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Biomedical subjects

B K Hall

Publications and source records attributed to B K Hall.

At least 91 records · Page 5Linked to original sources
PubMed1987

Development of the mandibular skeleton in the embryonic chick as evaluated using the DNA-inhibiting agent 5-fluoro-2'-deoxyuridine.

Mandibular development was examined in embryonic chicks following administration of 5-fluoro-2'-deoxyuridine (FUDR, 0.001-1.0 microgram/egg), an inhibitor of both DNA synthesis and of cell division. FUDR was injected in ovo at one of three developmental stages corresponding to 1) the migration of mandible-destined, midbrain-level neural crest cells (Hamburger and Hamilton [H.H.] stage 10); 2) midway through the epithelial-mesenchymal interaction required to initiate mandibular osteogenesis (H.H. stage 22), which is also after the epithelial-neural crest cell interaction required for the initiation of chondrogenesis in Meckel's cartilage; and 3) when prechondroblasts of Meckel's cartilage are beginning to differentiate (H.H. stage 25). Micromelia was induced following the administration of FUDR at either H.H. stages 22 or 25 but not when FUDR was given at H.H. stage 10. Although the micromelic mandibles were shorter than normal, Meckel's cartilage and the mandibular membrane bones both differentiated and grew along the full proximodistal length of the shortened mandibles. In contrast to the situation previously described by Ferguson for alligator embryos exposed to FUDR, the migration of neural crest cells in the embryonic chick was not inhibited by FUDR. In contrast to the situation previously described for rat embryos exposed to FUDR, differentiation of Meckel's cartilage was not inhibited in embryonic chicks exposed to FUDR. Differentiation of the membrane bones was also normal following either in ovo administration of FUDR or when mandibular processes were maintained in FUDR in vitro. Therefore, FUDR does not produce micromelia in the embryonic chick by interfering with the epithelial-mesenchymal/neural crest cell interactions, which are prerequisites or differentiation of cartilage or bone, nor by inhibiting the differentiation of chondrogenic or osteogenic mesenchymal cells after completion of these tissue interactions. Neither did the growth-inhibiting action of FUDR result from an inhibition of growth of Meckel's cartilage during the several days following initial chondrogenic differentiation. Rather, subsequent growth of the entire mandibular process was delayed. This mechanism of action differs from that in the alligator embryo, in which FUDR inhibits mandibular growth by removing mandible-destined, migrating neural crest cells, and in the rat, in which FUDR inhibits the differentiation of Meckel's cartilage but catch-up growth restores growth of the mandible to normal.

Abnormalities, Drug-Induced↗
PubMed1987

Earliest evidence of cartilage and bone development in embryonic life.

Some aspects of the development of cartilage and bone during embryonic life are discussed in this review and an attempt is made to show that studies of development, even when performed on species far removed from humans, are relevant to clinical orthopedic surgery. Initially, some definitions of skeletal tissues and cells are presented to illustrate the nontrivial problem of how to tell whether cells are capable of becoming osteoblasts or chondroblasts and of depositing bone or cartilage. This leads to a discussion of the best criteria to use to identify differentiating osteogenic and chondrogenic cells. Cytodifferentiation is immediately preceded by the appearance of the membranous skeleton, consisting of the mesenchymal condensations in which bone and cartilage will develop. Condensation formation in normal development and defective condensations leading to abnormal skeletogenesis are related to cellular properties of mesenchymal cells. The remainder of the review is on the development of membrane bone in the craniofacial skeleton, subperiosteal bone in embryonic avian long bones, and subperiosteal and endochondral bone in developing mammalian long bones. In each case the emphasis is on the embryologic origins of the skeletogenic cells, cell migration, and the factors and influences involved in the initiation of cell differentiation. The relevance of developing systems to clinical practice is stressed throughout.

Animals↗
PubMed1986

Enhanced penetration of nitrosonornicotine across oral mucosa in the presence of ethanol.

