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PubMed2002

Experimental study on effects of vitamin B(6) on dexamethason-induced palatal cleft formation in the rat.

OBJECTIVE: To evaluate whether or not administration of vitamin B(6) (vitB(6)) has preventive effects on cleft palate formation. METHODS: On the 14, 15 day of gestation, the pregnant rats were treated with administration of vitB(6) (10 mg/kg weight im) before and simultaneously with dexamethason (DEX). Compared the palatal cleft incidence of their fetuses with those whose mother were given DEX only. RESULTS: Treatment with administration of vitB(6) before and simultaneously with DEX, the palatal cleft incidence of subject group fetuses (32.35%) was significantly less than that given DEX only (64.52%). The proportion of the palatal cleft type was also changed significantly. CONCLUSIONS: VitB(6) decrease both the incidence and the severity of cleft palate induced by DEX in rats, which indicates VitB(6) may have preventive effects on cleft palate formation.

Animals↗
PubMed1976

The teratogenic effects of hydrocortisone on palatal development in the hamster.

The effect of different doses of hydrocortisone, administered at various times during gestation, on the fetal hamster and its palatal development was studied. Both the frequency of cleft palate and that of resorption depended upon the dose of hydrocortisone and the time of its administration. Two peaks in the incidence of cleft palate were observed, which appeared to be due to inhibition of different events. Incidence of morphologically different types of cleft palate was related to the doses and gestational time of hydrocortisone treatment. A close association was observed between the frequency of cleft palate and fetal growth retardation and between the latter and the dose and time of drug administration. It was suggested that maternal physiology and the placental barrier may play a crucial role in cleft palate induction.

Animals↗
PubMed1989

The management of the cleft lip and palate patient.

We believe that early closure of the hard palate defect with a palatal appliance and surgical closure of the lip and soft palate according to the rule of tens are very important. Delaying the hard palate closure allows for maximal growth of the palatal shelves. We also feel that pressure equalizing tubes placed in the ears at the initial surgical procedure allows for more normal function of the middle ear, less middle ear infections, better hearing, and ultimately better speech. We feel that early closure of the soft palate may decrease velopharyngeal incompetence by normalizing the position of the pterygoid plates. It may also help to reduce serous otitis media by improving eustachian tube function.

Cleft Lip↗
PubMed1988

Repair of surgical clefts of the hard palate in beagles.

The biological responses to the repair of palatal clefts has been evaluated principally by monitoring craniofacial growth. Little is known about the regenerative ability of the repaired palate. In the present study, 18 Beagle pups (51 to 58 days old) were assigned to one of three groups: (1) control group, having no surgery; (2) cleft group, having a surgically created cleft of the posterior hard palate (mean bony measurement: 3.1 x 11.7 mm) at 8 weeks of age; and (3) repaired group, same as group 2, and followed by soft-tissue closure at 12 weeks of age. Craniofacial growth was monitored by cephalometric and dental cast measurements. Records were taken at 6-week intervals. Animals were sacrificed either 16 or 28 weeks after time of cleft creation. Routine histologic examination and histochemical detection of alkaline phosphatase activity were performed to examine the quality and extent of soft-tissue repair and bone formation. Analysis of the cleft palate group revealed that the size of the bony cleft increased with time. The histologic examination demonstrated at 24 weeks of age (12 weeks after the repair) active reduction of medial margin of the bony palate as evidenced by osteoclastic activity. At 36 weeks of age, neither osteoblastic nor osteoclastic activity was detected. The mean dimensions of the bony cleft, in the cleft group at 36 weeks, were 7.9 x 18.8 mm. In the repaired group, partial bone repair occurred. However, no consistency was seen in predicting extent or location of repair. Histochemical detection of alkaline phosphatase activity indicated that the repaired group had greater amounts of new bone formation. In some sites, suture regeneration was seen. As with the amount of bone formation, the amount of suture regeneration was variable. This study revealed that the presence of a cleft inhibits osteoblastic activity along the margin of the cleft, and there is limited potential for regeneration of the palate subsequent to the repair.

