Osteomalacia
(Adult rickets) |  |
| Osteomalacia has a pathogenesis similar to that of rickets but it is seen in mature bones. Because bones mature at different rates, both rickets and osteomalacia can be seen in the same animal. Osteomalacia is characterized by an accumulation of excessive unmineralized osteoid on trabecular surfaces. |
| Clinical Findings: |
| Affected animals are unthrifty, may have abnormal estrus, and may exhibit pica. Nonspecific shifting lamenesses are common. Fractures can be seen, especially in the ribs, pelvis, and long bones. Spinal deformation such as lordosis or kyphosis may be seen. |
| In horses, nutritional osteodystrophy is known as
bran disease,
miller’s disease, and “big head.” The diet of pampered horses is often too high in grains and low in forage; such a diet is high in phosphorus and low in calcium. Many of the obscure lamenesses of horses have been attributed to nutritional osteodystrophy. The pathologic changes are similar to those in other species, with the provisos that the bones of the head are particularly affected in severe cases and that gross or
microscopic fractures of subchondral bone (with consequent degeneration of articular cartilage and tearing of ligaments from periosteal attachments) are dominant clinical signs. Unilateral facial deformity due to secondary (nutritional) hypoparathyroidism was recently reported in a 1-yr-old filly. |
| Nutritional osteodystrophy is uncommon in cattle and sheep but is seen occasionally in feedlots. Marrow fibroplasia is not a feature of the condition in these species. Osteoporosis is the dominant lesion, but “big head” may be seen in goats. Bone deformities in recovered animals can cause obstipation or dystocia. |
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| Diagnosis: |
| To establish a firm diagnosis, the diet should be evaluated for calcium, phosphorus, and vitamin D content. There is radiographic evidence of generalized skeletal demineralization, loss of lamina dura dentes, subperiosteal cortical bone resorption, bowing deformities, and multiple folding fractures of long bones due to intense localized osteoclast proliferation. Laboratory values used to assess renal function should be within normal limits in animals with nutritional
osteodystrophy. |
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| Treatment: |
| Affected animals should be confined for several weeks after initiation of the supplemental diet. Response to therapy is rapid; within 1 wk the animals become more active, and their attitude improves. Jumping or climbing must be prevented because the skeleton is still susceptible to fractures. Restrictions can be lessened after 3 wk, but confinement with limited movement is indicated until the skeleton returns to normal (response to treatment should be monitored
radiographically). |
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