There is evidence for synergy between tobacco and alcohol in the etiology of oral cancer but the reason for such an effect is unclear. One possible explanation is that alcohol enhances the penetration of carcinogens through the oral lining. We measured the permeability in vitro of three regions of porcine oral mucosa to the tobacco associated carcinogen, nitrosonornicotine (NNN) alone and in the presence of 5% or 50% ethanol. 50% ethanol did not significantly alter the permeability of oral mucosa to NNN except for buccal mucosa, where it was reduced. However, there was a significant increase in the permeability of gingiva and floor of mouth mucosa (but not buccal mucosa) in the presence of 5% ethanol; this increase occurred after far shorter exposures for floor of mouth than for gingiva. These results accord well with studies showing that the floor of mouth is a "high risk area" for oral carcinoma and that there is an increased relative risk of oral cancer for heavy smokers and drinkers and, in particular, for those individuals who consume beverages with a low alcohol content.

Animals↗
PubMed1986

The role of movement and tissue interactions in the development and growth of bone and secondary cartilage in the clavicle of the embryonic chick.

There has been debate in the literature concerning whether the clavicle arises by intramembranous ossification, i.e. is a membrane bone, and whether secondary cartilage develops from its periosteal cells. A histological study of carefully staged embryos revealed that pre-clavicular mesenchyme undergoes condensation at H.H. stage 31-32, bone forms by H.H. stage 33 and that a transitory secondary cartilage appears late in H.H. stage 35, only to disappear by H.H. stage 36. Except for the transitory nature of the secondary cartilage, this histogenetic sequence is as seen in craniofacial membrane bones. Enzymic removal of the epithelium overlying clavicular mesenchyme from embryos of H.H. stages 26-34 and chorioallantoic grafting of the isolated mesenchyme, revealed an epithelial requirement for initiation of intramembranous ossification during H.H. stages 26-29, again similar to initiation of craniofacial osteogenesis. Secondary chondrogenesis was initiated neither in embryos paralysed with decamethonium iodide nor when clavicular mesenchyme (H.H. stages 29-33.5) was grafted to the chorioallantoic membranes of paralysed embryos, but did form in a small percentage (16-23%) of clavicles grafted to the membranes of mobile embryos. Failure of chondrogenesis in the former was attributed to a requirement for movement as a proximate chondrogenic stimulus and the low incidence of chondrogenesis in the latter to the stimulus provided by amniotic movements which persist in paralysed embryos. Secondary cartilage did form when clavicles were organ cultured, either submerged, or at the air-medium interface. This stands in contrast to craniofacial membrane bone such as the quadratojugal, which only forms secondary cartilage in vitro when cultured submerged. Growth of the clavicle was shown to increase 53-fold between 10 and 11 days of incubation, an increase which was diminished but not eliminated in paralysed embryos, and which correlated closely with the dramatic increase in embryonic movement which occurs between 10 and 11 days of incubation. Thus, the clavicle of the embryonic chick shares all of the features and epigenetic requirements of the craniofacial the embryonic chick shares all of the features and epigenetic requirements of of the craniofacial membrane bones, but is more dependent upon biomechanical factors for its growth.

Age Factors↗
PubMed1985

Critical periods during development as assessed by thallium-induced inhibition of growth of embryonic chick tibiae in vitro.

In ovo application of thallium sulfate has been shown to produce a characteristic shortening and angulation of the tibia of the embryonic chick. The critical period for susceptibility to thallium-induced inhibition of tibial growth ends at 8 2/3 days of incubation, a time when the growth rate of the embryo declines by 55%. The aim of the present study was to expose tibiae to thallium in vitro to determine whether this response was intrinsic to the tibia. A 4-hour exposure to 400 micrograms thallium was found to be most effective. Growth of tibiae from 8-day-old embryos was inhibited, growth of tibiae from 9-day-old embryos was not, and the response of tibiae isolated from embryos of 8 2/3 days of incubation was intermediate. Therefore, the response of the tibia to thallium represents an intrinsic property and is not secondary to inhibited nerve growth as has been suggested. The critical period and its termination is also an intrinsic property of the tibia. Tibiae were exposed to thallium for 4 hours at various times after the tibiae had been established in vitro. Susceptibility to growth inhibition was shown to decline as tibiae developed beyond the critical period, a decline that could be correlated with a declining growth rate. Emphasis is placed upon critical events during development as a more useful concept than critical periods for explaining susceptibility to teratogens.

