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Biomedical subjects

A M Burrows

Publications and source records attributed to A M Burrows.

32 records · Page 2Linked to original sources
PubMed1997

Sutural bone frequency in synostotic rabbit crania.

This study tests the hypothesis that crania with synostosed sutures will have a significantly higher incidence of calvarial sutural bones than normal crania. Sutural bones were counted in seven calvarial sutures and compared among four groups of adult New Zealand white rabbit skulls: normal in-colony (NI) controls (N = 14), normal out-colony (NO) controls (N = 12), skulls with familial delayed onset (DO) coronal synostosis (N = 25), and skulls with experimentally immobilized coronal sutures (EI) (N = 20). Comparisons among groups were made with a Kruskal-Wallis one-way ANOVA and between groups with a Mann-Whitney U-test, using a Bonferroni correction for multiple comparisons. Significant differences (P < 0.05) were noted only in the coronal and sagittal sutures, with EI crania having the greatest number of coronal sutural bones; between group differences were undetectable for sagittal sutural bones. A post hoc two-sample binomial test for equal proportions showed that the distribution of coronal sutural bones among individuals across groups was even, while the distribution of sagittal sutural bones was significantly higher in EI crania. These results suggest that altered sutural forces of the calvaria contribute to an increased occurrence of sutural bones. However, the influence of inheritance on increased occurrence of sutural bones cannot be discounted, as reflected in the equivalent number of individuals across groups that possessed coronal sutural bones.

Analysis of Variance↗
PubMed1997

Prenatal growth of the human vomeronasal organ.

BACKGROUND: Vomeronasal organs (VNOs) are paired epithelial structures located adjacent to the nasal septum that form in the late first trimester of human fetal development. Although VNOs have long been known to exist in fetal and adult humans, some studies continue to suggest that these structures may be degenerative or functionless. Little is known of the growth of the VNO. METHODS: The present study examined length and volume changes of the human VNO in 26 "normal" (10 female, 16 male) histologically prepared fetuses from the University of Pittsburgh and the University of Michigan across three trimesters (8-30 weeks postmenstrual age). A computer reconstruction technique was used to quantify lengths and volumes of right and left VNOs, and regression equations were generated to assess growth rates. RESULTS: A linear increase in VNO length and a logarithmic increase in VNO volume with increasing postmenstrual age was found. Volume increase was noted for both the vomeronasal epithelium and the lumen of the VNO. A comparison with most estimates of adult human VNO length suggested that further prenatal or postnatal size increase occurs. The growth curves also suggested a more rapid growth in VNO length and volume for females than for males. CONCLUSIONS: The present study demonstrates that the fetal human VNO commences volumetric increase in the early second trimester but does not achieve maximum size during fetal development. Further investigation is needed to determine whether the human VNO is sexually dimorphic in size.

Female↗
PubMed1997

Ultrasonic prenatal diagnosis of coronal suture synostosis.

The present study was designed to assess the utility and validity of standard prenatal ultrasonography in identifying individuals with coronal suture synostosis by examining sutural abnormalities before the development of secondary craniofacial dysmorphologies. An Accusson 128 XP ultrasound machine was used to scan the coronal sutures of 31 twenty-five-day-old fetuses (term = 31 days) from four timed-pregnant New Zealand White rabbits with simple, nonsyndromic craniosynostosis. Each mother was sedated with general anesthesia, and the gravid uterine horns were exposed via a laparotomy procedure. The fetal calvariae were examined using a no. 7 transducer at 7.0 mHz. Each coronal suture was scanned using ultrasonography by first identifying bregma (the anterior fontanelle) at the intersection of the sagittal, interfrontal, and coronal sutures and then following the coronal sutures laterally. Seventeen of the 31 fetuses were diagnosed with unilateral or bilateral coronal suture fusion. In fetuses with synostosis, the suture was echolucent and patent in the midline but then rapidly tapered off to fused bone as it progressed laterally. This finding is in accordance with the natural history of the synostotic foci and coronal suture fusion progression in these rabbits. In addition, the sagittal and interfrontal sutures in each synostotic rabbit appeared wider along their course compared with normal. This reflects early enhanced compensatory transverse growth resulting from the anteroposterior growth restrictions from coronal suture fusion. No other cranial shape abnormalities were recognizable at this stage of fetal development. The validity of the ultrasound diagnoses was tested by direct ex utero inspection of 9 of the 17 synostotic fetuses. Gross morphological examination showed that 8 of 9 rabbit fetuses (89%) had fused coronal sutures. Statistical analysis revealed no significant difference (chi 2 = 0.22, P > 0.05) between the diagnostic accuracy of standard ultrasonography and direct examination. In conclusion, we have shown that standard ultrasonography of the calvarial sutures, in the absence of other craniofacial malformations, may be a feasible method of diagnosing simple, nonsyndromic craniosynostosis in utero, a condition that is typically missed during routine prenatal ultrasonic screening examinations.

