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Rickets was the first environmental disease. Although it was first described in the 1600s, the disorder reached epidemic proportions by the end of the 1800s. Many children in industrialized Europe and North America began developing a variety of physical deformities including bow legs, pigeon chests, broad heads, and poor tooth development. Eventually scientists discovered that these abnormalities resulted from a deficiency of vitamin D. For urban children of past centuries, this deficiency was often caused by their living conditions. Sunless city streets darkened by industrial smog provided insufficient exposure to sunlight. However, the abnormalities associated with rickets and a related disorder, osteomalacia, have other etiologies in addition to vitamin D deficiency. Although treatments exist for some of these syndromes, others continue to present therapeutic challenges. In 1645, Daniel Whistler published a thesis describing rickets. Unfortunately though, Francis Glisson defined rickets in a book in 1650. The book immediately became quite popular and Glisson's work quickly overshadowed that of Whistler (Gibbs 729-732). Several centuries later, by the end of the 1800s, rickets had reached epidemic proportions. Indeed, scientists estimated that the majority of children living in the northern cities of England, Scotland, and Germany had developed rachitic abnormalities (Wilton 1516-1517). Such observations were confirmed by autopsy studies perfor
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s exhibit considerable order. From the epiphyseal side to the metaphyseal side, there is a progressive increase in the number and size of the cartilage cells. Moreover, the cells also begin to arrange into columns aligned with the long axis of the bony shaft. The various zones of development include the reserve zone, the proliferating zone, the hypertrophic zone, and the zones of primary and secondary spongiosa. Adjacent to the epiphysis, the reserve zone contains only a few spherical cartilage cells. In contrast, the proliferating zone is an area of cellular proliferation and matrix production. It is in this zone that the chondrocytes become flattened and arranged into longitudinal, parallel columns. There is a marked change in cell structure from the proliferative to the hypertrophic zones. In the hypertrophic zone, the cells increase in both size and sphericity. This region may be further subdivided into the zones of maturation, degeneration, and provisional calcification. Near the metaphyseal side of the growth plate, the large and vacuolated cells become nonviable and there is calcification of the intervening cartilage matrix. Last, the zones of primary and secondary spongiosa are located in the metaphysis next to
Category: Medical - R
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Klein Simmons, Ricket Prevention, Isles Scandinavian, North America, Type II, Leiden Netherlands, Additionally Mellanby, Kurt Huldschinsky, Middle East, Whistler Gibbs, rickets osteomalacia, pitt 97-115, growth plate, holick 1-22, growth plates, klein simmons, vitamin d-deficiency rickets, d-deficiency rickets, 97-115 rickets, gibbs 729-732, wilton 1516-1517, pitt 97-115 rickets, klein simmons 379-382, classic vitamin d-deficiency, primary secondary spongiosa,
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= 9 (250 words per page)
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