Metabolic Bone Disease

Metabolic bone disease, or MBD, is a preventable problem that can occur in animals we rehabilitate. MBD has also been seen in wild animals with no prior human contact, though this is rare. A knowledge of this condition, and it's causes, can help us care properly for those species particularly at risk.

MBD is most often caused by improper diet. Vitamin D, which under normal circumstances the body produces on it's own (needing sunlight to do so), is vital to the body's ability to absorb calcium. Sun received through windows and window screens is not adequate because these filter the important UV rays necessary for this to take place. Professionally formulated milk replacers have vitamin D in them, but as the animal is weaning they are receiving less and less of this vital nutrient so 20 minutes of full sun a day is recommended, or all spectrum or full spectrum bulbs can be used if the former is not possible. Because the formula we feed is balanced with *all* the vitamins necessary, the weaning diet is critical.

Since MBD can get started in as little as 5 days time, an animal that is not eating needs to be monitored closely. Often the signs are slight, and by the time it is obvious what is going on, correcting it becomes more difficult. MBD also affects the internal organs as well; so what we see on the outside is just the tip of the iceberg.

Some of the more subtle signs of MBD are excessive sleeping, not wanting to move around or jump and climb. (Birds may limp, favor one leg, become reluctant to stand, or acquire unexplained fractures). MBD hurts! The bones (being effected the most), and muscles become weak and the animal is in pain. Swollen joints and improper bone growth (legs splaying in or out) are also sign of MBD's progression. In more drastic cases there are seizures and lack of use of the back legs. Because MBD is the thinning of the bone, a fall that would not normally have any effect can cause a leg or the spine to fracture or break.

One way to tell if you are dealing with MBD is a radiograph (advanced cases) however the stress factor on the animal must be taken into account. The other is to watch how they move and observe their abilities. Can they hang upside down without discomfort? Are they using the full extension of their legs and body, (in other words moving *freely*)? It is important for you to know what *normal* is so that you can identify the possible onset of MBD in the early stages.

In rare cases, MBD is not caused by incorrect diet but by genetics. The body doesn't synthesize sun properly to create vitamin D, or the body doesn't process calcium correctly. While this is extremely rare, it has happened. Another possible cause of MBD, when a correct diet is being fed, is hierarchy. Even young animals have a pecking order and often the one at the bottom doesn't get the adequate food needed to keep calcium/phosphorus at the proper levels. Again, a good commercial diet that makes up 80% of their daily food will go a long way in preventing this. Monitoring weight gain, growth and overall health will let you know if this is happening.

MBD can be treated, but the sooner it is caught the better. Correcting the diet, if that is the problem, is the first order of business. Adding additional calcium, along with making sure there is adequate access to vitamin D through natural sunlight or lighting mentioned above has proven to work well. Supplementing with actual vitamin D should only be done under the supervision of veterinarian; vitaimin D is a fat soluble and can build up and become toxic (more is *not* always better).

The most important thing to remember is an ounce of prevention is worth a pound of cure. In a perfect world Ca/Ph should be at 2:1 and a good commercial diet that is balanced is the place to start. For the other 20% of the daily foods there are many dietary books on the market that will help you in keeping the Ca/Ph ratios close to the exceptable level. Also see Vitamin/Mineral Sources

These are just the very basics, and depending on the severity of the MBD, other steps may also be necessary. If you have never dealt with MBD before it is important that you check with your veterinarian and/or another rehabilitator that is familiar with the problem and procedure.

It is important that we understand what part calcium and phosphorus play in the body. Below is a straight forward explanation of the very important rolls these two minerals, (also known as macroelements) have in bone growth and overall development of the animals in our care.

"They are major mineral constituents of the animals body and are largely associated with skeletal formation. Calcium is also important in blood clotting, excitability of nerves and muscles, acid-base balance, enzyme activation and muscle contraction, whereas phosphorus is involved in almost every aspect of animal metabolism, such as energy metabolism, muscle contractions, nerve tissue metabolism, transport of metabolites, nucleic acid structure,and carbohydrate, fat, and amino acid metabolism."
Source: Robbins, Wildlife Feeding and Nutrition, Second Edition.

