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Palatal dimensions and some inherited factors (body height and metacarpal index).

The relationship between the palatal dimensions and inherited factors such as body height and arachnodactyly, i.e., spider fingers, were studied in a sample of 87 patients with high and narrow palatal vaults, chosen from 1008 randomly selected patients at an orthodontic clinic. The patients with high palates were significantly taller than Swedes of the same sex and age (p < 0.001). Established arachnodactyly was not found in the examined sample. Sucking habits neither seem to influence crowding nor the palatal dimension at the molar region. Mouthbreathing strengthened but was not a pre-requisite for the significant correlation between palatal height and body height. The predominant orthodontic diagnoses included crowding, extreme maxillary overjet and postnormal occlusion as can be expected in a sample of orthodontic patients. The study will serve as a reference material for further investigations of patients with the Marfan syndrome where high palate, high stature and arachnodactyly are important features.

Adolescent↗

[Association of the genetic variation of (MSX1-7) and non syndromic cleft lip palate in Chilean subjects].

BACKGROUND: Homeotic genes have regulatory functions during development. It has been postulated that the human Msx-1 homeotic gene can be involved in the etiology of non syndromic cleft lip palate, since its homologous Msx-1 is involved in cleft palate of mice. AIM: To perform an association analysis between the genetic variation of Msx-1 and non syndromic cleft lip palate in Chilean subjects. PATIENTS AND METHODS: Seventy patients with non syndromic cleft lip palate, 136 healthy relatives of these patients and 69 non related normal individuals were studied. CA microsatellite in Msx-gene, that was amplified with PCR, was studied. RESULTS: No differences in the genetic frequencies of Msx-1 alleles, were observed in the three groups studied. Allelic heterogeneity for allele 2 seems to be related to cases of non syndromic cleft lip palate from multiplex families and heterogeneity for allele 3 is related with simplex families cases. CONCLUSIONS: These results seem to support the hypothesis of genetic heterogeneity in the etiology of non syndromic cleft lip palate.

Alleles↗

A randomised prospective clinical trial into the effect of infant orthopaedics on maxillary arch dimensions in unilateral cleft lip and palate (Dutchcleft).

Aim of the study was to evaluate the effect of infant orthopaedics (IO) on maxillary dimensions in infants with unilateral cleft lip and palate (UCLP). The study design was a prospective two-arm randomised controlled trial in parallel with three participating academic Cleft Palate Centres. Treatment was assigned by means of a computerised balanced allocation method. One group (IO+) wore passive maxillary plates during the first year of life, the other group (IO-) did not. Maxillary casts, made at birth, and at 15, 24, 48, 78 wk were digitised three-dimensionally. Before lip closure alveolar, midpalatal and posterior cleft width reduced significantly more in IO(+) than in IO(-). After lip closure, the alveolar cleft width reduced significantly more in IO(-). Until soft palate closure the slope of the palatal vault flattened significantly by IO. It is concluded that IO only has a temporary effect on maxillary arch dimensions that does not last beyond surgical soft palate closure. Therefore, infant orthopaedics as a tool to improve maxillary arch form could be abandoned. However, other outcome variables like facial and dental appearance, speech outcome, and cost-effectiveness need to be investigated further in order to assess the comprehensive effect of infant orthopaedics.

Alveolar Process↗

Data-objective diagnosis of infant cleft lip, alveolus, and palate. Morphologic data guiding understanding and treatment concepts.

Maxillary plaster models of untreated infants with various cleft lip and palate forms have been studied under the Reflex Microscope. From the three- dimensional data processed by a PC, the specific dimensions of various cleft forms can be determined. Unexpected findings are that skeletal maxillary changes are present in infant velar clefts. The mid-sagittal maxillary length in particular becomes shorter with more severe clefting of the bony palate. From the morphologic point of view, Robin's sequence does not represent a specific entity, but usually a severe cleft of the hard palate. Unilateral clefts of lip, alveolus, and palate with a partial cleft lip reveal worse malformations than complete unilateral clefts. The morphologic changes recorded can be explained by a varying degree of lingual malposition. This reveals that displacements and malformations of infant cleft lip and palate are in fact secondary in nature. In correcting these secondary surface manifestations as soon as indicated by physiologic criteria one could hope for early normalization of sensation, perception, and function. Three-dimensional high-precision measurements are crucial for data-objective diagnoses, timing of therapy, choice of treatment, and in later evaluation of the results.

Alveolar Process↗

Evidence for cleft palate as a postfusion phenomenon.

