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At least 487 records · Page 27Linked to original sources
PubMed1998

A fiberscopic analysis of velopharyngeal movement before and after primary palatoplasty in cleft palate infants.

There have been few studies done on the abnormal function of velopharyngeal muscles in unrepaired cleft palate infants. To examine and assess velopharyngeal movement before primary palatoplasty offers supposedly any valuable information for the successful operation and the restoration of excellent velopharyngeal function. We designed to investigate and analyze velopharyngeal movement before and after primary palatoplasty in 26 cleft palate infants with a fine nasopharyngeal fiberscope. We found three different patterns of velopharyngeal movement in unrepaired cleft palate infants when crying or strangulation reflex occurred: (1) posterior movement type (10 cases, 38.5 percent), where the soft palates moved only posteriorly and cephalically and did not move medially; (2) medial movement type (10 cases, 38.5 percent), where the soft palates moved only medially and did not move posteriorly or cephalically; and (3) posteromedial movement type (6 cases, 23.0 percent), where the soft palates moved both posteriorly and cephalically as well as medially. Postoperative velopharyngeal closure was classified into three patterns: (1) the soft palate type, in which the soft palate mainly operates; (2) the lateral wall type, in which compensational medial movement of the lateral pharyngeal wall is mainly observed; and (3) the mixed type, in which both the soft palate and the lateral pharyngeal wall operate. Also, we demonstrated a close relationship between velopharyngeal movement before and after primary palatoplasty in cleft palate infants. In total, 10 of 16 cleft palate infants with the posterior movement type or posteromedial movement type, in which posterior movement of the soft palates was observed before primary palatoplasty, postoperatively showed the soft palate type of velopharyngeal closure. On the other hand, only 2 of 10 cleft palate infants with the medial movement type, in which the soft palates did not move posteriorly but medially before primary palatoplasty, postoperatively showed the soft palate type of velopharyngeal closure. The Fisher's exact probability test clarified that cleft palate infants with the posterior movement type or posteromedial movement type were more likely to show postoperatively the soft palate type of the velopharyngeal closure compared with those with the medial movement type (p = 0.051). This is the first trial to examine velopharyngeal movement in unrepaired cleft palate infants. Our findings indicate the probability that velopharyngeal closure mechanism in repaired cleft palate infants is able to be predicted by velopharyngeal movement behavior before primary palatoplasty. Next, we must clarify a correlation between preoperative velopharyngeal movement and postoperative velopharyngeal function and speech outcome.

Cleft Lip↗
PubMed1996

Submucous cleft palate: diagnostic methods and outcomes of surgical treatment.

The following statements summarize our interpretation of the literature regarding submucous cleft palate: Incidence and Diagnosis of Submucous Cleft Palate 1. In surveys of classic stigmata of submucous cleft palate among the general population, the incidence has been reported to be 0.02 to 0.08 percent. In the larger of these series, the incidence of velopharyngeal inadequacy among patients identified to have submucous cleft palate was 1 to 9. The incidence of occult submucous cleft palate is not known, since these patients will only be detected during the evaluation of patients who present with velopharyngeal inadequacy. 2. The diagnosis of submucous cleft palate is made by identification of the classic stigmata on physical examination. The diagnosis of occult submucous cleft palate is only pursued if the patient has velopharyngeal inadequacy. 3. For consistency in evaluating and reporting data, patients with an overt cleft of the secondary palate that extends beyond the uvula should be reported as having a cleft palate, and not a submucous cleft palate, even if a submucous cleft exists in a portion of the palate anterior to the overt cleft. 4. The true incidence of otitis media with effusion in the presence of submucous cleft palate has yet to be determined using a prospective study. Surgical Treatment of Velopharyngeal Inadequacy in Patients with Submucous Cleft Palate 1. The technique that has most consistently been documented to result in a significant correction of velopharyngeal inadequacy is the pharyngeal flap. There is recent evidence from one large center supporting the efficacy of the Furlow Z-plasty in selected patients with submucous cleft palate. Both these procedures appear to be most effective in patients with good lateral pharyngeal wall motion. 2. If a pharyngeal flap is performed as the primary procedure to act as an obturator against which the lateral pharyngeal walls appose for closure, we do not see the need for adjunctive palatal procedures. The dynamic component of velopharyngeal competence following such a pharyngeal flap consists of lateral wall motion, which is not enhanced by further surgical manipulation of the palate. However, a pharyngeal flap may be performed as an adjunctive procedure to a palatal pushback in order to provide lining for the resultant defect in the nasal mucosa. 3. The present literature does not support "prophylactic" operations on patients who present with the physical stigmata of submucous cleft palate prior to reaching an age at which it can be demonstrated by perceptual speech assessment that velopharyngeal inadequacy remained refractory to speech therapy. A significant number of patients will never develop velopharyngeal inadequacy; therefore, surgery would be unnecessary. In addition, objective data regarding the outcomes of different surgical techniques cannot be gathered if patients with submucous cleft palate are operated on without having had velopharyngeal inadequacy documented prior to those operations. 4. In order to objectively compare the outcomes of different surgical techniques, any future studies should be prospective and utilize uniform means of assessment. As minimum criteria, these would include preoperative and postoperative perceptual speech assessments performed by a trained speech pathologist and preoperative nasopharyngoscopy and multiview videofluoroscopy. The latter two studies should be repeated postoperatively only in those patients who have persistent velopharyngeal inadequacy.

