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B K Hall

Publications and source records attributed to B K Hall.

At least 109 records · Page 6Linked to original sources
PubMed1983

Retention of epithelial basal lamina allows isolated mandibular mesenchyme to form bone.

The initiation of bone formation in the avian mandible requires that neural crest-derived cells undergo an inductive interaction with mandibular epithelium. To examine the role of the epithelial basal lamina in that interaction, mandibles were separated into their epithelial and mesenchymal components following exposure to the chelating agent, EDTA. Transmission and scanning electron microscopy was used to show that the basal lamina was retained as a continuous layer over the mesenchyme. Osteogenesis was initiated when such EDTA-isolated mesenchyme was grafted to the chorioallantoic membranes of host embryos. In contrast, mesenchyme isolated using trypsin and pancreatin failed to form bone. It is concluded that the property of mandibular epithelium which permits osteogenesis resides within the basal lamina.

Animals↗
PubMed1983

The origin of the ectomesenchymal condensations which precede the development of the bony scleral ossicles in the eyes of embryonic chicks.

The origin of neural crest-derived ectomesenchymal condensations located subjacent to scleral papillae and the development of the more deeply situated scleral ossicles were investigated in scleral tissues explanted from the eyes of chick embryos at Hamburger & Hamilton (1952) stages 30-38 (6 1/2-12 days of incubation). Explants were pulse labelled with [3H]thymidine for 4h in vitro. Nuclear counts and % labelling indices were calculated for standardized areas within and between the condensations. At all stages exhibiting condensations, the % labelling indices were higher within the condensations than in tissues between condensations. % labelling declined with maturity, but the decline was greater between than within condensations. Regional differences in intensity of proliferation in the ectomesenchyme centred about the scleral papillae seemed to be the best explanation for the development of these condensations. The condensations disappeared concomitant with the complete degeneration of the adjacent papillae. A new distribution of labelled nuclei 70-100 micrometer deep in the tissue and beneath the original sites of the condensations preceded the appearance of ossicle primordia. The roles of the scleral papillae, the ectomesenchymal condensations and deeper primordia in the development of scleral ossicles are discussed.

Animals↗
PubMed1982

Ultrastructural quantitation of connective tissue changes in phenytoin-induced gingival overgrowth in the ferret.

The gingival overgrowth obtained after maintaining ferrets on PHT appeared to be due entirely to the effect of the drug, for inflammation induced by banding had no influence on the action of PHT in eliciting the overgrowth. The significant change observed was an increase in relative volume of interstitial material (ground substance) in response to PHT. Although there was no appreciable alteration in numbers of cells present in the lesion, PHT had a significant effect on the ultrastructure of fibroblasts. These cells showed a decrease in the relative volume of phagosomes, although organelles concerned with synthesis (the rough endoplasmic reticulum and Golgi zones) were not affected. This suggests that the relative increase in ground substance may reflect decreased breakdown of extracellular material within fibroblasts, while synthetic activity is maintained at a constant level. As a consequence, there is an increase in connective tissue volume--an increase which is manifested as an overgrowth.

Animals↗
PubMed1982

Mandibular morphogenesis and craniofacial malformations.

Four questions have been addressed in this review. What is morphogenesis? I conclude that morphogenesis is simply development or change of shape and distinguish morphogenesis both from differentiation and from growth, although predominant growth along one axis can alter shape. Morphogenesis can be considered at all levels from the molecule to the population. I concentrated on cells, tissues, and organs. How does the mandible develop? A brief overview of the origin, migration, and differentiation of the neural crest and other cells which constitute the mandible has been provided. How is mandibular morphogenesis controlled? Several lines of evidence are presented to show that basic elements of morphogenesis, eg number and shape of skeletal elements in the mandible, are a property possessed by the mesenchymal cells which will form those tissues, before they differentiate into cartilage or bone. Reaggregated mesenchymal cells form site-specific-shaped cartilages. First arch neural crest, transplanted to sites of presumptive second and third arch neural crest, migrates to the second arch region but forms first branchial arch skeletal and muscle elements in that ectopic site. Morphogenesis is an intrinsic property of the neural crest and of the mesenchymal cells which arise from the crest. What is the developmental basis of craniofacial malformations? Evidence is presented to show that defects at any stage of mandibular development can lead to craniofacial malformations. Absence of the neural crest, abnormal migration of neural crest-derived cells, abnormal extracellular environments, defective interactions between or differentiation of mesenchymal cells, altered inductive tissue interactions, and deficiencies in epigenetic interactions between components of the mandible can all lead to craniofacial malformations. The challenge for the clinical and basic craniofacial biologist is to identify the defective cellular process which has produced the malformation and to devise preventative or corrective procedures which restore that process to normality.

