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At least 649 records · Page 36Linked to original sources
PubMed2006

Evaluation of potential modifiers of the palatal phenotype in the 22q11.2 deletion syndrome.

OBJECTIVE: To evaluate potential modifiers of the palatal phenotype in individuals with the 22q11.2 deletion syndrome. DESIGN: Data from 356 subjects enrolled in a study of the 22q11.2 deletion syndrome were used to evaluate potential modifiers of the palatal phenotype. Specifically, subjects with and without velopharyngeal inadequacy and/or structural malformations of the palate were compared with respect to gender, race, and genotype for variants of seven genes that may influence palatal development. METHODS: The chi-square test or Fisher exact test was used to evaluate the association between palatal phenotype and each potential modifier. Odds ratios and their associated 95% confidence intervals were used to measure the magnitude of the association between palatal phenotype, subject gender and race, and each of the bi-allelic variants. RESULTS: The palatal phenotype observed in individuals with the 22q11.2 deletion syndrome was significantly associated with both gender and race. In addition, there was tentative evidence that the palatal phenotype may be influenced by variation within the gene that encodes methionine synthase. CONCLUSIONS: Variation in the palatal phenotype observed between individuals with the 22q11.2 deletion syndrome may be related to personal characteristics such as gender and race as well as variation within genes that reside outside of the 22q11.2 region.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed2000

[Comparative histomorphological study on the craniomaxillary development of the trisomy-18 with cleft palate and euploid mice].

OBJECTIVE: The aim of this study is to compare histological morphology of craniomaxillary complex of Trisomy 18 with cleft palate (Ts + CP) and euploid mouse foetuses to understand whether cleft palate is associated with maldevelopment of the craniomaxillary complex or with hypoplasia of the adjacent tissues. METHODS: Thirty pairs of Ts + CP and euploid mouse foetuses with about equal body weight were selected, and sixty craniomaxillary complex were precisely orientated in the coronal plane, then serially sectioned with 7 microns thickness through the primary palate, the whole hard palate and the soft palate. Finally six sections were selected for comparative histomorphological study based on anatomical landmarks. RESULTS: The trisomy with cleft palate mouse foetuses had significantly developmental hypoplasia in the primary palatal shelves. The palatal shelves, vomer, palatal bone and nasal septal cartilage in cleft samples showed significantly developmental hypoplasia with a relatively wider nasal septum, nasal capsule and a bigger nasal airway volume, nasopharyngeal cavity. CONCLUSION: The hard tissues of the craniomaxillary complex in Ts + CP mouse foetuses, including bone and cartilage show serious maldevelopment or developmental hypoplasia, and these may be closely related to the autosomal trisomic condition.

Animals↗
PubMed1985

The influence of the epithelium on palate shelf reorientation.

The intrinsic forces necessary for directing the reorientation of the secondary palate appear to reside in the anterior two thirds of the palate or presumptive hard palate. The hard palate could reorient regardless of whether it was intact or separated from the posterior third or presumptive soft palate. The soft palate could only reorient if the palate shelves are left intact. These intrinsic forces, within the hard palate, may be mediated by the mesenchymal cells, their extracellular matrix, or the epithelium surrounding the shelves. This latter possibly was tested by removing the epithelium, from either the presumptive oral or nasal surface followed by measurement of reorientation in vitro. Only after removal of the oral epithelium was a significant inhibition in reorientation observed. The treatment used to remove the epithelium, EDTA and scraping, was shown to remove 41% of the oral epithelium leaving the majority of the basement membrane intact. The observed inhibition of reorientation did not appear to be a consequence of wound healing. Creation of wounds twice the area that was observed after treatment with EDTA and scraping inhibited reorientation minimally. These results suggest that the epithelium and particularly the anterior oral epithelium plays a major role in the reorientation of the murine secondary palate.

Animals↗
PubMed2001

A new approach to classify cleft lip and palate.

OBJECTIVE: To propose a new method, which allows for a complete description of primary and secondary cleft palates, incorporating elements that are related to the palate, lip, and nose that will also reflect the complexity of this problem. METHOD: To describe the type of cleft, two embryonic structures were considered: (1) the primary palate, formed by the prolabium, premaxilla, and columella and (2) the secondary palate, which begins at the incisive foramen and is formed by a horizontal portion of the maxilla, the horizontal portion of the palatine bones, and the soft palate. Anatomical characteristics to be considered were defined, and a new method is proposed to more fully describe any cleft. RESULTS: A description of five cases was made using the method proposed in this work and compared with other published methods for the classification and description of clefts. CONCLUSIONS: A mathematical expression was developed to characterize clefts of the primary palate, including the magnitude of palatal segment separation and the added complexity of bilateral clefts, yielding a numerical score that reflects overall complexity of the cleft. Clefts of the secondary palate are also considered in a separate score. Using this method, it is possible to incorporate elements that are not considered in other approaches and to describe all possible clefts that may exist.