Animals↗
PubMed1997

Age related changes in intracranial volume in rabbits with craniosynostosis.

Neurocapsular growth is highly heritable and determines neurocranial form. Although craniosynostosis alters brain growth direction, resulting in compensatory changes in the neurocranium, it is believed that such compensations occur without reduction in intracranial volume. This hypothesis was tested in a rabbit model with nonsyndromic, familial coronal suture synostosis. Skulls of 56 rabbits (20 normals, 20 with delayed onset synostosis, and 16 with complete synostosis) were scanned using three-dimensional computed tomography at 6 and 18 weeks of age. Intracranial contents were reconstructed, and indirect intracranial volume was calculated. Qualitatively, re-formations of intracranial contents from completely synostosed rabbit skulls exhibited the typical "copper beaten" morphology. Quantitatively, intracranial volume was significantly (p < 0.05) reduced in rabbit skulls with complete synostosis compared with both control rabbit skulls and rabbit skulls with delayed onset synostosis at 6 weeks by 11 percent and 14 percent, respectively). By 18 weeks, intracranial volume in rabbit skulls with synostosis was significantly (p < 0.05) reduced (by 12 percent in complete synostosis and 8 percent in delayed onset synostosis) compared with normal rabbits. Results suggest that in rabbits with uncorrected craniosynostosis, compensatory changes in the neurocranium were not adequate to allow normal expansion of the neurocapsular matrix. Further research is needed to determine whether reduction in intracranial volume was a result of neural tissue deficiency or cerebrospinal fluid (i.e., ventricular or subarachnoid) space compression in this model.

Aging↗
PubMed1997

Formation and enlargement of the paranasal sinuses in normal and cleft lip and palate human fetuses.

OBJECTIVE: Comparisons of paranasal sinus morphology between humans with and without cleft lip and palate (CLP) have yielded conflicting opinions regarding size differences. Although postnatal samples have been investigated, no studies have compared paranasal sinus volumes between cleft and noncleft human fetuses. METHOD: The nasal cavities of 20 'normal' and 9 CLP human fetuses (8-21 weeks' postmenstrual age) were examined to assess prenatal volumetric changes of the maxillary sinuses, anterior and posterior ethmoidal air cells, and sphenoidal sinuses. Lengths and volumes of right and left maxillary and sphenoidal sinuses were calculated from histologically prepared sections using a computer reconstruction technique, and regression equations were generated to assess the enlargement rates. RESULTS: All paranasal sinuses were found among both normal and CLP specimens in the same locations and in similar age ranges. However, greater shape asymmetry was noted for all sinuses in CLP compared to normal specimens. In the normal sample, results indicated significant (p < .05) correlations between right or left maxillary sinus length (R2 = 0.49, 0.54) and volume (R2 = 0.67, 0.68), and increasing postmenstrual age, but no significant (p > .05) correlations were observed for right or left sphenoidal sinus length or volumes and postmenstrual age. Maxillary sinus length changes were best described by second-order polynomial regression equations, and volume changes were best described by logarithmic equations. When individual right or left sinuses of CLP specimens were compared to the mean of the normal sample, one maxillary sinus was significantly (p < .05) larger, and 9 maxillary sinuses were not significantly (p > .05) different. Sphenoidal sinus lengths and volumes of CLP specimens were within the same range compared to these dimensions for the normal sample. CONCLUSION: Results on normal specimens indicate that maxillary sinuses exhibit second-trimester length and volume increases, whereas sphenoidal sinuses are more variable. This study suggests a similar timing of sinus formation in normal and CLP fetuses, but shape asymmetries are frequently detected among CLP specimens. In particular, the sphenoidal sinuses may be altered in shape and size by adjacent, hypertrophic cartilaginous structures in CLP fetuses. These results indicate that the maxillary sinuses of CLP fetuses are not deficient in size compared to noncleft fetuses.