Animals↗
PubMed1982

Distribution of osteo- and chondrogenic neural crest-derived cells and of osteogenically inductive epithelia in mandibular arches of embryonic chicks.

Mandibular arches of H.H. stage-22 embryonic chicks were divided into halves (lateral/medial; cephalad/caudal; or proximal/distal) and grafted to the chorioallantoic membranes of host embryos. All six halves formed both cartilage and membrane bone. Epithelial-mesenchymal recombinations performed between half mandibles showed (a), that the cephalad half of the mandible contained more chondrogenic cells than did the caudal half, (b), that the proximocaudal quarter of the mandible contained more osteogenic cells than the remainder of the mandible, and, (c), that the epithelium of the caudal half was more osteogenically inductive than was the cephalad epithelium. Differential distribution of mesenchymal cells and differentially inductively active epithelia are both components of this epithelial-mesenchymal interaction.

Animals↗
PubMed1982

Induction of bone by epithelial cell products.

The bones of the head and face of vertebrate embryos only form after their progenitor cells have undergone an inductive interaction with embryonic epithelia. We have investigated whether epithelial cell products can substitute for epithelia in allowing mandibular ectomesenchyme to form bone. Mandibular epithelia from embryonic chicks were cultured on Millipore filters for 28 days to allow them to deposit an extracellular matrix, shown by electron microscopy to be a basal lamina-like material. Mandibular ectomesenchymal cells formed bone when placed on to these epithelial extracellular products and grafted to chorioallantoic membranes of host embryos. Treatment of epithelial cultures with trypsin or L-azetidine-carboxylic acid removed both the extracellular products and their ability to induce bone formation. Hyaluronidase treatment did neither. We concluded that a proteinaceous component of epithelial basal lamina provides a sufficient inductive stimulus to initiate differentiation of bone within mandibular ectomesenchyme.

Animals↗
PubMed1981

A scanning electron microscopic study of the developing epithelial scleral papillae in the eye of the embryonic chick.

Eyes of early embryonic chicks possess 14 scleral papillae, derived from the conjunctival epithelium and present as transient structures between seven and 11 days of incubation. These papillae induce the formation of the 14 scleral ossicles, which develop in the adjacent, neural crest-derived ectomesenchyme. Each papilla undergoes a predictable series of developmental changes, divided by Murray ('43) into six morphological stages (M stages 1-6). We have confirmed his staging, and provide a scanning electron microscopic (SEM) evaluation of papilla development. The earliest stage that can be visualized with the S.E.M. is M stage 2. We describe the initial modifications of the surface of papilla cells, the presence of large microvilli and the asymmetrical morphogenesis and growth of the papillae. Papillae are shed by a mechanism that involves elongation of the cells at the base of the papilla. Such moribund papillae consist of necrotic cells coated with fibers.

Animals↗
PubMed1981

Intracellular and extracellular control of the differentiation of cartilage and bone.

This paper provides an overview of one aspect of the differentiation of cartilage and bone, namely, the degree of control provided by the extracellular matrix and microenvironment. A brief review of the diagnostic features of cartilage and bone is followed by a discussion of stem cells, emphasizing how to identify them using cytochemical, ultrastructural or experimental procedures. The role of extracellular matrices in the initiation of differentiation is discussed with reference to the initiation of chondrogenesis in the vertebral skeleton of the embryonic chick and of osteogenesis in the mandibular skeletons of embryonic chick and mice. The role of extracellular matrices in the maintenance of the differentiated state is discussed with reference to the ability of chondrocytes to compensate for depletion of their extracellular matrices and to the maintenance of altered differentiated states in achondroplasia. Some emphasis is placed on the notion that skeletal cells can neither be considered nor studied in isolation. The epigenetic approach used in studies of growth and morphogenesis needs to be applied to studies on both the initiation and the maintenance of cytodifferentiation.

Animals↗
PubMed1981

Modulation of chondrocyte activity in vitro in response to ascorbic acid.

