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At least 55 records · Page 3Linked to original sources
PubMed1997

The influence of different types of hard palate closure in two-stage palatoplasty upon palatal growth: dental cast analysis.

We investigated the influence of different types of hard palate closure in two-stage palatoplasty. In 12 cases the lip and soft palate were closed at the age of 3 to 7 months; these 12 were then divided into two groups. The hard palate was closed at the age of 1 year 5-11 months by the vomer flap with skin graft in the vomer flap (VF) Group (Osada's two-stage palatoplasty), and by push-back procedure of the mucoperiosteal flap in the push-back (PB) Group. Dental casts of the two groups were measured and compared at the ages of 0, 1, 3-4, and after 10 years. 1) In spite of apparent differences in palatal configurations at the age of 3-4 years, no significant differences in palatal size and area were noted between the groups. The cross-sectional areas in the VF Group were significantly larger than those in the PB Group in all the sections. 2) When the two groups were compared for rates of growth from 1 to 3-4 years, no significant differences in palatal size were noted, except in palatal width 1, although palatal growth from 1 to 3-4 years was more consistent and favorable in the VF Group. The rates of growth or change in palatal area and cross sectional-area 2 were significantly larger in the VF Group. 3) In spite of the apparent difference in palatal configuration, after age 10, no significant differences in palatal size, area, and depth were noted except in cross-sectional area 2.

Adolescent↗
PubMed2000

Investigations on the palatal rugae pattern in cleft patients. Part II: Changes in the distances from the palatal rugae to maxillary points.

The study investigated the relationship of the palatal rugae to points and distances of the cleft palate during the time period from birth to early mixed dentition in subjects with unilateral and bilateral cleft lip and palate by means of a three-dimensional measuring system. The changes identified in the distances from the lateral palatal rugae points of the first and third rugae to the incisal point, the canine point and the tuberosity line made it possible to assess how growth and the various forms of therapy applied affected the position of the palatal rugae during the study period (from birth to early mixed dentition). Changes in the linear distances from the palatal rugae to the maxillary measuring points were identified during preoperative therapy, after lip surgery, and after palate surgery. A comparison of the distances from the palatal rugae with distances between equivalent points (incisal point-canine point, canine point-tuberosity line, canine point-canine point) revealed differences in some instances. The results suggest that the palatal rugae in combination with measuring points of the cleft palate can serve to depict the changes occurring in the anterior palate during various stages of therapy and growth.

Cephalometry↗
PubMed2006

The fetal cleft palate: IV. Midfacial growth and bony palatal development following in utero and neonatal repair of the congenital caprine model.

BACKGROUND: Midfacial hypoplasia and growth disturbances following cleft palate repair are well-known consequences of the maxillary scarring inherent with each repair technique. The present study investigated the influence of in utero palatoplasty, and cleft repair in 6-week-old goats, on midfacial growth and bony palatal development in the authors' congenital caprine cleft palate model in an effort to identify an inherent component of facial growth impairment associated with the cleft anomaly. METHODS: At 85 days' gestation, eight clefted fetuses underwent in utero cleft palate repair using a modified von Langenbeck technique; eight fetuses remained as unrepaired controls. At 6 weeks of age, eight goats underwent cleft palate repair using the same technique. All goats were euthanized at 6 months of age; dry skull measurements and cephalometric analyses were performed. RESULTS: Fetal Repairs: Both repaired and unrepaired clefted goats demonstrated significant evidence of maxillary hypoplasia compared with unclefted controls. Repaired goats showed a decrease of 15.7 percent in maxillary length, and unrepaired clefted goats showed a decrease of 18.0 percent in maxillary length, compared with unclefted controls. There was no significant difference in maxillary growth between the repaired and unrepaired clefted groups. Bony cleft width was reduced by 48 percent anteriorly and 60 percent posteriorly. Thirty-seven percent of repaired congenital clefts demonstrated partial bony fusion involving 10 to 70 percent of the palatal length. This was accompanied by an 8.8 percent decrease in maxillary width at the level of the third molar crown compared with unclefted controls and an 18.3 percent decrease in maxillary width compared with unrepaired clefted goats. Unrepaired clefted goats demonstrated neither a decrease in maxillary width nor any narrowing or fusion of the bony cleft. Newborn Repairs: Significant midfacial growth impairment was seen in animals that underwent cleft palate repair at 6 weeks of age compared with those repaired in utero and with unclefted controls. Repaired clefted goats demonstrated a significant decrease in maxillary length by 29.5 percent compared with unclefted controls and 16.4 percent compared with the group repaired in utero. Repaired goats also demonstrated a significant decrease in maxillary width in the transverse dimension at the level of the third molar. A decrease in maxillary width of 25.3 percent was seen compared with the unclefted controls and 18.1 percent compared with the fetal repairs. Bony cleft width was reduced by 32 percent anteriorly and 27 percent posteriorly following repair at 6 weeks of age. Although all goats demonstrated narrowing following repair, partial bony palatal fusion was not seen in this group. CONCLUSIONS: In utero cleft palate repair does not contribute to impairment of midfacial growth. The authors attribute this finding to the scarless nature of mucoperiosteal healing in the privileged fetal environment. However, the cleft palate anomaly does have an inherent component of facial dysmorphology that is evidenced as maxillary hypoplasia or retrusion in unrepaired clefted animals. Cleft repair in the newborn period, or thereafter, results in midfacial growth impairment in a manner similar to that seen clinically. The authors attribute this finding to the scarring that routinely accompanies conventional palatoplasty. The combination of the growth impairment inherent in the cleft anomaly and that attributable to postnatal repair scarring yields the midfacial retrusion commonly associated with cleft palate.

