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PubMed2000

Local injection of IFN-gamma reduces the number of myofibroblasts and the collagen content in palatal wounds.

Wound contraction and scar formation after cleft palate surgery impair maxillary growth and dentoalveolar development. Since myofibroblast numbers and scar formation are reduced by interferon-gamma (IFN-gamma) in the healing of dermal wounds, the hypothesis was tested that local administration of IFN-gamma reduces the numbers of myofibroblasts and the elevated amount of collagen during palatal mucoperiosteal wound healing. Standardized mucoperiosteal excision wounds were made in the palatal mucoperiosteum of young rats. Either IFN-gamma or vehicle alone (sham group) was repeatedly injected into the wound site between 4 and 29 days post-wounding. The results were compared with unmanipulated control wounds. Samples of wound tissue were prepared for biochemical and microscopic analysis. The hydroxyproline, sulfated glycosaminoglycan and DNA contents of the wound tissues were analyzed biochemically. The degree of re-epithelialization, tissue thickness, the numbers of myofibroblasts, and the amounts of elastin and collagen types I and III were evaluated on histological sections. Injection of vehicle alone affected almost all healing parameters, compared with the controls, and delayed the wound-healing process. IFN-gamma stimulated re-epithelialization and decreased the numbers of myofibroblasts when compared with vehicle-treated wounds. It also decreased the hydroxyproline and glycosaminoglycan contents of 60-day-old wound tissue, but the histological characteristics of scar tissue persisted. Therefore, IFN-gamma is able to reduce the numbers of myofibroblasts and the collagen content of scar tissue after palatal wound healing. It may be a promising pharmaceutical agent for the reduction of wound contraction and scarring after cleft palate surgery.

Actin Cytoskeleton↗
PubMed1999

Myogenic determination and differentiation of the mouse palatal muscle in relation to the developing mandibular nerve.

The vertebrate palatal muscles are derived from the cranial paraxial mesoderm and start myogenesis by the expression of myogenic regulatory factors (MRFs). Predetermined myogenic cells migrate from the cranial paraxial mesoderm into the branchial arches, followed by myogenic differentiation. The objective of this study was to elucidate whether the determination, migration, and differentiation of myogenic cells during the myogenesis of the palatal muscles, particularly the tensor veli palatini (TVP), are related to the extending mandibular nerve in mouse embryos. By immunohistochemical staining at embryonic day (E) 9.5, MyoD1 and myogenin have been expressed in the mandibular arch, into which the mandibular nerve had not yet extended. At E11.5, these myogenic cells encircled the extending mandibular nerve and were distributed from the distal and lateral to the trigeminal ganglion and into the mandibular arch to form the muscle plate, a girdle-like structure. By E12.5, these myogenic cells lost their girdle-like pattern, vacated the trunk area of the mandibular nerve, and were separated into several incompletely divided masses encircling the collateral branches of the mandibular nerve. The TVP started differentiation at E13.5 with the appearance of myofilaments and acetylcholinesterase (AchE), whereas the other palatal muscles began differentiation at E14.5. We defined the differentiation process of mouse palatal muscles into five stages based on the present findings. These results suggest that the determination and initial migration of the palatal myogenic cells into the mandibular arch occur before the mandibular nerve extends out of the trigeminal ganglion, whereas the myogenic cells migrating into the final sites of differentiation intimately relate to the extending nerve.

Acetylcholinesterase↗
PubMedDate not supplied

Follicular lymphoid hyperplasia of the hard palate simulating lymphoma.

