Outline of Veterinary Skeletal Pathology

contents Ch 2, p 1 Chapter 2, Page 2 Ch 2, p 3 



Outline of Veterinary Skeletal Pathology

Chapter 2 - Bone - Pathologic Conditions

metabolic bone disease


(3) causes.
(a) vitamin D deficiency is considered the classic cause.
(b) calcium deficiency is a fundamental cause; but in actual practice, this seldom causes classic lesions, probably because longitudinal bone growth declines with calcium deficiency.
(i) failure to absorb calcium from the intestinal tract because it has combined with fatty acids from unassimilated fat (celiac rickets) may occur.
(ii) formation of other insoluble complexes between calcium and oxalate or phytate can prevent calcium absorption.
(c) deficiency of phosphorus is obviously able to cause rickets, since this element is essential in forming calcium phosphate.
(i) phosphorus deficiency occurs in herbivorous animals in certain parts of the world (Gulf Coast of the United States and in South Africa) where the soil is deficient in this element.
(ii) phosphorus deficiency also can arise from: steatorrhea, formation of insoluble complexes, and changes in the pH of intestinal contents.
(d) A severely unbalanced calcium-phosphorus ratio in the diet is entirely capable of causing rickets.
(e) Strontium interferes with the conversion of 25-hydroxycholecalciferol to the most active form of vitamin D (1,25-dihydroxycholecalciferol) by the kidneys, and strontium has been used experimentally to produce rickets.
(f) Drugs or disease may interfere with vitamin D hydroxylation in the liver.
(i) Certain drugs such as bisphosphonates can interfere with cartilage matrix mineralization.
(g) Rickets may be an inherited disease.
(i) Vitamin D-resistant rickets is caused by failure of renal absorption of phosphorus or by renal tubular acidosis. There is a persistent hypophosphatemia, but bone lesions can be partially prevented with pharmacologic doses of vitamin D.
(ii) Vitamin D-dependent rickets is caused by a deficiency of the 1-α hydroxylase enzyme (enzyme that converts 25-OH D3 synthesized in the liver to the hormonal form of 1,25 (OH)2 D3) in renal tubules or a failure of the end organ to respond to normal levels of vitamin D hormone.
(4) Pathogenesis.
(a) The lesions or rickets develop because there is inadequate mineralization of physeal cartilage.
(b) When this cartilage does not mineralize:
(i) Metaphyseal blood vessels fail to penetrate the maturing cartilage zone, and
(ii) There is a lack of resorption of cartilage cells.
(c) The result is an increase in the depth of the hypertrophic cartilage cell zone.
(d) In addition, the osteoid forming on the trabeculae of the primary spongiosa fails to mineralize.
(e) Biomechanical stress causes molding of the pliable cartilage and microfractures.
(f) A reparative response leads to:
(i) fibrous tissue deposition,
(ii) more cartilage formation and
(iii) deposition of additional osteoid.
(iv) Finally, low serum calcium concentrations stimulate the parathyroid glands and produce secondary hyperparathyroidism.
(5) Significance and Effect.
(a) Supporting weight on the poorly calcified bones is painful and results in lameness or disinclination to move.
(b) Pathological fractures, even of the vertebral column, are frequent.
(c) In birds, there is reduced hatchability of eggs.

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