Age Factors↗
PubMed2005

Regional regulation of palatal growth and patterning along the anterior-posterior axis in mice.

Cleft palate is a congenital disorder arising from a failure in the multistep process of palate development. In its mildest form the cleft affects only the posterior soft palate. In more severe cases the cleft includes the soft (posterior) and hard (anterior) palate. In mice a number of genes show differential expression along the anterior-posterior axis of the palate. Mesenchymal heterogeneity is established early, as evident from Bmp4-mediated induction of Msx1 and cell proliferation exclusively in the anterior and Fgf8-specific induction of Pax9 in the posterior palate alone. In addition, the anterior palatal epithelium has the unique ability to induce Shox2 expression in the anterior mesenchyme in vivo and the posterior mesenchyme in vitro. Therefore, the induction and competence potentials of the epithelium and mesenchyme in the anterior are clearly distinct from those in the posterior. Defective growth in the anterior palate of Msx1-/- and Fgf10-/- mice leads to a complete cleft palate and supports the anterior-to-posterior direction of palatal closure. By contrast, the Shox2-/- mice exhibit incomplete clefts in the anterior presumptive hard palate with an intact posterior palate. This phenotype cannot be explained by the prevailing model of palatal closure. The ability of the posterior palate to fuse independent of the anterior palate in Shox2-/- mice underscores the intrinsic differences along the anterior-posterior axis of the palate. We must hitherto consider the heterogeneity of gene expression and function in the palate to understand better the aetiology and pathogenesis of non-syndromic cleft palate and the mechanics of normal palatogenesis.

Animals↗
PubMed2004

Odd-skipped related 2 (Osr2) encodes a key intrinsic regulator of secondary palate growth and morphogenesis.

Development of the mammalian secondary palate involves multiple steps of highly regulated morphogenetic processes that are frequently disturbed during human development, resulting in the common birth defect of cleft palate. Neither the molecular processes governing normal palatogenesis nor the causes of cleft palate is well understood. In an expression screen to identify new transcription factors regulating palate development, we previously isolated the odd-skipped related 2 (Osr2) gene, encoding a zinc-finger protein homologous to the Drosophila odd-skipped gene product, and showed that Osr2 mRNA expression is specifically activated in the nascent palatal mesenchyme at the onset of palatal outgrowth. We report that a targeted null mutation in Osr2 impairs palatal shelf growth and causes delay in palatal shelf elevation, resulting in cleft palate. Whereas palatal outgrowth initiates normally in the Osr2 mutant embryos, a significant reduction in palatal mesenchyme proliferation occurs specifically in the medial halves of the downward growing palatal shelves at E13.5, which results in retarded, mediolaterally symmetric palatal shelves before palatal shelf elevation. The developmental timing of palatal growth retardation correlates exactly with the spatiotemporal pattern of Osr1 gene expression during palate development. Furthermore, we show that the Osr2 mutants exhibit altered gene expression patterns, including those of Osr1, Pax9 and Tgfb3, during palate development. These data identify Osr2 as a key intrinsic regulator of palatal growth and patterning.

Animals↗
PubMed1991

Comparative biochemistry of mouse and chick secondary-palate development in vivo and in vitro with particular emphasis on extracellular matrix molecules and the effects of growth factors on their synthesis.