Some clefts of the lip and palate appear to result from the rupture after fusion has occurred. This possibility is suggested by (1) epithelial remnants found in the palatal shelves, (2) regenerating epithelium found in the palatal clefts of human fetuses older than 13 weeks, (3) immature epithelium visible on the margin of the cleft, (4) nasopalatine ducts cut off by clefts, (5) perforation type cleft found in the hard palate, (6) a Simonart band visible in six cleft mouse fetuses, (7) duplicated upper lateral incisors enclosing a lip-jaw cleft, and (8) rodent cavities in the lip or palate related to cleft formation.

Animals↗

Labial-lingual double articulations in speakers with cleft palate.

OBJECTIVE: Labial-lingual double articulations (LLDAs) are speech errors involving simultaneous valving at the lips and in the linguapalatal region. This study investigates the frequency of LLDAs occurring for /p/, /b/, and /m/ targets and describes the linguapalatal contact patterns involved in these abnormal articulations. DESIGN: A retrospective study involving analysis of articulatory data from all speakers with cleft palate recorded at a research center over a 10-year period. PARTICIPANTS: Twenty-seven speakers aged 5 to 62 years (median 11 years) with compensatory speech errors associated with repaired cleft palate. MEASURES: The lingual component of LLDAs was identified using electropalatography (EPG). EPG data were recorded simultaneously with acoustic data. Fifteen bilabial targets (/p/, /b/, /m/) per participant were analyzed. LLDAs were identified in cases where complete linguapalatal constriction (as observed from EPG data) occurred throughout the closure phase of bilabial targets. The labial component of LLDAs was identified from clinical observations of the speakers made during productions of bilabial targets. RESULTS: Three speakers (11%) frequently produced LLDAs for bilabial targets. The configuration of tongue-palate contacts involved in the lingual component of the LLDAs differed in each of the three speakers: one speaker had velar constriction, another had alveolar constriction, and the third had simultaneous alveolar-velar constriction. LLDAs did not similarly affect bilabial targets in the three speakers. One speaker produced LLDAs for /p/ and /b/ targets only. Another produced LLDAs for all /m/ targets but inconsistently for /p/ and /b/ targets. The third speaker produced LLDAs for all /b/ targets but inconsistently for /p/ and /m/ targets. CONCLUSION: LLDAs occurred in a minority of speakers investigated. Nevertheless, it is argued that it is important to identify LLDAs for clinical decision making and for research purposes. The results from this study add to current knowledge about abnormal articulations in cleft palate speech, but further research is needed into the precise timing of lip and tongue-palate closures and into the airflow and acoustic characteristics of LLDAs.

Adolescent↗

[The facial artery-buccinator musculo-mucosal flap for reconstruction of the palate].

Since may 1999, 5 facial artery musculo-mucosal (FAMM) flaps have been used for mucosal reconstruction of the top of the mouth. The FAMM flap, first described by Pribaz in 1993 is a modification of the naso-labial cutaneous flap. The flap can be inferiorly based on the facial vessels (orthograde flow) or superiorly based (retrograde flow). It can easily reconstruct palate, alveolus and soft palate defects. The are of rotation has its pivot point inferiorly at the retromolar trigone, superiorly at the gingival labial sulcus. The FAMM flap has been used for 2 palatal fistula after facial blast injuries and 1 secondary cleft palate surgery. For the cleft palate surgery an Lefort 1 osteotomy with iliac crest graft was associated. All the flap but one survive with primary healing. One partial necrosis was noted but spontaneously healed secondarily. The FAMM flap is a reliable flap for mucosal reconstructions of the top of the mouth. The flap dissection is easy and the donor site morbidity is low.

Adolescent↗

Two-stage closure of cleft palate (progress report).

In order to achieve palatal closure with the least possible impediment to maxillary growth, the two-stage repair seems to be the best procedure in our hands. The technique and timing of closure of soft and hard palate are described. For soft palate closure a modification of Widmaier's (1959) technique is used. Of the 216 cases operated upon this manner, usually at the age of 18 months (total and partial clefts included), the great majority show a soft palate of sufficient length and good elevation, a definite improvement in comparison with the one-stage procedure used formerly. Hard palate closure is postponed until between 5 and 8 years, the timing of surgery is chosen individually on the assessments of speech and dento-maxillary development.

Age Factors↗

Velopharyngeal inadequacy in the absence of overt cleft palate.

