Outline of Veterinary Skeletal Pathology

contents Ch 2, p 3 Chapter 2, Page 4 Ch 2, p 5 



Outline of Veterinary Skeletal Pathology

Chapter 2 - Bone, Pathologic Conditions

C. Nutritional and Toxic Disorders
1. Vitamin D.
a. Deficiency. Vitamin D deficiency may be a cause of rickets in young animals (see metabolic bone disease). However, the lesions of vitamin D-deficiency rickets may not develop when there is inadequate dietary vitamin D or lack of skin synthesis, because the young are born with sufficient liver stores of vitamin D to maintain them through their growth period. Vitamin-D deficiency becomes particularly apparent if animals are fed diets that lack proper calcium and phosphorus concentrations. If vitamin-D deficient animals have parathyroid hyperplasia, fibrous osteodystrophy may occur (see metabolic bone disease).
b. Toxicity.
(1) Incidence. Vitamin-D toxicosis is rare except under special circumstances.
(2) Sources. Fatal poisonings are seen following the ingestion of vitamin-D containing rodenticides and overenthusiastic or inadvertent dietary supplementation. Several plants, Solanum malacoxylon, Cestrum diurnum, and Trisetum flavescens, contain vitamin-D compounds that are highly toxic.
(3) Mechanisms
(a) ingestion of vitamin D or toxic plants containing vitamin-D compounds increases serum concentrations of vitamin-D hormone (1,25(OH)2D3).
(b) hormonal action on enterocytes causes increased absorption of calcium from the gastrointestinal tract.
(4) Pathology.
(a) macroscopic appearance. Soft tissue calcification may vary, but there is a predilection for deposition in fibroelastic tissues of organs, in particular the arteries and heart, pulmonary alveolar septa, the mucosa and muscularis of the stomach, splenic capsule and the kidney.
(b) microscopic appearance. Excess of vitamin-D hormone causes exuberant osteoblastic activity that results in an increased volume of osteoid on trabecular surfaces (fig. Ib3-1).
(i) there is a mineralization defect that is transitory and results in unmineralized foci in osteons (fig. Ib3-2).
(ii) after mineralization, trabecular thickness is increased, and there is an increased volume density of bone in the spongiosa.
(iii) the mineralization defect leads to accumulation of basophilic bone matrix (fig. Ib3-3) and development of rib infractions (incomplete fractures) in young horses (fig. Ib3-4).

2. Vitamin-C deficiency (Scurvy).
a. Domestic animals normally are capable of synthesizing vitamin C in the liver and are not subject to deficiency. Certain species, including primates, some birds, guinea pigs and fish, are incapable of synthesizing the vitamin and develop scurvy (fig. Ib3-5).
b. Deficiency causes a marked reduction in the synthesis of collagen, and formation of bone matrix ceases.
c. Scurvy occurs infrequently when rations are stored improperly or for too long a period in laboratory animal facilities.
d. The disease can have devastating effects on animals in experiments.
e. The condition is characterized in young animals by muscle and periosteal hemorrhages (fig. Ib3-6) and in adult nonhuman primates by bleeding of the gums or cephalohematomas (figs. Ib3-7, Ib3-8).
(1) in growing animals, the bones develop metaphyseal fractures (fig. Ib3-6) with primitive appearing reparative tissue (figs. Ib3-9, Ib3-10); and
(2) in adults, bones become osteopenic.

3. Vitamin A.
a. Deficiency. Although vitamin A is not synthesized by the body, the ingested compound acts as a hormone.
(1) deficiency affects bone growth and retards bone development.
(2) disproportionate growth of the central nervous system and its surrounding bone leads to the skull compressing the brain resulting in herniation of the cerebellum into the foramen magnum.
(3) vertebral compression of the spinal cord causes spinal roots to herniate into intervertebral foramina.
(4) retarded bone resorption (bone modeling) of the internal auditory meatus in the dog causes deafness.
(5) in neonatal calves and weanling pigs, failure of the optic foramina to enlarge to accommodate the optic nerves, results in their compression and blindness.
b. Toxicity. Vitamin A toxicity in weanling pigs and neonatal calves causes focal premature closure of the physeal plate.
(1) may result in disproportionate shortening of the limbs and abnormal contour of the articular surfaces (see hyena disease in calves).
(2) it causes a hyperostotic bone disease in cats (fig. Ic-63).

4. Fluorosis is the condition caused by ingesting toxic amounts of fluoride
a. Incidence. All species are susceptible, but because of the manner in which chronic poisoning occurs, fluorosis usually is restricted to sheep and cattle.
b. Sources.
(1) toxicity occurs from drinking contaminated subsurface water often in areas where rock phosphates are plentiful.
(2) it also occurs when feed, usually contaminated from industrial effluents, is eaten.
c. Mechanism.
(1) upon absorption, fluoride is partly deposited in bone and developing teeth and partly excreted in urine.
(a) fluoride ions have the ability to replace hydroxyl ions in the hydroxy apatite crystal lattice.
(b) when the content of fluoride in bone reaches 2,500 ppm, major pathological changes begin to occur.
d. Pathology.
(1) macroscopic appearance. Dental lesions occur only if intoxication occurs while the teeth are in their developmental stages (figs. Ib3-11, Ib3-12). Changes in the teeth begin in the enamel.
(a) this is normally glistening but in affected teeth is mottled with small dry and chalky foci.
(b) large areas of mottling lead to uneven wear, attrition, and chip fractures.
(c) the teeth become discolored yellow, brown or black.
(d) the bones show evidence of exostoses that occurs most commonly in the mandible and metatarsals (fig. Ib3-13).
(e) joint surfaces are usually normal, but there may be ossification of tendinous and ligamental insertions on bone.
(2) microscopic appearance.
(a) changes in the osteons appear (mottling), which are characterized by:
(i) hypomineralization,
(ii) enlarged osteocyte lacunae in the periphery of the Haversian system (osteon),
(iii) tangled canaliculi,
(iv) increased numbers of peripheral Haversian osteocytes, and
(v) loss of osteocytes in the remainder of the osteon (fig. Ib3-14).
(b) the cortex becomes osteoporotic and may become reinforced by formation of new periosteal bone (fig. Ib3-15).

5. Lead poisoning results from accidental ingestion or occupational exposure
a. Incidence. Lead poisoning use to be more common and fatal in cattle and less common in sheep. It is rarely observed in pet animals.
b. Source. Paint, metallic lead in storage batteries, and putty cans from rubbish dumps are sources.
c. Mechanism. The principal sites of lead deposition are the red cells, the liver, and the skeleton. Over 90% of this lead accumulates in bone because of the relatively low exchange in bone. Lead is incorporated into bone during its mineralization.
d. Pathology.
(1) macroscopic appearance. Lead poisoning may cause bone lesions in growing animals. Lack of adequate osteoclastic resorption of metaphyseal trabeculae leads to osteosclerosis, and radiographs may show transverse lines of increased density below the physeal plates (lead lines) (fig. Ib3-16).
(2) microscopic appearance. When bone containing lead is resorbed by osteoclasts, they develop ultrastructural alterations including lead inclusions that are morphologically similar to those produced in other body organs such as the kidney. When lead-containing matrix is taken up by the osteoclast, the lead interferes with the osteoclast's ability to resorb bone, and this may result in failure to resorb the primary spongiosa. The result in growing dogs that consume sufficient amounts of lead is that the mineralized cartilage and bone of the primary spongiosa is retained, and this is responsible for the osteosclerosis ("lead lines") seen radiographically.

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