Age Factors↗
PubMed1985

In-vitro permeability of porcine oral mucosa after epithelial separation, stripping and hydration.

The permeability of porcine skin, gingiva, floor of mouth and buccal mucosa was measured in perfusion chambers using isotopically-labelled water and horseradish peroxidase. Values obtained for the permeability of the epithelium of each of these regions, after separation from the connective tissue with EDTA, did not differ significantly from those obtained for the intact tissue; however, the connective tissue alone had a permeability 2-8 times greater than that of the whole tissue. Stripping the surface layers of the floor of mouth mucosa increased its permeability to that of connective tissue. These results indicate that the functional permeability barrier of the oral mucosa, like that of skin, is located in the epithelium and occupies the superficial layers. After exposure to an aqueous environment for up to 67 h, the permeability of skin and keratinized oral mucosa showed similar but slight increases whereas that of non-keratinized mucosa showed a more rapid rise. These differences may reflect the different composition of the intercellular permeability barrier in keratinized and non-keratinized oral tissues.

Animals↗
PubMed1985

The permeability of skin and oral mucosa to water and horseradish peroxidase as related to the thickness of the permeability barrier.

The permeability of porcine skin and keratinized and nonkeratinized oral mucosa to tritium-labeled water and horseradish peroxidase (HRPO) was determined using perfusion chambers. Small blocks from each tissue were also incubated with HRPO and the extent of penetration visualized microscopically; this enabled measurements to be made of the thickness of the permeability barrier to this water-soluble tracer. Results obtained after inverting the oral mucosa in the chambers or adding metabolic inhibitors indicated that both compounds diffuse across the tissue. The permeability constants derived directly in the study showed that skin was less permeable than oral mucosa and that the floor of the mouth was significantly more permeable than all other regions. When these constants were normalized in terms of a standard permeability barrier thickness and the different tissues compared, the values obtained for skin were again less than those of the oral regions but, of these, the buccal mucosa was significantly higher. The difference in permeability between epidermis and keratinized oral epithelium may be due to differences in the volume density of membrane-coating granules known to exist between the tissues; differences between the oral mucosal regions may reflect differences in the nature of the intercellular barrier material.

Animals↗
PubMed1985

The permeability of hyperplastic oral epithelium.

An epithelial hyperplasia is one of the reactions of skin and oral mucosa to chemical and mechanical insult. It is usually assumed that this reaction produces a more effective epithelial barrier, but there is no information as to whether a less permeable tissue results. To examine this question, hyperplasia was induced in the cheek pouches of hamsters by either chemical treatment with 0.0025% TPA in acetone or by mechanical abrasion with a rotating mop; untreated hamsters served as controls. The animals were killed and the cheek pouches were removed, mounted in diffusion chambers and the permeability to labelled water and horseradish peroxidase (HRPO) determined. The results showed that higher values were obtained for the permeability constant of hyperplastic epithelia than for that of control tissue, suggesting that an increased epithelial thickness is not necessarily associated with an improved permeability barrier function. The presence of an inferior barrier layer in hyperplastic epithelia may be related to the increased rate of turnover of this tissue.

Animals↗
PubMed1984

The permeability of mammalian nonkeratinized oral epithelia to horseradish peroxidase applied in vivo and in vitro.

