Nutritional Secondary Hyperparathyroidism in the Horse

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70 Expcrirnental Nutritional Secondary Hyperparathyroidism in the I-Iorse . . . Hemosiderosis. Hemosiderin in macrophages of the connective tissue were present in the maxilla and the mandible of all NSH horses, but it was rare. Hemosiderosis of osteoclasts was observed in very rare instances. Brown nodes. Clear-cut examples of brownnodes werenot recorded. At the site of the fracture of the eighth right rib of NSH 2 a picture somewhat similar to a brown node did occur, but the hemorrhages, hemosiderosis, and accumulation of giant cells were believed to be associated with the fracture rather than with osteitis tibrosa per se. Cj~ts. Microscopic cysts were of rare occurrence in the jawbones and absent elsewhere. They appeared to be derived from hemorrhages rather than from mucoid degeneration. Osteoid apposition. Osteoblastic activity was observed in cancellous as well as in compact bone. In the jawbones, where the resorption was most advanced, osteoid bars of different thicknesses and of haphazard distribution were quite common (Figs. 28, 29, and 30). Osteoblasts were usually present in a single layer. Most of these bars stained diffusely pink with hematoxylin and eosin, and the deep-purple center seen in old bone was not present. Osteoclasts were absent along or within such osteoid bars. On the other hand, highly active osteoclastic resorption with the formation of numerous HOWHIP’S lacunae and deep excavations into trabeculae was frequently observed occurring simultaneously with apposition on the other surface of the same trabeculae (Fig. 29). Osteoid formation along the trabeculae of ribs was likewise rather pronounced (Fig. 31) with osteoblasts sometimes present in several layers. As before, the osteoid was light pink in color with hematoxylin and eosin. The formation of new osteons in areas of previous resorption was frequently observed in cortical bone (Figs. 33,34,37, and 38). Lamellae were laid down in an orderly manner, and a single layer of osteoblasts was usually present internally. All NSH horses exhibited the changes just described. The degree varied somewhat, however, NSI-I 2 presented the most advanced changes, then NSI-I 3, and finally NSH 1. Morpbologic diagnosis: GeneraliTed osteitis jbrosa. c) Other Tissues No changes were observed in any other tissues. There was no soft tissue calcinosis. Downloaded from vet.sagepub.com by guest on April 14, 2010
V. Experimental Nutritional Secondary Hyperparathyroidism in the Horse: Discussion 1. Clinical Course The clinical symptoms observed in NSH horses agreed in general with those of earlier descriptions (see Chapter 11). The time of onset differed, however. This will be discussed later under the bone changes. 2. Serum Phosphorus, Calcium, and hlltaline Phosphatase Interpretation of the changes in serum phosphorus and calcium and of the product of total calcium and serum phosphorus requires appreciation of two facts: i) Serum calcium and phosphorus are interrelated according to the law of constant ion product in a saturated solution at a given pH: Ca++ x HP04-- CaHP04 = kpFI (“this being the only logical means of correlating calcium and phosphorus”-T~o~so~ and COLLIP, 1932). ii) The solubility of calcium and phosphorus in the blood serum increases in hyperparathyroidism. The importance of additional effects of the parathormone such as resorption of bone and increased renal excretion of phosphorus is self-evident. The interrelationship between calcium and phosphorus in the blood serum has long been a question of debate. COLLID (1926) showed that, following injections of parathormone at 4-hour intervals into dogs, serum calcium rose from 12 to about 20 mg. per 100 ml. and that whole blood phosphorus increased, after a slight initial decrease, from 6 to 13 mg. per 100 ml. Similar results were reported by THOMSON and PTJGSLEY (1932), LOGAN (1939), MCLEAN et al. (1946), and others. Downloaded from vet.sagepub.com by guest on April 14, 2010
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Pathologia Veterinaria Online http:
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Supplementum ad Vol. 1 (1964) Patho
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V . Experimental Nritritional Secon
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Introduction and Object of Investig
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I. The Anatomy of the Parathyroid G
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Comparative Aspects of the Embryolo
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The Aracroscopic Anatomy of the Equ
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The Microscopic Anatomy of the Equi
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'I'hc hlicroscopic Anatomy of the E
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’The I\licroscopic Anatomy of the
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10 . 9 . a . 7 0 + 6 . 5 . 0 ’I
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‘The hl icroscopic Anatomy of the
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Page 31 and 32: Discussion 25 7bbic 1 .. Avcragc si
Page 33 and 34: Discussion 27 Table VZZ. Nuclear si
Page 35 and 36: 11. Nutritional Secondary Hyperpara
Page 37 and 38: The Nature of the Osteopathy 31 Fig
Page 39 and 40: ’The Nature of the Osteopathy 33
Page 41 and 42: Etiology 35 Experiments and clinica
Page 43 and 44: Clinical Pathology 37 Table X. Seru
Page 45 and 46: 111. Experimental Nutritional Secon
Page 47 and 48: Ration 41 Table XI/. Calcium and ph
Page 49 and 50: Necrops y 43 6. Necropsy The animal
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Page 57 and 58: (:linico-pathologic Determinations
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Page 81 and 82: Serum Phosphorus, Calcium, and Alka
Page 83 and 84: Serum Phosphorus, Calcium, and Alka
Page 85 and 86: The Parathyroid Glands 79 should be
Page 87 and 88: The Skeleton 81 5. The Skeleton The
Page 89 and 90: The Skeleton 83 ary hyperparathyroi
Page 91 and 92: Summary and Conclusions The thesis
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Page 95 and 96: References 89 COILIP, J. B.: 'I'hc
Page 97 and 98: Refereiices 91 ~~CILAN, F. C. and U
Page 99 and 100: Appendix Tables and Statistical Ana
Page 101 and 102: Tables and Statistical Analyses 95
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Nutritional Secondary Hyperparathyroidism in the Horse

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