The aim of this study was to examine the response of secondary cartilage to ascorbic acid in vitro. Cells which had not attained the prechondroblast stage when cultured, did not chondrify in vitro, even when exposed to high levels (400 microgram/ml) of ascorbic acid. On the other hand, prechondroblasts cultured in the presence of low levels (100 microgram/ml) of ascorbic acid did chondrify. Once cytodifferentiation commenced, chondrogenesis was independent of the presence of ascorbic acid in the medium. Cartilage which differentiated in the presence of continuous high levels ( greater than 200 microgram/ml) of ascorbic acid modulated to a tissue which consisted of hypertropic chondrocytes in a highly collagenous extracellular matrix. At the light-microscopic level, this tissue was classified as chondroid bone. At the ultrastructural level, the collagen was seen to be in the form of cross-banded fibres more typical of bone than cartilage. Prelabelling of cultures with either [3H]-thymidine or [3H]-proline showed that neither dedifferentiation of chondrocytes nor the resumption of mitotic activity was responsible for the alterations in the extracellular matrix. The differentiated chondrocytes can secrete an altered extracellular matrix without undergoing cytological dedifferentiation. The role of ascorbic acid in the attainment and maintenance of the differentiated state is briefly discussed.

Animals↗
PubMed1981

The induction of neural crest-derived cartilage and bone by embryonic epithelia: an analysis of the mode of action of an epithelial-mesenchymal interaction.

The formation of membrane bone from neural crest-derived mesenchyme of the maxillary and mandibular processes of the embryonic chick depends upon prior interactions between the mesenchyme and maxillary or mandibular epithelia. The present study explores the specificity of these interactions using tissue recombinations between heterotypic epithelia and mesenchyme. Mandibular and maxillary mesenchyme responded to maxillary and mandibular epithelia by forming bone. A third osteogenically inductive epithelium, the scleral epithelium with its specialized scleral papillae, also allowed mandibular mesenchyme to form bone, indicating that mesenchyme can form bone in response to osteogenic epithelia other than its own. Epithelia which normally do not induce membrane bone formation in situ (wing and leg bud, back and abdominal epithelia) also allowed mandibular epithelia to ossify as did mandibular epithelia from the 10-day-old foetal mouse. Thus this tissue interaction is neither site nor species specific. Mandibular epithelium allowed bone to form in osteogenic mesenchyme from the maxilla and the sclera of the chick and from the mouse mandible but would not induce bone formation from normally non-osteogenic mesenchyme of the limb buds, chorioallantoic membrane or trunk neural crest. The results obtained with all of the tissue recombinations were consistent with the epithelial-mesenchyme interactions that initiate osteogenesis in both the mandibular and the maxillary processes being permissive interactions. The distinction between permissive and instructive interactions is discussed.

Animals↗
PubMed1981

Specificity in the differentiation and morphogenesis of neural crest-derived scleral ossicles and of epithelial scleral papillae in the eye of the embryonic chick.

Enzymatic digestion followed by recombination of epithelia and ectomesenchyme from embryonic sclera and mandibles has been used to demonstrate that isolated scleral ectomesenchyme is only able to form scleral ossicles if in prior contact with scleral epithelium until H.H. stage 36 (10 days of incubation); that this induction by epithelial scleral papillae is a prolonged one, commencing as early as H.H. stage 30 (6.5-7 days); that scleral ectomesenchyme can respond to mandibular epithelium by forming bony ossicles and that mandibular ectomesenchyme can respond to scleral epithelium by forming bony rods, i.e. these interactions are not site, time or tissue specific. Scleral epithelia did not form scleral papillae when maintained alone in vitro or when recombined with scleral ectomesenchyme and maintained in vitro. Nor did papillae form when mandibular epithelia were cultured with scleral ectomesenchyme. These results, coupled with data from the literature, are used to argue that papillae will only form when scleral epithelia are under the tension generated by normal intraocular pressure of the growing eye.

Animals↗
PubMed1980

The role of epithelial collagen and proteoglycan in the initiation of osteogenesis by avian neural crest cells.

Osteogenesis was inhibited when mandibular processes from 3 1/2-day-old embryos were cultured in BUdR, LACA, alpha, alpha'-Dipyridyl, 4-Methylumbelliferone, and 4-Methylumbelliferyl-beta-D-glucoside or beta-D-xyloside. Mandibular processes were then cultured in the test substances for 3 days, enzymatically separated into their epithelial and ectomesenchymal components, combined with mandibular components from untreated embros, and either organ-cultured or grafted to chorioallantoic membranes of host embryos. Osteogenesis was inhibited when treated epithelium, but not when treated ectomesenchyme, was present in the tissue recombinations. Analysis of the known action of these inhibitors indicates that proliferation, hydroxylation of collagen, and synthesis of proteoglycans by epithelial cells are all necessary components of this osteogenic epithelial-ectomesenchymal interaction.

