Biomedical subjects
Publications and source records attributed to B M Eley.
An unusual case of multiple idiopathic external apical root resorption affecting all four quadrants, in a patient with a history of narcotic intravenous drug addiction and liver disease, is reported. The literature relating to a systemic etiology for external root resorption is briefly reviewed.
Twenty-four guinea pigs were subcutaneously implanted with 2 X 25 mg of powdered dental amalgam for between 1 and 24 months. Four animals served as controls. All animals were fed a standard diet containing 0.2 microgram/g selenium (Se). Mercury (Hg) was released from the implants at an average rate of 21.7 micrograms/d and 4.35-16.94 micrograms of Se were consumed daily in the diet. The renal Hg rose to a maximum of 263 micrograms/g at 11 months in implanted animals and 6.65 mg Hg was excreted over 2 yr. The renal proximal tubular cells of implanted animals contained visible Hg deposits in secondary lysosomes and within nuclei containing both Hg and Se. No other signs of obvious renal pathology were seen in implanted animals as compared with controls. It would seem likely that the low Se levels present within this standard laboratory diet were sufficient to protect against Hg toxicity.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
With both types of amalgam there was initial loss of material during healing of the implantation wounds. The rate of Hg release from the healed lesion was estimated by linear regression analysis of the content of implants when removed sequentially over 2 years. There were no significant differences between the amalgams, when expressed in absolute terms or as a percentage of the Hg content of the lesions immediately after healing, probably because gamma 1 (Ag2Hg3) phase breakdown was largely or solely responsible for Hg release with both materials. Hg levels in the blood, liver, renal cortex and faeces were all significantly lower with high-Cu amalgam which might be explained by the interference by Cu with Hg retention. There was no significant difference in urinary Hg excretion by the two groups of animals over the greater part of the study.
With each material, there was only a mild early inflammatory response; particles were taken up by macrophages and giant cells. By 1.5 to 3 months, chronic granulomas had developed. With conventional amalgam, there were early changes in the intracellular material, associated with the rapid degradation of Sn-Hg particles, corresponding to the gamma 2 phase. Thereafter, intracellular particles from both types of amalgam underwent progressive degradation, producing halos of secondary material containing Ag and S. Apart from an initial loss of Cu and Sn from some high-Cu amalgam particles, there were no qualitative differences in the later changes between the two materials, although conventional amalgam particles appeared to degrade faster. With both, vast numbers of fine secondary particles containing Ag and S became widely distributed throughout the lesions and gave rise to macroscopic tattooing of the skin. Secondary material and small degrading primary particles from both types of amalgam were detected in the submandibular lymph nodes where they caused localized staining.
The cysteine proteinases cathepsins B and L have collagenolytic potential and so have been implicated in connective-tissue breakdown in chronic periodontitis. Synthetic peptide substrates are often used to detect proteolytic enzymes. The action of homogenates of inflamed gingiva tissue against three such substrates of cathepsin B have been characterized here by protease inhibitors. Using the selective reagents ZPheAlaCHN2, BzValLysLysArgAFC, ZAlaArgArgAFC and ZPheArgAFC were susceptible to both cysteine and non-cysteine proteinase activity; the two types of enzymes had acidic and alkaline pH optima, respectively. The action of other inhibitors at acidic pH indicated the involvement of cathepsin B and, to a lesser extent, cathepsin L. The enzyme active at alkaline pH was a serine proteinase; it resembled glandular kallikrein in its inhibitor response and its ability to hydrolyse a fourth substrate, DValLeuArgAFC, but its greater reactivity with BzValLysLysArgAFC and ZAlaArgArgAFC was not consistent with kallikrein. ZPheArgAFC, though less sensitive than BzValLysLysArgAFC to cysteine proteinase action, was far less susceptible to hydrolysis by the serine proteinase and thus appears the best choice for selective assays of cathepsins B and L.
Powdered dental amalgam that had passed through either a 106 microns or a 45 microns sieve was implanted subcutaneously in guinea pigs for periods of up to 2 yr. The renal cortical mercury levels associated with the 106 microns material were on average 16% of those produced by the 45 microns material. A reduction in the amount of 45 microns powder implanted, by a factor of 75%, resulted in a fall of only 27% in renal mercury concentrations. The marked effect of particle size on mercury release may be explained by the large increase in the proportion of implanted material that was degraded within phagocytic cells in the local lesions.
The subcutaneous implantation in guinea pigs of powdered gamma 1 phase induced a severe initial tissue response and the majority of the material was extruded from the healing wounds. This process was accompanied by the release of significant amounts of mercury which appeared in the body organs and excreta. The small numbers of particles which remained in the tissues were handled quite differently, undergoing slow degradation in macrophages and giant cells in chronic granulomata. Minute secondary particles containing silver and sulphur were deposited in the tissues and gave rise to macroscopic tattooing of the skin above the implants.
