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PubMed1998

Our treatment of cleft lip and cleft palate.

Our principle in cleft lip and cleft palate repair is all-round personal treatment. That is, treatment concentrates not only on cleft lip and cleft palate repair, but also considers the patient comprehensively in terms of his or her personality. In this report, we present patients with cleft lips and/or cleft palates for whom we performed surgical treatments in the past 25 years. We performed primary operations for 402 patients and secondary operations for 120. Cleft lip and cleft palate should be managed with consideration for otolaryngeal aspects as well as plastic surgical ones because of the nature of the disease. We therefore treated our patients from the standpoints of both medical fields, and gained much appreciation from parents whose children suffered from the congenital anomaly.

Child↗
PubMed1996

Developmental expression and CORT-regulation of TGF-beta and EGF receptor mRNA during mouse palatal morphogenesis: correlation between CORT-induced cleft palate and TGF-beta 2 mRNA expression.

Glucocorticoids (CORT) have been shown to induce cleft palate in mice. Although the pathogenetic pathway of CORT-induced cleft palate has been investigated for several decades, the molecular details remain to be elucidated. Since growth factors have been shown to regulate palate morphogenesis, and the expression of several growth factors or their receptors, e.g. TGF-beta, EGF receptor (EGF-R), are known to be modulated by CORT, we postulate that CORT modulation of growth factor (or receptor) gene expression is a key mechanism involved in CORT-induced cleft palate. To test this hypothesis, we analyzed the steady-state levels (Northern and RNase protection) and developmental expression (in situ hybridization) of four CORT-responsive genes--TGF-Beta 1, TGF- beta 2, TGF-beta 3, and EGF receptor (EGF-R)--in developing mouse palates in the presence or absence of exogenous CORT. Pregnant B10.A dams were injected on day 12 of gestation with CORT or sham-injected and embryonic palates were collected at 1, 2, and 3 days postinjection (E13-E15). During mouse palate development, significant increases in TGF-beta 1 and TGF-beta 3 mRNA levels, as well as significant decrease in TGF-beta 2 mRNA levels, are detected; no significant difference in EGF-R transcript level is observed with progressive development. In CORT-exposed palates, we demonstrate no significant differences in the direction or magnitude of change with time in TGF-beta 1, TGF-beta 3, and EGF-R mRNA levels compared to controls. However, CORT delays by 1 day the down-regulation of palatal TGF-beta 2 transcript normally seen on day 14 of gestation. TGF-beta 2 is known to inhibit cell proliferation. The level of TGF-beta 2 mRNA, the only isoform primarily expressed in the palatal mesenchyme, significantly decreases with progressive palatal development; this down-regulation of TGF-beta 2 expression is associated with increased mesenchymal cell proliferation and palatal shelf growth. CORT, at a critical stage of palatogenesis, induces a delay in the normal down-regulation of TGF-beta 2 gene expression. Given that CORT is known to inhibit mesenchymal cell proliferation and palatal shelf growth, we conclude that the CORT-induced delay in the normal down-regulation of TGF-beta 2 gene expression is probably key event in the pathogenesis of CORT-induced cleft palate.

Animals↗
PubMedDate not supplied

Growth impairment of children with different types of lip and palate clefts in the first 2 years of life: a cross-sectional study.

OBJECTIVE: To analyze the differences in growth impairment according to sex in the 2 first years of life in children with three types of clefts. METHODS: This was a cross-sectional study of 881 children (58.9% boys and 41.1% girls) with cleft lip and palate treated at the Craniofacial Anomaly Rehabilitation Hospital, (University of São Paulo, Bauru, SP), Brazil. Age ranged from 1 to 24 months. Three types of clefts were evaluated: isolated cleft lip (181/20.5%), isolated cleft palate (157/17.8%) and cleft lip + palate (543/61.6%). Weight and length measurements and data regarding breast-feeding and socioeconomic level were obtained. Children with weight and length below the 10th percentile of the NCHS reference were considered to have impaired growth. RESULTS: Sample distribution according to cleft type and sex was similar to that observed in other epidemiological studies. Breast-feeding was more frequent in the isolated cleft lip group (45.9%) then in the isolated cleft palate (12.1%) or cleft lip + palate group (10.5%). Isolated cleft lip children showed less marked impairment of weight (23.8%) and length (19.3%) compared to the cleft lip + palate group (35.7% and 33.1%, respectively). In the latter group, the proportion of children with weight and length below the 10th percentile was very close to that of the isolated cleft palate group (34.4% and 38.9%). CONCLUSIONS: The impairment in weight and length was more severe in cleft lip + palate and isolated cleft palate children and may be attributed to feeding difficulties compared to the isolated cleft lip group.