Animals↗
PubMed1999

Periodontal disease in patients with cleft palate and patients with unilateral and bilateral clefts of lip, palate, and alveolus.

BACKGROUND: Long-term health of the stomatognathic system, as well as esthetics, is the therapeutic goal in patients with facial clefts. The aim of this study was to analyze the periodontal situation of patients with cleft palate (CP) and cleft lip, palate, and alveolus (CLPA) to elicit the differing degrees and localization of periodontal disease. METHODS: In 30 patients with unilateral cleft lip, palate, and alveolus (UCLPA), 30 patients with cleft palate (CP), and 20 patients with bilateral cleft lip, palate, and alveolus (BCLPA), the gingival situation was identified and classified according to the sulcus bleeding index (SBI). Periodontal attachment loss and pathological loosening of teeth were noted for identification of periodontal lesions. The state of oral hygiene was recorded by the approximal plaque index (API). RESULTS: In general, poor oral hygiene was found in all patients. The SBI showed a high incidence of gingivitis in patients with cleft lip, palate, and alveolus. Patients with cleft palate had a minor extent of sulcus bleeding. Periodontal disease was found to a similar extent to that in the general population in patients with cleft palate, whereas patients with cleft lip, palate, and alveolus had a predisposition to deep periodontal destruction of teeth adjacent to the cleft. The registration of pathological loosening of teeth, a result of attachment loss, corresponded to the degree of periodontal disease shown by the attachment loss. CONCLUSIONS: A critical periodontal situation was found in patients with unilateral and bilateral cleft lip, palate, and alveolus, ultimately leading to tooth loss in the front tooth region. In contrast, patients with cleft palate exhibited periodontal situations similar to that found in the general population with additional damage, which may be attributed to orthodontic treatment.

Adolescent↗
PubMed1998

Development of the residual cleft in the hard palate after velar repair in a 2-stage palatal repair regimen.

Delayed closure of the hard palate is believed to improve maxillary growth and facial appearance in cleft lip and palate patients. However, the cleft opening in the hard palate after velar closure might impair speech development. The aim of this investigation was to study the development of the residual cleft in the hard palate after 2-stage palatal repair (TSPR) in children born with complete cleft lip and palate (bilateral [BCLP]; n = 7 or unilateral [UCLP]; n = 22) or isolated cleft palate (CP; n = 9). Moreover, we aimed to investigate whether any morphologic factors before surgery might predict development of the residual cleft. Dental casts obtained prior to velar repair (mean age 7 months) and postoperatively at 1 1/2, 3, 4, 5 and 7 years were analyzed with a Reflex Microscope regarding the width, length and area of the cleft in the hard palate. The palatal cleft varied in size both pre- and postoperatively in all 3 types of cleft patients. The width of the cleft in the UCLP subgroup showed a marked reduction immediately after velar repair, but then, on average, remained stable until final surgical closure of the hard palate. In the BCLP subgroup the initially rather narrow width of the clefts remained unchanged postoperatively. Clefts in the CP subgroup, especially in those with a complete cleft, remained large after veloplasty. In 4 of the UCLP and 2 of the BCLP patients, the cleft width increased gradually. In some other subjects, both in the UCLP and BCLP subgroups, the residual cleft closed functionally with time, but this development could not be foreseen.