Follicular lymphoid hyperplasia of the hard palate is a slowly growing, soft, nontender swelling that may grow to involve the entire hard palate. The overlying mucosa is normal. This appearance naturally prompts biopsy, and both clinically and microscopically might be confused with lymphoma. Four case histories are presented with histologic description: normal palatal submucosal structures are replaced with benign reactive lymphoid tissue replete with well-developed germinal centers. Surrounding these centers are dense populations of small, regular, bland lymphocytes. Minor salivary glands, except for some atrophied residue, are notably absent; also absent are the epimyoepithelial islands characteristic of the benign lymphoepithelial lesion (Mikulicz's disease). Etiologic factors remain obscure. One of our patients had two recurrences following local excision; in another patient nodules of benign lymphoid hyperplasia developed in the cheek and upper neck. These four patients are alive and free of any malignant process 4, 7, 9, and 12 years after the onset of their palatal swellings. We urge caution in distinguishing these lesions from palatal lymphoma, and recommend local excision as the treatment of choice.

Aged↗
PubMed1993

Preliminary characterization of mucin from effusions of cleft palate patients.

Middle ear effusions from children undergoing myringotomy were classified into three groups-cleft palate, thick (mucoid), and thin (serous). Mucin was purified from each of the three groups using CsCI equilibrium density gradient centrifugation. Analysis of the cleft palate mucin on Sepharose CL-2B showed it was excluded and therefore of large molecular weight. It could be broken down into smaller glycopeptide units by proteolysis and these glycopeptides had, based on elution position, a larger hydrodynamic size than those from the thick mucin. Intrinsic viscosity measurements demonstrated that the intact mucins could be ranked in order of molecular space occupancy; cleft palate > thick > thin. Amino acid analysis showed the cleft palate mucin to have an amino acid composition similar to other mucins, with serine, threonine, and proline constituting 41% by weight of the protein core. Thiol analysis gave evidence of a possible difference in polymerization between the three mucins, in that thin (the smallest mucin) contained the lowest number of thiols. This preliminary analysis of cleft palate mucin suggests a mucin with larger glycopeptide units forming an intact mucin of larger hydrodynamic size than either thick or thin middle ear mucins from anatomically normal children.

Amino Acids↗
PubMed1994

Recovery of eustachian tube function and hearing outcome in patients with cleft palate.

Eustachian tube dysfunction is a nearly universal complication of cleft palate, resulting in chronic ear disease and conductive hearing loss. Cleft palate repair is thought to result in recovery of eustachian tube function, but the length of time between repair and recovery of eustachian tube function is not known. Furthermore, the efficacy of tympanostomy tubes in the treatment of eustachian tube dysfunction and hearing sequelae has not been examined in a systematic way. To answer these questions, we performed a retrospective study that used serial audiometric data and tympanometry on 81 patients with cleft palates (162 ears), with follow-up ranging from 1 to 17.3 years. Average time to recovery of eustachian tube function was 6.0 years (range, 1.0 to 10.3 years) after cleft palate surgery. For children followed up for at least 6 years (longest follow-up, 17.3 years), 70% (67 of 85) had normal eustachian tube function at their last follow-up visit. Ears treated with Armstrong tympanostomy tubes required an average of 3.1 tubes per ear until recovery of eustachian tube function, whereas ears treated with Goode T tubes required only 1.1 tubes per ear (p < 0.05). Hearing evaluation revealed that 67% of ears had abnormal hearing thresholds (> 20 dB) before tympanostomy tube placement, whereas only 7.5% of ears demonstrated this loss after tube placement. Furthermore, more than 90% of ears maintained normal thresholds after recovery of eustachian tube function. These data indicate that most children with cleft palates eventually recover normal eustachian tube function after palatoplasty, but for the majority of children, this does not occur for many years.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

Increased glucose metabolism in the medulla of patients with palatal myoclonus.

Hypertrophic degeneration of the inferior olivary nuclei is the pathologic substrate for palatal myoclonus, but the physiologic correlate of this finding is uncertain. Using the 2-[18F]fluoro-2-deoxy-D-glucose and PET method, we determined the local cerebral metabolic rate of glucose utilization in seven patients with palatal myoclonus (following stroke or infection, or idiopathic), one patient with oculopalatal myoclonus (following a stroke affecting the brainstem), and nine normal subjects. The metabolism of glucose in the medulla of the patients with palatal myoclonus was significantly greater than that of the normal subjects. This may well have been due to increased metabolism of the inferior olivary nuclei. Glucose metabolism in the medulla of the patient with oculopalatal myoclonus was normal. These findings suggest that the inferior olivary nuclei, or a region of the brainstem encompassing the inferior olivary nuclei, are hypermetabolic in palatal myoclonus and may be the generators of the involuntary movements in palatal myoclonus.

