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 hormone), 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 these minerals. These include the type of food, pH within the intestines, 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. Abnormalities of the bones can result, as well as other nutritional and metabolic complications.
Rickets is a disease of young, growing animals that causes soft and deformed bones. It is commonly caused by insufficient phosphorus or vitamin D in the diet. More rarely, calcium deficiencies are to blame. As in most diets causing defective bone formation, the cause is typically an imbalance in the ratio of calcium to phosphorus. Animals fed all-meat diets are commonly affected.
In affected kittens, the most common signs are a reluctance to move, lameness in the hind legs, bowing of the legs, and the inability to control muscle movements. The skeletal disease becomes progressively more severe after 5 to 14 weeks. The kittens become quiet and reluctant to play; they assume a sitting position or lie down with the hind legs stretched out away from the body. Normal activities may result in the sudden onset of severe lameness due to incomplete or folding fractures of one or more bones. In folding fractures, pressure on the bones causes them to slowly “fold” over and deform instead of fracturing. Joints may also appear swollen.
Rickets is diagnosed based on history, signs, physical examination, blood tests, and x-rays. The outlook for treating rickets is good if there are no broken bones or irreversible damage to the bone. The primary treatment is to correct the diet. Exposure to sunlight (ultraviolet radiation) will also increase the production of vitamin D.
Recent studies show that many homemade diets for cats are deficient in minerals and fail to achieve a proper calcium-to-phosphorus ratio. Therefore a high-quality commercial food, or one designed by a credentialed veterinary nutritionist, is recommended.
Osteomalacia develops similarly to rickets but in mature bones. It may be seen in cats that remain indoors and that consume an all-meat diet. The signs are similar to those seen in kittens but may be less severe. Affected animals may fail to thrive, have poor quality fur, and may eat non-food objects. Deformities may also be seen in the spine, including an abnormal inward curving of the spine in the lower area of the back (lordosis) or an abnormal outward curving of the spine (kyphosis). Over time, the bones become brittle and fracture easily. Because bones mature at different rates, both rickets and osteomalacia can be seen in the same animal.
To establish a firm diagnosis, veterinarians will evaluate a cat’s diet to make sure it provides enough calcium, phosphorus, and vitamin D for healthy bones. X-rays can reveal the effects of osteomalacia on the skeleton.
Affected animals should be confined for the first few weeks while the diet is corrected. The response to proper nutrition is rapid. Within 1 week the animals become more active and show an improved attitude. Jumping or climbing must be prevented because the skeleton is still susceptible to fractures. Restrictions can usually be relaxed after 3 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 animals with no or only minor limb and joint deformities.
Rubber jaw syndrome (fibrous osteodystrophy) is a condition in which calcium in bone is replaced by softer connective tissue. It is caused by high levels of a hormone from the parathyroid gland. Hyperparathyroidism refers to elevated levels of parathyroid hormone in the blood. Parathyroid hormone controls the metabolism of calcium and phosphorus in the body. Excessive amounts of the hormone can occur due to overproduction by an abnormal parathyroid gland (primary hyperparathyroidism) or due to abnormally low levels of calcium in the blood (secondary hyperparathyroidism) When too much parathyroid hormone is released over a long period of time, minerals are leached from the skeleton and replaced by immature fibrous connective tissue. Fibrous osteodystrophy affects the entire skeleton but tends to concentrate in the bones of the skull, including the jaw.
In primary hyperparathyroidism, the parathyroid gland produces too much parathyroid hormone, usually because of a benign (non-spreading) but functional tumor. The elevated levels of parathyroid hormone weaken bones, causing lameness and bones that break easily. In some cases, the condition causes a thickening of facial bones. Nasal cavities may be damaged and teeth loosened. Some animals lose the ability to close the mouth properly and develop slow-healing sores in the gums. Often, the jaw bones become coarsely thickened, whereas bones in the skull grow thin. The name “rubber jaw” syndrome refers to advanced cases in which the jaw can be twisted gently due to the degeneration of the bone.
Tests on animals with primary hyperparathyroidism will show an abnormally high level of calcium in the blood. Other tests can be performed to determine phosphorus and parathyroid hormone levels. Because abnormally high levels of calcium in the blood may be associated with many other diseases, additional tests may be necessary to confirm a diagnosis of primary hyperparathyroidism.
The goal of treatment is to eliminate the source of excessive parathyroid hormone production. If one or more tumors is causing the increased parathyroid hormone levels, it must be removed. However, removing the source of the increased hormone production results in a rapid decrease in circulating hormone levels. Calcium levels can drop below normal within 12 to 24 hours after surgery, so the veterinarian must monitor levels closely and correct them if needed. If high levels of calcium persist a week or longer after surgery or recur after initial improvement, a second tumor or the spread of cancer from a malignant tumor may be causing the problem.
An excess of parathyroid hormone (hyperparathyroidism) can also occur due to longterm kidney disease or failure. This type is more common than primary hyperparathyroidism. With progressive kidney disease, excess phosphate in the blood leads to lower calcium levels. Decreased calcium levels in turn trigger an increase in parathyroid hormone levels. In addition, the kidneys are necessary to produce the active form of vitamin D (calcitriol). Too little calcitriol leads to further increases in parathyroid hormone levels.
The most obvious signs include those related to kidney malfunction (vomiting, dehydration, excessive thirst and urination, depression). Bony changes vary with the severity of the kidney disease. Teeth can become loose and may fall out while chewing, and jawbones can become softened and pliable (rubber jaw syndrome) and fail to close properly. Lameness, a stiff gait, and fractures can occur because of weakened bones of the legs.
This type of hyperparathyroidism is diagnosed when laboratory test results show abnormalities consistent with kidney malfunction. Tests will also reveal increased levels of parathyroid hormone in the blood.
Treatment options include modifying the diet, supplementing it with active vitamin D (calcitriol), and giving medication that binds phosphate. Any underlying kidney disease must be managed as well. Prescription diets with restricted dietary phosphorus are available. Your veterinarian can give you specific recommendations for proper treatment options for your cat. Be sure to follow those recommendations and any prescriptions precisely as directed.
Also see professional content regarding disorders associated with calcium, phosphorus, and Vitamin D Dystrophies Associated with Calcium, Phosphorus, and Vitamin Din Animals The principal causes of osteodystrophies are deficiencies or imbalances of dietary calcium, phosphorus, and vitamin D, as well as dysregulation of parathyroid hormone (PTH) activity. Their interrelationships... read more .