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The existence of a median palatal cyst has been questioned. Such a lesion would represent an unusual anomaly of a unique embryological process. The radiologic and pathologic criteria necessary to establish such a diagnosis are inconclusive in the ten case reports that have appeared in the English language literature. A median palatal cyst that is distinct from other palatal defects would have specific characteristics that included: 1) a true epithelial-lined cyst; 2) no salivary gland, vascular, or neural elements in the cyst wall; and 3) location in the palate at a distance sufficiently posterior to avoid confusion with structures of the nasal palatine region. We report the findings of a palate lesion excised from a 27-year-old male which by location and histology were consistent only with a median palatal cyst. These data appear to authenticate, for the first time, the median palatal cyst as a distinct pathological entity.
A new inbred mouse strain, SW/Fr, developed from a random-bred SW stock has a 6% incidence of spontaneous cleft palate without cleft lip. SW/Fr mice close their palates comparatively late in development. After cortisone treatment, the mean of the distribution (mean time to reach palate stage 5) is shifted towards later gestational ages. There is no change in the variance of the distribution. These data lend further support to the hypothesis that cleft palate in mice may fit a model where a continuous distribution is separated into discontinuous parts by a developmental threshold, and that time of palate closure is an important component of liability to cleft palate.
The concentration of cAMP was measured in palatal shelves and tongues of 14.5-day old foetuses, 14.5-day old foetuses from steroid treated mothers, and 15.5-day old foetuses from four inbred lines of mice which represent the four possible combinations of two H-2 alleles and two residual genetic backgrounds. The incidence of spontaneous and steroid-induced cleft palate in these four strains was also determined. Analyses of variance of the cAMP data reveal that both the H-2 region and residual genetic background determine cAMP concentrations in both tissues and on both days of development. Similar analyses of cAMP concentrations after steroid treatments of the mother indicate that the interaction between H-2 and residual genetic background is significantly different in the injected than in the uninjected mice in both palatal shelves and tongues. The incidence of steroid-induced cleft palate parallels the palatal shelf concentration of cAMP before steroid treatment of the mother with one exception. These data suggest that a portion of the H-2 controlled component of susceptibility to steroid-induced cleft palate is mediated through alterations in the metabolism of cAMP.
A method is described for rapidly measuring the surface area of the palate by adapting a piece of soft plastic to a model of the upper jaw using a vacuum moulding technique. Tests with a hemisphere of known surface area showed the method to be consistent and to have a low degree of systematic error. When measuring models with unrepaired cleft palates, the error was found to be 2.1 per cent (compared with 3 per cent using stereophotogrammetry) but 7.1 percent when measuring intact palates. Because of the consistency of the method, the true palatal area could be calculated from the measured area by the use of a multiplying factor. These findings are described, and the application of the technique to the pretreatment assessment of cleft cases is illustrated by showing that, in a series of 30 cleft palate and 30 normal infants, a tissue deficiency of 16.8 per cent existed in the cleft subjects at birth.
Administration of the cleft palate teratogen chlorcyclizine or norchlorcyclizine to pregnant rats causes an alteration in glycosaminoglycans (GAGs) in embryonic palatal shelves. Pulse-chase experiments in vitro indicate that norchlorcyclizine enhances the degradation of hyaluronic acid and chondroitin sulfate but has little or no effect on their synthesis. These changes in GAGs are caused by concentrations of norchlorcyclizine that have no appreciable effect on DNA or protein synthesis. These findings suggest that degradation of palatal GAGs may be the primary biochemical defect responsible for the inhibition of palatal shelf elevation by norchlorcyclizine.
Both normal Wistar rat fetuses and those with cleft palate induced by 5-Fluoro-2-Desoxyuridine were studied with a view to elucidating the mechanism of palatal shelf elevation and the pathogenesis of cleft palate. It was postulated that normal shelf elevation is brought about rapidly by an intrinsic turgor shelf force generated by binding of water to mucopolysaccharides. Interference with mucopolysaccharide synthesis would seem to be an important factor in the pathogenesis of some types of cleft palate.
Closure between the secondary palate and the primary palate and between the former and the nasal septum was studied in the Syrian golden hamster at light- and electron-microscopic level. Sequential changes in the epithelia before, during and after the closure of the primary and the secondary palate were described. A characteristic epithelial thickening was observed prior to epithelial fusion between the nasal septum and the secondary palatal shelf. Fusion of the opposing epithelia was characterized by formation of desmosomes. An unilateral or bilateral empty space was observed on each side of the epithelial seam, and it was suggested that this may represent the incisive foramen in the adult.
