Bone grafts and biomaterials substitutes for bone defect repair: A review.

Magnesium and the inflammatory response: Potential physiopathological implications

This chapter presents an electron-microscopic study of the epiphyseal cell and its histological disposition with an emphasis on the morphological evidence of secretion. Detection of histological design in the pineal body is complicated by divergent results of fixation by immersion and perfusion. Cytological preservation is suboptimal, following immersion fixation, and it is indicated by the vesiculation of cytoplasmic membranes, the extraction of lipid droplets, the appearance of nuclear inclusions, and the slight swelling of the cells without conspicuous dilution of their cytoplasm. Such subtle swelling generates an artifactitious histological compactness resembling the texture of a gland or epithelioid body. Fixation of the epiphysis by intravascular perfusion yields the best cytoplasmic preservation, even when accompanied by a variable widening of the clefts between epiphyseal cells and the diminution of amorphous interstitial material, a phenomenon that occurs chiefly in the central portion of the pineal body.

The epiphyseal cell: an electron-microscopic study of its intercellular relationships and intracellular morphology in the pineal body of the albino rat.

Bone formation controlled by biologically relevant inorganic ions: role and controlled delivery from phosphate-based glasses.

An elevated blood eosinophil count may be associated with a number of reactive conditions and with clonal disorders of the bone marrow. When the blood eosinophil count is persistently greater than 1Æ5 · 10 ⁄ l for a period of 6 months, and damage to end organs such as the heart, lungs, skin, joints and nervous system can be demonstrated then, in the absence of any clonal abnormality or reactive cause, the term idiopathic hypereosinophilic syndrome (HES) is used. There is evidence to suggest that, in some patients, clonal T-cell populations are present. Treatment of the idiopathic hypereosinophilic syndrome has been varied and has included steroids, hydroxyurea, interferon and Tcell agents, and chemotherapy. Recently, patients have been treated successfully with imatinib mesylate and a trial of its use in HES is planned.

https://onlinelibrary.wiley.com/doi/pdf/10.1046/j.1365-2141.2003.04195.x

The eosinophilias, including the idiopathic hypereosinophilic syndrome.

The fact that magnesium is essential for growth has been known for some time. Leroy' was the first to demonstrate that growth was arrested after 9-15 days in mice maintained on a magnesium-deficient diet and that the deficient animals resumed their growth when magnesium was restored. Kruse, Orent, and McCollum2 were the first to describe the effects of this deficiency in rats. Since that time the biological function of magnesium, its pharmacological properties, and its function as an essential nutrient for animals have been frequently studied and have been reviewed by Wacker and Vallee.3 In a review of the available literature, there has been a scarcity of histological studies of growing bone and dentin in magnesium-deficient animals. Chemical studies on bone4 have shown that magnesium concentration was decreased in the bone and calcium was increased in the early stages of the deficiency. Yamana and Singer5 have observed that the bony trabecular of the metaphysis was lost and the zone of preliminary calcification just below the epiphysis was atrophic or absent. Irving,6 Becks and Furuta,7 and Yamana and Singer5 have described the changes in the dentin of rats and hamsters. Typical striations occurred in the dentin, which appeared to be imperfectly calcified. The present investigation was undertaken to determine by various histochemical reactions the components of bone and dentin that were affected by the magnesium deficiency.

Effect of Dietary Magnesium Deficiency on the Bones and Teeth of Rats

Results and conclusionsThe acute phase of the magnesium deficient syndrome is characterized by a dermal hyperemia(6) in rats and dermal mast cells degranulate in this phase(3). The blood eosinophilia which occurs in the acute phase of magnesium deficiency (Table I, Group 8) is highly significant (P = < .01) and may be caused by the endogenous release of mast cell secretory products. However, administration of commercial histamine, (Table I, Groups 1, 2, 3) in a variety of doses, routes and time intervals (some not reported here) failed to duplicate the eosinophilia produced by magnesium deficiency. Administration of 48/80 in gradually increasing doses for 3 days produced a significant (P = < .01) eosinophilia (Table I, Group 11) of comparable magnitude to that produced by dietary magnesium deficiency. One large dose of 48/80 (Table I, Group 10) proved fatal to 50% of the animals. Since 48/80 is supposed to be a fairly specific mast cell degranulating agent (7), one would assume that a mast cell product or...

Role of histamine in producing the eosinophilia of magnesium deficiency.

Pineal fat stainable with oil red 0 was markedly depleted in intact and adrenalectomized rats maintained on a diet deficient in sodium. Pineal fat was mildly depleted by adrenalectomy alone. The zona glomerulosa of the adrenal gland widened in response to the sodium deficient regimen in both intact and pinealectomized rats. These alterations were taken to indicate that the pineal gland may elaborate a hormone which is involved in salt regulation.

Response of the pineal and adrenal glands to sodium restriction.

The eosinophilia of magnesium deficiency.

The effect of hormone imbalances on the amount of fat stainable with oil red 0 in the pineal gland of the rat was studied. It was found that treatment with angiotensin II or propylthiouracil depleted pineal lipid. Removal of the pituitary or combined castration and adrenalectomy also severely depleted pineal fat. On the other hand, the administration of desoxycorticosterone acetate tended to augment the amount of pineal lipid. Other treatments which were found to be without effect in altering the amount of pineal lipid included: thyroxine, testosterone, hydrocortisone, adrenaline, serotonin, ACTH, B-MSH, alloxan and castration. All the procedures which defatted the pineal gland had some effect on sodium metabolism. While it was concluded that the pineal gland may be implicated in sodium homeostasis, the mechanism remains unknown.

Gerald F. Hungerford

Papers

Effect of Dietary Magnesium Deficiency on the Bones and Teeth of Rats

Role of histamine in producing the eosinophilia of magnesium deficiency.

Response of the pineal and adrenal glands to sodium restriction.

The eosinophilia of magnesium deficiency.

Response of pineal lipid to hormone imbalances.