Alkaline Phosphatase↗
PubMed1985

Palatal development and the arachidonic acid cascade.

The production of cleft palate by glucocorticoids and phenytoin is a complicated interference of a complex developmental program involving many genetic and biochemical processes. The H-2 histocompatibility region includes genes which affect susceptibility to glucocorticoid- and phenytoin-induced cleft palate; glucocorticoid receptor level in a variety of tissues including maternal and embryonic palates, adult thymuses and lungs; and the degree of inhibition of prostaglandin and thromboxane production by glucocorticoids and phenytoin in thymocytes. A gene linked to a minor histocompatibility locus (H-3) on the second chromosome also influences susceptibility to glucocorticoid and phenytoin-induced cleft palate. Phenytoin is an alternate ligand for the glucocorticoid receptor affecting prostaglandin and/or thromboxane production. The capacity of glucocorticoids to induce cleft palate is correlated with their anti-inflammatory potency. At least some of the anti-inflammatory effects of glucocorticoids can be explained by the inhibition of prostaglandin and/or thromboxane release, which in turn could be caused by inhibition of arachidonic acid release from phospholipids. Similar mechanisms may be involved in cleft palate induction, as exogenous arachidonic acid injected into pregnant rats and mice at the same time as glucocorticoids reduces the teratogenic potency of the steroids and indomethacin, and inhibitor of cyclooxygenase, blocks the corrective action of arachidonic acid. Glucocorticoids and phenytoin cause a delay in shelf elevation, and this delay is promoted by fetal membranes and the tongue. However, the cells of the medial edge epithelium are programmed to die whether contact is made with the apposing shelf or not. Glucocorticoids and phenytoin interfere with this programmed cell death, and this interference by both drugs seems to be a glucocorticoid receptor mediated event, to require protein synthesis and to be related to arachidonic acid release.

Animals↗
PubMed1984

Rare total and partial palatal clefts experimentally induced in the rat.

Clefts of the hard palate with soft palate integrity can be produced through amniocentesis in Sprague-Dawley rats. This study attempted to induce exotic partial clefts of the palate and to describe their type, frequency and possible genesis. Palatal closure, i.e., elevation and fusion of the anterior zone, remodelling of the middle zone, and fusion in the posterior zone, occurs in rats between 16.0 and 17.5 days of fetal age. Withdrawing a small amount of amniotic fluid produced a series of total and rare partial clefts. The upper jaws of 95 of 410 fetuses of precisely determined age were examined in the scanning electron microscope. Total clefts occurred in 48.9% of viable fetuses examined at day 17.8 and in 21.8% of those examined at day 19.3. Partial clefts were observed in 14.1 and 18.5% of viable fetuses at days 17.8 and 19.3, respectively. Total clefts were most frequent in fetuses treated between day 15.21 and 15.40, while Partial clefts were distributed rather equally over the various age groups. Total clefts occurred in at least four different varieties, while partial clefting involved variable portions of the hard palate or both the hard and the soft palate, with six different forms being distinguished. The induction of partial clefts was dependent on the developmental point in time at which experimentation took place.

Abnormalities, Multiple↗
PubMed1982

A comparative study of craniofacial growth during secondary palate development in four strains of mice.

Different inbred strains of mice have different timing of palatal shelf elevation, and strains with normally late shelf elevation have been shown to be more susceptible to induction of cleft palate. However, the major factors controlling the timing of elevation remain unknown. The objective of this study was to analyze different strains of mice morphometrically in order to identify characteristics or changes that corresponded with and contributed to shelf elevation. The four strains--A/J, SWV, C3H, and C57BL/6J (C57)--were studied between days 13 and 16 of gestation. Similar patterns of facial development were present in the strains, with C57 fetuses most advanced and A/J fetuses least advanced, relative to chronological age. Lifting of the head away from the thorax was also most retarded in the A/J fetuses. Palatal shelf elevation occurred between 200 and 240 mg body weight, with C57 fetuses smaller than A/J fetuses. The time of shelf elevation corresponded with the time that Meckel's cartilage became longer than the oronasal cavity, and the time that the head position lifted rapidly. Simultaneously with elevation, the height of the oral cavity increased and the width of the oral cavity decreased. The decrease in maxillary width appeared to facilitate shelf contact during palatal closure. The results demonstrated the need for normal growth of Meckel's cartilage for shelf elevation when a normal tongue was present between the palatal shelves. The results also showed that facial growth is one of the important factors that determine the time of palatal shelf elevation in mice.

