Osteomalacia is a disturbance of the bone metabolism of adult animals. The primary cause is an inadequate mineral supply over prolonged periods of time. Diagnosis is based on clinical presentation in combination with the presence of predisposing nutrient deficiencies. Serum biochemical tests, radiography of long bones, and bone biopsies can help confirm the diagnosis. Treatment consists of addressing dietary imbalances.
Osteomalacia has a pathogenesis similar to that of rickets; however, it occurs in mature bones and is associated with disruption of normal bone remodeling. Because bones mature at different rates, both rickets and osteomalacia can occur in the same animal.
Osteomalacia is characterized by an accumulation of excessive unmineralized osteoid on trabecular surfaces. Osteomalacia caused by nutritional deficiencies in adult animals is a chronic disease with protracted development of clinical signs, whereas rickets affects primarily fast-growing juvenile animals.
In horses, nutritional osteodystrophy is known as bran disease, Miller disease, or big head. The diet of pampered horses is often too high in grains and low in forage, and thus high in phosphorus and low in calcium. Nutritional osteodystrophy can cause obscure lameness in horses.
Nutritional osteodystrophy can occur in cattle that graze on arid, infertile soils deficient in phosphorus, if they are not given adequate mineral supplementation.
In mature pigs, bone demineralization typically occurs during lactation or after weaning in herds that have an inadequate supply of dietary calcium, phosphorus, or vitamin D. Affected herds show increased occurrence of lameness and spontaneous bone fractures. Osteomalacia in lactating sows is considered a primary cause of "downer sow syndrome."
Acidogenic diets with excessively low dietary cation-anion difference consumed for a period 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
Animals with osteomalacia are unthrifty and might exhibit pica. Nonspecific shifting lamenesses are common. Fractures can occur, especially fractures of the ribs, pelvis, and long bones. Spinal deformation such as lordosis or kyphosis might be evident.
The pathological 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. Facial deformity can also occur.
Cattle with osteomalacia caused by phosphorus deprivation are unthrifty and have a rough coat. Weight loss, shifting limb lameness, limb deformities, and spontaneous fractures are the most common clinical findings.
Pica can predispose affected animals to esophageal obstruction, reticuloperitonitis, botulism, or other intoxications.
Diagnosis of Osteomalacia
Clinical signs
Serum biochemical analysis
Radiography
Bone biopsy
To establish a firm diagnosis of osteomalacia, the patient's diet should be evaluated for calcium, phosphorus, and vitamin D content. Radiography of affected animals shows 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 measured in blood or urine to assess the extent of ongoing bone mobilization. If dietary calcium and phosphorus content cannot readily be determined (eg, in grazing animals), soil or fecal samples can be analyzed as crude proxies for estimating the dietary intake of these minerals.
No single unambiguous biochemical parameters indicate a diagnosis of osteomalacia. Laboratory testing is used to differentiate dietary etiologies from disturbances of renal mineral handling.
Depending on the primary cause of osteomalacia, patients might display hypocalcemia or hypophosphatemia. The activity of alkaline phosphatase is typically markedly elevated, which only reflects an increase in bone turnover.
Laboratory values used to assess renal function, such as the fractional excretion of minerals in urine, should be within normal limits in animals with nutritional osteodystrophy. In contrast, excessive amounts of calcium or phosphorus in urine indicate disturbed renal handling of minerals.
Treatment of Osteomalacia
Identification and management of underlying etiology
Identifying and addressing the underlying etiology through dietary supplementation is the primary approach to treating osteomalacia. Affected animals should be confined for several weeks after initiation of the supplemental diet. The response to treatment is rapid; usually within 1 week, animals become more active, and their attitude improves.
Even after treatment for osteomalacia begins, animals must be prevented from jumping or climbing, because the skeleton remains susceptible to fractures for a while. Restrictions can be lessened after 3 weeks; however, confinement with limited movement is recommended until the skeleton returns to normal (response to treatment should be monitored radiographically).
Complete recovery from osteomalacia can be achieved within months in animals with no or only minor limb and joint deformities.
Key Points
Osteomalacia is softening of bone that results from calcium, phosphorus or vitamin D imbalance in adult animals.
Causes include absolute dietary insufficiency or increased mineral mobilization from bone due to production losses, such as during lactation.
Treatment requires identification and treatment of the primary cause of calcium, phosphorus, or vitamin D imbalance.
For More Information
Francis RM, Selby PL. Osteomalacia. Baillières Clin Endocrinol Metab. 1997;11(1):145-163.
Also see pet owner content regarding disorders associated with calcium, phosphorus, and vitamin D in dogs, cats, and horses.
