Bone is composed of a tough organic matrix that is greatly strengthened by deposits of calcium salts. The average compact bone contains approximately 30% matrix and 70% salts by weight. The crystalline salts are composed primarilly of calcium and phosphate.

When there is interference in the deposition of calcium salts in bone, then Metabolic Bone Disease (MBD) will result. The most common cause of MBD is a dietary deficiency of calcium (Ca) or Vitamin D. Less common causes of MBD include kidney, liver, intestinal, thyroid, or parathyroid disease.

MBD is most commonly seen in rapidly growing reptiles and amphibians. Adult animals that have normally developed bones are much more resistant to MBD since they already have a reservoir of Ca in their bones. Up to 99% of an animal’s Ca is contained within their bones. Calcium is necessary for bone contraction, blood clotting, and nervous impulse conduction as well as other physiological processes. When blood calcium levels are high, calcitonin released from the thyroid gland stimulates bone cells (osteoblasts) to form more bone tissue, effectively storing the excess calcium in the extracellular matrix of bone. When blood is low in calcium, the parathyroid gland releases a hormone called parathormone (PTH), instructing bone cells (osteoclasts) to break down bone tissue to release the needed calcium into the bloodstream.

Diets lacking in calcium are often fed to captive reptiles and amphibians. Carnivorous reptiles are often fed hamburger or worse, organ meats. The Ca:P ratio of a diet describes the level of calcium compared to phosphorous found within the food. Hamburger has a Ca:P ratio of 1:16, while beef heart has a Ca:P ratio of 1:38. Diets containing whole rodents, birds or fish have a positive Ca:P ratio of 1:1 - 1:4 because of the skeletal bones that contain calcium within the prey and are a more natural diet for most reptiles. MBD is unheard of in snakes because they are fed whole, small prey animals.

Insects also have a negative Ca:P ratio and therefore reptiles and amphibians fed insects are also prone to MBD. A balanced diet for insect eating herps should usually include baby mice or whole fish to narrow the Ca:P imbalance. Insects may also be dusted with Ca carbonate but coating insects in dust is usually not enough.

Herbivorous diets often contain low amounts of Ca and excessive P as well. Most fruits and various types of lettuces are typically low in Ca. Calcium rich vegetation includes alfalfa hay, beet greens, broccoli leaves, and the outer green leaves of cabbage. Mustard and turnip greens as well as collards have a medium level of calcium. Dried figs are about the only fruit with a high level of calcium.

Lack of vitamin D or insufficient exposure to sunlight may also result in MBD. The inactive form of vitamin D is 7-dehydrocholesterol which is converted by exposure to sunlight or ultraviolet (UV) radiation to the active form 1,25-Dihydroxycholecalciferol or vitamin D3 in reptilian skin. Although exposure to unfiltered sunlight is the best form of ultraviolet light necessary for vitamin D conversion, there is lighting available for reptile enclosures. Sunlight filtered through glass or plastic is essentially devoid of UV radiation. Lighting for reptiles must include ultraviolet radiation. Fluorescent tubes are available that produce UVB wavelengths in the range of 290-320 nm, which are the most appropriate for Vitamin D conversion. Mercury vapor lamps are the only non-fluorescent bulbs available that can also provide the necessary UV light. UV-producing bulbs should be placed within an 18 inch range of resting or basking surfaces so that the reptile can obtain adequate UV exposure. Mercury vapor lamps may be placed up to several feet from the basking area.   

Reptiles and amphibians require active vitamin D3 for several important reasons including increased absorption of Ca from the intestinal tract, bone deposition, and bone adsorption. Normally, the rate of bone deposition and absorption are equal to each other so that the total mass of bone will remain constant. In a young growing animal, the rate of bone deposition should be much greater than the rate of absorption due to the demand for the construction of additional bone.

There are two distinct forms of MBD. The classical form of MBD is more common and has symptoms referable to the skeletal system. When dietary calcium is lacking, the bone will be composed primarily of an organic matrix lacking the calcium salts needed for an increase in strength. Animals with classical MBD will have weak and rubbery bones that are prone to fractures. The second form, hypocalcemic MBD, is more prevalent in adult iguanas and exhibits symptoms secondary to a lack of metabolic Ca and include paresis, muscle tremors, and possible seizures.

In classical MBD affecting iguanas, the most consistent sign of a problem is the complete lack of truncal lifting. During normal locomotion an iguana will lift the body or trunk as well as the tail off the ground. Early in MBD, the iguana will drag its pelvis and tail along the ground and eventually fail to lift the entire body while walking until they can no longer ambulate.

Anther common clinical sign seen in all lizards is a mandible or maxilla that is pliable. As the disease worsens, an underbite may develop. The mandible is often aggravated by a fibrous osteodystrophy (the manufacturing of defective bone) that will bow the mandible laterally. Juvenile iguanas often retain a rounded shape to the skull because there is a failure of the skull to grow and lengthen.

The presence of a single or multiple fractures without a history of trauma should be suspect of MBD. Fibrous osteodystrophy generally affects the long bones or jawbones. It results from the deposition of the fibrous bony matrix without a resulting deposition of Ca salts. The leg areas will appear well-muscled but will feel more reminiscent of bone rather than muscle. Paresis (slight or incomplete paralysis) generally improves with treatment.

Lack of growth or weight gain in a juvenile lizard may be another indication of MBD. There may be little definition between bone and soft tissue on radiographs. Plasma levels of Ca and P may or may not be affected in classical MBD.

In hypocalcemic MBD, serum calcium levels are low while phosphorous levels are often high. Symptoms usually start out as intermittent muscle tremors in the digits, progressing to the tail and legs, and finally causing tetani (stiffness in the limbs) and seizures.

The most important aspect of treatment is the correction of the poor husbandry practices that caused the deficiency to begin with. Diet and lighting must both be corrected and medical problems such as fractures and dehydration should be dealt with. Tube feeding may be necessary for anorectic animals. Calcium glubionate syrup at a level of 1 ml/kg should be given every 12 hours for literally months. Vitamin D3 injectable should be given every 7 days for two treatments.

Once calcium has been supplemented for a one to two week period and serum calcium levels are adequate, calcitonin may be given to speed calcium deposition on the bone. If however the Ca level is not between 8 and 11 mg/dl in the blood, the administration of calcitonin may result in the death of the animal by dropping the Ca levels in the blood stream and thereby causing Ca to be unavailable for metabolic physiologic processes such as nerve transmission and blood clotting. Calcitonin used before there are adequate blood levels of Ca will actually induce the hypocalcemic form of MBD.

Without treatment these patients generally die. The more severe the clinical signs are to start with, the worse the prognosis. Mild fibrous osteodystrophy will resolve with therapy while the more severe cases may be permanent. Prognosis of animals with serum hypocalcemia is guarded and dependent on the underlying cause of the condition.


References:

Shier, David, Jackie Butler and Ricki Lewis. Essentials of Human Anatomy and Physiology. Ninth Edition. 2006. Pp. 132-133.A

Mader, Douglas DVM. Reptile Medicine and Surgery. W.B. Saunders Co. 1996. Pp.385-392.

Guyton, Arthur. Textbook of Medical Physiology. 5th Edition. Saunders Co. 1976. Pp. 1052-1057.

Kahn, Cynthia Editor. The Merck Veterinary Manual. Ninth Edition 2005. Merck and Co. Pp. 1591.