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 maintaining strong, healthy bones.
The primary source of calcium and phosphorus is the diet, but a number of factors affect how the body absorbs calcium and phosphorus. These include the source of the minerals as well as the levels of vitamin D in the body. Vitamin D is obtained either through the diet or by exposure to sunlight. Vitamin D must also be activated within the liver and kidney. Because of the role it plays in the body, if the vitamin or its activity is decreased, calcium and phosphorus absorption are reduced. Bone deformities can result, as well as other nutritional and metabolic complications.
Osteomalacia causes soft and deformed bones, commonly due to insufficient phosphorus or vitamin D in the diet. It develops similarly to rickets (which affects the growth plate in growing animals) but in mature bones.
In horses, osteomalacia is sometimes known as bran disease, miller’s disease, and “big head.” The diet of pampered horses often contains too much grain and too little forage, making it high in phosphorus and low in calcium. In cases where a horse becomes lame for no apparent reason, the cause is frequently attributed to osteomalacia. In severe cases the disease may cause structural changes and swelling of the bones of the head. Signs may include microscopic and obvious breaks in bone beneath cartilage (followed by degeneration of the joint cartilage and tearing of ligaments).
To establish a firm diagnosis, your veterinarian will evaluate your horse’s diet to make sure it provides enough calcium, phosphorus, and vitamin D for healthy bones. X-rays will reveal the effects of osteomalacia on the skeleton. Blood or fecal tests may also be necessary.
Affected horses should be confined for the first few weeks after the diet is corrected. The response to proper nutrition is rapid. Within 1 week the horses become more active and show an improved attitude. Restrictions on activity can usually be relaxed after several weeks, but confinement with limited movement is recommended until the skeleton returns to normal. Response to treatment can be monitored using x-rays. Complete recovery can be achieved within months in horses with no or only minor limb and joint deformities.
In enzootic calcinosis large deposits of calcium in the body contribute to the hardening of soft body tissues (such as the heart, lungs, kidneys, and tendons). The condition can be caused by plant poisoning or less commonly mineral imbalances in the soil.
Wild jasmine, day-blooming jessamine, king-of-the-day (Cestrum diurnum); golden oats or yellow oat grass (Trisetum flavescens); as well as some other plants (Nierembergia veitchii, Solanum species) contain a substance in their leaves that bypasses the body’s feedback mechanism for regulating levels of the active form of vitamin D (calcitriol). An excess of vitamin D in turn may trigger the deposit of excessive calcium in the soft tissues called calcinosis. Dietary mineral imbalances such as excessive phosphate or calcium, as well as deficiencies of magnesium, potassium, and nitrogen, may worsen the tissue hardening that is caused by plant poisoning. Calcinosis caused by the ingestion of Cestrum diurnum can also impair the formation of bone (osteodystrophy). Enzootic calcinosis is most common in certain areas of Hawaii, India, Brazil, Argentina, Papua-New Guinea, and Jamaica, especially at higher altitudes (up to 5,000 feet above sea level).
Calcinosis progressively worsens over weeks or months. The earliest signs are a stiffened and painful gait, which is most obvious when the horse rises after prolonged rest. Severely affected horses stand with their forelimbs rotated outward and displaced at the shoulder joints. The flexor tendons, particularly the suspensory ligaments, are painfully sensitive. The fetlock joints are overextended to varying degrees. When affected horses are forced to walk, they take short steps, and their gait is awkward, stiff, and slow. After walking only short distances, the horse may display labored breathing. Examination by a veterinarian often reveals a heart murmur and rapid heart rate as well.
As the disease progresses, the horse loses weight and becomes weak and listless. The coat may become shaggy, dull, and faded. As the animal loses muscle mass, the skeleton may become pronounced and the abdomen tucked up. The spine may curve upward (causing the animal to appear hunched over), and the tailhead may rise. Appetite is usually unaffected, although it may become poor.
Diagnosis may be difficult at early stages but is usually based on a medical history and examination of physical changes to the horse. Abnormal levels of minerals in the blood and the presence of poisonous plants in the feed or on pasture are additional clues. X-rays and electrocardiography help confirm the diagnosis by identifying calcium deposits in soft tissues.
If poisonous plants are to blame, they must be removed from the pasture or feed. When the disease is associated with the mineral content of the soil, however, control may be more difficult. A change of pasture, forage, and environment may reduce the signs. No treatments are currently available to reverse the soft-tissue mineral deposits.
Also see professional content regarding disorders associated with calcium, phosphorus, and vitamin D.