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Intraoperative rapid expansion in cleft palate repair.

Intraoperative rapid expansion in cleft palate repair increases surface area by distension of the palate and recruitment of the surrounding palate tissue. A 5-cc Foley catheter with the distal tip trimmed is employed as the tissue expander. Intraoperative rapid palate expansion is proposed for closure with less tension of large gaps between cleft borders. This procedure has not demonstrated any deleterious clinical effects in cleft palate repair.

Catheterization↗

Cleft palate with autosomal recessive transmission in Brittany spaniels.

In the course of maintaining a large colony of Brittany spaniels for studying a dominantly inherited motor neuron trait, cases of sporadic complete cleft palate were observed. Without intervention, the pups with cleft palate that attempt to nurse, aspirate and die. In this study, we report on the incidence of cleft palate in this dog kindred, describe the gross morphologic characteristics of the cleft, and present a morphometric analysis of the skull of two of the cleft palate pups and one unaffected pup that died at birth. Our data thus far indicate 26.9% incidence of cleft palate in the colony. Pedigree analysis indicates that this cleft palate trait is inherited as an autosomal recessive. High resolution computed tomography scans of the pup heads were used in morphometric comparison of normal and cleft palate pups. We found specific morphologic differences between the cranial base and palate of normal and cleft palate pups. Plans for future studies of the genetics and growth and development of this animal model are discussed. This canine cleft palate trait provides an ideal model for studying a malformation common in humans.

Animals↗

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

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

Breast Feeding↗

Overexpression of iNOS and down-regulation of BMPs-2, 4 and 7 in retinoic acid induced cleft palate formation.

The present work studied the induction of cleft palate formation in embryos developed from pregnant BALB/c mice treated orally with retinoic acid (RA). Previous studies on mature somatic cell types showed that RA exerted inhibitory effects on inducible nitric oxide synthase (iNOS) production. For the first time, our study has shown that RA actually stimulates significant expression of iNOS at specific zones of the affected embryonic palatal tissues at three consecutive stages, from gestation day 13 (GD13) to day 16 (GD16). Enzymatically, iNOS facilitates intracellular nitric oxide (NO) synthesis from L-arginine. When NO reacts with reactive superoxides it may result in irreparable cell injury. NO was also reported to induce apoptosis in some mammalian cell systems. Based on our findings, we propose that such an increase in NO production might be associated with apoptosis in the embryonic palatal tissues in the RA-treated mice. The detrimental effects of NO resulted in a reduction in proliferating palatal cells and therefore disturbed the normal plasticity of the palatal shelves. With iNOS overexpression, our findings also showed that there was significant concomitant down-regulation in the expressions of Bone Morphogenetic Proteins (BMPs) -2, 4, and 7 with regional variations particularly in the palatal mesenchymal cells for those embryos developing cleft palate. Since specific spatial and temporal expressions of BMPs -2, 4, and 7 are critical during normal palatal morphogenesis, any deficiency in the epithelial-mesenchymal interaction may result in retarding growth at the embryonic palatal shelves. Taken together, our study has demonstrated cleft palate formation in the BALB/c embryos involved overexpression of iNOS and down-regulation of BMPs-2, 4 and 7.

Animals↗

Speech results following late palatal surgery in previously unoperated Sri Lankan adolescents with cleft palate.

The speech of 18 Sinhala speaking patients over 11 years of age with previously unrepaired palatal clefts is presented preoperatively, 8 months postoperatively, and after two brief courses of speech therapy (8 and 12 months postoperatively). Speech was usually severely disordered in the unoperated patient. The postoperative results show that speech often remains disordered following surgery, but there is the potential for change in some patients when supported by intensive goal directed therapy.

Adolescent↗

[Repair of hard cleft palate with absorbable membranes made by poly-DL-lactic acid: a feasibility study].

OBJECTIVE: To investigate the feasibility and clinical results of applying poly-DL-lactic acid (PDLLA) biomembranes in cleft palate repair. METHODS: 68 cleft palate patients were divided into study group and control group. The traditional surgical method was used to control group to close the soft cleft palate, and the PDLLA biomembrane was used to study group and implanted into the surgical gap between the periosteum and bone at the hard palate, and fixed with suture. The duration, blood loss at operation, post-operative complication, wound healing and recovery were recorded and compared to conventional cleft palate repair. RESULTS: Operations were successfully completed on all 34 patients. Wound healing of soft palate and uvula was uneventful with no incidence of fistula or dehiscence. The primary healing on tissue defect of hard palate occurred in 29 patients, secondary healing occurred in 3 patients, permanent fistula between the oral cavity and the nasal cavity occurred in only one patients, and 3 patients left over fistula on alveolar process. Compared to traditional cleft palate repair, blood loss and incidence of fistula on alveolar process were decreased; the average surgical time was 89.25 minutes and was not prolonged; and there was no significant increase in post-operative complication. CONCLUSION: Hard cleft palate repair with PDLLA biomembranes is safe, simple and practical with good clinical results and is beneficial to minimize the bad influences towards the development and growth for maxilla of cleft palate patients.