Body Height↗
PubMed1999

A cephalometric study of the relationship between the level of velopharyngeal closure and the palatal plane in patients with repaired cleft palate and controls without clefts.

To find out whether the palatal plane is a useful indicator for evaluating the level of velopharyngeal closure, we did a cross-sectional study from early childhood to puberty of the vertical relationship between the palatal plane and the level of velarpharyngeal contact during velopharyngeal functioning in 61 patients with repaired cleft palate (unilateral cleft lip and palate = cleft group) and 82 controls without clefts (control group). Measurements on the vertical dimension were derived from a coordinate system and landmarks on lateral cephalograms, and the significance of differences in measurements was analysed using Student's t-test. Changes in the points of velarpharyngeal contact in relation to the palatal plane with growth showed a consistent tendency though differed between the two groups. In the control group, the PPW (point where palatal plane extension intersects the posterior pharyngeal wall) was maintained at a level that did not differ significantly from the level of midpoint of velarpharyngeal contact during phonation of /a/, and was maintained at a level that did not differ significantly from the level of the inferior point of velarpharyngeal contact. In the cleft group, however, it was maintained at a level that was slightly higher than the superior point of velarpharyngeal contact both during phonation of /a/ and during blowing. These results suggest that the palatal plane is useful as an indicator for evaluating the level of velopharyngeal closure.

Adolescent↗
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↗
PubMedDate not supplied

The double transposition flap for closure of the extremely wide hard palate cleft.

Repair of the extremely wide hard palate cleft can be done effectively with a double transposition flap. All cases referred for closure of cleft palates from 1997 to 2005 were considered for this study. Of these, 6 were classified as extremely wide cleft palates thought not to be treatable with standard closure techniques. A double transposition flap was used in each case. All patients tolerated the procedure well; no flap failure or dehiscence was noted; and none has required secondary repair. All patients tolerated an appropriate diet following flap repair. Two patients who were gastrostomy tube dependent preoperatively no longer required gastrosotomy tubes postoperatively.

Cleft Palate↗
PubMed2005

Morphology of the auditory tube and palatal muscles in a case of bilateral cleft palate.

OBJECTIVE: There is an increased incidence of otitis media in children with cleft palate, which may be related to the pathology of the auditory tube and palatal muscles. In the present study, the head of a human on term born fetus with bilateral palatal cleft was serially sectioned and the anatomy of the auditory tube and palatal muscles were studied by computer-aided three-dimensional reconstruction. RESULTS: The results showed a nearly horizontal course of the auditory tube. The tensor veli palatini muscle had a bony attachment on either side. The levator veli palatini muscle also showed an abnormal course. CONCLUSIONS: This abnormal course may result in obstruction of the auditory tube during contraction. These pathological findings may explain the higher frequency of otitis media in children with cleft palate.

Anatomy, Cross-Sectional↗
PubMed1994

Histochemical analysis of cleft palate muscle.

Research has clarified the abnormal insertions and orientations of the involved musculature in cleft palate. However, little is known about the physiologic aspects of these muscles, specifically from a histochemical perspective. In this study, 30 muscle specimens were removed from the palatal cleft margin in patients undergoing primary palatoplasty. Nine patients had combined cleft lip and palate deformity, and seven had an isolated cleft palate. Biopsies were taken from the area of the musculus uvulus in all specimens and examined by histochemical techniques. The percentage of type 1 and type 2 fibers was different in isolated cleft palate as compared with cleft lip and palate specimens, being, respectively, 56.7 percent type 1 and 43.3 percent type 2 and 62.0 percent type 1 and 38.0 percent type 2 fibers. This is the opposite ratio from other facial muscles but is in line with the literature regarding normal palatal muscle. Isolated cleft palate muscle fibers also were minimally decreased in diameter as compared with normal facial muscle. Fiber diameters of the combined cleft lip and palate muscles were severely decreased in size compared with those muscles found in the cleft lip. Abnormal mitochondrial accumulations also were found in cleft lip and palate muscle specimens but not in isolated cleft palate muscle specimens. We consider the decrease in muscle diameter found in isolated cleft palate to be secondary to functional atrophy, while that in the cleft lip and palate specimens is secondary to a primary hypoplasia together with a functional atrophy.(ABSTRACT TRUNCATED AT 250 WORDS)

