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Musculoskeletal System
Dystrophies Associated with Calcium, Phosphorus, and Vitamin D
Rickets
Clinical Findings and Lesions
Treatment
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Sections in Veterinary Professionals
  • Behavior
  • Circulatory System
  • Clinical Pathology and Procedures
  • Digestive System
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  • Exotic and Laboratory Animals
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Chapters in Musculoskeletal System
  • Musculoskeletal System Introduction
  • Congenital and Inherited Anomalies of the Musculoskeletal System
  • Dystrophies Associated with Calcium, Phosphorus, and Vitamin D
  • Arthropathies in Large Animals
  • Lameness in Cattle
  • Lameness in Goats
  • Lameness in Horses
  • Lameness in Pigs
  • Lameness in Sheep
  • Myopathies in Ruminants and Pigs
  • Myopathies in Horses
  • Bovine Secondary Recumbency
  • Lameness in Small Animals
  • Arthropathies and Related Disorders in Small Animals
  • Myopathies in Small Animals
  • Osteopathies in Small Animals
  • Sarcocystosis
Topics in Dystrophies Associated with Calcium, Phosphorus, and Vitamin D
  • Overview of Dystrophies Associated with Calcium, Phosphorus, and Vitamin D
  • Rickets
  • Osteomalacia
  • Enzootic Calcinosis
  • Vitamin D3 Toxicity
  • Fibrous Osteodystrophy
  • Hypoparathyroidism
 
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Rickets

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Rickets is a disease of young, growing animals. The most common causes are dietary insufficiencies of phosphorus or vitamin D. Calcium deficiencies can also cause rickets, and while this rarely occurs naturally, poorly balanced diets that are deficient in calcium have been said to cause the disease. As in most diets causing osteodystrophies, the abnormal calcium:phosphorus ratio is most likely the cause.

Clinical Findings and Lesions

The characteristic lesions of rickets are failure of both vascular invasion and mineralization in the area of provisional calcification of the physis. This pathology is most obvious in the metaphyses of the long bones. There may be a wide variety of clinical signs, including bone pain, stiff gait, swelling in the area of the metaphyses, difficulty in rising, bowed limbs, and pathologic fractures. On radiographic examination, the width of the physes is increased, the nonmineralized physeal area is distorted, and the bone may show decreased radiopacity. In advanced cases, angular limb deformity can be seen due to asynchronous bone growth.

Animals fed all-meat diets are commonly affected. Kittens that are fed beef heart exclusively develop locomotor disturbances within 4 wk, even though the high content of digestible protein (>50% on a weight basis) and fat promotes rapid growth, the animals appear well nourished, and their coat maintains a good luster. The predominant clinical signs are reluctance to move, posterior lameness, and ataxia. The kittens often stand with characteristic deviation of the paws. The skeletal disease becomes progressively more severe after 5–14 wk. The kittens become quiet and reluctant to play; they assume a sitting position or sternal recumbency with the hindlimbs abducted. Normal activities may result in the sudden onset of severe lameness due to incomplete or folding fractures of 1 or more bones. Lameness is the initial functional disturbance in growing dogs and may vary from a slight limp to inability to walk. The bones are painful on palpation, and folding fractures of long bones and vertebrae are common.

Rickets and other bone pathologies have been reported in young pigs housed indoors and fed processed feed. Processing of the feed removes natural vitamin D and other fat-soluble vitamins. Without vitamin supplementation, nutritional osteodystrophy may result.

Diets with excessive amounts of calcium (3× normal concentrations) have caused ricket-like signs in growing Great Danes. Several other bone pathologies such as retained cartilaginous cores, osteochondrosis, and stunted growth were seen in these dogs as well.

Treatment

Correction of the diet is the primary treatment. The prognosis is good in the absence of pathologic fractures or irreversible damage to the physes. If the animals are housed, exposure to sunlight (ultraviolet radiation) will also increase the production of vitamin D3 precursors.

Recent studies show that many homemade diets for dogs are deficient in minerals and have altered calcium:phosphorus ratios. Therefore a high-quality commercial food, or one designed by a credentialed veterinary nutritionist, is recommended.

Last full review/revision March 2012 by Walter Gruenberg, DrMedVet, MS, PhD, DECAR, DECBHM

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