Child↗
PubMed2007

One- or two-stage palate closure in patients with unilateral cleft lip and palate: comparing cephalometric and occlusal outcomes.

OBJECTIVE: To assess facial growth and dentoalveolar development in two groups of patients with complete unilateral cleft lip and palate. Primary surgical treatment differed in the timing of hard palate closure. DESIGN: Forty-three patients with unilateral cleft lip and palate were examined. Twenty-two patients underwent early one-stage closure of the hard and soft palate cleft (mean age 23.0 +/- 4.7 months); in 21 patients, the hard palate closure was delayed to 86.3 +/- 39.2 months of age. Lateral cephalograms and dental casts were consecutively analyzed at four stages between 6 and 18 years of age. RESULTS: Lateral cephalometric analysis revealed no significant intergroup differences in the sagittal and vertical craniofacial dimensions at any time. Dental cast analysis showed constriction of the upper anterior arch width at the ages of 6 and 10 years in patients with one-stage surgical palate closure, but a difference could no longer be verified at the ages of 15 and 18 years. CONCLUSIONS: The transverse distances in the upper jaw developed initially more positively in the group with delayed hard palate closure, but it became apparent later that the transverse deficiency after one-stage palate closure could be compensated for. When considering surgical treatment in general, the advantages of the delayed hard palate closure must be weighed against criteria favoring the early one-stage closure of the hard and soft palate.

Adolescent↗
PubMed1983

Occurrence of cleft palate, palatal slit, and fetal death in mice treated with a glucocorticoid: an embryo transfer experiment.

SWV and C57BL/6 (C57BL) mice were treated subcutaneously with triamcinolone acetonide in a single dose of 2.5 mg/kg on day 12 of pregnancy (vaginal plug = day 0), and the palate of their fetuses was examined at term. Cleft palate was seen in some SWV and C57BL fetuses; its frequency was significantly higher in the former. Closer examination revealed palatal slit in some C57BL, but in no SWV fetuses. In addition, fetal mortality was significantly increased in SWV, but not in C57BL, exposed to triamcinolone. These strain differences in cleft palate, palatal slit, and fetal mortality were investigated by embryo transfer. The results showed that, in cleft palate induction, the effects of uterine environment were more important than those of fetal genotype. On the other hand, after transfer, palatal slit still occurred in C57BL but not in SWV fetuses; thus, in palatal slit occurrence, the fetal genotype played a more important role than the uterine environment. Accordingly, it is suggested that the nature of the participation of fetal genotype and uterine environment in palatal slit occurrence is different from that in cleft palate induction. In regard to fetal mortality, embryo transfer procedures influenced it in SWV dams and the effect of triamcinolone could not be detected after embryo transfer.

Abnormalities, Drug-Induced↗
PubMed1985

Epithelial changes of the nasal columella of the palatal slit and cleft palate defects in C57BL/6 mouse fetuses.

Palatal slit and cleft palate are induced in fetuses of C57BL/6 female mice treated with triamcinolone acetonide. In this study, the progressive changes in the epithelia of the presumptive fusion areas of the nasal columella and the anterodorsal part of the secondary palate were examined histologically. No difference was seen in the epithelial changes of the nasal columella of fetuses with palatal slit and those with cleft palate. In the treated palates the basal cuboidal epithelial cells in the presumptive fusion area of the nasal columella extended further toward the nasal cavity, and the vacuolization of the nasal epithelial cells appeared earlier than in the untreated palates. Although the treatment produced epithelial changes of the presumptive fusion area, its primary effect does not seem to be the disturbance of the epithelial fusion processes. The induction of palatal slit may be due to a failure of the primary and secondary palates to make adequate contact and fuse at the appropriate developmental stage because the secondary palate closure is delayed.

Animals↗
PubMed2003

Normal palatal sutures in newborns and fetuses: a critical fact for successful palatal distraction.