Animals↗
PubMedDate not supplied

The CORT-GR signal transduction pathway and CORT-induced cleft palate in H-2 congenic mice.

A significant association between genes at or near the H-2 complex and glucocorticoid (CORT)-induced cleft palate in mice has been conclusively demonstrated. In addition, the frequency of CORT-induced cleft palate in heterozygous offspring from reciprocal crosses has been shown to be dependent on maternal H-2 haplotype. Although CORT responses are known to be mediated through the glucocorticoid receptor (GR), the involvement of H-2 haplotype-specific variation in the embryonic CORT-GR signal transduction pathway in CORT responsiveness remains uncertain. In this study, we characterized the embryonic (E13 to E15) CORT-GR pathway in developing B10 (H-2b) and B10.A (H-2a) mouse palates. Northern analysis demonstrates similar GR transcripts and mRNA steady-state levels in embryonic B10 and B10.A mouse palates. Palatal GR M(r) and pI, as determined by Western analysis, are similar between strains and among gestational days. We also analyzed possible haplotype-specific qualitative or quantitative differences in the ability of the GR to bind a glucocorticoid response element (GRE); no significant differences in the GR-GRE complex or in the levels of activated GR are seen between strains or among gestational days. Based on these results, we conclude that H-2 associated differences in susceptibility to CORT-induced cleft palate are not associated with either variation in embryonic GR or increasing gestational age. To determine if endogenous differences in maternal circulating corticosterone levels are related to differential embryonic CORT responsiveness, the levels of serum corticosterone were determined by RIA in pregnant dams on day 13 of gestation.(ABSTRACT TRUNCATED AT 250 WORDS)

Abnormalities, Drug-Induced↗
PubMedDate not supplied

Glucocorticoid receptor expression during the development of the embryonic mouse secondary palate.

The role of glucocorticoids and their interaction with the glucocorticoid receptor (GR) during embryonic growth and development has been a topic of interest and research for many years. Glucocorticoids are known to be teratogenic, and administration of these compounds during pregnancy produces cleft palate in the offspring. In the mouse, induction of cleft palate correlates with the level of palatal glucocorticoid receptor (GR) expression. However, the specific patterns of GR expression during critical stages of palatal morphogenesis remain to be examined. In the present study, GR expression was evaluated in the developing palates of C57BL/6N mouse embryos on gestation days (GD) 12, 13, 14, and 15 by both in situ hybridization and immunohistochemistry. On GD 12, GR mRNA was locally expressed in the region of palatal shelf outgrowth in both mesenchymal and epithelial cells, and GR was expressed uniformly throughout the developing shelf. A similar pattern of distribution occurred on GD 13 as the shelf became larger and elevated. By GD 14, GR was regionally expressed with higher levels in epithelial cells relative to mesenchyme. Chondrogenic regions strongly expressed GR. In different regions of oral and nasal epithelia localized patterns of expression were noted and may be related to differentiated state. Correspondingly, GR mRNA was expressed in epithelia and became regional in mesenchyme with abundant mRNA in regions of bone formation. On GD 15, oral and nasal epithelial cells showed mRNA, but mesenchymal levels were low except for chondrogenic regions. This pattern correlated with immunohistochemical localization of GR on GD 15. During palatogenesis the expression of mRNA correlated with immunodetectable GR peptide. GR localized initially within regions of active morphogenesis and subsequently within differentiating cells. This specificity of spatial and temporal expression supports the idea that GR is involved in regulation of regional growth and differentiation during palatogenesis.

Animals↗
PubMed1993

Issues and controversies in the management of cleft palate.