Absorbable Implants↗

Indications on suitable scaffold as carrier of stem cells in the alveoloplasty of cleft palate.

Autologous iliac crest bone is used to close the residual alveolar bone defect in cleft palate patients during late mixed dentition. Surgery involves physical and anaesthesiologic risks, long-time hospitalization, high costs and not always good results (15% failure rate). Alternatives to iliac crest bone grafting are going to be evaluated: synthetic, xenograft and allograft matrices combined with platelet-rich plasma or recombined bone morphogenic proteins for osteoinductivity are commercially available. These alternatives have not yet been determined to be equivalent to the previous treatment. A new field of research is represented by stem cells, which have been also used to regenerate ischaemic cardiac tissue after heart attack, to treat hypophosphatasia and osteoporosis. Our aim was to use osteoblasts from stem cells to close the residual palate cleft in association with a suitable carrier. Stem cells are expanded in the Aastrom bioreactor, differentiated into osteoblasts and positioned in the bone defect by means of a Spongostan scaffold. This scaffold has the best characteristics as commercial availability, low cost, good manageability, absence of allergic reactions or other side effects on patient, biocompatibility, imbibition, radiotransparency, reabsorbability and osteoinductivity. Previous studies encourage Spongostan scaffold application.

Alveoloplasty↗

Dental abnormalities and ectopic eruption in patients with isolated cleft palate.

The aim of this study was to evaluate the influence of cleft size and surgical treatment on the development of permanent teeth in patients with isolated cleft palate. The series comprised 109 children with isolated cleft palate, 70 girls and 39 boys, including 14 patients with Robin sequence. The patients were grouped according to the sagittal extent of the palatal cleft, measured on dental casts obtained before the primary palate surgery. Forty-six children were treated by one-stage palatoplasty, and 63 in two stages. The dentition was studied on orthopantomograms taken at 5, 8, 11, and 14 years of age. Congenitally missing permanent teeth (third molars excluded) were found in 33 subjects (30%). Children with large clefts had significantly more missing teeth than children with small clefts. The tooth most usually missing was the mandibular second premolar, followed by the maxillary lateral incisor, and the upper second premolar. The incidence of dental malformation was 23%, mostly mild forms. Ectopic eruption of the upper first permanent molars was seen in 23 (45%) of the subjects with large clefts, and in 18 (31%) of those with small clefts. The surgical method did not significantly affect the direction of the eruption. There is a correlation between cleft size and hypodontia, dental deformity, and ectopic eruption. Children with Robin sequence had almost the same incidence of hypodontia, malformed teeth, and ectopic eruption as children with large clefts. There was no correlation between surgical method and ectopic eruption of the maxillary first permanent molars.

Adolescent↗

Alterations in vascular pattern of the developing palate in normal and spontaneous cleft palate mouse embryos.

The alterations in the vascularization of the developing palate were studied through the use of resin cast images of vascular networks in normal and spontaneous cleft lip and palate (CL/Fr) mouse embryos (crown rump [CR] Length 9-18 mm, body wt. 0.11-0.65 g). A more dense vascular plexus was observed in the oral side than in the nasal side before the reorientation of the palatal shelves. Prominent terminal dilatations of the vascular plexus were observed in the extreme medial edge of the elevating palatal shelves which may exert significant force for palatal shelf elevation. The vascular plexus showed a lateral extension. Many small spherical masses of resin were observed in the medial edge of the palatal shelves at the time of medial extension and during fusion, indicating some changes occurring in the capillary wall leading to the resin leakage. In the spontaneous cleft group, a similar vascular pattern was observed, but the greater palatine artery showed discontinuity in the premaxillary region at an early stage. At the same time, terminal dilatations were delayed and frequently absent in the contralateral shelf. After the reorientation of the palatal shelves, the vascular plexus formed an irregular lattice pattern. Dilated vasculature was apparent in the anterior nasopalatine region, indicating the persistence of a more primitive vascular structure in the spontaneous cleft embryos. However, the area where capillary dilatation occurred was different between unilateral and bilateral cleft embryos. In conclusion, blood vessels in the palatal shelves are underdeveloped and remained immature in cleft lip and palate embryos and showed different patterns in the anterior nasopalatine region between unilateral and bilateral cleft embryos. These variant vascular patterns may be due to the inadequate blood supply to the nasopalatine region from the early embryonic stages possibly resulting from the discontinuity of the greater palatine artery.

Animals↗

Radiographic demonstration of oronasal fistulas in patients with cleft palate with the use of barium sulfate contrast.