Horseradish peroxidase, an intercellular tracer, was injected sub-epithelially beneath keratinized gingiva and a variety of nonkeratinized oral epithelia. Fresh tissue biopsies from the same regions were also incubated with this tracer for 1 h. In separate experiments, horseradish peroxidase was applied topically to biopsies of oral mucosa maintained in tissue culture for periods up to 12 h. All specimens were treated so as to visualize the site of peroxidase penetration and the tissues were examined with the light and electron microscopes. In all the epithelia, a surface barrier was evident from which the tracer had been excluded. This was often narrow in the thin, nonkeratinized epithelia and could only be identified unambiguously with the electron microscope. Membrane-coating granules of the so-called nonkeratinized type were invariably associated with superficial plasma membrane of epithelial cells at the level where the barrier was first seen. The results suggest that a permeability barrier exists to horseradish peroxidase in all nonkeratinized oral epithelia with a similar location to that seen in the keratinized oral tissues. However, results obtained with a water-soluble tracer such as horseradish peroxidase may not apply to many drugs, the ready absorption of which may reflect their high lipid solubility.

Animals↗
PubMed1984

Effects of chlorhexidine on the structure and permeability of hamster cheek pouch mucosa.

This study examined the effects of chlorhexidine (CHD) on the clinical appearance, morphology, and in vitro permeability of hamster cheek pouch mucosa. The cheek pouches were treated daily for 3 weeks with topical applications of saline, 0.2% CHD, or 2.0% CHD. Treatment with 2.0% CHD resulted in the formation of discrete white lesions in every animal in the group, whereas no changes were identified in any animal treated with 0.2% CHD or saline. Upon microscopic examination it was determined that treatment with 2.0% CHD resulted in a statistically significant (P less than 0.01) increase in epithelial thickness, when compared to the other groups, and the lesions were found to consist of hyperplastic areas of epithelium with associated inflammatory cell accumulations. Daily treatments with 2.0% CHD, 0.2% CHD or saline had no effect on the very low permeability of cheek pouch mucosa to 14C-CHD. However, treatment with 2.0% CHD resulted in decreased permeability to 3H2O (P less than 0.05) when compared to the other groups. Treatment with 2.0% CHD also resulted in a thickened permeability barrier (P less than 0.01), as determined using a tracer, horseradish peroxidase. It is concluded that topical applications of 0.2% T CHD have no detectable effect on cheek-pouch mucosa while applications of 2.0% CHD result in hyperplasia and a decrease in mucosal permeability. Our results suggest that CHD should be used with caution clinically and at a concentration of 0.2% or less.

Administration, Topical↗
PubMed1984

Genetic and epigenetic control of connective tissues in the craniofacial structures.

The connective tissues of the craniofacial region can neither develop nor be maintained independently of their local environment. I have stressed such epigenetic control in the present brief review of the origin, differentiation, morphogenesis, and growth of selected craniofacial tissues. I began by discussing the origin of these tissues in the neural crest. The extensive migration of neural crest cells to form the craniofacial region of the embryo is epigenetically regulated by extracellular matrix products such as fibronectin, and by basal laminae of the epithelia along which some cells migrate. The trigger which initiates differentiation of these mesenchymal cells is provided by epithelia with which they come into contact either before, during, or after migration, as illustrated by the differentiation of both Meckel cartilage and mandibular dermal bones. Subsequent differentiation of secondary cartilage is also shown to be epigenetically initiated, in this case by the mechanical environment created by muscle action. Both secondary cartilages on avian dermal bones and the condylar cartilage of the mammalian dentary are discussed. The interplay between genetic and epigenetic factors in morphogenesis and growth of craniofacial connective tissues is then very briefly discussed.

Animals↗
PubMed1984

Epithelial induction of osteogenesis in embryonic chick mandibular mesenchyme studied by transfilter tissue recombinations.