Cartilage↗
PubMed1996

Coronal suture pathology and synostotic progression in rabbits with congenital craniosynostosis.

The purpose of the present study was to describe coronal suture pathology and cross sectional synostotic progression in an inbred strain of rabbits with congenital craniosynostosis. Calvaria from 102 perinatal rabbits (39 unaffected; 63 bilateral or unilateral synostosis) were collected at fetal days 21 (n = 12), 25 (n = 20), 27 (n = 22), 30 (term) (n = 32), and 3 days post-term (n = 16) for gross morphologic and histologic examination. Synostotic foci, the extent of relative bony bridging, and suture morphology were evaluated qualitatively and quantitatively. Of the 204 coronal sutures examined, 91 sutures were synostosed, and 113 were patent. All synostosed sutures showed similar foci by day 25, which originated as bony bridges in the middle of each suture on the ectocortic surface. Bony bridging width increased significantly (p < .001) from day 25 through 3 days post-term, and was best described by a linear regression equation. Osteogenic front areas of synostosed sutures were up to 2.5 times greater than patent sutures in term fetuses. Findings demonstrate that coronal suture synostosis in the congenital rabbit model (1) begins early during suture morphogenesis (before 25 days of gestation); (2) consistently radiates from a single focus corresponding to a normal interdigitating region (i.e., a high-tension environment); (3) varies in onset and rate as evidenced by low R2 value between age and extent of bony bridging; and (4) is the result of early hyperostosis of the osteogenic fronts and sutural agenesis. A number of possible pathogenetic mechanisms are discussed.

Analysis of Variance↗
PubMed1996

Development of plagiocephaly in rabbits with unicoronal synostosis.

Human unicoronal synostosis results in plagiocephaly of the cranial vault due to predictable compensatory growth patterns of the contralateral coronal, sagittal, and ipsilateral squamosal sutures. The present study describes the development of plagiocephaly and tests compensatory growth predictions in a naturally occurring rabbit model of uncorrected unicoronal synostosis. Cranial vault and sutural growth data were collected from serial x-ray films in 70 normal rabbits and 19 rabbits with congenital unicoronal synostosis from 1.5 to 18 weeks of age. One-way analysis of variance results revealed that rabbits with unicoronal synostosis had significant (p < 0.05) growth inhibition at both coronal sutures and the contralateral frontonasal suture and a significantly wider (p < 0.05) cranial vault compared to controls. Paired Student's t-tests between affected and unaffected sides of the vault in rabbits with synostosis revealed significant (p < 0.05) asymmetry, with ipsilateral coronal sutures growing less than contralateral ones. Gross qualitative examination of the adult brains revealed severe asymmetry and anteroposterior reduction on the ipsilateral side. These results demonstrate that this congenital rabbit model effectively simulates human cranial vault growth predictions from unicoronal synostosis and produces a plagiocephalic morphology.

Age Factors↗
PubMed1995

Growth of the cranial vault in rabbits with congenital coronal suture synostosis.