Adult↗
PubMed1992

Epithelial-mesenchymal transformation during palatal fusion: carboxyfluorescein traces cells at light and electron microscopic levels.

During the fusion of rodent embryo palatal shelves, the cells of the outer epithelial layer slough off, allowing the cells of the medial edge basal layer to form a midline seam that undergoes epithelial-mesenchymal transformation, as judged by electron microscopy and immunohistochemistry. In this study, we analyze the fate of the transformed cells using a lipid soluble dye to label the medial edge epithelium in situ. Prefusion E14 mouse palates were exposed in vitro or in vivo to a fluoresceinated lipid soluble marker, carboxydichlorofluorescein diacetate succinimidyl ester (CCFSE), which localizes in epithelia as a lipid insoluble compound that does not pass into the connective tissue compartment. The midline seam that formed after 24 hours contained labelled epithelial cells that were replaced by individually labelled mesenchymal cells where the seam transformed. By light microscopy, the labelled cells were seen to contain intensely fluorescent bodies that do not react for acid phosphatase. We were able for the first time to identify these structures by electron microscopy as CCFSE isolation bodies. The cells with isolation bodies are clearly healthy and able to participate in subsequent development of the palate. At 4 days after labelling, individual CCFSE containing cells present in the palate mesenchyme occupy both midline and lateral areas and can clearly be classified as fibroblasts by electron microscopy. CCFSE is a far more useful marker than another lipid soluble marker, DiI, for following cells, because the cells can be fixed and identified both at the light and electron microscope levels. Interestingly, if labelled palatal shelves are not allowed to fuse in vitro, the basal epithelial cells do not form mesenchyme after sloughing, indicating that formation of the epithelial midline seam is necessary to trigger its epithelial-mesenchymal transformation.

Animals↗
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↗
PubMed1992

[Spontaneous cleft palate in CF#1/Ohu mice].

We found a spontaneous cleft palate in a mouse of CF#1/Ohu (Ohu University, Japan). Further, the frequency of the spontaneous cleft palate in strains of CF#1/Jms (Institute of Medical Science, University of Tokyo, Japan) and CF#1/Jah (National Institute of Animal Health, Japan) were about 3%, respectively. The frequency and the types of spontaneous cleft palate in CF#1 were clearly different from those in A/J and CL/Fr strains which were used as model animals of lip and cleft palate. We think that CF#1 is the new animal models to analyze a cleft palate genetically and biochemically.

Animals↗
PubMed2003

Cleft palate repair in spondyloepiphyseal dysplasia congenita: minimizing the risk of cervical cord compression.

OBJECTIVE: Spondyloepiphyseal dysplasia congenita (SEDC) is a rare, inheritable condition that can include dwarfism, cleft palate, and C(1-2) instability. When repairing a cleft palate in a patient with SEDC, there is a significant risk of cord compression at the C(1-2) level because of neck hyperextension required for the operation. This reports presents a patient with SEDC who underwent surgery for a cleft palate, using a Ferno vacuum splint to immobilize the spine. INTERVENTION: The patient underwent general anesthesia. Good access was gained to the palate, and it was repaired without any complications. Particular attention was paid to maintaining the neck in a neutral position. CONCLUSIONS: The described technique provides the patient with the safest possible situation during anesthesia for cleft palate repair.

Cervical Vertebrae↗
PubMed2004

Mandibular morphology in complete unilateral cleft lip and palate.

