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Biomedical subjects

J Kirkham

Publications and source records attributed to J Kirkham.

88 records · Page 5Linked to original sources

Spurious high birth defect rate on the island of Lanai and an unexpected indication of a high incidence of adverse pregnancy outcomes in Kohala on the Big Island.

The previously reported high birth defect rate from 1968-1982 on the island of Lanai in Hawaii was found to be due to incomplete recording of birth defects on birth certificates elsewhere in the state. The elevated birth defect rate and low birth weight rate for the area of Kohala on the big island were without obvious explanations and were sufficiently high to warrant further study.

Americas↗

Distribution and uptake of magnesium by developing deciduous bovine incisor enamel.

Magnesium concentrations determined in deciduous bovine enamel at different stages of development were similar to those previously published for human and rat enamel ranging from 0.1 to 0.4 per cent. Highest concentrations, i.e. greatest uptake, occurred after secretion, in the transitional and maturing enamel. Uptake had occurred throughout the tissue thickness and was not confined to the surface. Magnesium probably enters enamel in the tissue fluid which replaces the organic matrix. Some magnesium is lost as fluid is replaced by calcium and phosphate but part is retained probably on or near crystal surfaces.

Animals↗

Computed tomographic demonstration of "coronary" collateral vein calcification and patent spleno-renal shunt--a case report.

A case of hepatoma associated with previously treated portal hypertension and calcification of the portal veins, collaterals, and superior mesenteric veins was demonstrated by CT, as was the patent splenorenal shunt and ascites. Computed tomography successfully demonstrated all these aspects of the case by plain scans and the use of angiotomography with rapid sequential sections using the multiple bolus technique of contrast enhancement.

Aged↗

Changes in the protein components of rat incisor enamel during tooth development.

Enamel-matrix components from rat incisor enamel were extracted from tissue at different stages of development on single teeth. Separations of proteins using urea and SDS acrylamide gel electrophoresis were compared. The bulk of the matrix exhibited SDS mol. wt of 25-30,000 with smaller amounts at approximately 18,000 and about 10-12,000. Trace amounts of material at -50,000 and 70,000 were detected. These were presumably associated with the mineral phase as their yield increased after demineralization. The proportion of small molecular weight components increased with tissue age. Using urea, many more proteins were separated (up to 20) into fast, intermediate and slowly-migrating components. Disappearance of small bands of intermediate mobility at the end of matrix secretion suggested that they were early ameloblast products which were rapidly degraded after secretion. Both slowly- and rapidly-migrating components increased with tissue age indicating progressive degradation of parent molecules of intermediate mobility into highly charged and relatively uncharged molecules.

Animals↗

Serum histidine in rheumatoid arthritis: a family study.

We have compared free serum histidine in patients with rheumatoid arthritis, their blood relatives, and their non-blood relatives. The hypohistidinaemia of rheumatoid arthritis is acquired with the disease and does not provide a biochemical marker of those at risk.

Arthritis, Rheumatoid↗

Non-steroidal anti-inflammatory drugs and the Sigma SR in rheumatic diseases.

Sigma SR and erythrocyte sedimentation rate (ESR) were compared before and after treatment with non-steroidal anti-inflammatory agents in 6 patients with rheumatic diseases. No evidence was found that either was altered by this kind of drug therapy, though there was considerable variation in the shape of sedimentation rate curves (obtained by plotting erythrocyte sedimentation rate every 5 minutes over 150 minutes), between individuals with the same disease.

Adult↗

Distribution of exogenous proteins in caries lesions in relation to the pattern of demineralisation.

While it is believed that proteins may protect enamel from demineralisation, recent work has indicated that such material may also hinder remineralisation. For example, albumin will inhibit apatite crystal growth in vitro and is present in carious enamel in vivo. However, it is not clear whether (1) the distribution of proteins within lesions is restricted to specific lesion zones or (2) the origin of such proteins is endogenous (i.e. as a remnant of the developmental process) or exogenous, originating in the saliva or gingival crevicular fluid. The present study used a combination of immunohistochemistry and microradiography to determine the distribution of two proteins, serum albumin and salivary amylase, within natural white-spot carious lesions in relation to specific levels of demineralisation. The results indicated that albumin is found primarily in a region of between 10 and 20% demineralisation (an area of transition between the 'dark' zone and lesion 'body'), with smaller quantities occurring in the region between 0 and 10% demineralisation and trace amounts in the zone indistinguishable from sound enamel by microradiography. A similar distribution was found for amylase in that the heaviest labelling was within the 10-20% demineralisation zone, although little if any was present in the 0-10% zone. The presence of these molecules in a region of the lesion where some potential for reprecipitation may exist will have important implications with respect to lesion progression.