Cleft palate management is complex. There is no current agreement on the appropriate treatment strategy. Extensive disagreement on the pathophysiology, timing of intervention, and techniques of surgical repair have added to the confusion. To provide a comprehensive guide to the management of cleft palate is difficult. However, several main points should be emphasized. Normal speech should be the most important consideration in the therapeutic plan. Growth disturbance should be minimized, but not at the expense of speech impairment, because the facial distortion can be satisfactorily managed with further surgery, whereas speech impairment can often be irreversible. We believe repair of cleft palate to establish a competent velopharyngeal sphincter should be completed from 6 to 12 months of age. This is done early enough to minimize the development of an often irreversible pathologic compensatory speech pattern, but late enough not to increase significantly the surgical risk to the infant. Surgical interventions should be designed to cause minimal disruption of the palate, to decrease the severity of subsequent growth problems. There is a need for well-controlled, prospective studies to establish the validity of the widely different claims of superior results from various techniques. We believe strongly that cleft patients should be managed in a center with a multidisciplinary team. The benefits of these teams have been elaborated. Cleft palate embodies one of the major tenets of plastic surgery, the achievement of an aesthetic result with minimal interference with function. Cleft palate remains a significant and interesting challenge for current and future plastic surgeons.

Cleft Palate↗
PubMed1977

Mandibular growth retardation as a cause of cleft palate in mice homozygous for the chondrodysplasia gene.

Defective chondrogenesis in C57BL mice homozygous for the chondrodysplasia gene leads to deformity of limbs, ribs, trachea, mandible and palate. Since formation of the secondary palate depends upon coordinated development of several craniofacial structures, the presence of micrognathia and cleft palate in cho/cho newborn mice suggested a cause-and-effect relation between these two deformities. To determine whether or not lower jaw shortening coincided with the time of palate closure, heads from mutant control littermates previously rated morphologically were examined in median sagittal section. Of six parameters analyzed, growth rates for mutant mandible and anterior vertical dimension were significantly less than those of controls from the beginning of control palate closure. Since there is evidence that intrinsic shelf force is normal, these observations suggested that, during palatogenesis, growth retardation of Meckel's cartilage did not allow forward displacement of the tongue, and that the consequent failure to straighten the tongue impaired shelf movement. The data support the concept that growth of Meckel's cartilage is necessary for normal palate formation.

Animals↗
PubMed2006

A modified procedure for velopharyngeal sphincteroplasty in primary cleft palate repair and secondary velopharyngeal incompetence treatment and its preliminary results.

During cleft repair, velopharyngeal sphincter reconstruction is still a challenge to plastic surgeons. To improve the surgical treatment for cleft palate and secondary velopharyngeal incompetence (VPI), a carefully designed modified procedure for primary palatoplasty and secondary VPI was presented. Fifty-six patients (48 for primary cleft palate repair and eight for secondary VPI of previously repaired clefts) underwent this procedure from 1988 to 2001. The modified procedure is a combination of the tunnelled palatopharyngeus myomucosal flap for dynamic circular reconstruction of the pharyngeal element of the velopharyngeal sphincter and the double-reversing Z-plasty with levator velo palatini muscles reposition in the velar element of the sphincter. The satisfactory velopharyngeal competence (complete velopharyngeal closure and marginal velopharyngeal closure) was achieved in 23 of 25 patients with primary cleft palate repair examined by nasendoscopy and the nasality, speech articulation and intelligibility are also assessed in 25 primary cleft palate repaired patients with 92% satisfactory result (normal speech and speech with mild VPI) in single word test and 88% in continuous speech evaluation. Based on our experience, we believe that this modified procedure is a reasonable choice for primary cleft repair and secondary VPI treatment because it is in accord with normal physiology and anatomy of the velopharyngeal sphincter, can lengthen the soft palate, decrease the enlarged velopharynx, augment the posterior pharyngeal wall, and enhance the relationship between the muscles of velopharyngeal sphincter which results in a dynamic neo-sphincter in palatopharyngoplasty. Further study of the procedure is needed. The theoretical basis, operative highlights, velopharyngeal function, advantages and disadvantages of the modified procedure were discussed.

