Calcium Article #1

Melissa Kaplan's
Herp Care Collection
Last updated April 19, 2007

Calcium metabolism and metabolic bone disease
©1995, 2002 Melissa Kaplan
Secondary nutritional hyperparathyroidism.
Fibrous osteodystrophy.

While the terms may differ depending upon the orientation of the user (veterinarian, pathologist, radiologist) they all refer to something which strikes fear into (or should!) the hearts and minds of reptile owners: calcium deficiency.

Calcium deficiency is actually a sort of generic term which represents only one of the possible causes for metabolic bone disease. MBD is generally caused by too little calcium, too much phosphorus, too little or too much vitamin D3, too little ultraviolet light (UV B), too little protein or a combination of these factors. Less common is MBD caused by disease of the kidneys, liver, small intestine, or of the parathyroid or thyroid glands When any of these deficiencies, excesses or organ dysfunctions occur, the normal metabolic processes of the body are disrupted and, as they say, bad things happen.

Probably the most troubling thing about metabolic bone disease is that it is something which is caused by our mismanagement of the reptile's diet or environment, or both. Living in the wild, a healthy animal in a normal environment would not get MBD. It is only after being brought into or being raised in captivity, where the animal is not provided a balanced diet (a diet that meets its needs, not the needs of another type of animal or the convenience of the owner) nor with enough environmental stimuli (photoperiod and regular ultraviolet exposure) that this weakening of the bone occurs.

While much research has been done on the calcium metabolism in mammals and, to a lesser extent, in birds, little has been done in other vertebrates. Thus, discussions of the metabolic process reflects that known for mammals. Reptilian calcium metabolism may be different from mammals, and there may be differences between different types of reptiles. (Snakes are rarely subject to calcium deficiencies as they do not require exposure to ultraviolet radiation for Vitamin D synthesis and their consumption of healthy whole prey ensures an adequate amount of calcium.)


Balancing Act
There are multiple entities involved in the metabolism of calcium: the hormones parathyroid (PTH), calcitonin (thyrocalcitonin or TCT), 1,25-dihydroxycholecalciferol (1,25-DHCC, a biologically active form of vitamin D3), and the intestine, kidney, liver, thyroid gland, parathyroid gland, and, of course, bone. Each plays one or more roles in the metabolism and bone formation/resorption.

In the many articles and discussions about calcium deficiency, the importance of getting enough but not too much calcium, not too much phosphorus, and getting enough but not too much vitamin D3 , is frequently discussed. Just exactly what role these and the organs and glands play often remain shrouded in mystery to all but the initiated. So get ready: you're about to be initiated!

Calcium is a chemical element (symbol Ca) and is the most abundant mineral in the body. It interacts with phosphorus to form calcium phosphate; this is the hard, dense material which forms bone and teeth. Calcium is a positively charge ion element (cation) and is essential in intra- and extracellular fluid exchange, blood clotting, and maintaining a regular heartbeat. It is also important in the initiation of neuromuscular as well as metabolic functions. Unsurprisingly, most of the calcium in the body is stored in a very usable form: bone. The balance of the calcium is found in the serum (that fluid which is left after all blood solids have been removed) and is either ionized and ready for use, or is bound to protein and not ionized.

Calcium needs some assistance to cross through cell membranes. While very small amounts of calcium can be absorbed through cellular membranes throughout the small intestine, 1,25-DHCC enables the calcium absorption across the membranes of the duodenum. Fusion absorption, that done without the assistance of 1,25-DHCC, is not nearly as effective in maintaining proper calcium levels as is calcium absorbed with that form of vitamin D.

Calcium absorption is also affected by the degree to which it is soluble and thus usable. Acidic levels of the ingested food, and the presence of substances such as oxalates (found in spinach, soy, rhubarb, beet greens, and to a lesser extent in collards and carrots) binds the calcium, rendering it unusable. Diets high in fat (such as found in tofu, bird seeds such as sunflower or rapeseed) relative to the levels consumed in the wild, can impede calcium absorption; faulty fat metabolism can adversely affect the metabolism of vitamin D. Diets high in oxalates or fats, in other words, both lead to metabolic bone disease, coming by different routes.

The kidneys represent the one of the body's waste management centers. Not only are certain elements recycled through the body, those no longer useful or unusable are gotten rid of through excretion. The kidneys can only handle a certain amount of input, and so can only put out a certain amount. When there is too much calcium in the system, the kidneys cannot excrete out any more than it does when the body is carrying a normal load.

Phosphorus is a chemical element and, when combined with calcium (in the form of calcium phosphate), forms the majority of the bone in the body. In addition, it is used in nearly all of the body's metabolic processes and is important in cellular function It is extracted from foods, and its use is controlled by vitamin D and calcium.

Phosphates, other than the calcium phosphate found in bone, is not retained in the body, but is continually being excreted (in urine and feces) and so much be replaced. It is utilized to maintain the acid-base balance in blood, saliva, urine and other bodily fluids.