Distraction osteogenesis (DO) has recently been applied to the palate. Successful posterior lengthening and medial advancement of the palates was continuously reported. Based on these studies, it is obvious that DO will play a major role in the management of problems related to palatal defects in the near future. Although the results are appealing, they may not be applicable for humans due to anatomic differences. All experimental studies used normal palatal sutures of young dogs for size expansion. Therefore, it is necessary to know normal palatal sutures in infants before one can clinically apply this new technique. With consent, palates of fetuses and neonates who died of various causes were examined. Eight fresh cadavers were available for the dissection, with two being skeletonized using the boiling process. There were three fetal deaths in utero (33-41 weeks of gestational age) and five postnatal deaths (aged between 5 hours and 6 months). All specimens were grossly normal in shape and size except for one with a unilateral complete cleft of lip and palate. A midline palatal suture was found in every noncleft specimen, while premaxillary and transverse palatomaxillary sutures were present in every specimen. Laterally, there was no true suture except for the most posterior portion, which was contiguous with the greater palatine foramen. The palatal sutures of third-trimester fetuses and neonates are not different from adult ones. There is no lateral suture that will allow distraction in the medial direction. It is only the posterior hard palate (palatine bones) that can potentially be moved medially and posteriorly by sutural expansion with DO.

Animals↗
PubMed2000

Palatal distraction in a canine cleft palate model.

The purpose of this study was to determine whether the canine hard palate can be lengthened by distraction osteogenesis in a cleft palate model using a mostly submucosal distractor. Five mongrel dogs were used. After raising mucoperiosteal flaps, a midline strip of bone was removed from the hard palate of each dog to simulate the bony defect seen in a cleft palate. A transverse osteotomy was then made to separate the posterior segment of the hard palate from the anterior segment. Posterior osteotomies were also made laterally parallel to the teeth so that the 2 posterior segments (one on either side of the bony cleft) were mobile. An intraoral distractor that was mostly submucosal was attached to the anterior hard palate and both segments of the mobilized posterior hard palate. Radiopaque bone markers were placed, and x-rays were obtained. After a 10-day latency period, the distractor was expanded 0.675 mm per day until it had been lengthened 10.125 mm. Distractors were left in place for an additional 8 weeks. After distractor removal, animals were observed for an additional 8 weeks before euthanization. Follow-up x-rays and histologic examinations were performed. New bone formation was found at the site of distraction in all dogs at the time of death. This new bone was seen on the follow-up x-rays and on histologic examination of the hard palates using both hematoxylin and eosin staining and Masson's trichrome stain. Distraction osteogenesis using a mostly submucosal device is an effective technique for lengthening the hard palate in a canine cleft palate model. The technique may eventually provide an alternative treatment for velopharyngeal incompetence in humans that is more precise and involves less morbidity than existing treatments.

Animals↗
PubMed1992

Early palatal changes in complete and incomplete cleft lip and/or palate.

Early palatal development in various complete and incomplete forms of cleft lip and/or palate (CLP) was studied from birth to 3 months of age by means of dental casts. Palatal morphology (shape) and dimensions--based on reproducible reference points--were determined in a group of 128 CLP children and 68 normal children who served as controls. Substantial normal palatal growth during the first 3 months of life was observed. Round arch forms changed into oval arch forms. Growth mainly takes place in the sagittal direction (+4 mm) (transverse: +1 mm). Palates of CLP children differed significantly dependent on the type of cleft and whether the cleft was complete or incomplete. Cleft lip and alveolus children and bilateral cleft lip and palate children had more elongated palatal arches, whereas unilateral cleft lip and palate children and cleft palate children had wider palatal arches than the control group. Incomplete clefts differed from the control group in the same direction as their complete cleft forms, though less distinctly. Preoperative orthopedics used in CLP patients does not stimulate growth. On the contrary, it even restricts growth.

Cleft Lip↗
PubMed2006

Hard palate repair timing and facial growth in unilateral cleft lip and palate: a longitudinal study.

OBJECTIVE: To investigate whether timing of hard palate repair had a significant effect on facial growth in patients with unilateral cleft lip and palate (UCLP). DESIGN: Retrospective longitudinal study. SETTING: Sri Lankan Cleft Lip and Palate Project. PATIENTS: A total of 104 patients with nonsyndromic UCLP who had hard palate repair by age 13 years, with their 290 cephalometric radiographs taken after lip and palate repair. MAIN OUTCOME MEASURES: Clinical notes were used to record surgical treatment histories. Cephalometry was used to determine facial morphology and growth rate. RESULTS: Timing of hard palate repair had a significant effect on the length and protrusion of the alveolar maxilla (PMP-A and SNA, respectively) and the anteroposterior alveolar jaw relation (ANB) at age 20 years but not on their growth rates. CONCLUSION: Timing of hard palate repair significantly affects the growth of the maxilla in patients with UCLP. Late hard palate repair has a smaller adverse effect than does early hard palate repair on the growth of the maxilla. This timing effect primarily affects the anteroposterior development of the maxillary dentoalveolus and is attributed to the development being undisturbed before closure of the hard palate.