OBJECTIVE: The purpose of this study was to evaluate and compare mandibular morphology and spatial position in children with complete unilateral cleft lip and palate (UCLP) treated at two different cleft centers (Hannover and Brussels) following different surgical treatment protocols. PATIENTS: A total of 62 Caucasian children (40 boys, 22 girls) with nonsyndromic complete unilateral cleft lip and palate (UCLP) were evaluated by means of conventional cephalometric analysis at approximately the age of 10 years. Data of both cleft groups were compared with a control, noncleft group (n = 40) matched according to age and sex. INTERVENTIONS: The Hannover children with cleft (n = 36) underwent lip repair at a mean age of 5.83 +/- 1.16 months. The hard and soft palates were closed at a mean age of 29.08 +/- 4.68 and 32.25 +/- 4.29 months, respectively. The Brussels children with cleft (n = 26) were treated according to the Malek surgical protocol with soft palate repair at a mean age of 3.04 +/- 0.20 months and simultaneous lip and hard palate repair at a mean age of 6.15 +/- 0.68 months. RESULTS: Statistical analysis (analysis of variance with post hoc Tukey's test) showed a significant (p =.001) smaller mandibular ramus length (Co-Go) in the Brussels cleft group, compared with the control group. The Hannover-Brussels comparison data revealed that the S-N-B angle was significantly (p =.047) less in the Brussels cleft group. CONCLUSIONS: The influence of surgical procedures in patients with UCLP might not be restricted to the maxilla but could influence mandibular spatial position to the cranial base. Because of these positional changes of the mandible, both cleft groups showed facial balance.

Analysis of Variance↗
PubMed2004

Predisposing factors to formation of cleft lip and palate: inherited craniofacial skeletal morphology.

OBJECTIVE: To identify inherited craniofacial morphologic features in individuals at high risk for cleft of the lip, cleft palate, or both. SUBJECTS: Twins without cleft from 33 pairs of monozygotic twins discordant for cleft lip, cleft palate, or both were studied. There were 17 males and 16 females of Caucasian origin, ranging from 3 to 18 years (15 with cleft lip and palate [CLP], 10 with cleft lip [CL], and 8 with cleft palate [CP]), collected from five craniofacial centers (United States and Canada). DESIGN: The twin without cleft (noncleft) from each set was compared with an age- and sex-matched control individual from the Burlington Growth Centre, Toronto, Ontario. Posteroanterior and lateral cephalograms were traced and digitized using a computer custom analysis. Descriptive statistics, Student's t tests, and analysis of variance were used to test 40 variables in a pilot study comparing the noncleft twin groups with the controls. Preliminary analysis permitted pooling of the CLP and CL groups (n = 25). To minimize false-positive significance, only 14 variables (from the maxillofacial area) were tested. RESULTS: Using the raw probabilities, eight variables showed significant differences between the pooled noncleft CLP and CL (CL[P]) twin group and the controls. However, when the level of significance was adjusted, only four (nasal width [p < .01], cranial base length [p < .05], cranial base width/length ratio [p < .001], and maxillary width/length ratio [p < .05]) were significantly different. No significant differences were confirmed between the noncleft CP twin group and the controls. CONCLUSIONS: The noncleft member of a discordant monozygotic pair has a number of facial characteristics that differ from the general population. These may predispose to the formation of a cleft lip or palate and may result from a deficiency or distortion of the mesenchyme that forms the craniofacial structures.

Adolescent↗
PubMed2005

The bacteriology of children before primary cleft lip and palate surgery.