The initiation of osteogenesis in the mandibular mesenchyme of the embryonic chick at 7 days is dependent upon an epithelial induction which occurs in the mandible up to the fourth day in ovo. In the present study, transfilter tissue recombinations were used to study this inductive mechanism. The epithelial and mesenchymal components of the mandibles were separated before the completion of the induction and recombined to form transfilter explants which were either cultured for 9 days or grafted onto the chorioallantoic membrane for host embryos for 7 days. Control experiments demonstrated that the tissue separation and recombination techniques did not interfere with the normal epithelial induction, and confirmed that mandibular mesenchyme isolated at this stage was incapable of forming bone. Bone was observed in 86% of the CAM-grafted intact mandible controls and in 80% of the cultured intact mandible controls. Bone failed to form in the mesenchyme of transfilter explants when Millipore filters with 0.45 micrometer pores were used. Bone was observed as frequently as in control explants when the mandibular mesenchyme was separated from its epithelium by 0.8 micrometer or 0.4 micrometer porosity Nuclepore filters. Only about 30% of the transfilter explants prepared with 0.1 micrometer porosity Nuclepore filters formed bone and none of the explants prepared with 0.03 micrometer porosity Nuclepore filters formed bone. SEM studies demonstrated a distinct correlation between the formation of bone in transfilter explants and the ability of the epithelium and mesenchyme to penetrate the pores of the filters. Thus, the present study provides evidence that the site of the induction is restricted to the epithelial-mesenchymal interface, and that the induction is not mediated by a diffusible substance. The nature of the inductive mechanism is discussed with respect to this and other recent studies which suggest that the induction may be mediated by a non-diffusible epithelial cell product resident in the epithelial basal lamina.

Animals↗
PubMed1984

An SEM analysis of the epithelial--mesenchymal interface in the mandible of the embryonic chick.

In this paper the ultrastructural features of the epithelial-mesenchymal interface in mandibular processes of embryonic chicks have been examined using scanning electron microscopy. Mandibular epithelium is required for the mesenchyme to differentiate as osteoblasts and to deposit the membrane bones of the mandible. The surface morphology of the epithelium changes from the lateral to the medial face of the mandible from rounded cells, each with a central cilium to flattened cells with numerous microvilli. Treatment with trypsin and pancreatin was used to digest the basal lamina so as to separate epithelium from mesenchyme. This exposed a thick, fibrillar basement membrane (reticular lamina), which was thicker underlying the caudal epithelium than under the cephalad epithelium. Addition of collagenase to the trypsin/pancreatin solution degraded some of the basement lamella, especially that underlying epithelium on the caudal portion of each mandibular process. Selective degradation of basement lamella is postulated as one means of regulating inductive epithelial-mesenchymal interactions. EDTA was used to isolate basal laminae on mandibular mesenchyme. SEM was used to confirm the integrity of the basal lamina, its structure, and its association with overlying epithelial cells and underlying basement lamella.

Animals↗
PubMed1983

Epithelial induction of osteogenesis in embryonic chick mandibular mesenchyme: a possible role for basal lamina.

The initiation of osteogenesis at 7 days in the embryonic chick mandibular mesenchyme depends on an epithelial induction in the mandible to day 4. This article reviews a series of experiments conducted to study the nature of this inductive mechanism. Transfilter tissue recombinations were used to determine whether direct tissue apposition was required for induction. Ultrastructural studies of the epithelial-mesenchymal interface were conducted to see if direct epithelial-mesenchymal cell-cell contacts occurred during the inductive stage in vivo. Epithelial cells were cultured on Millipore filters for 28 days and allowed to deposit extracellular products. These products were tested for inductive activity. Findings from these three sets of experiments were discussed with respect to the inductive mechanism. Our results indicate that the induction is not mediated by a diffusible substance and that direct apposition of the two tissues is required. The mechanism of induction, however, does not require direct epithelial-mesenchymal cell to cell contacts. This suggests that a nondiffusible component of the extracellular matrix may be involved. Epithelial extracellular products are inductively active and have the appearance of basal lamina. The active component of the extracellular product is proteinaceous, perhaps collagen, and appears to be situated in the epithelial basal lamina. The role of basal lamina in epithelial-mesenchymal interactions is discussed.

Animals↗