Velopharyngeal inadequacy in the absence of overt cleft palate may be due to any one, of any combination, of the following: intraorally visible stigmata associated with submucous defects (any combination of bifid uvula, muscular diastasis of the soft palate, bony defect of the hard palate); "occult" anatomical defects of the levator palatini or musculus uvulae, detectable only by nasopharyngoscopy or by operative dissection; anatomic disproportion between the size of the nasopharynx and the length of the hard and/or soft palate; mechanical interference with motion of the velopharyngeal system occurring as a result of scarring or contracture, and possibly as a result of interposition of the upper poles of the faucial tonsils between the velum and the posterior pharyngeal wall; a wide variety of neuromotor deficits, either congenital or acquired, causing reduced and/or incoordinated movement of the velopharyngeal musculature; a learning error of unknown origin which results in velopharyngeal inadequacy only on specific phonemes with all other pressure consonants emitted orally. Submucous defects of the secondary palate do not necessarily produce velopharyngeal inadequacy. Thus, our estimates of both the incidence of submucous defects and of the frequency of genes for clefting in any given population are undoubtedly low. Finally, "stress velopharyngeal inadequacy" in wind instrument players has been linked to a variety of anatomic findings and is not necessarily accompanied by velopharyngeal inadequacy in speech. This paper will review the historic aspects of velopharyngeal inadequacy and will discuss and analyze the causes outlined above.

Adenoids↗

Independent effects of palatability and within-meal pauses on intake and appetite ratings in human volunteers.

The effects of the introduction of timed pauses within meals and palatability on food intake and changes in rated appetite during a meal were assessed in three experiments in which volunteers ate a lunch of pasta with a tomato sauce. Eating was monitored using a disguised electronic balance attached to a micro-computer, which also allowed the introduction of timed pauses within meals. In the first experiment, 16 subjects were tested with both a bland and palatable food (with 0.27% oregano), with eating uninterrupted or with pauses after every 50 g consumed during which appetite ratings were completed. Both the addition of oregano and the introduction of regular within-meal pauses enhanced overall intake. Rated hunger increased in the early stages of eating the palatable food in the interrupted condition, and then declined, whereas hunger declined throughout with the bland food. Similarly, the linear function relating intake to time in the uninterrupted condition was greater with the palatable food. In the second experiment, nine subjects ate the palatable food with no pauses within meals, with 30-second pauses with appetite ratings or with 30-second pauses in a non-appetite task. Intake was greater in both pause conditions than when eating was uninterrupted. In Experiment 3, the effect of pause duration was investigated in a further 16 subjects, with either no pause or a pause of 5, 30 or 60 seconds. Subjects ate more in all pause conditions than with no pauses, while ratings of hunger and fullness suggested that subjects were less satisfied at the end of the meal with longer pauses. These data confirm previous work which suggests that palatability exerts its effect by stimulating appetite and eating rate, but also suggest that the introduction of pauses within meals enhances intake as well, contradicting the idea that pausing within meals should reduce intake by allowing more time for post-ingestive satiety to develop.

Adolescent↗

Dissociation of palatability and calorie effects in learned flavor preferences.

Rats acquire a preference for a flavor paired with a caloric solution over a flavor paired with a solution providing fewer or no calories. Because the palatability and the caloric value of the solutions typically covary, it is unclear which property of the high-calorie solution reinforces the flavor preference. Two studies were conducted to assess the independent effects of palatability and calories in flavor preference conditioning. In Experiment 1, rats consumed two distinctively flavored solutions having equal palatability but different caloric value. The flavor paired with ingestion of more calories was subsequently preferred, indicating that a caloric advantage is sufficient to establish a flavor preference (flavor-calorie conditioning). In Experiment 2, rats consumed two distinctively flavored solutions having equal calories but different palatability. The flavor paired with the more palatable solution was subsequently preferred, indicating that a palatability advantage is sufficient to establish a flavor preference (flavor-flavor conditioning). This finding demonstrates flavor-flavor conditioning in the context of postingestive stimulation by calories. Taken together, these results demonstrate both flavor-calorie and flavor-flavor conditioning in the context of normal ingestion (i.e., self-paced oral intake of nutritive solutions).

Animals↗

Benzodiazepines, appetite, and taste palatability.

Benzodiazepine agonists stimulate feeding in animals. This paper reviews evidence which indicates that benzodiazepine-induced feeding is due to a specific enhancement of the perceived palatability of food and fluids, and is not a mere secondary consequence of anxiety reduction. In studies of the effect of benzodiazepines on affective reactions that are naturally elicited from rats by tastes, we have shown that (a) benzodiazepines enhance hedonic taste palatability in a receptor-specific fashion; (b) the relevant receptors and the minimal neural circuitry required to mediate benzodiazepine-induced palatability enhancement both exist complete in the decerebrate brain stem; and (c) even in normal brains, receptors in the brain stem, not forebrain, are the primary substrate for the benzodiazepine-induced enhancement of taste palatability. We conclude that a 'benzodiazepine-GABA' neural system in the brain stem constitutes an important component of the neural hierarchy responsible for taste pleasure. The reason why benzodiazepine tranquilizers have not been reported to enhance palatability for humans may be that the appropriate studies have not yet been done, that human doses are low, and that the brain stem palatability system is less responsive to commonly prescribed agonists that are anxiety/arousal benzodiazepine systems. Finally, in keeping with the purpose of the symposium in which this paper was originally presented, we discuss a number of issues regarding the measurement and interpretation of taste reactivity data.