Generally, equal amounts of soluble calcium and phosphorus ions are required for balance; ideally, the ratio of calcium to phosphorus should be 2:1. Too much calcium results in a phosphorus deficiency and impaired metabolic function. Too much phosphorus in the diet forms insoluble calcium phosphate which renders the calcium unusable; as the body continues to absorb the phosphorus, hypocalcemia—metabolic bone disease—results.

We tend to think of bone as a solid, fixed substance subject only to growth as we grow from infancy, and becoming weakened and subject to breaks in old age. In fact, bone is a sort o rigid connective tissue composed of a component of collagen and salts, including calcium phosphate.

Bone matter is constantly being resorbed and new deposits are being laid down so in a very real dense, bone is a dynamic, not a fixed, process. The deposition and resorption are regulated by the serum mineral levels and PTH and 1,25-DHCC.

Parathyroid Hormone (PTH)
The parathyroid glands are small bodies near the thyroid gland. They secrete parathyroid hormone (PTH). The secretion of this hormone is regulated by the serum calcium level: if the serum calcium level falls, the parathyroid secretes the hormone; if the serum calcium level is high, PTH production is inhibited.

PTH serves two functions. PTH promotes the normal bone resorption process and is adversely affected by calcitonin. PTH also stimulates the excretion of phosphates by the kidneys; this inhibition of phosphate resorption in turn enables calcium resorption.

Calcitonin is a hormone produced by the thyroid gland (in reptiles, it is by the ultimobranchial glands). Its secretion is regulated by serum calcium levels: elevated serum calcium levels stimulates the secretion of calcitonin. Thus, calcitonin acts counter to PTH. Calcitonin inhibits bone resorption thus causing serum calcium levels to fall.

Vitamin D
Studies have shown that Vitamin D is produced by a steroid hormone, 1,25-DHCC. There are two forms of Vitamin D. Plants produce ergosterol, which has been synthesized into ergocalciferol, Vitamin D2, which is used as an animal feed supplement. Cholecalciferol, or Vitamin D3, is created by the synthesis of 7-dehydrocholesterol in the skin by ultraviolet radiation (UV B).

Cholecalciferol is bound with serum protein and transported to the liver (where it is transformed into 25-hydroxycholecalciferol (25-HCC). This in turn is bound to serum protein and transported to the liver, where it is transformed into 1,25-dihydroxycholecalciferol (1,25-DHCC).

(Plant sources of Vitamin D2 are not sufficient for proper calcium metabolism; it is thought that this form of D is metabolized too quickly. Vitamin D3 is best obtained through regular exposure to ultraviolet radiation; in studies of iguanas [Bernard et al.], those iguanas receiving Vitamin D3 injections or diet supplements fared less well than those iguanas whose main source of D3 was from ultraviolet radiation.)


Diagnosing MBD
Most diagnoses are made based on a combination of the physical presentation of the iguana and information provided by the owner relating to diet and environment. Swollen limbs and soft or swollen jaws are the most common presentations, as are lameness, partial paralysis, tremors (hypocalcemic tetany) and painful movement. Anorexia and emaciation are common when the jaws have become so weakened that eating is difficult or impossible. Blood serum tests may be less effective; lizards with even severe MBD often present normal serum levels.

Radiographs may show weakened bones; the bones show more faintly than healthy solid bone material. They are useful in determining the degree to which bone loss has occurred, and are helpful in assessing the efficacy of treatment.


Metabolic Bone Diseases
As mentioned earlier, calcium deficiency is just one type of metabolic bone disease. What follows is a brief description of the most commonly seen metabolic bone diseases.

Osteoporosis is a disease well known in humans as well as in certain captive animals. This is a thinning of the bone matrix as more calcium is resorbed into the blood than is deposited into the bone.

Rather than being caused strictly by a deficiency in calcium or excess of phosphorus, true osteoporosis may be related to protein deficiency (both dietary and due to prolonged anorexia),or through disuse of bones. This may be as a result of being confined in too-small spaces, or enforced inactivity such as that experienced when fractures have been immobilized, or as a result of long-term paralysis.

Bones become brittle, light, and easily broken.

This is softening of the bone and decreased bone density due to decreased mineralization. The body tries to compensate by depositing bone material at the sites of greatest tension. Folding fractures and bowed bones are common.

Rickets is similar to osteomalacia, and occurs in the young. The differences are most noticeable in x-rays as it affects the bones in different ways. Bowing of the long bones, sometimes severely deformed long bones, is the most common outward signs of rickets.

Secondary Nutritional Hyperparathyroidism
Low levels of serum calcium stimulate the production of PTH (parathyroid hormone), which causes the bones to release calcium and phosphate, as well as stimulating 1,25-dihydroxycolecalciferol, which increases calcium absorbtion in the gut. The result is bones stripped of calcium, with insufficient calcium available to replace the calcium lost from the bone, and so the bone weakens. This results in osteomalacia in adults and rickets in the young.