Nonda Surratt
Special thanks to Dr. Anne Hiss & Pat Chamberlain


  • SQ 0.5-1 mL/kg of a 5 mg/mL calcium gluconate + mg/mL calcium lactate solution, and maintained with an oral supplement *1
  • Birds do not use vitamin D2 efficiently; vitamin d3 should be used when vitamin D is added to avian diets. *2
  • Rickets has been reported in...vitamin-D-deficient diets, even though they contained normal amount of calcium and phosphorus. *3
  • Animals that are exposed to sunlight for as little as 1 hr/day synthesize ample vitamin D in the skin and do not require high levels in their feed. *4
  • Calcium, phosphorus, and vitamin D are related closely in metabolism. Vitamin D, which is produced in the skin as vitamin D3 or eaten in the diet as vitamin D2, is essential for adequate absorption of calcium and phosphorus. It is important to realize that vitamin D3 is much more potent...than is D2 *5
  • However, feeding diets that contain >2.5% Ca during the growing period produces a high incidence of nephrosis, visceral gout, calcium urate deposits in the ureters, and at times, high mortality. *6

References: The Merck Veterinary Manual, Seventh Edition, p. 1011 *1, p. 1211 *2; 1165 *3; *4 1190; 1200 *5; 1268 *6

Dairy Council Digest on Calcium

According to a recent review of calcium preparations, there are at least a dozen common calcium preparations and hundreds of different formulations available. Calcium carbonate is the most common preparation; some others include tricalcium phosphate, dicalcium phosphate, bone meal, calcium citrate-malate, oyster shell, calcium lactate, and calcium gluconate. These calcium preparations differ in a variety of ways. Calcium carbonate has the highest concentration of calcium by weight (40%), whereas calcium citrate has 21% calcium and calcium phosphate has 8% calcium by weight.


Although calcium carbonate has the highest concentration of calcium by weight, this form of calcium is relatively insoluble, especially at a neutral pH. In contrast, calcium citrate, although containing about half as much calcium by weight, is a more soluble form of calcium. Because calcium citrate does not require gastric acid for absorption, it is a better choice for patients with achlorhydria (i.e., limited gastric acid production).

In addition to the amount (dosage) of calcium in various supplements, the solubility and absorption of calcium must be considered. In general, there are not large differences in the absorption of calcium from different calcium supplements or foods. However, the solubility of calcium supplement preparations needs to be considered. Prior to absorption, calcium preparations must dissociate into elemental calcium. The more soluble a calcium supplement product is in vitro (i.e., measured by the ability to dissolve in 6 ounces of vinegar within 30 minutes), the more soluble the calcium preparation is in the body. Because of better manufacturing processes, name brand supplements may be more bioavailable than generic products.

While dosage and solubility can influence the bioavailability of calcium from calcium supplements, the timing of intake and meal conditions also are important. Calcium from supplements appears to be more efficiently absorbed when consumed in divided doses, each containing less than 500 mg of elemental calcium. The NIH Consensus Conference recommends consuming calcium supplements between meals to increase calcium bioavailabilty.

The long-term safety of consuming large doses of single nutrients including calcium is of concern. Although calcium intakes up to 2,000 mg/day appear to be safe for most individuals, potential adverse effects can occur as a result of chronic high intakes or intakes of specific calcium preparations. Potential adverse effects include gastrointestinal problems such as constipation. Certain preparations of calcium (e.g., bone meal, dolomite) may contain contaminants such as lead, aluminum, arsenic, mercury, and cadmium. Significant amounts were identified in calcium carbonate supplements labeled oyster shell or natural source. Chronic intake of these supplements may pose an unnecessary risk. Most commercial calcium preparations are tested for heavy metal contamination.

High intakes of calcium supplements may interfere with the absorption of other nutrients such as iron and zinc. Intake of calcium supplements also may interfere with the absorption of concurrently consumed medications, and vice versa. Other potential adverse effects of chronic intakes of high doses of calcium include milk-alkali syndrome (ectopic calcium deposition), hypervitaminosis D (i.e., in the case of supplements containing calcium and vitamin D), and possible hypercalciuria leading to kidney stone formation. However, recent studies indicate that increased intake of calcium does not increase risk of kidney stones. Moreover, restricting dietary calcium may increase urinary excretion of oxalate which in turn increases risk of kidney stones.

Source: Dairy Council Digest, January/February 1995, Volume 66, Number 1


Additional Data

Additional Data on Calcium/Phosphorus/D3 ratios and dietary sources

Hypercalcemia and Vitamin D Toxicity

V. Hypercalcemia and Vitamin D Toxicity

Excessive consumption
Abnormal conversion of vitamin D to its biologically active metabolites (sarcoidosis, lymphoma, other granulomatous diseases - 1-hydroxylase present in macrophages of granulomas)
Laboratory findings

Elevated 25-hydroxyvitamin D (e.g., excessive consumption) and/or 1,25-dihydroxyvitamin D (e.g., sarcoidosis)
Hypercalciuria (often greater than seen in primary hyperparathyroidism) -PTH is suppressed

Treatment: glucocorticoids (dexamethasone, prednisone, etc) inhibit calcium absorption in the GI tract and inhibit conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D


Source:Pathophysiology of Calcium Metabolism Hypercalcemia, Hypocalcemia, Osteoporosis;
Allan D. Marks, MD