Craniofacial growth data from craniosynostotic children have shown that suture immobilization results in predictable restrictions of cranial vault growth in a direction perpendicular to the affected suture and compensatory growth at sutures perpendicular to the affected one. This study tests these predictions by using rabbits with nonsyndromic congenital coronal suture synostosis. Data were collected from 96 rabbits divided into three groups: 42 unaffected litter mate controls, 33 partially synostosed rabbits, and 21 completely synostosed rabbits. Markers were placed bilaterally on either side of the vault sutures at 1.5 weeks of age. Serial radiographs were taken at 1.5, 6, 12, and 18 weeks of age for assessment of growth at the vault sutures and of various cranial landmarks. Results revealed that completely synostosed animals had significantly (p < .05) shorter cranial vaults, reduced growth at the coronal suture, and increased growth at the sagittal, frontal, and squamosal sutures compared with unaffected rabbits. Results also showed that the calvarial growth observed in this craniosynostotic rabbit model closely reflects predicted compensatory patterns seen in human clinical populations and that this rabbit model is valuable for understanding the pathogeneses and craniofacial growth patterns of humans with premature cranial suture synostosis.

Adaptation, Physiological↗
PubMed1994

Development of a strain of rabbits with congenital simple nonsyndromic coronal suture synostosis. Part I: Breeding demographics, inheritance pattern, and craniofacial anomalies.

The lack of an animal model of congenital coronal suture (CS) synostosis has prompted the widespread use of an experimental rabbit model using adhesive immobilization of the CS. Such postnatal models have helped make significant scientific contributions but may still not fully represent all aspects of the human congenital condition. In the March 1993 issue of The Cleft Palate-Craniofacial Journal we reported a female rabbit born in our laboratory with complete bilateral CS synostosis. This follow-up study presents our attempts to breed this animal and establish a strain of craniosynostotic rabbits. To date, we have accomplished 10 back- and intercrosses with these animals and have produced a total of 71 live offspring; 10 animals exhibited complete nonsyndromic unilateral (plagiocephalic) or bilateral (brachycephalic) CS synostotic deformities at birth, and 19 animals exhibited partial CS synostosis that showed more than 75% growth retardation across the CS (well below the 95% confidence interval for normals). Results revealed that gestational time and litter size averages were consistent with those reported for the strain, although the average litter size decreased with increased inbreeding. By 1.5 weeks of age the completely synostosed animals already exhibited brachycephalic cranial vaults and midfacial hypoplasia compared to unaffected siblings. Initial pedigree analysis suggested an autosomal dominant inheritance pattern with incomplete penetrance and variable expressivity. The development of such a congenital rabbit model may prove useful in helping to understand the etiopathogenesis of this condition in human populations.

Animals↗
PubMed1994

Development of a strain of rabbits with congenital simple nonsyndromic coronal suture synostosis. Part II: Somatic and craniofacial growth patterns.

In the March 1993 issue of The Cleft Palate-Craniofacial Journal we reported a female rabbit born in our laboratory with complete bilateral coronal suture (CS) synostosis. This follow-up study presents our attempts to breed the animal and establish a strain of craniosynostotic rabbits. The second part of this study presents longitudinal somatic and craniofacial growth data in offspring with coronal suture synostosis. Serial growth data from 72 animals were collected for the present study. The sample consisted of 11 animals (10 offspring and the original female) with complete nonsyndromic unilateral (plagiocephalic) or bilateral (brachycephalic) CS synostosis, 19 animals with partial CS synostosis, and 42 unaffected control litter mates. At 10 days of age, all animals had radiopaque amalgam markers placed on either side of the frontonasal, coronal, anterior lambdoidal, and sagittal sutures. Body weights and serial lateral and dorsoventral head radiographs were taken at 1.5 (10 days), 6, 12, and 18 weeks of age. All animals showed similar body weights at 1.5 weeks of age, while completely synostosed animals exhibited a slight (about 12%), but significantly (p < .001) lowered body weight by 18 weeks of age. Results revealed that by 1.5 weeks of age the completely synostosed animals already exhibited brachycephalic cranial vaults, midfacial hypoplasia, and increased flattening of the cranial base compared to unaffected siblings. This pattern continued through 18 weeks of age, with the partially synostosed animals exhibiting intermediate morphologies.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Positional changes of the frontoparietal ossification centers in perinatal craniosynostotic rabbits.

