Nutritional Secondary Hyperparathyroidism in the Horse

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32 Nutritional Secondary Hyperparathyroidism in the Horse right mandibular ramus appeared like pumice stone. There can be little doubt that the lesions of the skull bones were those of osteitis ilbrosa cystica. RYCHNER did not commit himself to a diagnosis. The disease exhibited, he stated, some similarities to osteomalacia and some to osteoporosis. HAUBNER (1854) gave a most detailed account of the condition in an 8-year-old riding horse, which had been developing the symptoms for 2 years. His description of the necropsy emphasized the generalized nature of the skeletal changes: “All bones, without exception, show signs of the disease. The lesions are most pronounced in the flat (Fig. 17) and so-called mixed bones and are less striking in the long bones.” The following is quoted from his histologic description : “The microscopic examination of thin slices of different bones always reveals one change in the bone. This change is that the Haversian canals of the compact bone are considerably larger than normal. On longitudinal section it is observed that the widcning of these canals is not uniform; in some areas the canals arc two or three times as wide as in others.” In the same communication HAUBNER described the disease in a pig. His histologic observations are remarkable : “With the help of my colleague PISCIIEL it was proved that an osteoporosis was present here also. It was concluded, however, that the osteoporosis was of a peculiar nature, hitherto never described in textbooks on pathologic anatomy. It differed as I have already pointed out, from the medullary porosis, which it otherwise resembled very closely, mainly in the respect that a firm fibrous cellular tissue occupied the bone space and, which I like to add, contributed to the enlargement of the bones, although it may not have been the only cause of this enlargement.” This is a clear-cut description of generalized osteitis fibrosa. It was given in 1854, 4 years before VIRCHOW’S Cellzdar Pathology appeared, 19 years before KOLLIKER published his classical treatise on resorption of bone, and it anticipated VON RECKLINGHAUSEN’S description of generalized osteitis f-ibrosa in man by 37 years. In agreement with HAUBNER, DOR (1902) showed that the osteopathy in maladie dzt son is generalized; he applied the term “rarefying osteitis”. He believed that the horse disease was comparable to PAGET’S (1877) osteitis deformans but noted a difference between the two conditions. In PAGET’S disease the cranial bones are more commonly involved than the jaws, which DOR, like earlier and later investigators, found to be most severely affected in the horse. Downloaded from vet.sagepub.com by guest on April 14, 2010
’The Nature of the Osteopathy 33 The term “osteitis fibrosa” for the osseous lesions in nutritional secondary hyperparathyroidism in the horse was first used by JOST (1910). He gave a detailed description of the histologic changes in the skull bones of a 6-year-old horse. He described all anatomical characteristics of osteitis fibrosa and presented several photomicrographs to support his diagnosis. JOEST and ZUMPE (1924) showed that other bones (cervical vertebra, humerus, femur) exhibit the same changes. The investigations by JOST and by JOEST and ZUMPE thus revealed that the osteopathy in bran disease is a generalized osteitis fibrosa. Nevertheless, the later literature does not show any uniformity in nomenclature. The disease continued and continues to be described as
Page 1 and 2: Pathologia Veterinaria Online http:
Page 3 and 4: Supplementum ad Vol. 1 (1964) Patho
Page 5 and 6: V . Experimental Nritritional Secon
Page 7 and 8: Introduction and Object of Investig
Page 9 and 10: I. The Anatomy of the Parathyroid G
Page 11 and 12: Comparative Aspects of the Embryolo
Page 13 and 14: The Aracroscopic Anatomy of the Equ
Page 15 and 16: The Microscopic Anatomy of the Equi
Page 17 and 18: 'I'hc hlicroscopic Anatomy of the E
Page 19 and 20: ’The I\licroscopic Anatomy of the
Page 21 and 22: 10 . 9 . a . 7 0 + 6 . 5 . 0 ’I
Page 23 and 24: ‘The hl icroscopic Anatomy of the
Page 25 and 26: ’I’hc hlicroscopic Anatomy of t
Page 27 and 28: ‘I’lic ihlrcroscopic Anatomy of
Page 29 and 30: ‘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: The Nature of the Osteopathy 31 Fig
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 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
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The Skeleton 83 ary hyperparathyroi
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Summary and Conclusions The thesis
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Siimmary and Conclusions 87 Rocntgc
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References 89 COILIP, J. B.: 'I'hc
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Refereiices 91 ~~CILAN, F. C. and U
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Appendix Tables and Statistical Ana
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Tables and Statistical Analyses 95
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’Tablcs and Statistical Analyscs
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Nutritional Secondary Hyperparathyroidism in the Horse

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