Adolescent↗
PubMed1998

Measurement of palatal surface sensation by neuro-sensory tests in the postoperative cleft palate patients.

To clarify the effects of abnormal sensation on the palatal surface on speech sounds in postoperative cleft palate patients, we measured palatal surface sensation in these patients. Tactile and vibratory sensation were measured quantitatively using a SW sensemeter and a vibrometer. The obtained values were compared with those in controls. The following results were obtained. In both the postoperative cleft palate patients and controls, the sensation in the anterior region of the hard palate was more numb than that in the anterior region of the soft palate or the premolar alveolar region. The tactile sensation in the postoperative cleft palate patients was more numb than that in the controls. In particular, a marked difference was observed in the premolar alveolar mucosa. The vibratory sensation in the postoperative cleft palate patients, however, did not clearly differ from that in the controls. There was a positive correlation between the tactile sensory threshold and the vibratory sensory threshold in the controls. No association between the two thresholds was observed in the postoperative cleft palate patients. The authors concluded that the tactile sensation at premolar alveolar region in the postoperative cleft palate patients was more numb than in the controls. This abnormality may affect speech development.

Adolescent↗
PubMed2003

[Comparative morphometrical study on development of palatal shelves in cleft and non-cleft palate mice].

OBJECTIVE: To quantitatively compare the relationship between the congenital cleft palate and development of the palatal shelf. METHODS: Fifty two pairs palatal shelves were macroscopic measured, and 60 series coronal sections were microscopically measured, which were precisely orientated in the coronal plane and serially sectioned at 7 micro m thickness. With the aid of computer imaging analysis system the widths and areas of the palatal shelves in vertical and coronal direction, the maximal areas of the palatal bone and palatal process and alveolar process were measured and compared quantitatively between the cleft group and non-cleft group. RESULTS: The widths and areas of palatal shelves in cleft foetuses showed significant reduction macroscopically and microscopically as well as the maximal areas of the palatal bone, in addition, both of two processes of the maxilla showed significant developmental deficiency. CONCLUSIONS: The palatal shelves show significant developmental hypoplasia in three dimension directions, which have significant correlation between palatal cleft and trisomic condition.

Animals↗
PubMedDate not supplied

Mouse palatal width growth rates as an "at risk" factor in the development of cleft palate induced by hypervitaminosis A.

Epidemiological studies revealed population differences in the frequency of cleft lip and palate, with wide faced, rapid growing populations having the highest incidence: Mongoloids > Caucasoids > Blacks. Laboratory studies have also demonstrated higher incidence of vitamin A-induced cleft palate in both rats and mice with rapid somatic growth rates compared to those with slower rates. The present study was designed to test the hypothesis that palatal width growth rates are significantly correlated with frequencies of cleft palate induced by hypervitaminosis A in seven strains of mice. Palatal width growth rates were calculated using 158 fetuses from 26 timed pregnant mice. Anterior and posterior palatal width growth rates during secondary palatogenesis were calculated between day 15 (n = 88) and day 18 (n = 70) gestational age. Anterior palatal width rates ranged from 0.106 mm/day (BALB/cByJ) to 0.219 mm/day (C57BL/6J), and rates for the posterior measure ranged from 0.111 mm/day (BALB/cByJ) to 0.179 mm/day (CBA/J). Vitamin A (10,000 IU/kg) was administered to an additional 26 timed pregnant mice on day 10 of gestation. The frequency of clefting, calculated from 181 fetuses at day 18 of gestation, was found to range from 52.4% +/- 9.7 (C3H/HeJ) to 96.3 +/- 6.4 (CBA/J). No significant correlation (P > 0.05) was found between palatal width growth rates and the frequencies of vitamin A induced cleft palate. It is concluded that if the rate of growth in the width of the palate is causative in clefting, it must be a pre-clefting (i.e., pre-shelf elevation) event and may only be detectable earlier than day 15 of gestation in the mouse.

Animals↗
PubMed2002

Dental arches and occlusion in bilateral cleft lip and palate patients after two different routines for palatal surgery.