Following the subcutaneous implantation in guinea pigs of powdered gamma 2 phase with a mercury content only slightly greater than that indicated by the stoichiometric formula Sn7Hg, there was a limited initial release of mercury from extracellular material. Thereafter, chronic granulomata developed around the implants and particles degraded slowly in macrophages and giant cells. Vast numbers of fine secondary particles containing tin were produced and these were associated with macroscopic staining. Mercury seemed to be lost as the result of intracellular particle breakdown but it did not accumulate in the body organs or appear to any great extent in the excreta.
Examination of light microscopical sections of the kidneys of guinea pigs with chronic exposure to mercury as the result of the breakdown of subcutaneous implants of powdered dental amalgam demonstrated the development of black, refractile deposits in the cytoplasm and nuclei of cells in both the straight and convoluted portions of the proximal tubule. The more numerous cytoplasmic deposits were of a particulate nature with dimensions of approximately 1 microgram. The nuclear deposits, which appeared later but which were relatively more common in longer-term animals, took the form of prominent inclusions, 1 to 3 micrograms in diameter. The ratio of nuclear to cytoplasmic deposits was higher in animals receiving high copper as compared with conventional amalgam. At electron microscopical level, the cytoplasmic deposits were seen to consist of collections of fine particles within lysosomes. Similar deposits were also found in far smaller numbers in lysosomes in collecting duct cells. The nuclear inclusions in proximal tubular cells were made up of closely packed electron dense granules. X-ray microanalysis showed both lysosomal and nuclear deposits to contain mercury and selenium. The association of mercury with selenium, which was present in the animals' diet at low levels, probably aided the microscopical visualisation of the deposits.
Following the subcutaneous implantation of powdered dental amalgam in guinea pigs, there was an initial extrusion of material from the healing implantation wounds. Longer-term release of mercury from the lesions was demonstrated by linear regression analysis of the mercury contents of implant sites removed after time periods of up to 2 years. Raised mercury levels were detected in the blood, bile, kidneys, liver, spleen and lungs of implanted animals; by far the highest concentrations were found in the renal cortex. Mercury was excreted with the urine and, to a lesser extent, the faeces. The pattern of mercury redistribution resembled that seen following chronic exposure to mercuric compounds.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Soft tissue degradation of the 3 principal amalgam phases have been investigated in relation to their role in the formation of the amalgam tattoo. Each phase, finely powdered, was implanted subcutaneously into the submandibular region of guinea-pigs for periods ranging from 1 week to 1 year. The rates of breakdown were assessed radiographically and the final lesions were examined by light and electron microscopy and X-ray microanalysis. gamma 2 (Sn7Hg) phase degraded rapidly, mainly extracellularly, and did not produce a tattoo. Both mercury and tin disappeared from the lesion. gamma 1 (Ag2Hg3) phase degraded less rapidly, both extra and intracellularly, and produced a small tattoo. Mercury was lost from the lesion. gamma (Ag3Sn) phase degraded slowly, intracellularly, and produced a large tattoo. Tattoos always resulted from persistence of minute particles of silver and sulphur associated with basal lamina and connective tissue.
Dental amalgam, either in the form of a solid rod or as a fine powder was implanted subcutaneously into guinea-pigs and the tissue reactions were examined after varying time periods. The solid rods were enclosed by fibrous capsules within which only extremely limited breakdown occurred. This appears to result from electrolytic corrosion of the gamma 2 (SnHg) phase of the rod's surface. Powdered amalgam induced granulomata and most of the particles of amalgam were actively digested by macrophages and giant cells. This resulted in the progressive loss of mercury and tin from the lesion and the formation of minute particles containing silver and sulphur which became widely distributed throughout the lesion, being associated with basal lamina, collagen and elastic tissue and giving rise to the formation of a tattoo. In contrast, some particles of amalgam, too large to be interiorised, were encapsulated by collagen and persisted almost unchanged. Intracellular small amalgam particles and aggregates of fine particles, resulting from their degradation, were seen within lymph node macrophages. It is extremely likely that the sequence of events leadng to the formation of an amalgam tattoo of the oral mucosa in Man are the same.
The soft tissue reaction to amalgam depended on whether it was finely ground or a solid mass. Finely ground amalgam was actively digested within macrophages and giant-cells with loss of mercury and the formation of the fine particles of silver and sulphur. Larger masses became surrounded by a fibrous capsule.
Implantation of amalgam induced a cellular reaction, and a rapid loss of copper and zinc and a more gradual loss of tin and mercury occurred. The silver remaining was generally associated with sulphur and was present either as a diffuse fuzz around remaining masses or in a finely particulate form.