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Biomedical subjects

V M Diewert

Publications and source records attributed to V M Diewert.

At least 37 records · Page 2Linked to original sources
PubMed1983

Abnormal head posture associated with induction of cleft palate by methylmercury in C57BL/6J mice.

Maternal treatment with methylmercury (MeHg) has been shown to induce a high frequency of cleft palate and produce growth retardation in rat and mouse fetuses, but the relation between these effects is unknown. The objective of this study was to determine if mandibular growth retardation was a factor that contributed to induction of cleft palate in C57BL/6J mice. Two doses of MeHg (10 mg/kg maternal body weight) were given subcutaneously on days 10 and 11 of gestation, and the fetuses were morphometrically studied on days 14, 15, and 18. Full clefts of the secondary palate were present in approximately half of the treated day 15 and 18 fetuses; therefore, the cleft palate (CP) and noncleft palate (NCP) groups were analyzed separately to facilitate identification of morphologic changes associated with the clefting. The results showed that, compared with controls, the day 14 MeHg-treated fetuses had significantly smaller placental weights, but only half of the fetuses had delayed palatal shelf elevation, reduced body weight, and delayed morphological development. However on day 15, the CP and the NCP groups had similar reductions in body weight and placental weight. A striking downward and forward positioning of the head was present in the MeHg-treated fetuses with the CP group more severely affected than the NCP group. Significant differences between the three groups (control, NCP, and CP) were present with mean head-to-body angles of 67 degrees, 60 degrees and 51 degrees, respectively. The absence of normal head lifting resulted in a relative mandibular retrognathia that when combined with a decrease in mandibular length produced alterations in spatial relations that were most severe in the CP fetuses. The results suggest that after exposure to MeHg, palatal closure is affected by altered tongue posture associated with the abnormal head positioning and shortening of the mandible that develop following placental and embryonic growth retardation.

Animals↗
PubMed1982

Contributions of differential growth of cartilages to changes in craniofacial morphology.

During the late embryonic and early fetal periods of mammalian development, the cartilages of the chondrocranium and Meckel's cartilage form the major skeletal system in the craniofacial complex. Growth of craniofacial structures and changes in their spatial relations were morphometrically analyzed in normal human embryos and fetuses and in normal and abnormal rodent fetuses. The results showed that rodent and human specimens had similar patterns of differential facial growth which appeared to be related to regional growth of cartilages. Facial structures grew primarily in length with limited increases in height and in width. During the late embryonic period, the position of the head lifted rapidly relative to the body and the lower facial region became prominent. The predominantly sagittal direction of growth in Meckel's cartilage contributed to extension of the tongue and mandible beneath the primary palate at the time of secondary palatal closure. Growth of Meckel's cartilage was more rapid than other craniofacial cartilages and its growth appeared to be more sensitive to inhibition than other cartilages. The results of these studies suggest that differential growth of cartilages contributes significantly to changes in facial morphology and craniofacial relations during periods of development prior to extensive bone formation.

Animals↗
PubMed1982

A comparative study of craniofacial growth during secondary palate development in four strains of mice.

Different inbred strains of mice have different timing of palatal shelf elevation, and strains with normally late shelf elevation have been shown to be more susceptible to induction of cleft palate. However, the major factors controlling the timing of elevation remain unknown. The objective of this study was to analyze different strains of mice morphometrically in order to identify characteristics or changes that corresponded with and contributed to shelf elevation. The four strains--A/J, SWV, C3H, and C57BL/6J (C57)--were studied between days 13 and 16 of gestation. Similar patterns of facial development were present in the strains, with C57 fetuses most advanced and A/J fetuses least advanced, relative to chronological age. Lifting of the head away from the thorax was also most retarded in the A/J fetuses. Palatal shelf elevation occurred between 200 and 240 mg body weight, with C57 fetuses smaller than A/J fetuses. The time of shelf elevation corresponded with the time that Meckel's cartilage became longer than the oronasal cavity, and the time that the head position lifted rapidly. Simultaneously with elevation, the height of the oral cavity increased and the width of the oral cavity decreased. The decrease in maxillary width appeared to facilitate shelf contact during palatal closure. The results demonstrated the need for normal growth of Meckel's cartilage for shelf elevation when a normal tongue was present between the palatal shelves. The results also showed that facial growth is one of the important factors that determine the time of palatal shelf elevation in mice.

Animals↗
PubMed1981

Correlation between alterations in Meckel's cartilage and induction of cleft palate with beta-aminoproprionitrile in the rat.