A biochemical study analysing the wet weight, dry weight, water, protein and DNA content, collagen and GAG composition of all stages of the developing secondary palate in vivo and in vitro was undertaken to investigate differences between a species in which the palatal shelves elevate (mouse) and one in which they do not (chick). The effects of EGF, bFGF, PDGF and TFG-beta 1 on collagen and GAG synthesis by cultured mouse and chick palatal shelves of different embryonic stages were also studied. The total GAG content of developing mouse palatal shelves decreased with developmental time; heparan sulphate proteoglycan formed the major species in early palates but hyaluronan was the major species in mid-late palates. There was a peak of hyaluronan synthesis in embryonic palatal shelves in vitro at day 13 (T.21), i.e. immediately before shelf elevation. By contrast the total GAG content of chick palates increased with development; chondroitin-6-sulphate formed the major GAG species and there was no peak in hyaluronan synthesis. The water content of developing murine palates rose rapidly at day 14 (T.22), i.e. the time of shelf elevation. No such peak was seen in the chick, where the water content rose exponentially with developmental time. Mouse palates synthesized chondroitin-4-sulphate and novel proteins around the time of shelf elevation; chick palates synthesized chondroitin-6-sulphate and no novel proteins at any developmental stage. Collagen synthesis also peaked in vitro in T.21 murine palates. EGF markedly stimulated murine palatal collagens and GAG synthesis between stages T.20-T.22, but had no effect thereafter. Basic FGF had similar but smaller stage-related effects. PDGF had no effect on mouse palatal collagen and GAG synthesis whilst TGF-beta 1 inhibited GAG synthesis at T.21. The ratios of collagens I, III and V produced by mouse palates were unaltered by the growth factors. All the growth factors had no effect on chick palatal collagen synthesis at any stage and minimal effect on GAG synthesis; TGF-beta 1 stimulated it in early but inhibited it in mid- to late-stage chick palates. These data indicate that extracellular matrix molecule metabolism within the palate is markedly different in the two species studied and suggest that the differing profiles of such molecules may be regulated at certain developmental stages by specific growth factors.

Animals↗
PubMed1981

Glutamine synthetase activity in the developing secondary palate and induction by dexamethasone.

Glutamine synthetase (EC 6.3.1.2) (GS) and glutamyltransferase (EC 2.3.2.1) (GT) specific activity were examined in developing A/Jax and C57BL/6J (C57) mouse fetal secondary palates. In addition, the induction of palatal GS was also examined after maternal injection of dexamethasone. Palatal GT activity was uniformly higher in A/J than C57 palates with both strains showing highest activity late on day 13 of gestation and a drop in activity by early day 14. In contrast, A/J palatal GS activity peaked transiently late on day 13, dropped by early day 14 and remained lower throughout the remaining period of palatal development. Palatal GS activity in C57 mouse fetuses, although failing to show a discrete transient peak of activity, remained at a constant elevated level from early day 13 to late day 14 and did not decrease until day 15 of gestation. These elevated levels of palatal GS and GT activity correspond to the gestation period of maximal palatal glycoconjugate biosynthesis. Thus, palatal GS activity may play an important regulatory role in the synthesis of these macromolecules. A/J and C57BL/6J mice exhibit different susceptibilities to glucocorticoid-induced cleft palate. However, maternal administration of a non-teratogenic dose of dexamethasone on either late day 12 or late day 13 resulted in a dramatic stimulation of both A/J and C57 fetal palatal GS but not GT activity when assay 18 h later. A/J palatal tissue responded to dexamethasone with greater induction of palatal GS activity than enzyme activity in C57 palates. Palatal GS, sensitive to glucocorticoid stimulation, may thus be an important link in expressing hormonal control of normal palatal differentiation.

Animals↗
PubMed1986

Arterial venous and lymphatic pathways intrinsic to the palate and fauces (implicated routes for metastatic lesions).