Biopsy↗
PubMed1999

Dentoalveolar growth inhibition induced by bone denudation on palates: a study of two isolated cleft palates with asymmetric scar tissue distribution.

OBJECTIVE: This report presents two cases of isolated cleft palate with asymmetric distribution of postsurgical scar tissue determined by laser Doppler flowmetry. To determine the effect of mucoperiosteal denudation of the bone on maxillary alveolar growth, the analysis of dentoalveolar structures compared the affected side to the unaffected side of each case. METHOD: Two Japanese girls with isolated cleft palates were examined. Both subjects had undergone pushback operations (a modified version of the procedure of Wardill) for palatal repair at 18 months of age. Palatal blood flow was examined by laser Doppler flowmetry when the girls were 12 years old to determine the extent of postsurgical scar tissue over the denuded bone. To analyze the maxillary dentoalveolar structures three dimensionally, the whole surface of the upper dental cast was measured and recorded by an optical measuring device when the girls were 7 years old. RESULTS AND CONCLUSIONS: Analysis via flowmetry showed that the palatal scar tissue area was limited to the anterior tooth region on the right (unaffected) side but extended posteriorly to the premolar region on the left (affected) side in both subjects. The two girls had similar dentoalveolar structures, with the dental and alveolar arches deflected lingually at the deciduous molar area on the affected side. There were no differences in the buccolingual inclination of deciduous molars or in the vertical growth of the alveolar processes between the affected and unaffected sides. In both girls, bone denudation in the premolar region appeared to result in less than 3 mm of displacement of the teeth palatally, with no change in lingual inclination. Any effects of scar tissue on the vertical development of the alveolus were not substantiated.

Alveolar Process↗
PubMed2001

An electropalatographic investigation of middorsum palatal stops in an adult with repaired cleft palate.

OBJECTIVE: Middorsum palatal stops are compensatory articulations that occur relatively frequently in cleft palate speech. This study used electropalatographic (EPG) and acoustic data to investigate /t/ and /k/ targets produced as middorsum palatal stops ([c]) by an adult with an articulation disorder associated with a repaired cleft palate. RESULTS: Two novel observations were made from the instrumental data. First, although /t/ and /k/ targets were judged by phonetically trained listeners as homophonous (i.e., both produced as [c]), the EPG data revealed that the place of articulation for the [c] produced for /t/ was more anterior than the place of articulation for the [c] produced for /k/. Second, production of palatal stops involved lateral release followed by a variable period of lateral friction. Measurements made from the instrumental data quantified the temporal extent of lateral friction during the aspiration period. CONCLUSIONS: These observations merit further systematic investigation in cleft palate speech, and the procedures reported in this study are considered appropriate for such future research.

Adult↗
PubMed1995

The effect of very early cleft palate closure on the need for ventilation tubes in the first years of life.

The otologic consequences associated with cleft palates are well known. Closure of palatal clefts within the first weeks of life has many potential benefits, including improved feeding and cosmesis. The potential otologic benefits of very early closure are not known. Eighteen newborns have undergone closure of their palatal clefts within the first month of life with subsequent otolaryngology follow-up through our craniofacial center. Thirteen (72%) of the 18 still required placement of ventilation tubes during their first 3 years of life because of persistent effusion (for more than 120 days) or recurrent infection (more than four episodes in 6 months or more than six episodes in 12 months). Very early cleft palate closure may not significantly alter the need for ventilation tubes in children with palatal clefts.