Using planimetric measurements of projections of the space between the palatal processes of ICR-Velaz mouse embryos, we indirectly demonstrated that the pre-horizontalization size of the palatal processes after the i.m. administration of 7.5 mg cortsone acetate on the 12th day of gestation was smaller than in the controls. After horizontalization, the inadequate palatal processes were unable to meet in the midline as they do in the majority of normal embryos. The administration of 0.5 mg 6-amino-nicotinamide on the 14th day of gestation did not significantly affect the size of the palatal processes.
Cleft lip and cleft palate are two possible effects of fusion failure of embryonic facial processes. Aberrant facial morphogenesis suggest aberrant arterial distribution. Prompted by surgical need, studies detailing major branches of the third or pterygopalatine portion of the maxillary artery acquire practical significance. Therefore postomortem arteriographic studies were undertaken to ascertain location of these major arteries and their branches in twelve near-term human fetuses. Comparison was made between arterial distributions in three cleft and nine non-cleft fetal palates. The question of bilateral symmetry was examined. It is known that these major branches are commonly present on both sides, but the study revealed numberous variations in each facial half in both cleft and non-cleft palates. Variation implies morphologic contradiction with sterotype presentations. So numberous are the variations that occasionally they may account for sudden and unexpected hemorrhage during surgery/and retarded healing or sphacelus of flaps following surgery.
A combinaation vomer mucoperiosteal flap and nasal floor mucoperiosteal flap is described which is used to achieve nasal coverage in unilateral cleft palate patients requiring pushbacks. A posteriorly based readily accessible vomer flap is raised on the cleft side and used as nasal lining for the palatal mucoperiosteal flap on the non-cleft side. On the cleft side, a symmetrically sized nasal floor flap is easily elevated under direct vision and used to cover the nasal aspect of the corresponding mucoperiosteal palatal flap.
A quantitative histological investigation was carried out on biopsy specimens taken from patients suffering from denture sore mouth. The results were compared with those obtained in investigations on denture and non-denture wearers. The sections were studied by standardized quantitative morphometric methods. After 4 years the denture bearing palatal epithelium from both groups, normal denture wearers and the patients suffering from denture sore mouth did not show changes in mean thickness of the epithelium as compared with the controls. The mitotic index in denture bearing epithelium from patients suffering from denture sore mouth was three times lower than in the epithelium of the normal denture wearers. The number of Langerhans cells correlated with the mitotic indices of the group of denture wearers and non-denture wearers. The group of denture sore mouth patients showing a low mitotic index showed a high number of Langerhans cells in their palatal epithelium. The three groups of patients investigated did not show differences in density of mast cells in the lamina propria of their palatal epithelium.
A mixed longitudinal study of the occlusion and arch dimensions from 4 to 11 years of age was made on fifty-five children with solitary palatal clefts. A cephalometric study was also made on thirty of these patients when they were approximately 10 years of age. The palatal closure was made by means of a modified von Langenbeck procedure at a mean age of 1 year 9 months. The frequency of cross-bite in the deciduous dentition was comparable with that in children without clefts. As in other studies, an impairment of the occlusion was seen with increasing age. The children showed retrognathic faces and the difference between the cleft children and the noncleft children was of the same magnitude as in other studies. It was found that the arch dimensions and the craniofacial morphology were influenced by the size of the cleft, while the occlusion was not. The craniofacial morphology in the present investigation was comparable to that in other studies where a push-back technique had been used, but the frequency of cross-bite was lower. Thus, it would appear that the type of surgery influences the occlusion more than it affects the craniofacial morphology.
Dessection of the musculature of the palate, pharynx, and styloid process was carried out in a cadaver aged 78 years with an unrepaired complete cleft palate. A new muscle named "the accessory stylohyoid" was found to be attached to the styloid process and the lesser cornu of the hyoid bone bilaterally. Anatomical changes in other muscles especially the stylopharyngeus and palatopharyngeus are described. The functions of these muscles are discussed on the basis of the anatomical findings and previous observations of other investigators.
This article has described a technique to achieve maxillary orthopedics for the infant with a bilateral cleft lip, protruded premaxilla, and intact palate. Both maxillary expansion and retraction of the premaxilla can be accomplished with the same prosthesis.
The "D. E. F.-syndromes" consist of ectodermal dysplasia, cleft of the lip and/or palate (fente labiale et/ou palatine). This group includes the A. E. C.- and the E. E. C.-syndromes. We are reporting two cases of D. E. F.-syndrome, in which there was a very particular hair dysplasia, which we named "scrubbing-brush hair". The first case was a boy. The disease was probably transmitted on the dominant autosomal mode. The ectodermal dysplasia was of hypohidrotic type. The second case was also observed in a boy. There was no similar genetic abnormality in the family. The ectodermal dysplasia was of hidrotic types. The embryological findings account for the association between the ectodermal dysplasia and the medial dysraphia of the face.
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