The primary vitamin D deficiency disease is a bone disorder called rickets in young animals, generally characterized by a decreased concentration of calcium and phosphorus in the organic matrices of cartilage and bone. Vitamin D results in clinical signs similar to those indicating a lack of calcium or phosphorus or both, as all three are concerned with proper bone formation. In the adult, osteomalacia is the counterpart of rickets and, since cartilage growth has ceased, is characterized by a decreased concentration of calcium and phosphorus in the bone matrix. Outward signs of rickets include the following skeletal changes, varying somewhat with species depending on anatomy and severity: (a) weak bones causing curving and bending of bones, (b) enlarged hock and knee joints, (c) tendency to drag hind legs and (d) beaded ribs and deformed thorax.
Although there appear to be differences among species in the susceptibility of different bones to such degenerative changes, as well as differences that probably reflect bodily conformation (e.g., dog compared with sheep), there is nevertheless an apparent common pattern (Abrams, 1978). Spongy parts of individual bones and bones relatively rich in such tissues are generally the first and most severely affected. As in simple calcium deficiency, the vertebrae and the bones of the head suffer the greatest degree of resorption. Next come the scapula, sternum and ribs. The most resistant bones are metatarsals and shafts of long bones.
Several methods have been used to assess nutritional status of animals deficient in vitamin D. Poor growth rates as well as bone abnormalities in both animals and humans are the chief indications when vitamin D deficiency is substantially advanced. The incomplete calcification of the skeleton is easily detectable with X-rays and reduced bone ash but, like other production-related signs, would not be specific for vitamin D deficiency versus other nutrient inadequacies (e.g., calcium and phosphorus). Deviations from normal in serum calcium, phosphorus and alkaline phosphatase are associated with rickets. For rickets in kittens, serum alkaline phosphatase activity increased markedly in the third month, peaked during the fifth to seventh months, and decreased through the twenty-first month. Serum calcium and inorganic phosphorus concentrations decreased markedly during the acute phase of rickets (Gershoff et al., 1957b).
