested by the mother and fed to the infant via an artificial feeder. Baseline clinical and sociodemographic characteristics and surveillance in the two groups of infants were comparable. CONCLUSIONS: Artificially fed breast milk provides variable protection against the development of otitis media in infants with cleft palate. This finding supports the likelihood of a similarly protective effect of breast milk in noncleft infants. The finding also suggests strongly that in infants with cleft palate, impaired eustachian tube function is not the only pathogenetic factor in the infants' initial development of middle-ear effusion.

Breast Feeding↗
PubMedDate not supplied

Changes in human palatine bone location and tongue position during prenatal palatal closure.

Closure of the palatal shelves during normal prenatal palate formation is commonly supposed to be the result of a complex interaction between tissue growth processes and functional factors such as mandibular and tongue movements. The purpose of the present study was to analyze tongue and palatine bone positions during palatal shelf closure. The material consisted of 40 normal human fetuses (CRL 26-57 mm). The series covers the developmental stages in which palatal shelf closure takes place. The spatial relation between the tip of the tongue and the lips was examined by visual inspection, and radiographic/cephalometric methods were used for analyzing palatine bone positions. On axial radiographs of the upper jaws, the angle in the horizontal plane between the vertical plates of the palatine bones was measured. The study revealed that the vertical plates of the palatine bones rotate on their vertical axes during palatal closure, the mean interpalatine angle changing from 23.7 degrees (SD 2.0 degrees) to 13.3 degrees (SD 3.2 degrees), P < 0.001. The rotation of the palatine bones occurred while the cranial base was still unossified. Moreover, the tip of the tongue became visible between the lips immediately after palate closure. In the present study the rotational changes observed in skeletal tissue provided information about soft tissue changes during palatal closure. These normal developmental aspects are discussed in relation to skeletal deviations in congenital cleft palate malformations.

Fetus↗
PubMedDate not supplied

Developmental regulation of various annexins in the embryonic palate of the mouse: dexamethasone affects expression of annexin-1.

The annexins are a group of structurally related proteins implicated in a number of cellular processes, including growth, membrane fusion, and the effects of glucocorticoids on cellular physiology, signal transduction, and regulation of activities of phospholipase A2. Though their exact role in cellular physiology is not clear, their properties make them candidate proteins for signal transduction pathways by which growth factors and glucocorticoids modulate development of the palate. We have determined the exact cellular location and development expression of various annexins in the embryonic murine palate as a first step in assessing their developmental function. Western blot analysis revealed an increased accumulation of selected annexins in elevated palates compared to vertical (unelevated) ones. This was particularly striking for lipocortin I1 (annexin I), whose mRNA accumulated as well. Lipocortin I was expressed primarily in the apical portion of the palatal epithelium at early stages of development, but throughout the epithelium at later stages. Also, there was increased immunoreactivity for lipocortin I in the mesenchyme as development proceeded. Immunoreactivity for the endonexins (annexins IV and V) was found in the palatal epithelium and mesenchyme, whereas immunoreactivity for the 67-kDa calelectrin (annexin VI) was found only in the mesenchyme. Treatment of pregnant A/J strain mice with a cleft-palate inducing regimen of dexamethasone stimulated accumulation of lipocortin I protein and mRNA, but not lipocortin II (annexin II) protein. In contrast, the same regimen of dexamethasone did not affect levels of lipocortin I protein in palates of the glucocorticoid-less sensitive C57BL/6J strain mouse embryo. These data permit the suggestion that lipocortin I plays some critical, but as yet undefined, role in modulating ontogeny of the murine palate.

Animals↗