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.
Clinical Findings of Osteomalacia in Animals
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 Esophageal Obstruction in Large Animals Esophageal obstruction, commonly known as choke, occurs secondary to obstruction of the esophagus with food or foreign objects. Symptoms include nasal discharge of feed, coughing, bloat, and... read more , reticuloperitonitis, botulism Botulism in Animals Botulism most commonly results from ingestion of toxin in food. The usual source of the toxin is decaying carcasses or vegetable material. Clinical signs are caused by flaccid muscle paralysis... read more , or other intoxications.
Diagnosis of Osteomalacia in Animals
Based on clinical signs and confirmed by serum biochemistry, radiographs, or bone biopsy
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.
Treatment of Osteomalacia in Animals
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.
Osteomalacia is a bone metabolic disturbance of adult animals.
Proper mineralization of bone is impaired through inadequate mineral supply.
For More Information
Also see pet health content regarding osteomalacia in dogs Adult Rickets (Osteomalacia) Also see professional content regarding disorders associated with calcium, phosphorus and Vitamin D. Defective bone formation is called osteodystrophy. It is caused in most cases by deficiencies... read more , osteomalacia in cats Adult Rickets (Osteomalacia) Defective bone formation is called osteodystrophy. It is caused in most cases by deficiencies or imbalances of calcium, phosphorus, and vitamin D, and the hormone that regulates them (parathyroid... read more , and osteomalacia in horses Osteomalacia (Adult Rickets, Bran Disease) Defective bone formation is called osteodystrophy. It is caused in most cases by deficiencies or imbalances of calcium, phosphorus, and vitamin D, all of which are important in creating and... read more .