2,2'-Dipyridyl↗
PubMed1980

Differentiative ability of the tibial periosteum for the embryonic chick.

The claim that the hypertrophic cartilage of a transversely divided 9-day chick tibia is able to induce the differentiation of osteoblasts when placed against the fibrous periosteum of a second, intact, 9-day tibia in vitro, is refuted. Tibia from 7- and 9-day-old chick embryos were transversely sectioned though either the diaphysis or epiphysis and these diaphyseal and epiphyseal grafts were then placed in close association with the fibrous periostea of intact, host tibiae of the same or different ages, at either the diaphyseal or epiphyseal level. All of the sixteen possible combinations of paired tibiae were established in organ culture for 7 days on three types of culture media and two types of atmospheres. In response to the close contact established when diaphyseal grafts were used, the fibrous layer of the periosteum underwent hyperplasia to form fibroblasts at the contact site. Contact of the graft with the periosteum as not sufficient to allow osteoprogenitor cells to accumulate, to differentiate into osteoblasts, or to deposit osteoid. We concluded that the outer, fibrous layer of the periosteum is fibroblastic and not osteblastic.

Animals↗
PubMed1980

Viability and proliferation of epithelia and the initiation of osteogenesis within mandibular ectomesenchyme in the embryonic chick.

Ectomesenchyme, a derivative of the embryonic neural crest, forms the membrane bones of the mandibular skeleton, but will only do so after undergoing an inductive interaction with mandibular epithelium. Previously, non-mandibular epithelia have been shown to act as effective substitutes for the mandibular epithelium in this interaction. The role of epithelial viability was examined by enzymatically separating the mandibular epithelium from its ectomesenchyme, killing the epithelium, recombining the epithelium with vital ectomesenchyme and either organ culturing the recombinant or grafting it to the chorioallantoic membrane of a host embryo. Epithelia killed by distilled water, air drying, 80% ethanol, freeze-thawing or with 2500 rad of gamma irradiation did not elicit osteogenesis from the ectomesenchyme while vital epithelia did. Exposure of epithelia to gamma irradiation at doses between zero and 2000 rad resulted in a progressive reduction in the incidence of osteogenesis in ectomesenchme. However, the incidence of osteogenesis progressively increased after irradiation of the mandibular epithelium with 3000 to 5000 rad, only to decrease again after 10000 rad. [3H]thymidine autoradiography was used to show that this pattern of induction of bone by irradiated epithelia could be correlated with the proliferative activity of the epithelia. A similar pattern of induced osteogenesis and epithelia proliferation was seen after epithelia were treated with colchicine. It was concluded that the ability of the mandibular epithelium to permit osteogenesis within mandibular ectomesenchyme was correlated with some property of epithelial proliferation. Several possibilities are discussed and related to other instances of induction of heterotopic bone by epithelia.

Animals↗
PubMed1980

Tissue interactions and the initiation of osteogenesis and chondrogenesis in the neural crest-derived mandibular skeleton of the embryonic mouse as seen in isolated murine tissues and in recombinations of murine and avian tissues.

Mandibular processes from 9- to 13-day-old embryonic mice formed both bone and cartilage when grafted to the chorioallantoic membranes of most embryonic chicks. Isolated ectomesenchyme, taken from 9-day-old embryos did not form bone or cartilage, while older ectomesenchyme formed both. Recombination of the epithelial and ectomesenchymal components confirmed that the presence of the epithelium was a sufficient stimulus for the initiation of both chondro- and osteogenesis. Recombinations between components of mouse and chick mandibular processes showed that 9-day-old mouse ectomesenchyme could respond to chick epithelium but that, although older murine epithelia could initiate osteogenesis from the avian ectomesenchyme, epithelia from 9-day-old embryos could not. These results indicated that an epithelial-ectomesenchymal interaction was responsible for the initiation of both osteo- and chondrogenesis within the mandibular arch of the mouse; that the interaction began at 20 days of gestation; that the ectomesenchyme was capable of responding at 9 days, but that the epithelium did not acquire its ability to act on the ectomesenchyme until 10 days of gestation.

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