Nutritional Secondary Hyperparathyroidism in the Horse

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76 Experimental Nutritional Secondary Hyperparathyroidism in the Horse. . . more subject to stresses and strains ; this will stimulate the osteoblasts to lay down more osteoid tissue.” The level of serum alkaline phosphatase would therefore be “an index not of the degree of hyperparathyroidism but merely of the degree of bone disease”. Concerning the alkaline phosphatase MAJNO and ROUILLER (1951) wrote : “Although theories concerning the mode of action have varied somewhat, the phosphatase remains the undisputed calcification enzyme” (free translation from the original German). As shown in Charts 6 and 8, an inverse relationship between serum calcium and serum alkaline phosphatase was demonstrated in all NSH horses, although the maximums and minimums of serum alkaline phosphatase were somewhat delayed compared to the minimums and maximums of serum calcium. The continuous changes described diphasic curves beginning, in the case of calcium, with a decrease and, in the case of alkaline phosphatase, with an increase. The initial increase of serum alkaline phosphatase, progressing over 18, 11, and 16 weeks in the three NSH horses, respectively, would theoretically be explained by the function of alkaline phosphatase as the calcification enzyme. The stresses and strains on the skeleton, weakened by resorption, would stimulate increased osteoblasticactivity in accordance with the quotation from ALBRIGHT and REIFENSTEIN. Such an explanation seems very unlikely. First, roentgenologic signs of resorption were evident only after 21, 11, and 21 weelis in the three NSH horses, respectively. Second, the mode of action of the parathyroid hormone on the osteoblasts is a depression [GAILLARD (1961)l. The stimulus from stresses and strains for osteoblastic activity would then have to overcome this action of the parathyroid hormone at this early time also. Third, even if the increased serum alkaline phosphatase levels were to be explained as evidence of increased osteoblastic activity, the value of such an explanation is definitely nullified by the sabseqzlent decrease in serum alkaline phosphatase. The demand for increased apposition could not possibly be lowered in any phase of the experiment, especially not in the last stage when radiologic, clinical, and morphologic changes were very dramatic. The explanation for the diphasic changes in serum alkaline phosphatase is rather to be found in the work by RUTISHAUSER and his associates. RUTISHAUSER and MAJNO (1 951) attributed great significance to the changes in the bone tissaeproper in resorption in addition to the sm-$acepherzomena on which the interest had been focused up to that time. They pointed out the evidence for considering the osteocyte and Downloaded from vet.sagepub.com by guest on April 14, 2010
Serum Phosphorus, Calcium, and Alkaline Phosphatase 77 the surrounding fundamental substance an entity: “If the former dies, the latter is destined to be resorbed. It is one of the principal laws of bone tissue.” RUTISHAUSER and MAJNO distinguished two types of osteocyte necrosis, viz., rapid necrosis and slow necrosis or oncosis. “Rapid necrosis apparentIy occurs in osteocytes which have been directly affected by traumatism, and evolves in approximately six hours.” The lacuna is not enlarged and presents clear-cut borders. In oncosis, on the other hand, the duration of the process is from 24 to 36 hours. The osteocyte undergoes swelling, its nucleus may divide, and the lacuna is enlarged and appears rounded. Enlargement of the canaliculi causes the lacuna to be indistinctly outlined. The alkaline phosphatase of the bone cells varies considerably [RUTISHAUSER and MAJNO (1951); MAJNO and ROUILLER (1951)l. The osteoblast gives a highly positive alkaline phosphatase reaction. The young osteocyte contains the enzyme to some degree, but the adult osteocyte lacks it. In the osteocyte undergoing oncosis the enzyme reappears and the staining intensity is comparable to that of the osteoblast. No enzyme activity is left in the empty lacuna after oncosis. RUTISHAUSER and MAJNO therefore concluded that oncosis is a vital phenomenon, caused by irritation of the osteocyte, which then “progresses toward its disease and death”. They referred to this oncosis not only as a regressive change in the osteocyte but also as a special form of bone resorption, the pericytic osteo&sis. The studies on alkaline phosphatase of the osteoclasts by MAJNO and ROUILLER (1951) added further information on the role of this enzyme in resorption of bone. Osteoclasts in the “osteolytic phase” showed an intense alkaline phosphatase staining reaction and so did adjacent bone under resorption. In the “resting phase”, i. e., when osteoclasts were not actively eroding bone but were located at some distance from the bone surface, the osteoclasts showed almost no alkaline phosphatase stain reaction. MAJNO and ROUILLER then concluded that the alkaline phosphatase is not on4 an en? yme of bone apposition but also of bone resorption. With the results of RUTISHAUSER and his associates at hand the interpretation of the serum alkaline phosphatase curves and their inverse relation to those of the serum calcium in our NSH horses offers no difficulties. As the hypocalcemia progresses because of progressing hyperphosphatemia, the demand for calcium removal from the skeleton becomes greater and greater. The induced hyperparathyroidism causes bone resorption, and calcium is liberated to a 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
Page 7 and 8:
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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’I’hc hlicroscopic Anatomy of t
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‘I’lic ihlrcroscopic Anatomy of
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‘I’hc Alicroscopic Anatomy of t
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
Page 51 and 52: Clinical Observations 45 During wee
Page 53 and 54: Clinico-pathologic Determinations 4
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Page 57 and 58: (:linico-pathologic Determinations
Page 59 and 60: Rocntgencilogic Observations 53 Fie
Page 61 and 62: lioentgcnologic Ohscrvntions 55 I,'
Page 63 and 64: Pathologic Anatomy 57 7bb/e XIS. Si
Page 65 and 66: Pathologic Anatomy 59 fhb/c. A’X.
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Page 75 and 76: Pathologic Anatomy 69 Fiq. 37. Cont
Page 77 and 78: V. Experimental Nutritional Seconda
Page 79 and 80: Scruin Phosphorus, Calciiiiii, and
Page 81: 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
Page 93 and 94: Siimmary and Conclusions 87 Rocntgc
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
Page 103 and 104: ’Tablcs and Statistical Analyscs
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Nutritional Secondary Hyperparathyroidism in the Horse

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