Algorithms↗
PubMed1998

In vivo and in vitro assessment of mitogen activated protein kinase involvement during quail secondary palate formation.

Spatiotemporally regulated cell proliferation and differentiation are crucial for the successful completion of morphogenesis of the vertebrate secondary palate. An understanding of the mechanisms by which these cellular phenomena are regulated during palate development involves the identification of the various signal transduction pathways. In the present study, the presence and activation of mitogen-activated protein (MAP) kinases were investigated during the development of quail secondary palate. The palatal shelves were dissected on days 5-9 of incubation, homogenized, and centrifuged, after which the samples were separated by anion exchange fast protein liquid chromatography. The fractions were analyzed for myelin basic protein (MBP) phosphorylation. In addition, primary cultures of quail palate mesenchymal cells (QPMCs) were treated with epidermal growth factor (EGF) and prepared for MBP phosphorylation assays. A temporally regulated pattern of phosphotransferase activity, characterized by a three-fold increase in phosphotransferase activity toward MBP between days 5 and 8 of incubation, was observed during quail palate development. Western blotting, using MAP kinase antibodies, demonstrated the presence of a 42-kDa isoform between days 5 and 9 of incubation, during which the level of protein remained constant. Antityrosine immunoblotting with 4G10 also detected a 42-kDa protein. Phosphotransferase assays, using either a MAP kinase-specific substrate peptide (S5) or a protein kinase C inhibitor (R3), further confirmed the presence of a MAP kinase in the developing palate of quail. Because diverse biological processes occur concurrently during in vivo palate morphogenesis, the involvement of MAP kinase was explored further in primary cell culture. The data showed that EGF stimulated proliferation and activated 42-kDa MAP kinase in QPMCs. It is suggested that MAP kinase cascade may be involved in growth factor-regulated cell proliferation during morphogenesis of quail secondary palate.

Animals↗
PubMed1988

Gross and cellular analysis of 6-mercaptopurine-induced cleft palate in hamster.

The present study analyzes the morphological, histochemical, and ultrastructural aspects of the pathogenesis of 6-mercaptopurine (6MP)-induced cleft palate in hamster fetuses. Gross and light microscopic observations indicated that 6MP stunts the growth of vertical palatal shelves and thus induces cleft palate. Ultrastructural analysis showed that, in contrast to controls, 6MP-induced alterations were first seen in the mesenchymal cells 24 hr after drug administration. The initial alterations were characterized by swelling of the nuclear membrane. During the next 12 hr, lysosomes were seen first in the mesenchymal cells and then in the cells of the medial edge epithelium (MEE) of the developing palatal primordia. The appearance of lysosomes was temporally abnormal and was interpreted as a sublethal response to 6MP treatment. Subsequently, the nuclear alterations and the lysosomes diminished; and 48 hr after 6MP administration, they were absent from the palatal tissues. Ninety hours after 6MP administration, unlike the controls (in which the palatal shelves were already fused), changes were seen at the epithelial-mesenchymal interface in the developing cleft palatal shelves. These changes were characterized by breakdown of the basal lamina and epithelial-mesenchymal contacts. Eventually, at term, the MEE of the vertical shelf stratified. It was suggested that 6MP affected cytodifferentiation in the palatal tissues during the critical phase of early vertical shelf development and thereby induced cleft palate.

Acid Phosphatase↗
PubMed1991

Genesis of hadacidin-induced cleft palate in hamster: morphogenesis, electron microscopy, and determination of DNA synthesis, cAMP, and enzyme acid phosphatase.