The lathyrogen beta-aminoproprionitrile (BAPN) induces cleft palate in rats when administered at a critical time in secondary palate formation. BAPN is known to inhibit the crosslinking of newly synthesized collagen, but its primary site of action in producing cleft palate is unknown. In this study time-mated Sprague-Dawley rats were given a single oral dose of 600 mg/kg BAPN at five known gestational ages in the 48 hours before palatal shelf elevation, and the fetuses were studied on days 16, 17 and 18. Evaluation of craniofacial relations and palate development in BAPN-treated heads revealed that delayed palatal shelf elevation and resulting cleft palate were related to retrognathia of the mandible. However, shortening of the mandible was due primarily to vertical and lateral bending of Meckel's cartilage. High and retruded tongue positions that were present with the deformities in Meckel's cartilage interfered with palatal shelf movement to the horizontal plane. The group treated with BAPN at 15 days 7 hours, approximately 24 hours before normal palatal shelf elevation, had the most severe defects in Meckel's cartilage, the longest delay in palatal shelf elevation and the highest incidence of cleft palate. Inhibition of crosslinking of collagen in Meckel's cartilage appeared to weaken the cartilage during the critical period in facial development when extention of the tongue and mandible beneath the primary palate is required to facilitate palatal shelf elevation.

Aminopropionitrile↗
PubMed1981

Cortisone-induced cleft palate in A/J mice: failure of palatal shelf contact.

Although cortisone treatment for induction of cleft palate in mice has been shown to delay the time of palatal shelf elevation, the effects of delayed elevation of shelf contact have not been critically evaluated in a cortisone-sensitive mouse strain. The objective of this study was to evaluated palatal development in cortisone-treated A/J mice in order to determine whether the shelves make contact upon elevation. Morphometric analysis of frozen sections revealed that cortisone-treated shelves were smaller than control shelves with apparent reductions in both the content of extracellular matrix and the number of cells. At a light microscopic level, thinning of medial epithelium in cortisone-treated palates appeared similar to that in untreated palates with spontaneous cleft lip and palate. Shelf elevation was delayed by approximately 12 hours and only half of the cortisone-treated palates achieved complete horizontal positioning of the shelves in all regions of the palate. Immediately after elevation, all control palates had extensive vertical contact along the complete length of the palate. In contrast, approximately 20% of the cortisone-treated fetuses had contact between the shelves in the middle palate region only, with the mean area of contact only 20% as large as in control fetuses. As result, the net shelf contact in all the cortisone-treated fetuses was only 4% of the potential contact shown in control fetuses. Therefore, failure of the palatal shelves to elevate and make extensive contact appeared to be the major factor contributing to cortisone-induced cleft palate in A/J mice.

Animals↗
PubMed1980

Differential changes in cartilage cell proliferation and cell density in the rat craniofacial complex during secondary palate development.

During mammalian secondary palate formation sagittal growth of the lower face has been shown to be more rapid than that of the upper face, and the tongue and mandible extend beneath the primary palate. In order to identify factors contributing to this differential growth pattern, cellular and morphologic growth of the major cartilages of the upper and lower facial regions were studied in radioautographic sections labeled with tritiated thymidine. Evaluation of cell-density recordings, labeling indices, and structural dimensions revealed significant differences between Meckel's cartilage in the lower face, and the nasal cartilage and anterior cranial base cartilage in the upper face. After formation of the precartilaginous blastema, labeling indices were high in Meckel's cartilage (20-30%), but very low in the nasal cartilage and the anterior cranial base (0-2%). During secondary palate formation the volume of Meckel's cartilage increased more rapidly than the other cartilages and its growth was primarily in the sagittal direction. Between days 15 and 17, the increase in the length of Meckel's cartilage (165%) was approximately twice as great as the increase in the combined length of the nasal cartilage and the anterior cranial base (77%). During this period induction of cleft palate with some teratogens has been shown to severely retard growth of Meckel's cartilage and produce mandibular retrognathia that contributes to delayed elevation of the palatal shelves. Therefore, extensive cell proliferation in Meckel's cartilage, during a period of limited proliferation in other craniofacial cartilages, appears to contribute to its rapid growth and its differential sensitivity to growth inhibition.

Animals↗
PubMed1980

Cortisone-induced cleft palate in the brachymorphic mouse.

Previous studies have shown that the autosomal recessive gene brachymorphic (bm/bm), which is maintained on a C57BL/6J (C57) background, reduces limb growth and sulfation of cartilage proteoglycans. Hydrocortisone administered on gestational days 11-14 resulted in 20% CP in the C57 mouse, but 95% CP in the bm/bm mouse. The bm/bm mouse had a median effective dose for CP of 45 mg/kg, compared to 325 mg/kg for C57 and 40 mg/kg for A/J. Morphometric analysis indicated that the time of palatal elevation was delayed in the bm/bm relative to the C57 mouse both with and without hydrocortisone treatment. The amount of cytoplasmic glucocorticoid receptor protein present in the bm/bm palate on day 14 was the same as the amount found in the C57 palate, and was not elevated as it is in the A/J palate. The levels of cyclic AMP in the bm/bm palate on day 14 were 30-70% higher than that found in the C57 palate with or without hydrocortisone. These results suggest that both bm/bm and A/J exhibit a delay in palatal shelf rotation and elevated levels of cyclic AMP, which appear to be predisposing factors for cortisone-induced cleft palate. These strains differ in that elevated levels of steroid receptors are present in A/J palate, whereas lower levels are found in the C57 and bm/bm mice.

