Osteomalacia has a pathogenesis similar to that of rickets but is seen in mature bones and associated with disruption of normal bone remodeling. Because bones mature at different rates, both rickets and osteomalacia can be seen in the same animal. Osteomalacia is characterized by an accumulation of excessive unmineralized osteoid on trabecular surfaces.
In horses, nutritional osteodystrophy is known as bran disease, miller’s disease, and “big head.” The diet of pampered horses is often too high in grains and low in forage; such a diet is high in phosphorus and low in calcium. Many of the obscure lamenesses of horses have been attributed to nutritional osteodystrophy.
Nutritional osteodystrophy can occur in cattle grazing on arid, infertile soils deficient in phosphorus if they are not given adequate mineral supplementation.
Acidogenic diets with excessively low dietary anion-cation difference consumed over a course of months can also result in demineralization and ensuing osteomalacia, because even mild but sustained metabolic acidosis tends to stimulate osteoclast activity.
Animals with osteomalacia are unthrifty and may exhibit pica. Nonspecific shifting lamenesses are common. Fractures can be seen, especially in the ribs, pelvis, and long bones. Spinal deformation such as lordosis or kyphosis may be seen.
The pathologic changes of bran disease in horses are similar to those in other species, with the provisos that the bones of the head are particularly affected in severe cases and that gross or microscopic fractures of subchondral bone (with consequent degeneration of articular cartilage and tearing of ligaments from periosteal attachments) are dominant clinical signs. Unilateral facial deformity due to secondary (nutritional) hypoparathyroidism has been reported in a 1-year-old filly.
Cattle with osteomalacia caused by phosphorus deprivation are unthrifty and have a rough hair coat. Weight loss, shifting limb lameness, limb deformities, and spontaneous fractures are the most common clinical findings. Pica may predispose affected animals to esophageal obstruction, reticuloperitonitis, botulism, or other intoxications.
To establish a firm diagnosis of osteomalacia, the diet should be evaluated for calcium, phosphorus, and vitamin D content. There is radiographic evidence of generalized skeletal demineralization, loss of lamina dura dentes, subperiosteal cortical bone resorption, bowing deformities, and multiple folding fractures of long bones due to intense localized osteoclast proliferation. Bone biomarkers such as hydroxyproline, an amino acid released into blood during bone mineralization can be determined to assess the extent of ongoing bone mobilization. If the dietary calcium and phosphorus content cannot readily be determined (eg, in grazing animals), soil or fecal samples can be analyzed as crude proxies for dietary intake of these minerals.
Laboratory values used to assess renal function should be within normal limits in animals with nutritional osteodystrophy.
Identify and address the underlying deficiencies
Animals with osteomalacia should be confined for several weeks after initiation of the supplemental diet. Response to therapy is rapid; within 1 week the animals become more active, and their attitude improves. Jumping or climbing must be prevented, because the skeleton is still susceptible to fractures. Restrictions can be lessened after 3 weeks, but confinement with limited movement is indicated until the skeleton returns to normal (response to treatment should be monitored radiographically). Complete recovery can be achieved within months in animals with no or only minor limb and joint deformities.