Animals↗

Influence of social norms and palatability on amount consumed and food choice.

In two parallel studies, we examined the effect of social influence and palatability on amount consumed and on food choice. In Experiment 1, which looked at amount consumed, participants were provided with either palatable or unpalatable food; they were also given information about how much previous participants had eaten (large or small amounts) or were given no information. In the case of palatable food, participants ate more when led to believe that prior participants had eaten a great deal than when led to believe that prior participants had eaten small amounts or when provided with no information. This social-influence effect was not present when participants received unpalatable food. In Experiment 2, which looked at food choice, some participants learned that prior participants had chosen the palatable food, others learned that prior participants had chosen the unpalatable food, while still others received no information about prior participants' choices. The social-influence manipulation had no effect on participants' food choices; nearly all of them chose the palatable food. The results were discussed in the context of Churchfield's (1995) distinction between judgments about matters of fact and judgments about preferences. The results were also used to illustrate the importance of palatability as a determinant of eating behavior.

Adult↗

Chronic withdrawal of a high-palatable obesity-inducing diet completely reverses metabolic and vascular abnormalities associated with dietary-obesity in the rat.

Chronic consumption of a high-palatable diet induces obesity and markedly impairs arterial relaxation. We have recently reported that endothelial function is only partially resorted after acute withdrawal of palatable diet. Therefore, this study was designed to investigate the effects of chronic withdrawal of high-palatable obesity-inducing diet on metabolic and vascular function in rats. Wistar rats were fed either standard laboratory chow throughout (controls) or given a highly-palatable diet (diet-fed) for 15 weeks; or fed the diet for 8 weeks and then returned to chow (diet-to-chow) for further 7 weeks before sacrifice. Diet-fed rats had higher body weight, fat mass, liver and heart weight than both chow-fed and diet-to-chow groups (P<0.01 for all). Compared with chow-fed and diet-to-chow groups, diet-fed rats had significantly raised fasting plasma levels of insulin, leptin and triglycerides levels (each +180%; P<0.0001), but not glucose or non-esterified fatty acids. There were no significant differences between any metabolic parameters between chow-fed and diet-to-chow groups. Mesenteric arteries showed no significant differences between any groups in KCl-induced tension generation, while diet-fed groups had significantly higher noradrenaline-induced vasoconstriction than both chow-fed and diet-to-chow groups. Maximum endothelial-dependent vasorelaxation responses to carbamylcholine (CCh) were significantly (by 23%; P<0.001) attenuated in the diet-fed group. This defect was abolished in the diet-to-chow group. There were no significant differences in endothelium-independent vasorelaxation responses to sodium nitroprusside between the three groups. In conclusion, palatable diet induces obesity and metabolic abnormalities as well as a marked endothelial dysfunction. These abnormalities are completely reversed by chronic withdrawal of the obesity-inducing high-palatable diet.

Animals↗

Allopregnanolone produces hyperphagia by reducing neophobia without altering food palatability.

The neurosteroid allopregnanolone may increase feeding by altering food palatability; however, it may also increase feeding by reducing anxiety (neophobia). Moreover, it is unclear whether this induced hyperphagia is selective to safe, palatable foods only. Male rats were injected with allopregnanolone 20 min prior to behavioral testing. The taste reactivity test was used to examine possible shifts in the palatability of a 0.3 M sucrose solution. A lickometer was used to monitor intake and licking of either a sucrose or sucrose-quinine solution. Sucrose palatability was not enhanced; however, allopregnanolone significantly increased sucrose intake and licking on Test Day 1 when the solution was novel, but not on Test Day 2 when the solution was familiar. Sucrose-quinine intake was not enhanced. Allopregnanolone-induced hyperphagia is not a result of altered sucrose palatability, but rather reflects a reduction in the neophobia elicited by a novel solution; an effect that further seems to be selective to safe, palatable foods.

Analysis of Variance↗

Energy density, diet composition and palatability: influences on overall food energy intake in humans.

