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. 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 (Adult Rickets, Bran Disease)
Osteomalacia causes soft and deformed bones, commonly due to insufficient phosphorus or vitamin D in the diet. It develops similarly to rickets 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 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.
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.
In enzootic calcinosis large deposits of calcium in the body contribute to the hardening of soft body tissues. 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. Certain soils in Hawaii, India, Austria, and elsewhere contain these mineral imbalances.
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 somewhat pulled away from the central line of the limb 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. Examination by a veterinarian often reveals a heart murmur as well.
As the disease progresses, the horse loses weight and becomes weak and listless. The coat becomes 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. X-rays and electrocardiography help confirm the diagnosis.
If poisonous plants are to blame, they must be removed from the pastures. 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 and even diminish the soft-tissue mineral deposits.
Last full review/revision July 2011 by Russell R. Hanson, DVM, DACVS, DACVECC; Joerg A. Auer, DrMedVet, Dr h c, MS, DACVS, DECVS; Andrew P. Bathe, MA, VetMB, DACVS, DEO, MRCVS; Leo B. Jeffcott, MA, BVM, PhD, FRCVS, DVSc, VD; Svend E. Kold, DMV, MRCVS, RCVS Specialist in Equine Surgery (Orthopedics); C. Wayne McIlwraith, BVSc, PhD, DSc, FRCVS, DACVS; Dale A. Moore, MS, DVM, MPVM, PhD; Sheldon Padgett, DVM, MS, DACVS; Tracy A. Turner, DVM, MS, DACVS, DABT; Stephanie J. Valberg, DVM, PhD, DACVIM; John F. Van Vleet, DVM, PhD