Osteodystrophia fibrosa is a bone disorder arising due to secondary calcium deficiency in horses, pigs and goats. The disease is characterized by painful weak bones due to defective mineralization.
Aetiology: Excessive phosphorous intake, associated with secondary calcium deficiency, is the common cause of osteodystrophia fibrosa in horses and probably in pigs. A low calcium intake (2-3 g per day) and calcium: phosphorous ratio of 1:1.3 is reported to produce disease in horses. The disease can even occur when calcium in diet is normal but calcium: phosphorous ratio is greater (1:1.5). Heavy work, racing, and feeding of diet rich in cereal hays or heavy grains or oxalates can predispose the disease. Army horses moved to new territory and those in age group of 2-7 years are most likely to be affected. In pigs, the disease is produced due to diet low in calcium and high in phosphorous or deficient in both calcium and phosphorous.
Clinical findings: Imbalance of calcium: phosphorous ratio due to excess phosphorous intake causes hyperparathyroidism and development of fibrous dysplasia and painful-weak bones. Characteristic signs in horses include shifting lameness, and sometimes arching of back. Many cases of obscure lameness in horses may be attributable to nutritional osteodystrophia. Horses may be mildly lame without apparent physical abnormality. While the horse walks, the joints creak badly due to relaxation of tendon and ligaments. Fracture and visible sprains of tendon are found in more advance cases. The disease is also known as ‘big head’ as there is local swelling of the lower and alveolar margins of mandible followed by soft symmetrical enlargement of facial bones. Swelling of joints, curvature of long bones and flattening of rib bones are also observed.Affected pigs show gross distortion of limbs and enlargement of joints and the face. Lameness, pain on standing, reluctance to rise and bending of legs are seen in less severe cases. In goats, prominent signs include symmetrical enlargement of the face and jaws, protrusion of tongue, tremors and outward symmetrical bending of hind limbs.
Diagnosis: Disease is diagnosed by history, clinical signs and laboratory analysis of diet, and clinico-pathological changes in blood (low calcium and high inorganic phosphorous values in serum). High incidence of lameness in horses needs to be investigated by detailed chemical analysis of ration for calcium: phosphorous ratio.
Treatment and Prevention: The affected animals are treated by correcting dietary imbalances. Cereal fodders are replaced by leguminous fodder. Calcium: phosphorous ratio should be maintained in the vicinity of 1:1 and not greater than 1:1.4. Finely ground limestone (30 g daily) may be added to cereal hay to correct imbalances