The purpose of this investigation was to determine the overlapping and unique contributions that radiographic techniques might provide for accurate characterization of hard palate fistulas associated with cleft palate. Five subjects with oronasal fistulas were selected for radiographic imaging, and their informed consent was obtained. Results indicated that radiographs with contrast can provide important supplemental and unique information. Qualitative descriptions of the inferior-superior course and location, and the size of the narrowest aperture could be obtained from the combination of maxillary occlusal, posteroanterior tomographic, and lateral tomographic projections. This information could not be obtained from the common clinical methods in use to describe fistulas. This technique can provide valuable information to all members of a multidisciplinary cleft palate team to document palatal fistulas for both clinical and research purposes.

Barium Sulfate↗

The impact of cleft type on early vocal development in babies with cleft palate.

OBJECTIVE: The purpose of the present investigation was to examine the impact of cleft type on early sound development in children with cleft palate (with or without cleft lip). PARTICIPANTS: The participants included 53 babies with unrepaired cleft palate aged 8 to 10 months. Thirty-five babies had cleft lip and palate (CLP) and 18 had cleft palate only (CPO). MAIN OUTCOME MEASURES: Spontaneous vocalizations of the CLP and CPO groups were compared to determine whether differences were evident in canonical babbling, size of consonant inventory as well as place and manner of consonant production, and frequency of vocalization. RESULTS: Student's t tests revealed no significant differences between the groups in canonical babbling, size of consonant inventory, place and manner of consonant production, or frequency of vocalization. However, there was a trend for babies in the CPO group to produce fewer compensatory stop consonants and more anterior place features. In addition, a larger percentage of children in the CPO group had entered the canonical babbling stage at the time of this study. CONCLUSIONS: In general, the findings of this study suggested that cleft type does not appear to play a significant role in early consonant development for babies with cleft palate. Additional study using a larger CPO group is recommended to further investigate the trend toward better performance noted in this group.

Articulation Disorders↗

Cell behaviour and cleft palate in the mutant mouse, amputated.

Cleft palate with a genetic origin normally arises because of a failure of the palatal shelves to elevate or fuse. Until now attention in studies of palatal development development has been focused on two critical phases, those of elevation and fusion. In the mutant mouse, amputated, however, cleft palate arise because of a failure of the palatal shelves to make any significant outgrowth between the 12th day after conception when the palatal shelves are first observed and the 14th day when elevation and fusion normally occur. When cell proliferation (mitotic index) was measured in the palatal shelves on days 12, 13 and 14 no difference was found between mutant and normal. The failure of the mutant palate to grow cannot be accounted for on grounds of reduced cell proliferation. For this reason the palatal mesenchyme in 12.5-day and 14.5-day normal and amputated mice has been studied wit the scanning electron microscope. This work shows that the mesenchymal cells in the mutant palate are clumped together and have much greater areas of cell contact than are observed in the normal palate. The abnormal cell behaviour described in mutant palatal mesenchyme is typical of amputated embryonic mesenchyme in general, and in other cases has been shown to cause abnormal morphogenesis. We propose that aberrant cell behaviour causing an aggregation through increased cell adhesion inhibits palatal outgrowth in the mutant, and for this reason the palatal shelves subsequently fail to elevate and fuse.

Animals↗

Correlations between microforms of the Van der Woude syndrome and cleft palate.

The lower lip was examined in 397 children with isolated cleft palate (CP), in 518 cleft lip children with or without cleft palate (CL(P)) and in 1000 noncleft children. Familial occurrence of clefts, other concomitant anomalies and the type and extension of the cleft were determined from the child's medical history. A total of 323 orthopantomograms, taken at the ages of 6-12 years, were available in the detection of hypodontia of the permanent teeth excluding the third molars in the CP group. The incidence of lower lip sinus and microforms (conical elevations, CE) was noted. The incidence of sinuses was 2.3% in the CP group, 2.5% in the CL(P) group and 0% in the noncleft group. The corresponding figures for CE were 39.3%, 0.8% and 0.7%, respectively. In the CP group with CE, the familial occurrence of clefts was statistically higher (30.0%) than in the group without CE (20.7%). The corresponding figures for hypodontia were 40.7% and 24.7%, respectively. Conical elevations are cleft palate related disturbances in the development of the lower lip. At least in certain cases the CE do represent microforms of the sinus syndrome. Thus the question arises: do the CE always represent microforms of the Van der Woude syndrome, or are they only pathogenic similarities of a variable etiology?

Adolescent↗

Optimal timing of cleft palate closure.

Treatment objectives for the cleft palate patient--normal speech, normal maxillofacial growth, and normal hearing--are closely related. Controversy about the timing of cleft palate surgery is directed at the need for early palatoplasty for improved speech and hearing versus delayed hard palate repair for undisturbed facial growth. This controversy as to the value of early versus delayed closure continues into the present. The authors present an updated argument regarding this controversy along with a comprehensive literature review. They also present a logical algorithm based on the literature and their personal experience.

Age Factors↗