Since metastatic lesions of the palate are known to spread primarily via lymphatics and secondarily via veins it would seem likely that knowledge of their distribution would be essential to clinico-pathologic interpretation. Arteries, veins and lymphatics intrinsic to human fetal and neonatal dog palates were ascertained by perfusing each vessel type with a different coloured dye. Stereomicroscopic observations determined that the three vessel types are so intricately intermingled that companionship in distribution does not exist. It was determined that the greater palatine and nerve enter the palatal area via the greater palatine foramen and are constant companions to one another as they ramify in the palatal mucoperiosteum. The palatal venous plexus converges in the posterior palate forming a single vein that descends to the pharynx where it joins the pharyngeal venous plexus. Hard and soft portions of the palate do not drain separately to infratemporal and pharyngeal venous plexuses. Arterial and venous networks form three strata (mucosal, submucosal and periosteal) but the lymphatic network forms only two strata (mucosal and submucosal). Images of blood and lymph vessels were observed coursing into the bony palate via canals of Volkmann but no images of lymph vessels were observed coursing into bone. The bony palate appears to be alymphatic. Fibrous connective tissue investing the bony palate (periosteum) and that surrounding neurovascular bundles (connective tissue sheaths) appears to function as a barrier to lymphatic ingrowth since both structures did not contain imaged lymphatic vessels. However, the fibrous connective tissue band at the palatal midline (median palatal raphe) does not present a barrier to lymphatic continuity since imaged lymphatic vessels were observed extending across the midline. Lymphatic afferentia exit the palatal area in stromata investing the palatoglossus and palatopharyngeus muscles and subsequently join lymphatic networks intrinsic to the tongue and pharynx. Hence arteries enter while veins and lymphatics exit the palatal area at separate locations in the posterior palate. Distribution of lymphatic vessels were found to coincide with clinical observations as to direction of spread of malignant lesions from the posterior palate and upper faucial area to the tongue and pharynx. The study also provided a vasculo-anatomic basis for surgical consideration specific to cleft palate reconstruction and palato-pharyngeal hiatus closure.

Animals↗
PubMed1983

Velopharyngeal incompetency in the absence of overt cleft palate: anatomic and surgical considerations.

Fifty-two patients with velopharyngeal incompetency without overt cleft palate underwent pharyngeal flap surgery. Surgery included exploration of the soft palate and reconstruction of the levator muscles. Four patients had a completely normal hard and soft palate. In two patients, the palatal musculature was normal but a U-shaped defect of the posterior hard palate was palpable. Seventeen patients had a diagnosis of submucous cleft palate made preoperatively and of these thirteen presented with the classic triad of a bifid uvula, a palpable abnormality of the hard palate and diastasis of the soft palate musculature. In thirteen patients a notch was found in the hard palate and in one patient a U-shaped defect was palpable at the posterior edge of the hard palate. Three patients presented no abnormality of the hard palate. One patient's uvula was normal. In the remaining twenty-nine patients, all demonstrated abnormal insertion of the palate muscles into the hard palate. In fifteen of these patients the hard palate was normal. In nine of the patients a U-shaped defect was palpable at the posterior hard palate and in three patients a notch was palpable. Thus, forty-eight of fifty-two patients (92%) demonstrated abnormal anatomy of the palate responsible for their velopharyngeal incompetency.

Humans↗
PubMed1999

A prospective evaluation of the prevalence of submucous cleft palate in patients with isolated cleft lip versus controls.

Although there is an established relationship between cleft lip and overt cleft palate, the relationship between isolated cleft lip and submucous cleft palate has not been investigated. To test the hypothesis that patients with isolated cleft lip have a greater association with submucous cleft palate, a double-armed prospective trial was designed. A study group of 25 consecutive children presenting with an isolated cleft lip, with or without extension through the alveolus but not involving the secondary palate, was compared with a control group of 25 children with no known facial clefts. Eligible patients were examined for the presence of physical criteria associated with classic submucous cleft palate, namely, (1) bifid uvula, (2) absence of the posterior nasal spine, and (3) zona pellucida. Nasoendoscopy was subsequently performed just after induction of general anesthesia, and the findings were correlated with digital palpation of the palatal muscles. Patients who did not satisfy all three physical criteria and in whom nasoendoscopy was distinctly abnormal relative to the control group were classified as having occult submucous cleft palate. Classic submucous cleft palate was found in three study group patients (12 percent), all of whom had flattening or a midline depression of the posterior palate and musculus uvulae on nasoendoscopy and palpable diastasis of the palatal muscles under general anesthesia. An additional six study group patients (24 percent) had similar nasoendoscopic criteria and palpable diastasis of the palatal muscles; they were classified as having occult submucous cleft palate. No submucous cleft palate was identified in the control group. Seventeen patients in the study group had an alveolar cleft with a 53 percent (9 of 17) prevalence of submucous cleft palate. In the present study, classic submucous cleft palate in association with isolated cleft lip was 150 to 600 times the reported prevalence in the general population. All children with an isolated cleft lip should undergo peroral examination and speech/resonance assessment no later than the age of 3 years. Any child with an isolated cleft lip with velopharyngeal inadequacy or before an adenoidectomy should be assessed by flexible nasal endoscopy to avoid missing an occult submucous cleft palate.

Adolescent↗