BACKGROUND: Delayed hard palate repair (DHPR) is believed by many researchers to improve maxillary growth and facial appearance in patients born with cleft lip and palate. However, only few studies dealing with the midfacial growth outcome after this type of surgery in bilateral cleft patients have been published. PATIENTS AND METHOD: The purpose of this retrospective study was to compare long-term results of maxillary morphology, dental arches and occlusion in two groups of patients with bilateral cleft lip and palate. The palatal surgery differed between the two groups, particularly with respect to the timing of hard palate repair. The DHPR group (n = 16) underwent soft palate closure at 12 months and hard palate repair at around 8 years, whereas the early palatal repair group (EPR) (n = 12) had completed two-stage palatal closure during the first year of life. These latter subjects had undergone more traditional palatal surgery with vomer flaps for repair of the anterior part and push-back closure for the posterior part of the cleft. Surgery was performed in both groups by the same surgical team at Sahlgrenska University Hospital, Göteborg, Sweden. Dental casts were used to analyze the pre- and postoperative maxillary morphology, dental arch dimensions, and occlusion of both samples, which were followed longitudinally from infancy to early adulthood. RESULTS: Differences recorded in both maxillary growth and occlusion were generally in favor of the DHPR group. However, major intragroup variations and relatively small sample sizes precluded statistical verification of the differences, except for development during the early stages.

Adolescent↗
PubMed1998

Classification, recording, and cleft palate surgery at the Uppsala Cleft Palate Centre.

This paper describes the classification system, method of recording, and surgical techniques used in Uppsala for children with isolated cleft palate. The classification is based on the system described by Kernahan and Stark and the more detailed system described by the American Cleft Palate Association. Separation of the hard palate into thirds, and into right and left sides, assures a detailed description of the cleft, and separates small morphological differences. The longitudinal registration system was introduced into the Uppsala Cleft Palate Centre in 1967. After the initial recording at the time of primary surgery, it is repeated at 5, 8, 11, 14, 17, and 20 years. By emphasising the therapeutic aspects of various stages of growth, it has been possible to limit the recording to once every third year. This has resulted in an important reduction in the dose of radiation without compromising the reliability of the results. Children born before 1975 had clefts of both the soft and hard palate closed at 18-24 months in a one-stage procedure. For children born in 1975 and later a two stage technique has been used, while clefts limited to the soft palate only have been closed entirely in the first operation. At first, the soft palate cleft was closed at 18 months of age and the hard palate at 4 to 5 years. The timing was changed in several steps to the present soft palate closure at 6 months and hard palate closure at 2 years of age.

Adolescent↗
PubMed2005

Palatal development of preterm and low birthweight infants compared to term infants - What do we know? Part 2: The palate of the preterm/low birthweight infant.

BACKGROUND: Well-designed clinical studies on the palatal development in preterm and low birthweight infants are desirable because the literature is characterized by contradictory results. It could be shown that knowledge about 'normal' palatal development is still weak as well (Part 1). The objective of this review is therefore to contribute a fundamental analysis of methodologies, confounding factors, and outcomes of studies on palatal development in preterm and low birthweight infants. METHODS: An electronic literature search as well as hand searches were performed based on Cochrane search strategies including sources of more than a century in English, German, and French. Original data were recalculated from studies which primarily dealt with both preterm and term infants. The extracted data, especially those from non-English paper sources, were provided unfiltered for comparison. RESULTS: Seventy-eight out of 155 included articles were analyzed for palatal morphology of preterm infants. Intubation, feeding tubes, feeding mode, tube characteristics, restriction of oral functions, kind of diet, cranial form and birthweight were seen as causes contributing to altered palatal morphology. Changes associated with intubation concern length, depth, width, asymmetry, crossbite, and contour of the palate. The phenomenon 'grooving' has also been described as a complication associated with oral intubation. However, this phenomenon suffers from lack of a clear-cut definition. Head flattening, pressure from the oral tube, pathologic or impaired tongue function, and broadening of the alveolar ridges adjacent to the tube have been raised as causes of 'grooving'. Metrically, the palates of intubated preterm infants remain narrower, which has been examined up to the age of the late mixed dentition. CONCLUSION: There is no evidence that would justify the exclusion of any of the raised causes contributing to palatal alteration. Thus, early orthodontic and logopedic control of formerly orally intubated preterm infants is recommended, as opposed to non-intubated infants. From the orthodontic point of view, nasal intubation should be favored. The role that palatal protection plates and pressure-dispersing pads for the head have in palatal development remains unclear.

Humans↗