Rickets is a disease of the bony growth plate and thus only affects 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 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.
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 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 one 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.
Swine kept in confined housing are susceptible to rickets because of their rapid growth rate combined with lack of exposure to sunlight. Furthermore, diets for market swine are formulated to maximize growth of lean muscle mass with little consideration of requirements for bone formation.
Diets with excessive amounts of calcium (three times normal concentrations) have caused rickets-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.
Typical microscopic lesions associated with rickets are impaired endochondral ossification, which are most prominent in fast-growing bones. Growth plates are widened and irregular, and joints appear enlarged. Trabecula of the spongiosa are thinner, predisposing to infarctions and hemorrhage. Radiographic examination of large bones and joints is the most reliable in vivo diagnostic tool for rickets. The radiopacity of rachitic bones is characteristically less than that of normal bone. Growth plates appear widened and irregular.
Plasma alkaline phosphatase activity is commonly increased. Concentrations of serum phosphorus and vitamin D may be altered depending on the primary cause of rickets. In cases associated with phosphorus or vitamin D deficiencies, concentrations of these compounds in serum are subnormal. Hypocalcemia is seen in advanced stages.
Correction of the diet is the primary treatment for rickets. 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 production of vitamin D3 precursors.
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.