OBJECTIVE: Bacterial infections can complicate any surgery. Knowledge of potentially pathogenic bacterial flora in children with cleft lip and palate allows appropriate risk management, including the need for prophylactic antibiotics. This project reviewed the bacteriology of children before primary cleft lip and palate surgery. DESIGN: A retrospective study of the results of nose, throat, and ear microbiological swabs taken from children, aged 1 to 26 months, before repair of primary cleft lip, cleft palate, or both was carried out. Swabs with Staphylococcus aureus and beta-hemolytic streptococcus were considered positive. RESULTS: From October 1987 to May 2002, 321 primary cleft lip or palate operations were performed in 250 patients. Results from 326 sets of preoperative swabs were available, including five repeat sets from patients whose operations were postponed. There were 235 (72.1%) negative sets and 91 (27.9%) positive sets. Of the positive swabs, 86 sets grew S. aureus, and 10 sets grew beta-hemolytic streptococcus. CONCLUSIONS: Children with unrepaired cleft lip and palate have a significant risk of carrying S. aureus and a small risk of carrying beta-hemolytic streptococci. These risks need to be considered when deciding on protocols for preoperative bacteriology tests and prophylactic antibiotics.

Antibiotic Prophylaxis↗
PubMed2005

Visual and statistical modeling of facial movement in patients with cleft lip and palate.

OBJECTIVE: To analyze and display facial movement data from noncleft subjects and from patients with cleft lip and palate by using a new dynamic approach. The hypothesis was that there are differences in facial movement between the patients with cleft lip and palate and the noncleft subjects. SETTING: Subjects were recruited from the University of North Carolina School of Dentistry Orthodontic and Craniofacial Clinics. PATIENTS, PARTICIPANTS: Sixteen patients with cleft lip and palate and eight noncleft "control" subjects. INTERVENTIONS: Video recordings and measurements in three dimensions of facial movement. MAIN OUTCOME MEASURES: Principal component (PC) scores for each of six animations or movements and dynamic modeling of mean animations. STATISTICS: Multivariate statistics were used to test for significant differences in the PC mean scores between the patient groups and the noncleft groups. RESULTS: No statistically significant differences were found in PC mean scores between the patient groups and the noncleft groups; however, the variability of the effect of clefting on the soft tissues during animation was noted when the noncleft data were used to establish a "normal" scale of movement. Compensatory movements were seen in some of the patients with cleft lip and palate, and the compensation was not unidirectional. CONCLUSION: Measures of mean movement differences as summarized by PC scores between patients with cleft lip and palate and noncleft subjects may be misleading because of extreme variations about the mean in the patient group that may neutralize group differences. It may be more appropriate to compare patients to a noncleft normal scale of movement.

Adolescent↗
PubMed2006

Speech in children with an isolated cleft palate: A longitudinal perspective.

OBJECTIVE: To describe articulation and speech symptoms related to velopharyngeal impairment in children born with an isolated cleft palate. DESIGN: Blind assessment of speech at 3, 5, 7, and 10 years of age was performed. Two subgroups were formed based on the results at age 5 years, the no-VPI group and the VPI group, and they were compared with controls. SETTING: A university hospital. PATIENTS: Twenty-six children born with isolated cleft palate. Seventeen children served as controls. INTERVENTIONS: Soft palate closure at 7 months and hard palate closure at a mean age of 3 years and 11 months if the cleft extended into the hard palate. MAIN OUTCOME MEASURES: Perceptual assessments of four variables related to velopharyngeal function and of articulation errors were performed at all ages. Phonetic transcriptions of target speech sounds were obtained at 5, 7, and 10 years and nasalance scores were obtained at age 10 years. RESULTS: The no-VPI group continued to have no or minor difficulties. The VPI group improved but continued to have moderate velopharyngeal impairment. Both groups differed significantly from the controls at age 10 years. Persistent velopharyngeal impairment, as well as glottal misarticulation, were mostly found in children with the cleft as a part of a syndrome or together with multiple malformations. CONCLUSION: Small changes in velopharyngeal impairment were found across ages. Improvement seemed to be related to surgical intervention, and persistent problems seemed to be related to the presence of additional multiple malformations or syndromes.

Articulation Disorders↗
PubMed2006

Epidemiology of Hoffmeister's "genetically determined predisposition to disturbed development of the dentition" in patients with cleft lip and palate.