Calcium deficiencies may be caused by kidney, intestinal and liver diseases as well as by dietary deficiencies. Diseases which affect the way in which nutrients are extracted from food and metabolized may ultimately affect how calcium is processed in the body.


Rugwort, ~3 years of age, permanently stunted and deformed from the long term severe MBD he had when he was finally obtained from his prior owners. The foreshortened skull and swollen lower jaw are typical of fibrous osteodystrophy.


Fibrous Osteodystrophy
This is most often seen in the jaw bones; they begin to soften and bow outward as they continue to be pulled upon by the muscles. The heads of some afflicted animals, such as iguanas, tend to look small and rounded, juvenile in appearance. Self-feeding becomes difficult, then impossible, as the jaw bones become too soft. Force feeding by tube is required in advanced cases.

The swelling of the jaw is sometimes mistaken for an abscess. Abscesses, however, are rarely bilateral, and quick a discussion of diet and environment are often all that is needed to confirm a diagnosis of fibrous osteodystrophy.

 As the bones weaken, the body tries to compensate, and a network of soft connective tissue forms, stretching across the weakened areas. This results in hard lumps. Most noticeable in the long bones of the legs, they can also be felt in the tail. Many owners mistakenly think their lizard is healthy and strong based on the appearance of the legs. In fact, the lizard is highly susceptible to broken bones, and such breaks may go unnoticed due to the overlying swelling.


Treating MBD
Treatment depends upon the cause of the problem. In most cases (other than those resulting from other diseases), changes in the animal's diet and environment are required in addition to whatever other treatment modalities are initiated.

In many instances, it may be just as difficult to make an owner see that there is a problem in these areas as it is to get an animal to eat foods which it is not accustomed to eating. The old, inappropriate foods may be mixed in with the proper foods, in decreasing quantities, if the animal absolutely will not make the switch to the proper foods.

Owners are encouraged to provide access to direct sunlight whenever possible, augmenting that on days which are too cold or overcast with adequate exposure to fluorescent lights developed to provide ultraviolet radiation. Many incandescent lights being marketed in the pet trade are claiming to provide ultraviolet radiation but they do not (Gehrmann). As fluorescent light bulbs do not provide much heat, many reptiles require both fluorescent lamps for ultraviolet radiation as well as lights or other equipment to provide heat. Proper temperature is just as important for digestion and metabolism as is diet and ultraviolet radiation.

Various drugs are available to administer to animals with MBD. Which drug or drugs are selected will depend upon the cause of the disease. Different forms of calcium (calcium glycerophosphate with calcium lactate [Calphosan], calcium glubionate [NeoCalglucon]), Vitamin D3, and calcitonin are used to help restore calcium balance. Calcitonin, which is used to reduce the resorption of calcium from bone to blood can only be given after initial treatment with calcium. Failure to do so can result in hypocalcemia as serum calcium levels fall.


Prevention, as always... better—and less expensive and less painful—than the cure. Be careful what you feed. When feeding omnivorous or herbivorous lizards and chelonians, feed a properly varied diet which is low in deficient foods, and be very sparing or avoid completely offering foods high in oxalates, fats and tannins, all of which impede calcium metabolism.

When raising rodent prey, don't skimp on their care and feed. The healthier they are, the more nutritious they will be. The same goes for arthropods and insect prey. If you buy them from a pet store, nutrient-load them before feeding them to your animals: set them aside for at least 24 hours after purchase and provide nutritious food for them to feed upon. Ground rodent block, tropical fish flakes, chicken egg layer feed, high protein baby cereal and slices of fruit or potato for moisture are excellent sources of nutrition. In addition, arthropod and insect prey can be sprinkled with or shaken in a bag of vitamin and calcium supplement powders just prior to feeding out.

The initial outlay for proper equipment and housing may be expensive, and preparing fresh foods may be time consuming, but all are worth it when weighed against a future of pain and deformity and, all too often, early death.


Literature Cited

Barten, S.L. (1993) The medical care of iguanas and other common pet lizards. Exotic Pet Medicine. VCNA: Small Animal Practice, 23(6):1213-1249

______ (1994) personal communication.

Bernard, J.S., O.T. Oftendal, P.S. Barboza, M.E. Allen, S.B. Citino, D.E. Ullry and R.J. Montali. (1991) The response of vitamin D deficient green iguanas (Iguana iguana) to artificial ultraviolet light. Proc Am Vet 1991:147-150.

Frye, F.L. (1992) Reptile Care: An Atlas of Diseases and Treatments. Malabar FL: Krieger Publishing. 637 p.

Gehrmann, W.H. (1992) No UV B from tungsten filament incandescent lamps. ARAV 2(2):5.

Blood, D.C. and V.P. Stoddert. (1988) Baillière's Comprehensive Veterinary Dictionary. London: Baillière and Tindall. 1124 p.

Fowler, M.E. (1986) Zoo & Wild Animal Medicine. Philadelphia PA: W.B. Saunders Company. 1087 p.
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