Cleft Palate↗
PubMed2000

Sutural expansion osteogenesis for management of the bony-tissue defect in cleft palate repair: experimental studies in dogs.

A series of experimental studies on sutural expansion osteogenesis for management of the bony-tissue defect in cleft palate repair was performed between 1995 and 1997. Forty-five young dogs in weaning were used in four experiments that were divided into two parts. Part I probed the possibility of closing the surgically constructed hard palate cleft not only with mucoperiosteum but also with bony tissue by the technique of sutural expansion of lateral palatine sutures. Part II explored the possibility of pushing the palatine bone posteriorly and advancing the maxillary segment anteriorly by transverse palatine suture expansion. In Part I, a ring-shaped suture expander made of nickel-titanium shape memory alloy was used to expand the lateral suture of palatine bones. Expansion forces of 200 G, 360 G, and 480 G were used for the first experiment. A force of 360 G was chosen for two other experiments; this force is equivalent to the distraction rate of 0.5 mm per day of a jackscrew device. The ring-shaped suture expander was opened and its two feet were fixed in the medial sides of residual horizontal plates of the palatine bones immediately after a hard palate cleft was constructed surgically under endotracheal general anesthesia. At the eighth postoperative day, under the traction of 360 G, the two sides of the 8-mm-wide hard palate cleft were brought into contact with each other, and 8 or 9 days later the closed palatal cleft had healed completely with mucosal tissue. This experiment was repeated twice and yielded the same results. Sutural expansion osteogenesis was evaluated physically, fluorescently, histologically, and ultrastructurally to examine the deposition of the regenerated bone in the suture areas. Additionally, the influence of sutural expansion osteogenesis of the palatal bones on other facial bones was also studied cephalometrically. In Part II, a bow-shaped suture expander made of nickel-titanium shape memory alloy was applied to expand either the left or the right side of the transverse palatal suture of each of the experimental dogs. At the postoperative week 4 to 6, the maxillary segment was moved forward 5 to 6 mm on the expanded side, and the palatal bone was pushed backward 5 mm. The changes of bone position were assessed radiographically and cephalometrically. Tissue response of circum-maxillary sutures was examined histologically. These experiments led to the following conclusions: (1) Bony closure of the surgically constructed hard palate cleft with a ring-shaped suture expander made of nickel-titanium shape memory alloy is possible. (2) Anterior advancement of the maxillary segment and posterior lengthening of the hard palate using a bow-shaped suture expander made of nickel-titanium shape memory alloy applied at the palatomaxillary suture (transverse palatal suture) of the hard palate are also possible. Thus, in humans, a new approach for cleft palate repair may be a worthwhile investigation.

Alloys↗
PubMed1990

TCDD-induced altered expression of growth factors may have a role in producing cleft palate and enhancing the incidence of clefts after coadministration of retinoic acid and TCDD.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is teratogenic in mice, inducing cleft palate and hydronephrosis at doses which are not overtly maternally toxic or embryotoxic. After TCDD exposure the palatal shelves of normal size come into contact, but fail to fuse due to altered differentiation of the medial epithelial cells. These cells continue to express EGF receptors, proliferate, and differentiate into an oral-like stratified squamous epithelium. The present study examines the effect of TCDD on the expression of growth factors which are believed to regulate differentiation and proliferation in the palate. This study also examined the combined effect of TCDD and retinoic acid (RA), since in teratology studies coadministration of these agents results in an enhancement of cleft palate incidence. Embryos were exposed in vivo on Gestation Day (GD) 10 or 12 to TCDD ot TCDD + RA and the palatal shelves were dissected on GD 14-16. Growth factor expression was determined immunohistochemically using antibodies to TGF-alpha, EGF, TGF-beta 1, or TGF-beta 2. The growth factors displayed specific spatial and temporal expression in the palatal shelves. TCDD reduced the expression of TGF-alpha, EGF, and TGF-beta 1 in epithelial and mesenchymal cells. The degree of reduction was generally greater after exposure on GD 10 to TCDD alone or in combination with RA when compared to that on GD 12. The abnormal proliferation and differentiation of TCDD-exposed medial cells may be a response to reduced expression of EGF and TGF-alpha. Low levels of these factors may be related to the previously observed elevated levels of EGF receptors in medial cells. In other systems, low levels of ligand have resulted in upregulation of the EGF receptor. Continued proliferation and altered differentiation could also be attributable to decreased levels of TGF-beta 1, a factor inhibitory to epithelial proliferation. Since TGF-beta 1 stimulates mesenchymal growth and TGF-alpha and EGF stimulate epithelial proliferation, the formation of small shelves after exposure to TCDD + RA on GD 10 may be due to the severe reduction in these factors. Only a slight to moderate reduction in growth factor expression occurs after exposure to TCDD + RA on GD 12 and in this case shelves of normal size form. Since TCDD and RA appear to act in part through pathways that involve TGF-beta 1, in vitro experiments were designed to examine the involvement of TGF-beta 1 in TCDD teratogenicity.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2002