A morphological, electron microscopic, and biochemical study was undertaken to analyze the genesis of hadacidin-induced cleft palate in hamster fetuses. Gross and light microscopic observations indicated that hadacidin affected the growth of vertical palatal shelves to induce cleft palate. Electron microscopic observations showed that initial hadacidin-induced changes were seen in the mesenchymal cells. Within 12 hr of drug administration, the perinuclear space was swollen and a lysosomal response injury was evident in the mesenchymal cells. Subsequently, 24 hr after hadacidin treatment, lysosomes appeared in the epithelial cells; changes were also seen in the basal lamina which included separation of the lamina densa from the basal cells, duplication of lamina densa, and complete loss of basal lamina. Between 36 and 42 hr post-treatment, the cellular and basal lamina changes subsided, and the epithelium of vertical shelves underwent stratification. Biochemical determination of enzyme acid phosphatase indicated that the levels of enzyme activity in both the control and treated palatal tissues corresponded to the appearance of lysosomes. Measurement of cAMP levels suggested that the peak activity of cAMP corresponded to that of enzyme acid phosphatase and cell injury. The cAMP activity in hadacidin-injured cells, however, was significantly lower in comparison to that of the dying cells of control palates. Hadacidin treatment also affected DNA synthesis in the developing primordia of the palate. It was suggested that hadacidin injures the precursor cells of the palate prior to the appearance of the primordia, and subsequently affects their proliferative behavior, stunting the vertical growth of the palatal shelves and inducing a cleft palate.

Acid Phosphatase↗
PubMed1989

Morphogenesis of the secondary palate in mouse embryos with special reference to the development of rugae.

Morphological studies of secondary palate formation, with special reference to the development of rugae, were carried out on Jcl:ICR mouse embryos. Three rugae were observed on the anterior part of the future oral surface of the vertically developing palatal shelves in 13-day embryos. Rugae increased in number as the development of the palatal shelves proceeded, and five to six prominent rugae were observed in 14-day embryos just prior to shelf elevation. The folding of these five to six rugae progressed in conjunction with the formation of a sharp, valley-like groove at the base of the anterior two-fifths of the vertical palatal shelves. As palatal shelves elevated, the groove disappeared gradually, and, accordingly, the folding of rugae loosened. In the groove region, the superficial epithelial cells were roundish, while the basal ones were elongated. Such characteristic features were no longer observed when the disappearance of the groove was completed. Eight rugae were observed on the future hard palate of 14-day embryos with already completed palatal fusion. An additional ruga was frequently found in 15-day embryos, and the pattern then was almost the same as that of an adult. Epithelial thickening and condensation at the rugae region, as well as mesenchymal condensation under the epithelium of the rugae, were confirmed in embryos both before and after elevation of the palatal shelves. There is a possibility that these structural characteristics observed in the epithelial and mesenchymal cells of the rugae and groove regions may be related to palatal shelf elevation.

Animals↗
PubMed2006

PDGF-C controls proliferation and is down-regulated by retinoic acid in mouse embryonic palatal mesenchymal cells.

BACKGROUND: Platelet-derived growth factor C (PDGF-C) was recently identified as a member of the PDGF ligand family. Some observation suggests that PDGF-C could play an important role in palatogenesis highlighted by the Pdgfc(-/-) mouse with cleft palate, which led us to examine the mechanism of PDGF-C signaling in palatogenesis. It is well known that retinoic acid (RA) is a teratogen that can effectively induce cleft palate in the mouse. Due to the critical roles of PDGF-C and RA in cleft palate, the link between cleft palate induced by RA and loss of PDGF-C was investigated. METHODS: Retarded mesenchymal proliferation is an important cause for cleft palate. To clarify the mechanism of PDGF-C in palatogenesis, we evaluated the effects of PDGF-C and anti-PDGF-C neutralizing antibody on proliferation activity in mouse embryonic palatal mesenchymal (MEPM) cells. RESULTS: Briefly, our results show PDGF-C promotes proliferation, anti-PDGF-C antibody inhibits it in MEPM cells, and RA downregulates the PDGF-C expression both at the mRNA and protein levels. CONCLUSIONS: These demonstrate that PDGF-C is a potent mitogen for MEPM cells, implying that inactivated PDGF-C by gene-targeting or reduced PDGF-C by RA may both cause inhibition of proliferation in palatal shelves, which might account for the pathogenesis of cleft palate in Pdgfc(-/-) mouse or RA-treated mouse. In conclusion, our results suggest that PDGF-C signaling is a new mechanism of cleft palate induced by RA.

Animals↗
PubMed1995

Developmental changes in phosphorylation of the transcription factor CREB in the embryonic murine palate.