Albumins↗

Fluoride profiles in dental plaque in vivo formed on fluoride pre-treated human enamel.

Using a novel device capable of generating plaque in vivo on a natural enamel substrate, it has been possible to determine fluoride profiles from the saliva-plaque interface towards the enamel surface. Fluoride profiles in dental plaques tended to fall from the saliva-plaque interface towards the enamel. The device also offered the possibility of examining fluoride distributions after pre-treatment of the enamel with fluoride in vitro. Fluoride profiles were determined in plaque generated in vivo on enamel surfaces, which had been previously treated with a 900-ppm fluoride solution. The results showed the previously reported fall from the plaque surface, but in addition, a further rise towards the enamel surface was seen. The data imply that enamel loaded with fluoride can release some of this fluoride back into the plaque and may act as a fluoride reservoir.

Calcium↗

Effect of experimental fluorosis on the surface topography of developing enamel crystals.

Dental fluorosis is an increasing problem, yet the precise mechanism by which fluoride exerts its effects remains obscure. In the present study, we have used atomic force microscopy to image and quantitate surface features of enamel crystals isolated from specific developmental stages of fluorotic and control rat incisors. The results showed a significant decrease in crystal surface roughness with development in control tissue. Crystals from fluorotic tissue were significantly rougher than controls at all stages of development, did not decrease in roughness during the later stages of their development and had many morphological abnormalities. These data clearly demonstrate an effect for fluoride on enamel crystal surfaces which could reflect changes in the nature and distribution of growth sites and/or in mineral-matrix interactions. These would be expected to affect crystal growth during maturation, resulting in the characteristic porous appearance of fluorotic lesions in mature teeth.

Animals↗

In vitro studies of the penetration of adhesive resins into artificial caries-like lesions.

Instead of removing the porous carious tissue at a relatively late stage in the disease process, attempts have been made to 'fill' the microporosities of lesions at a much earlier stage of lesion development. This would not only reduce the porosity and therefore access of acid and egress of dissolved material, but also afford some mechanical support to the tissue and perhaps inhibit further attack. Successful infiltration of materials into lesions has been demonstrated previously using resorcinol-formaldehyde which, however, was clinically unacceptable. The advent of dental adhesives with potentially suitable properties has prompted a re-examination of this concept. Artificial lesions of enamel were generated in extracted human teeth using acidified gels. A range of currently available adhesive materials was then used to infiltrate the porosities. The extent of occlusion of the lesion porosities was determined both qualitatively using light microscopy and quantitatively using a chloronaphthalene imbibition technique. The effect of such treatment upon subsequent exposure to acid gels was also investigated. Results showed that up to 60% of the lesion pore volume had been occluded following infiltration with some of the materials and that this treatment was capable of reducing further acid demineralization. The development of such treatment strategies could offer potential noninvasive means of treating early enamel lesions.

Adhesives↗

The effect of fluoride on the developing tooth.

This review aims to outline the effects of fluoride on the biological processes involved in the formation of tooth tissues, particularly dental enamel. Attention has been focused on mechanisms which, if compromised, could give rise to dental fluorosis. The literature is extensive and often confusing but a much clearer picture is emerging based on recent more detailed knowledge of odontogenesis. Opacity, characteristic of fluorotic enamel, results from incomplete apatite crystal growth. How this occurs is suggested by other changes brought about by fluoride. Matrix proteins, associated with the mineral phase, normally degraded and removed to permit final crystal growth, are to some extent retained in fluorotic tissue. Fluoride and magnesium concentrations increase while carbonate is reduced. Crystal surface morphology at the nano-scale is altered and functional ameloblast morphology at the maturation stage also changes. Fluoride incorporation into enamel apatite produces more stable crystals. Local supersaturation levels with regard to the fluoridated mineral will also be elevated facilitating crystal growth. Such changes in crystal chemistry and morphology, involving stronger ionic and hydrogen bonds, also lead to greater binding of modulating matrix proteins and proteolytic enzymes. This results in reduced degradation and enhanced retention of protein components in mature tissue. This is most likely responsible for porous fluorotic tissue, since matrix protein removal is necessary for unimpaired crystal growth. To resolve the outstanding problems of the role of cell changes and the precise reasons for protein retention more detailed studies will be required of alterations to cell function, effect on specific protein species and the nano-chemistry of the apatite crystal surfaces.