Adolescent↗
PubMed2002

Modifying the two-stage cleft palate surgical correction.

OBJECTIVE: This paper reports the experience with a two-stage approach to surgical correction of the complete cleft palate, wherein timing of the second stage is dependent on the judgment of the speech pathologist and the orthodontist together with the surgeon. PATIENTS: Of a total of 35 patients having complete unilateral clefts a sample of 22 were available for postsurgical assessment. The first-stage repair of the palate was carried out at an average age of 10.7 months (range 6 to 17 months), and the second-stage repair of the residual cleft was completed at an average age of 32.7 months (range 26 to 34 months). INTERVENTIONS: The first-stage repair of the soft palate defect involved mobilizing two short posteriorly based flaps, which extend onto the posterior quarter of the hard palate thus including up to 1 cm of mucoperiosteum. Careful freeing of the muscle is followed by an intravelar veloplasty. The later closure of the residual cleft involved turnover hinge flaps and small mucoperiosteal flaps. RESULTS: Eighty-seven percent of the sample had good to excellent speech as assessed by the Great Ormond Street screening method. Only two patients showed evidence of recessive maxillae with Class III malocclusions. CONCLUSIONS: A two-stage surgical closure of the palate using this procedure would appear to confer several valuable advantages to the patient. These include favorable outcomes for speech in the large majority of cases and minimal adverse effects on the growth of the midface region.

Child, Preschool↗
PubMed2001

[A primary clinical analysis of artificial bone implantation of cleft palate].

OBJECTIVE: To observe whether repairing the hard palate can improve velopharyngeal function. METHODS: 40 patients with hard palate cleft were randomly divided into two groups: the control group and the implantation group. Each group had 20 patients. The patients in the implantation group were implanted with compound artificial bone of HA--Bone cement. All patients hag been followed up for three months postoperatively. The patients in the repaired group were examined using computer tomography. All patients were examined using NPF. RESULTS: The implanted artificial bone had no rejection. The computer tomography showed that the implanted artificial bone in hard palate had no shifting, subsidence or breakage. The movement of soft palate of the implantation group was greater than the control group. The velopharyngeal function of the implantation group was much better than the control group. CONCLUSION: Repairing the hard palate cleft with artificial bone can improve velopharyngeal function.

Biocompatible Materials↗
PubMedDate not supplied

Decellularized dermal grafting in cleft palate repair.

OBJECTIVE: To assess the efficacy of decellularized dermal grafting used as an adjunct to the performance of primary repair of wide cleft palates. DESIGN: Retrospective review. SETTING: Tertiary referral center for large managed care organization. METHODS: Seven consecutive patients with clefts of the hard and soft palates wider than 15 mm as measured at the posterior edge of the hard palate. Palates were repaired in the standard 2-flap approach with intravelar veloplasty. The decellularized dermal graft (AlloDerm) was applied immediately deep to the oral mucosal closure. Patients were followed up with serial postoperative examination. Palates were assessed for dehiscence, fistula, infection, rejection, scarring, and contracture. RESULTS: There were no fistulas. In 2 patients, the oral mucosa dehisced, exposing the dermal graft. In 2 other cases, nasal mucosal tears were inadvertently created during closure of the nasal layer. In all cases, the decellularized dermal graft mucosalized and, by clinical examination, became incorporated into the wound. There were no cases of local inflammation or infection. The degree of scarring and contracture was indistinguishable from the adjacent scar. CONCLUSIONS: Decellularized dermal graft is safe and effective for use in primary closure of wide clefts involving the hard and soft palates. Its application to wide clefts otherwise at risk of fistula is justified. Its use in repair of an existing fistula is also promising.

Cleft Palate↗
PubMed1999

Considerations for free-flap reconstruction of the hard palate.