Cyclic AMP, via activation of cAMP-dependent protein kinase (PKA) and subsequent protein phosphorylation, regulates a number of cellular and tissue responses that are critical to normal development of the mammalian palate. The present study examines the expression, distribution, and phosphorylation in the developing murine palate of a substrate for PKA known as the cAMP-response element binding protein (CREB). This 43 x 10(3) M(r) protein functions as a regulator of cAMP-inducible gene expression. CREB is expressed constituitively throughout the palatal morphogenetic period and is ubiquitously distributed throughout palatal tissue. Immunofluorescent staining of palatal cells and tissues with an anti-CREB antibody revealed CREB to be localized to cell nuclei. Western blot analysis of extracts of staged palatal shelves with an antibody specific for phospho-ser 133-CREB demonstrated a steady increase in CREB phosphorylation at this residue during palate development. These observations show a temporal correlation with expression levels of cAMP-regulated genes in palate cells. The data indicate that CREB activity in the developing palate is most likely to be regulated at the level of protein phosphorylation as opposed to changes in levels of CREB protein expression.

Alternative Splicing↗
PubMed1983

Differentiation of the avian secondary palate.

The avian secondary palate exhibits the unique feature of a midline cleft. Cryostat sections indicated that although extensive contact between homologous shelves was present, chick palatal medial edge epithelium (MEE) failed to fuse. The failure of fusion and subsequent clefting of the avian palate were correlated with continued proliferation of the avian MEE, a failure of selective MEE cell death, and an absence of elevated levels of intracellular cAMP. Moreover, immunohistochemical staining for cAMP and microspectrophotometric quantitation of staining intensity indicated that staining of chick MEE was significantly (p less than .01) less than murine MEE at comparable gestational ages. These data indicate that differentiation of the avian secondary palate is fundamentally different than reported for the mammalian palate in that many developmental events known to be associated with normal mammalian palate formation (cessation of MEE proliferation, MEE cell death, elevated levels of MEE cAMP) fail to occur in the chick. The developing avian secondary palate, with its midline cleft, thus provides an interesting and useful model system with which to compare mammalian palate formation where the palate is normally fused in the midline.

Animals↗
PubMed1994

TGF beta 1 regulation of collagen metabolism by embryonic palate mesenchymal cells.

Proper metabolism of the extracellular matrix (ECM) in mammalian embryonic palatal tissue is required for normal development of the palate. In particular, perturbation of collagen metabolism in the embryonic orofacial region results in the production of cleft palate. Although several types of collagen have been localized in the embryonic palate, factors responsible for regulating their synthesis have not been identified. Transforming growth factor beta (TGF beta), shown to be capable of modulating ECM metabolism in other tissues, has been localized in the developing palate. Thus, we examined the ability of TGF beta 1 to modulate collagen synthesis and degradation in murine embryonic palate mesenchymal (MEPM) cells in vitro. Immunohistochemical analysis confirmed that type III collagen was predominant in the mesenchyme of the embryonic palate, whereas type I collagen was ubiquitous throughout palatal epithelium and mesenchyme. Total collagen production by TGF beta-treated confluent MEPM cells in serum-free conditioned medium was determined by measuring incorporation of L-[2-3-4-5-3H]proline into hydroxyproline. Treatment for 24 hr with TGF beta 1 stimulated incorporation into both cell layer and medium fractions. Quantification of collagen types by ELISA indicated that TGF beta 1 stimulated the accumulation of type III collagen as early as 3 hr after treatment. Northern blot analysis of MEPM cells treated with TGF beta 1 revealed that steady-state levels of mRNA encoding for procollagen alpha 1 (I) and alpha 1 (III) were increased and that these effects were ablated by cycloheximide but not actinomycin. The effects of TGF beta treatment on MEPM cell collagen levels also reflected alterations in collagen degradation. TGF beta-treated MEPM cells exhibited a significant diminution of total protease activity. Moreover, analysis by substrate gel electrophoresis indicated specific decreases in vertebrate collagenase and stromelysin. These data represent the first report of changing proteolytic profiles during palatogenesis. Thus, TGF beta regulates the amount of collagen present in embryonic palatal tissue at the level of synthesis and degradation.

Animals↗
PubMed1980

Cortisone-induced cleft palate in the brachymorphic mouse.