OBJECTIVE: Type and prevalence rates of the symptoms of Hoffmeister's "genetically determined predisposition to disturbed development of the dentition" were studied in patients with clefts. PATIENTS: Data of 263 patients with nonsyndromic clefts of lip (alveolus and palate) or isolated cleft palates were examined in a retrospective study. SETTING: The clefts were classified as cleft lip or cleft lip and alveolus, cleft palate, unilateral cleft lip and palate, and bilateral cleft lip and palate. All patients were scrutinized for 28 individual symptoms. Prevalences of the individual symptoms were statistically evaluated regarding cleft type and gender by using the chi-square test and were also compared with findings in patients without clefts. RESULTS: In 97.7% of the patients with clefts, at least one symptom was found. Microdontia of individual teeth, hypodontia, and hyperodontia were the symptoms most frequently recorded. Comparison of the different cleft types revealed differences regarding the prevalences of supernumerary lateral incisors (p = .051), infraposition of deciduous molars (p < .001), and atypical tooth bud position (p = .030). Comparison of the prevalences of 10 symptoms recorded in the patients with clefts with the prevalences recorded in patients without clefts showed nine symptoms were found much more frequently in the population with clefts. CONCLUSION: These findings support the hypothesis that clefting is part of a complex malformation associated with other dental anomalies resulting from disturbed development of the dentition. Patients with clefts are also likely to present other deficiencies of dental development and tooth eruption in both dentitions, even in regions not affected by the cleft.

Adolescent↗
PubMed2006

Contributions of PTCH gene variants to isolated cleft lip and palate.

OBJECTIVE: Mutations in patched (PTCH) cause the nevoid basal cell carcinoma syndrome (NBCCS), or Gorlin syndrome. Nevoid basal cell carcinoma syndrome may present with developmental anomalies, including rib and craniofacial abnormalities, and predisposes to several tumor types, including basal cell carcinoma and medulloblastoma. Cleft palate is found in 4% of individuals with nevoid basal cell carcinoma syndrome. Because there might be specific sequence alterations in PTCH that limit expression to orofacial clefting, a genetic study of PTCH was undertaken in cases with cleft lip and/or palate (CL/P) known not to have nevoid basal cell carcinoma syndrome. RESULTS: Seven new normal variants spread along the entire gene and three missense mutations were found among cases with cleft lip and/or palate. One of these variants (P295S) was not found in any of 1188 control samples. A second variant was found in a case and also in 1 of 1119 controls. The third missense (S827G) was found in 5 of 1369 cases and in 5 of 1104 controls and is likely a rare normal variant. Linkage and linkage desequilibrium also was assessed using normal variants in and adjacent to the PTCH gene in 220 families (1776 individuals), each with two or more individuals with isolated clefting. Although no statistically significant evidence of linkage (multipoint HLOD peak = 2.36) was uncovered, there was borderline evidence of significant transmission distortion for one haplotype of two single nucleotide polymorphisms located within the PTCH gene (p = .08). CONCLUSION: Missense mutations in PTCH may be rare causes of isolated cleft lip and/or palate. An as yet unidentified variant near PTCH may act as a modifier of cleft lip and/or palate.

Adenine↗
PubMed1990

A preliminary study of facial growth and morphology in unoperated male unilateral cleft lip and palate subjects over 13 years of age.

This paper investigates the effects of surgery on facial growth and morphology in Sri Lankan males with unilateral cleft lip and palate who were over 13 years of age at the time of study with cephalometry and dental study models. Three separate subgroups were analyzed: those who had totally unrepaired cleft lip and palate, those who received lip repair in infancy but not palatal repair, and those who had lip and palate repair in infancy. Twenty-three healthy noncleft Sri Lankan males over 13 years formed a control group from the same racial background. The results show that subjects who had no surgery had a potential for normal maxillary growth. Subjects who have had lip repair in early infancy show relatively normal maxillary growth, but maxillary hypoplasia is common when the palate has also been repaired early.

Adolescent↗