OBJECTIVE: To evaluate the use of microvascular free-tissue transfers in the reconstruction of hard palate defects. DESIGN: Retrospective review of a case series. SETTING: Two tertiary referral centers. PATIENTS: Thirty patients had hard palatal defects that resulted from ablative oncologic surgery: 10 total or subtotal palatal defects, 14 hemipalatal defects, and 6 anterior arch defects. INTERVENTION: Nine fibular, 11 rectus abdominus, 3 scapular, 6 radial forearm, and 1 latissimus dorsi free flaps were used to reconstruct these defects. MAIN OUTCOME MEASURES: Separation of the oral cavity from the nasal and sinus cavities, complications, oral diet, speech intelligibility, and overall quality of life. RESULTS: No flap failures occurred, and all palatal defects were ultimately sealed. Nineteen patients eat a regular diet, while the remainder maintain a soft diet. Twelve patients use a conventional dental prosthesis; 8 of the dental prostheses are supported by implants. Of 23 patients examined for speech, 18 have no disorders, 3 exhibit hyponasal speech, and 2 have hypernasal speech. Overall University of Washington, Seattle, quality of life scores were fair in 2 patients, good in 6, and excellent in 12. CONCLUSIONS: Free-flap reconstruction of the palate provides reliable permanent separation of the oral and sinonasal cavities in one stage. In addition, the potential for dental rehabilitation with the restoration of masticatory function and normal phonation exists. Flap choice is tailored to specific palatal defects as well as patient needs.

Adolescent↗
PubMed1989

Does maternal cigarette smoking during pregnancy cause cleft lip and palate in offspring?

To investigate the relationship between maternal cigarette smoking and the risk of oral clefts in offspring, we examined data from the Atlanta Birth Defects Case-Control Study, which included 238 cases of cleft lip with or without cleft palate and 107 cases of cleft palate ascertained by the Metropolitan Atlanta Congenital Defects Program from 1968 through 1980. In all, 2809 infants who served as controls were frequency matched to cases by race, period of birth, and hospital of birth. Maternal periconceptional exposures to smoking were investigated through use of a structured questionnaire. Smoking exposure was defined as reported maternal smoking during the periconceptional period (from 3 months before conception to 3 months after pregnancy began). Offspring of smoking mothers were 1.6 and 2.0 times more likely than offspring of nonsmoking mothers to have isolated cleft lip with or without cleft palate and cleft palate, respectively. On the other hand, offspring of smoking mothers were not at increased risk of having cleft palate or cleft lip with or without cleft palate that are associated with other defects. Adjustment for potential confounding variables did not alter these results. A relatively modest effect of smoking may be explained by the presence of underlying etiologic heterogeneity in oral clefts and differential susceptibility to smoking. Because of the inconsistencies in the literature on the relationship between smoking and oral clefts, these results suggest the need to refine oral clefts into more homogeneous subgroups in epidemiologic studies of these defects.

Adult↗
PubMed1997

Transforming growth factor-beta3 regulates transdifferentiation of medial edge epithelium during palatal fusion and associated degradation of the basement membrane.

Studies on transforming growth factor beta3 (TGF-beta3) deficient mice have shown that TGF-beta3 plays a critical role in palatogenesis. These null mutant mice have clefting of the secondary palate, caused by a defect in the process of fusion of the palatal shelves. A critical step in mammalian palatal fusion is removal of the medial edge epithelial cells from the midline seam and formation of continuous mesenchyme. To determine in more detail the role of TGF-beta3 in palatogenesis, we cultured TGF-beta3 null mutant and wild-type control palatal shelves in an organ culture system. The fate of the medial edge epithelial cells was studied in vitro using vital cell labeling and immunohistochemical techniques. Despite clear adherence, the null mutant palatal shelves did not fuse in vitro, but instead the medial edge epithelial cells survived at the midline position, and the basement membrane was resistant towards degradation. Supplementation of the culture medium with the mature form of TGF-beta3 was able to fully correct the defective fusion in the null mutant specimens. Our results demonstrate that the reason for the defective palatal fusion in TGF-beta3 (-/-) samples is not impaired adhesion. Our data define a specific role for TGF-beta3 in the events that control transdifferentiation of the medial edge epithelial cells including degradation of the underlying basement membrane.

Animals↗