Previous studies have shown that the autosomal recessive gene brachymorphic (bm/bm), which is maintained on a C57BL/6J (C57) background, reduces limb growth and sulfation of cartilage proteoglycans. Hydrocortisone administered on gestational days 11-14 resulted in 20% CP in the C57 mouse, but 95% CP in the bm/bm mouse. The bm/bm mouse had a median effective dose for CP of 45 mg/kg, compared to 325 mg/kg for C57 and 40 mg/kg for A/J. Morphometric analysis indicated that the time of palatal elevation was delayed in the bm/bm relative to the C57 mouse both with and without hydrocortisone treatment. The amount of cytoplasmic glucocorticoid receptor protein present in the bm/bm palate on day 14 was the same as the amount found in the C57 palate, and was not elevated as it is in the A/J palate. The levels of cyclic AMP in the bm/bm palate on day 14 were 30-70% higher than that found in the C57 palate with or without hydrocortisone. These results suggest that both bm/bm and A/J exhibit a delay in palatal shelf rotation and elevated levels of cyclic AMP, which appear to be predisposing factors for cortisone-induced cleft palate. These strains differ in that elevated levels of steroid receptors are present in A/J palate, whereas lower levels are found in the C57 and bm/bm mice.

Animals↗
PubMed1983

Involvement of GABA in palate morphogenesis and its relation to diazepam teratogenesis in two mouse strains.

Previous studies have indicated that serotonin and acetylcholine stimulate palate shelf reorientation. The present studies were undertaken to determine whether gamma-aminobutyric acid (GABA) functions as an inhibitory neurotransmitter in the palate and whether diazepam mimics GABA to inhibit shelf reorientation and cause cleft palate. First, it was shown that 10(-4) M GABA inhibits palate shelf reorientation in day 14.5 AJ embryos cultured for 2 hours. Anterior palate reorientation stimulated by 10(-5) M serotonin was decreased by GABA; 10(-5) M picrotoxin (GABA antagonist) stimulated anterior shelf reorientation and reversed the effect of GABA. Diazepam (10(-4) M) partially inhibited palate shelf reorientation and that stimulated by 10(-5) M serotonin. Diazepam (400 mg/kg) was administered to AJ mice at day 13.5 of gestation and embryos were cultured at day 14.5. The inhibition produced by diazepam was significantly reduced by 10(-5) M picrotoxin. The teratogenic effect of diazepam was compared with AJ and Swiss-Webster Vancouver (SWV) inbred strains. Diazepam produced greater clefting in SWV mice (57% net) than in the AJ (18% net) when compared to their water- and food-starved controls. The greater sensitivity of the SWV strain than the AJ strain to diazepam, as well as to GABA, was also observed in embryo culture. GABA (10(-5) M) markedly inhibited posterior palate reorientation and reversed the stimulation produced by bethanechol in SWV mice. The inhibitory effects of GABA on the posterior palate were partially reversed by picrotoxin. Furthermore, diazepam inhibited palate reorientation either when administered to the pregnant dam or added in embryo culture.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Maternal phenytoin administration affects DNA and protein synthesis in embryonic primary palates.

Recent studies have shown that phenytoin (Dilantin) administration to pregnant A/J mice on day 10 causes reduced growth in embryonic primary palates. The current investigation concentrates on biochemical and autoradiographic changes toward the end of primary palate formation (gestational day 11), which coincides with the developmental period used for the previously conducted morphological studies. On gestational day 10, one group of pregnant A/J mice was injected intraperitoneally (IP) with 60 mg/kg phenytoin and the other group with vehicle. Twenty-three hours after phenytoin administration, all animals were injected (IP) with either [3H]-thymidine or [3H]-leucine. After one hour of incorporation, animals were sacrificed, embryos removed and placed in ice-cold Eagle's minimum essential medium containing 0.02% NaN3 for biochemical assay or fixed immediately in Bouin's solution for autoradiography. For biochemical analyses, palates and limb buds were removed, homogenized, TCA precipitated, lyophilized, and acid hydrolyzed. Examination of the data revealed that DNA synthesis in control palates was 3.8-fold greater than in primary palates from embryos of phenytoin-treated mothers. Results were similar for limb buds from control embryos and from embryos of phenytoin-treated mothers. Experiments utilizing [3H]-leucine indicated that protein synthesis was 2.6-fold greater in primary palates from phenytoin-treated mothers than in control primary palates. Similar results were obtained for protein synthesis in limb-bud tissue from controls and embryos of phenytoin-treated mothers. Autoradiographic data supported the biochemical findings. DNA synthesis in primary palates from embryos of phenytoin-treated mothers decreased 3-fold; protein synthesis increased 2.2-fold compared with control primary palates.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Processes involved in retinoic acid production of small embryonic palatal shelves and limb defects.

