The primary disease of vitamin D deficiency is rickets, generally characterized by a decreased concentration of calcium and phosphorus in the organic matrices of cartilage and bone. A deficiency of vitamin D results in clinical signs similar to those of 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, it 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 cause 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., pig compared with sheep), there is nevertheless an apparent common pattern (Abrams, 1978). Spongy parts of individual bones and bones relatively rich in such tissue 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.
For swine specifically, a deficiency of vitamin D causes poor growth, stiffness, lameness (Illus. 1), stilted gait, a general tendency to "go down" or lose the use of the limbs (posterior paralysis), frequent cases of fractures, softness of bones, bone deformities, beading of the ribs, enlargement and erosion of joints and unthriftiness (Cunha, 1977). Bones may also be deformed by the weight of the animal and the pull of body muscles.