Amelogenesis↗

Enamel protein in smooth hypoplastic amelogenesis imperfecta.

Amelogenesis imperfecta (AI) remains a poorly understood group of hereditary enamel defects characterized by a wide array of clinical presentations. Although numerous reports have described the histological features of AI, knowledge concerning the biochemical composition of the affected enamel remains minimal. The purpose of this investigation was to examine the protein of smooth hypoplastic AI enamel. Exfoliated primary teeth were obtained from an individual with smooth hypoplastic AI together with exfoliated teeth from normal healthy individuals for controls. Enamel was dissected from the AI and control teeth to determine protein content and amino acid profile. The analyses showed that the hypoplastic AI teeth contained 2% protein, compared with 0.3% in normal primary enamel. The protein content of the hypoplastic AI enamel was similar to that reported for the late maturation stage of normal primary enamel. The amino acid profiles of both normal and AI enamel were similar although there appeared to be increased amounts of glycine in the AI enamel. Hypoplastic AI enamel showed an amino acid profile similar to normal mature primary enamel in contrast to hypomaturation AI that exhibits an amelogenin-like character. The amount of retained protein also was different from that reported for hypomaturation AI enamel which contains approximately 5% protein compared with the 2% seen in hypoplastic AI enamel. This study emphasizes the potential usefulness of protein characterization in delineating different AI types and illustrates how this information may lead to an understanding of the developmental defects responsible for producing abnormal enamel.

Amelogenesis Imperfecta↗

The mineral composition and enamel ultrastructure of hypocalcified amelogenesis imperfecta.

Hypocalcified amelogenesis imperfecta is characterized clinically by a yellow-brown colored enamel that is prone to severe attrition, often leading to rapid destruction of the crown. While the enamel is thought to be poorly mineralized few studies have evaluated the mineral content, or the histological or microradiographic features of this specific AI type. The purpose of this investigation was to examine teeth affected with autosomal dominant hypocalcified AI histologically using light microscopy (LM), scanning electron microscopy (SEM), and to evaluate the degree of enamel mineralization chemically and with microradiography. Four AI teeth were obtained from an affected individual for comparison with age-matched teeth from normal healthy individuals. Thin sections approximately 100 microns were cut with a diamond disc for examination by LM and microradiography. Using SEM, fractured enamel samples were examined either untreated or after removal of organic material using NaOCl or urea. Normal and AI enamel particles were dissected from thin sections to evaluate the mineral per volume and carbonate content. The enamel was not uniformly affected in all areas of the teeth with the lingual surfaces of the mandibular central incisors appearing clinically and histologically normal. The affected enamel was porous and appeared opaque with LM. Both SEM and LM showed the enamel to be prismatic with relatively normal prism morphology. However, the enamel crystallites were rough and granular compared with those of normal enamel. Extraction to remove organic material did not change the appearance of the crystallites indicating their granular appearance was due to mineral and not residual organic material such as enamel protein. Microradiography showed the enamel was less radiodense and therefore poorly mineralized compared with normal enamel. This was confirmed by chemical determination of the mineral per volume, which showed some areas of the AI enamel had as much as 30% less mineral compared with normal enamel. The carbonate content was found to be similar in AI and normal enamel. Hypocalcified AI is associated with decreased mineralization as well as ultrastructural defects in the crystallite structure. The combined histological and biochemical features of hypocalcified AI seen in this investigation indicate that this AI type is distinctly different from the hypoplastic and hypomaturation AI types.

Amelogenesis Imperfecta↗