All-trans-retinoic acid (RA) is teratogenic to the embryonic mouse, producing malformations in many developing systems, including the limb bud and palate. High incidences of limb defects and cleft palate are induced at doses which are not maternally toxic and do not increase resorptions. Exposure to RA on gestational day (GD) 10 results in small palatal shelves, which fail to make contact on GD 14. The formation of small shelves could be a consequence of increased cell death, reduced proliferation, a combination of these effects, or some other effect such as inhibition of extracellular matrix production. After exposure to 100 mg RA/kg on GD 10, proliferation in mesenchymal cells of the palatal shelves was not reduced from GD 12 to GD 14 and the levels of cell death in control and treated shelves did not differ when observed by light and electron microscopy. The present study examines the effects of RA on cell death and proliferation from GDs 10-12 and compares the effects in palatal shelves and limb buds. Embryonic mice were exposed to RA suspended in corn oil (100 mg/kg on GD 10), a dose that was teratogenic but not maternally toxic or embryolethal. Embryos were collected at 4, 12, 24, 36, or 48 hr postexposure, and tissues which form the palate or limb were dissected from the embryos, stained by a modified Feulgen procedure, and whole mounted on slides. Mitotic index (MI) and percentage dead cells were determined for mesenchymal cells of the first visceral arch, maxillary process, or palatal shelf (depending on stage of development) and forelimb buds. In the palatal tissues from GD 10 to GD 12, RA did not significantly alter MI and percentage dead cells was significantly increased only at 4 hr postexposure. Some whole embryos were prepared for scanning electron microscopy (SEM). At 48 hr (GD 12) a reduction in the size of the shelves was not apparent on SEM. In the limb buds, RA did not increase percentage dead cells, but MI was significantly decreased. A decreasing rate of proliferation was detected in control facial tissues as development progressed, and this agrees with findings in rat and chick. Thus it appears that mesenchymal cell death and reduced proliferation are not responsible for the small palatal shelves seen on GD 14. RA did not increase cell death but inhibited proliferation in the limb bud, and this effect may contribute to the retarded development and malformations occurring in the limb.

Abnormalities, Drug-Induced↗
PubMed1984

Middle ear function in cleft palate.

This study is based on an impedence audiometric evaluation of three groups of patients-20 with un-operated cleft palate, 28 normal subjects as controls and 20 operated cleft palate patients. Four major parameters have been analysed: middle ear pressure, static compliance, acoustic reflex and tympanometry. It was confirmed that in the normal child Eustachian tube function improves with growth and the critical age when the middle ear pressure becomes normal in almost all the normal children is 5 to 6 years. This process of improvement is disturbed in the presence of a cleft palate. Poor Eustachian tube function, evidenced by persistent negative middle ear pressure, continues to be commonly seen in the older subjects with un-operated cleft palates. The static compliance that reflects the elasticity of the conducting mechanism of the middle ear is poorer in cleft palate patients. It was also observed that when the cleft palate had been repaired before the age of 6 years, Eustachian tube function improved significantly in the older age group as shown by the lower incidence of negative middle ear pressure and Eustachian tube block. The high incidence of serous otitis media is apparently unaffected by surgery on the cleft palate and is responsible for some degree of hearing loss encountered in the older patients with operated cleft palates. Thus the incidence of hearing loss as studied by acoustic reflex is higher in all age groups in the presence of a cleft palate.

Acoustic Impedance Tests↗
PubMed1989

Pulp test response of the maxillary anterior teeth in cleft palate patients.

The relative pulpal responsiveness of the six maxillary incisors to electrical and cold thermal stimuli was tested in patients with complete unilateral and bilateral clefts. The six maxillary anterior teeth were tested at random to electrical stimuli. After a 5-minute interval, the same teeth were tested at random to cold stimuli with an ice pencil. Unilateral and bilateral cleft palate patients had statistically significant higher mean electrical pulp test thresholds for the maxillary anterior teeth than the noncleft palate patients. No statistically significant difference between unilateral and bilateral cleft palate patients was found in electric pulp test responses of the maxillary anterior teeth. No statistically differences in electric pulp test responses and cold test responses of the maxillary anterior teeth in both cleft palate and noncleft palate individuals based on differences in sex were observed. No statistically significant difference in cold test responses were observed between cleft palate and noncleft palate patients. Cleft palate patients who completed orthodontic treatment within 1 year of testing showed elevated mean electrical pulp test thresholds as did noncleft palate patients who received orthodontic treatment within 1 year of testing.

Adolescent↗