It has been suggested that craniosynostosis is caused by abnormally located ossification centers (i.e., bony tubers) in the developing skull prior to suture formation [Mathijssen et al., 1996, 1997]. The present study was designed to test this hypothesis in a rabbit model of human familial, nonsyndromic coronal suture (CS) synostosis. Calvariae were taken from 99 New Zealand White rabbit perinates (55 normal controls, 15 with delayed-onset CS synostosis, and 29 with bilateral or unilateral CS synostosis), ranging in age from 23 to 34 days postconception (synostosis occurs at approximately 23 days in this model). Frontoparietal, interfrontal, and interparietal ossification center distances were obtained using a Wild microscope with camera lucida attachment and a 2-D computer digitization technique. Linear regression analysis was used to compare age-related changes in the perinatal ossification centers among groups. Results revealed that frontoparietal ossification center regression line slopes had similar start points (24-day intercepts) with significantly (P < 0.05) diverging slopes over time. Normal and delayed-onset ossification center distance increased more rapidly than in synostosed perinates. No significant (P > 0.05) differences were noted in regression line slopes among groups for interparietal or interfrontal ossification center distances. Results demonstrated that, in synostosed perinates, frontoparietal ossification center location was similar to normals around the time of synostosis and became displaced later. These findings suggest that ossification center (i.e., bony tuber) displacement seen in infants with craniosynostosis is probably a secondary and compensatory, postsynostotic change and not a primary causal factor of synostosis in this rabbit model.

Animals↗
PubMedDate not supplied

Craniosynostosis with autosomal dominant transmission in New Zealand white rabbits.

Although great strides have been made recently in determining the etiology of a number of human craniosynostotic syndromes, pathogenic mechanisms for these conditions are still unclear, in part because of the lack of a genetic animal model with primary craniosynostosis. Recently, we developed an inbred colony of rabbits with congenital coronal suture synostosis. The present study describes long term breeding demographics, karyotypes, and pedigree analysis from this colony in an effort to characterize the genotype and mode of inheritance of craniosynostosis for future etiopathogenic studies. Seventy-six consecutive back- and intercrosses resulted in 46 fetal and term litters and produced 135 normal offspring and 163 affected offspring with either partial or complete coronal suture synostosis. Conception rate, litter size, and gestation length were normal, and karyotype analysis revealed no gross chromosomal abnormalities. Pedigree analysis of the segregation rates observed for each rabbit litter suggests that the craniosynostosis seen in this pedigree is inherited in an autosomal dominant fashion with reduced penetrance and variable expression. Results revealed that the mode of inheritance and phenotypic variability noted in this colony closely parallel the human craniosynostotic condition and several possible candidate gene families are discussed. The utility of developing such a congenital animal model is evident and may lead to a better understanding of gene expression, normal suture morphogenesis, and the pathogenesis of craniosynostosis.

Animals↗
PubMedDate not supplied

Postnatal changes in the cranial base in rabbits with congenital coronal suture synostosis.

Cranial base abnormalities are a common correlate of human craniosynostosis, although controversy exists as to whether they are primary malformations or secondary deformities. The current study assesses longitudinal cranial base growth and shape changes in rabbits with congenital coronal suture (CS) synostosis. Data were collected from 96 New Zealand White rabbits: 21 with complete bilateral or unilateral CS synostosis; 33 with partial CS synostosis; and 42 unaffected, "control" litter mates. Serial radiographs were taken at 1.5, 6, 12, and 18 weeks of age. Linear, angular, and shape measurements of the cranial base were compared among the three groups. Results revealed that at 1.5 weeks of age, rabbits with complete synostosis had significantly (P < 0.05) shortened anterior cranial bases, orthocephalic cranial base angeles, and acute, dysmorphic cribriform plate triangular shapes compared to the two other groups. Some significant differences persisted through 18 weeks of age. No significant differences were noted between partially synostosed and normal rabbits at any time period. If partial synostosis represents a continuum of the craniosynostotic phenotype, then the craniosynostosis may be seen as the primary deformity in this model and the cranial base abnormalaties as secondary, deformational changes. However, fetal data are still needed to more clearly delineate the role of the cranial base in this congenital rabbit model. Results reiterate the appropriateness and continued development of these rabbits for modeling cases of familial, human non-syndromic coronal suture synostoses.

Age Factors↗