Animals↗
PubMed1979

Correlation between mandibular retrognathia and induction of cleft palate with 6-aminonicotinamide in the rat.

A single injection of the niacin antimetabolite 6-aminonicotinamide (6-AN) late in gestation produces cleft palate in the rat. In order to achieve an understanding of the mechanism of induction of cleft palate, craniofacial growth and palate development were studied in Sprague-Dawley rats after treatment with 6-AN on day 15 of gestation. The rats were maintained on a high niacin diet (95 ppm) and subjected to three different teratogenic levels of 6-AN. The first group was injected with 8 mg/kg, the second was fasted and injected with 8 mg/kg and the third was treated with 16 mg/kg. The lowest teratogenic dose, 8 mg/kg, produced mild mandibular retrognathia on day 16, delayed shelf elevation a few hours and resulted in small rostral and small caudal clefts of the secondary palate. The moderate dose, 8 mg/kg with fasting, produced more severe mandibular retrognathia, delayed shelf elevation about 24 hours and resulted in 37% full clefts and 63% partial clefts of the palate. The highest teratogenic dose, 16 mg/kg, produced severe mandibular retrognathia, delayed shelf elevation by more than 24 hours and resulted in 100% full clefts of the palate. In each 6-AN group, the most severe mandibular retrognathia was present between days 16 and 17, the critical time for palate closure in the rat. Treatment with 6-AN also produced abnormality of the epithelial cells of the palate, the toothbuds and the nasal septum. Molar and incisor toothbuds were small and malformed, and the epithelial surfaces of the palate and the soft tissue nasal septum did not fuse.

6-Aminonicotinamide↗
PubMed1979

Selective inhibition of mandibular growth and induction of cleft palate by diazo-oxo-norleucine (DON) in the rat.

A high percentage of cleft palates can be induced in rat fetuses by a single injection of the glutamine analog diazo-oxo-norleucine (DON) on day 15 of gestation. The purpose of this study was to evaluate the effects of DON in vivo on craniofacial growth and spatial relations in order to identify factors that may contribute to the palatal defects. Sprague-Dawley rats in the experimental groups were given a single IP injection of 2.0 mg DON (6 mg/kg maternal body weight) on day 15 and were killed on day 16 or 17. Control fetuses were collected on days 15, 16 and 17. Fetal heads were fixed in Bouin's solution, embedded in Paraplast and serially-sectioned. Midsagittal and coronal sections were projected at 30 X and a series of linear and angular measurements were made. DON had limited effect on growth of the cranial base, nasomaxillary complex, and palatine processes, but dramatically reduced the length of Meckel's cartilage. Treatment with DON delayed shelf elevation approximately 24 hours, and tongue position remained high in the oronasal cavity. Growth retardation in Meckel's cartilage therefore may contribute to delayed shelf movement by retarding downward and forward positioning of the tongue-mandibular complex.

Animals↗
PubMed1979

Palatal process movement in the rat as demonstrated in frozen sections.

During mammalian secondary palate development, movement of the lateral palatine processes from the vertical plane to the horizontal plane involves a complex interaction of the palatine processes and the tongue within a dynamic growing oronasal cavity environment. This study of pre-fixation facial profile photographs and frozen sections was undertaken to evaluate external and internal changes in the oronasal complex during secondary palate elevation without the shrinkage known to be present with routinhistological preparation of embryonic tissues. Frozen sections of Sprague-Dawley rat embryos between 15 and 17 days of (conceptual) age were prepared by hexane quenching and cryostat cutting. The results showed that, during the stages of palate development prior to shelf elevation, the tongue and mandible became positioned beneath the primary palate, and the vertical dimension of the oronasal cavity increased by the lifting of the nasomaxillary complex. The tongue and mandible maintained contact with the primary palate, whereas a space developed above the tongue in the middle and posterior palate regions. As the vertical dimension increased the volume of the palatomaxillary processes increased rapidly, the tongue became squeezed, and the palatine processes bulged medially above the level of the tongue. After shelf elevation extensive contact between the palatine processes was present, and the tongue became flattened. The results of this study support the observations of Lazzaro (1940) that rapid increase in shelf volume owing to increased intercellular volume contributes to movement of the processes above the tongue. But, rapid increase in shelf volume occurred contemporaneously with the time when the tongue and mandible outgrew the oronasal cavity and became positioned beneath the primary palate. Therefore, it would appear that the simultaneous occurrence of a lower and more forward tongue position, and an increased palatomaxillary process volume without change in maxillary width, contributed to the medial movement of the processes above the tongue.