The effect of growth of nasopharyngeal structures in velopharyngeal closure in patients with repaired cleft palate and controls without clefts: a cephalometric study.

To clarify the changes with growth of nasopharyngeal structures involved in velopharyngeal closure, a cross-sectional study from early childhood to puberty was carried out in 61 patients with repaired unilateral cleft lip and palate showing complete velopharyngeal closure (cleft group) and 82 controls without clefts (control group). Measurements of the nasopharyngeal area were derived from a coordinate system and landmarks on lateral cephalograms, and results were analysed by multivariate analysis and t test. The adequate ratio (velar length to pharyngeal depth ratio) in the control group was maintained at a stable value, indicating that the ratio around 1.3 would be standard to maintain velopharyngeal closure. The vertical position of posterior maxilla, pharyngeal depth and velar length in the cleft group showed a different pattern of growth from those in the control group. There was, however, characteristic growth in both groups for maintenance of velopharyngeal closure.

Adolescent↗
PubMed1986

Synergistic interaction of 2,3,7,8,-tetrachlorodibenzo-p-dioxin and hydrocortisone in the induction of cleft palate in mice.

Glucocorticoids cause cleft palate in sensitive mouse strains by interfering with the proliferation of mesenchymal cells in the palatal shelves; 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) also causes cleft palate, but its effects involve the epithelial cells. The purpose of this study was to examine the interaction of TCDD and the glucocorticoid hydrocortisone in the induction of malformations. Pregnant C57BL/6N mice were treated on gestation days 10-13 with TCDD (0 or 3 micrograms/kg, p.o.), hydrocortisone (0, 25, 50, or 100 mg/kg, s.c.) or a combination of TCDD and hydrocortisone. The dams were killed on gestation day 18 and the mice were analyzed for maternal and fetal toxicity and soft tissue malformations. TCDD alone had no effect on litter size, fetal weight or viability, or maternal weight gain. This dose of TCDD is essentially a threshold dose and it did not produce cleft palate in this study, but all the TCDD-treated fetuses had hydronephrosis, the most sensitive indicator of TCDD teratogenicity. Hydrocortisone alone caused dose-related decreases in fetal weight and maternal liver/body weight ratios, and dose-related increases in cleft palate (0, 5, 10, and 30%). No effects of hydrocortisone were detected on litter size or fetal viability, but maternal weights were affected. Combination of all doses of hydrocortisone with TCDD resulted in a 100% incidence of cleft palate, accompanied by a decrease in litter size and fetal weight and an increase in fetal mortality related to the dose of hydrocortisone. TCDD tended to reverse the decrease in liver/body weight ratio seen with hydrocortisone alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Abnormalities, Drug-Induced↗
PubMed2001

New syndrome characterized by sparse hair, prominent nose, small mouth, micrognathia, cleft palate, crumpled upper helices, digit anomaly, and mild developmental delay.

A brother and a sister show very similar clinical features, including sparse hair in the first year of life, prominent nose, small mouth, micrognathia, high arched palate or cleft palate, crumpled upper helices, flexion limitation of the distal interphalangeal joint of the fingers, and mild developmental delay. Their clinical appearance suggests a premature aging phenotype, but is not really compatible with the hitherto known syndromes of that group. The mode of inheritance is likely autosomal recessive.

Abnormalities, Multiple↗