This paper considers the role of energy density (ED), diet composition and palatability in the control of energy intake (EI) in humans through several related considerations: (i) the relationship between ED and diet composition, (ii) the relationship between ED, diet composition and EI, (iii) the relationship between palatability and EI, (iv) the relationship between ED, palatability and EI, (v) the importance of postingestive factors in influencing palatability in the longer term, (vi) the contribution of sensory and nutritional factors to dietary hyperphagia and (vii) the implications these considerations have for people living their normal lives in their natural environment. The main factors influencing ED are the fat and water content of foods. Energy density does elevate EI, especially in short-term studies where it can account for >40% of the variance in EI. In real life, ED accounts for only approximately 7% of the variance in EI. This is because the determinants of EI are multifactorial and also because the short-term effects of ED on EI do not translate into the longer term. We argue that part of the longer term amelioration of short-term effects of ED on EI is due to learned compensation, based on the postingestive consequences of consuming familiar food that differ in ED. More energy-dense foods tend to be more palatable but we learn to consume them in smaller portion sizes. In the longer term, the perceived palatability of a food is strongly influenced by the postingestive consequences of eating it. This effect can override sensory factors alone. This implies that nutrient mimetics, if used continuously, would not be as efficacious as initially supposed and that their ad hoc use may undermine the stability of learned appetites and satieties for foods with different EDs and contribute to the poor weight control capability exhibited by consumers at large.

Diet↗

Overeating of palatable food is associated with blunted leptin and ghrelin responses.

Palatable food is rich in fat and/or sucrose. In this study we examined the long-term effects of such diets on food intake, body weight, adiposity and circulating levels of the satiety peptide leptin and the hunger peptide ghrelin. The experiments involved rats and mice and lasted 5 weeks. In rats, we examined the effect of diets rich in fat and/or sucrose and in mice the effect of a high fat diet with or without sucrose in the drinking water. Animals fed with the palatable diets had a larger intake of calories, gained more weight and became more adipose than animals fed standard rat chow. Fasted animals are known to have low serum leptin and high serum ghrelin and to display elevated serum leptin and lowered serum ghrelin postprandially. With time, a sucrose-rich diet was found to raise the fasting level of leptin and to lower the fasting level of ghrelin in rats. A fat-rich diet suppressed serum ghrelin without affecting serum leptin; high sucrose and high fat in combination greatly reduced serum ghrelin and raised serum leptin in the fasted state. The mRNA expression of leptin in the rat stomach was up-regulated by sucrose-rich (but not by fat-rich) diets, whereas the expression of ghrelin seemed not to be affected by the palatable diets. Mice responded to sucrose in the drinking water with elevated serum leptin (fasted state) and to all palatable diets with low serum ghrelin. The expression of both leptin and ghrelin mRNA in the stomach was suppressed in fasted mice that had received a high fat diet for 5 weeks. We conclude that the expression of leptin mRNA in stomach and the concentration of leptin in serum were elevated in response to sucrose-rich rather than fat-rich diets, linking leptin with sucrose metabolism. In contrast, the expression of ghrelin and the serum ghrelin concentration were suppressed by all palatable diets, sucrose and fat alike. In view of the increased body weight and adiposity neither elevated leptin nor suppressed ghrelin were able to control/restrain the overeating that is associated with palatable diets.

Adipose Tissue↗

Meal palatability, substrate oxidation and blood glucose in young and older men.

We investigated the effects of food palatability on the thermic effect of feeding (TEF), substrate oxidation and circulating glucose and insulin. Healthy young men (23.4+/-1.0, SD, years, n=10) and older men (69.4+/-1.3, years, n=9) were resident in a metabolic unit for two 2-day study periods. On the second day of each period, they consumed in random order either a palatable test meal containing 2.93 MJ or a nonpalatable control meal containing the same foods in identical amounts but blended and freeze-dried into biscuit form. TEF and respiratory quotient (RQ) were measured over 6 h and blood samples were taken for measurement of glucose and insulin. Age group had no effect on TEF, RQ or circulating glucose other than to delay the time of peak TEF (P<0.002 for both meals). There was no significant effect of meal type on TEF, but RQ and circulating glucose were higher following consumption of the palatable meal (P<0.001 for both parameters). These results suggest that over 6 h postprandial, consumption of palatable foods does not increase TEF, but is instead associated with increased glycemic response and increased carbohydrate oxidation. These changes, combined with previous work on the glycemic index, predict an accelerated return of hunger and increased energy intake at subsequent meals following consumption of palatable vs. control foods. Further studies are needed to examine the possible mechanism for this previously suggested "second meal" effect of diet palatability on energy intake.

Adult↗