Animals↗
PubMed1979

Experimental induction of premature movement of rat palatal shelves in vivo.

In order to enhance further knowledge of palatal shelf movement and the factors involved in palate closure, a method was developed for prematurely elevating palatal shelves in utero. Approximately 7 hours before expected shelf elevation, pregnant Sprague-Dawley rats were laparotomized and two medially directed squeezes were applied to the face of some of the embryos through the intact uterine wall. Palates from control (unsqueezed) and experimental animals were obtained immediately after the procedure and 2, 4, 7, 12 and 24 hours later. In the 0, 2 and 4 hours groups, 82% of experimental palates were elevated, whereas only 6% of control palates were elevated. At 0 hours only the hard palate in the experimental group had elevated, but at 2 and 4 hours almost half this group showed elevation of the soft palate as well, and, in addition, contact had been made between the elevated shelves.

Animals↗
PubMed1976

Graphic reconstructions of craniofacial structures during secondary palate development in rats.

Lateral and ventral graphic reconstructions of coronally sectioned rat fetuses at four stages of secondary palate development were made to illustrate the size, form, and spatial relations of craniofacial structures at each stage, and to indicate changes between stages. The results illustrated extensive changes in the nasomaxillary and tongue-mandibular complexes and spatial relations in the oronasal cavity during this 2-day period. During closure of the palate the palatine processes and molar dental laminae moved medially, the vertical dimension between the cranial base and Meckel's cartilage increased, and the Meckel's cartilage changed in shape from a "U" to a "V". During the 2-day period extensive increases in anteroposterior and vertical dimensions and limited changes in lateral dimensions resulted in a change in shape of the complete orofacial region. More extensive investigations, preferably quantitative, of the changes shown are indicated to identify the relative contribution of various craniofacial components and to establish the role of differential growth in secondary palate closure.

Animals↗
PubMedDate not supplied

A morphometric analysis of craniofacial growth in cleft lip and noncleft mice.

Differences in face shape are considered a factor in cleft lip malformation. The purpose of this study was to analyze craniofacial growth in two strains: A/WySn with 28% cleft lip and C57BL/6J without cleft lip. Standardized photographs of 27 A/WySn and 25 C57BL/6J embryos with 34-46 somites (S) were taken in the superior, frontal, and lateral views. Landmarks were located and digitized for computerized analysis of growth change relative to somite number and at stages of face development before, during, and after primary palate closure. The results showed that both strains had similar overall growth patterns with increases in head width and face width, and decreases in nasal pit width. During early palatal closure in C57BL/6J mice, the nasal pit width was unchanged as brain width increased rapidly; and then later, the nasal pit width decreased as brain width increased slowly. However, during early closure in A/WySn mice, the nasal pit width decreased rapidly as brain width increased slowly; and then later, the nasal pit width was unchanged as brain width increased more rapidly. During early palatal closure, the narrower nasal pit width in A/WySn mice appeared to result from delayed growth of the supporting forebrain as the nasal pits become more medially positioned with normal face development. From the lateral view, the maxillary prominence depth was also smaller in the A/WySn strain during early palatal closure. This deficient forward growth of the maxillary prominences and the narrower positioning of the medial nasal prominences in A/WySn embryos appear to reduce the contact between the prominences and thus predispose this strain to cleft lip malformation.

Animals↗
PubMedDate not supplied

A morphometric analysis of human embryonic craniofacial growth in the median plane during primary palate formation.

As the human primary palate develops between embryonic stages 15 and 18, the facial prominences are part of a rapidly growing craniofacial complex that undergoes extensive morphogenetic change. The purpose of this study was to analyze growth in the medial plane in order to identify regional changes that occur during changes in craniofacial morphology. Photographs of midsagittal sections of 35 human embryos of stages 15 to 19 from the Carnegie Embryology Collection were enlarged, and landmarks were digitized for angular and linear measurements and for finite element modeling (FEM) analysis. The results showed magnitudes and directions of growth required to change average stage 15 morphology to later stages. As the facial and cranial components increased in size, shape change was most pronounced in the posterior cranial and orofacial regions. Increases in cranial linear dimensions were significantly larger than those in the cranial base regions. Between stages 15 and 18, the posterior cranial angle decreased, the forebrain and midbrain rotated superiorly toward the hindbrain, the orofacial angle increased, and the face grew above the thorax. The results suggest that morphogenetic growth changes in the cranial regions are closely associated with facial regions during primary palate formation.

Facial Bones↗