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How to Prevent Metabolic Bone Disease - And Understanding the Role of Calcium and Phosphorus
Table of Contents
Trivia question for you herp fanciers…when is a serpentine spine a bad thing? When it’s in a lizard suffering from metabolic bone disease (MBD). A waving spine in a ball python is pretty normal, but not in a bearded dragon. While not exactly a catchall term, MBD is a condition caused by more than one deficiency or illness. In other words, MBD itself comes in various forms. For instance, the most common form diagnosed in captive reptiles and amphibians is nutritional secondary hyperparathyroidism (NSHP), caused by too little available calcium.
The Importance of Calcium
It is so important for vertebrate bodies to have the correct calcium that nature has developed an organ whose sole purpose is to regulate the amount of calcium circulating in the blood stream. The ideal range is very tight, with either too much or too little creating an enormous number of illnesses. Enter the parathyroids. These are the little quartermasters of the calcium allocated to bones, and therefore, they determine how strong and dense the bones are. Weirdly, although the parathyroid glands are located next to (and sometimes inside) the thyroid glands, they have no related function to those iodine regulating bodies.
Putting that aside, let’s return to the subject of calcium. This mineral is a vital biochemical messenger used in many metabolic pathways and not just bone structure and formation. Chronic calcium deficiency can result in:
- impaired nerve impulse transmission
- weakened muscle contractions (especially in the heart)
- brain disregulation
- decreased blood coagulation
For instance, in most vertebrates, if calcium levels drop extremely low, cardiac failure may occur (unfortunately, in neglected animals, I have seen this occur). So calcium in the right balance with other critical minerals is therefore vital to the health and longevity of a large number of lizards and chelonians (tortoises and turtles), and of course other pets as well. Why exactly is this the case?
Physiology of Insufficient Calcium Intake
Insufficient levels of dietary calcium cause the parathyroid glands to produce excess parathyroid hormone, which triggers decalcification of bones. And although this seems counter-intuitive in terms of fitness and survival, (because, after all, bones are pretty darned important), the brain is even more important.
The brain also needs to be supplied with calcium in just the right amount, all the time. So really, the parathyroid is making the choice between brain impairment and bone density. Tough job! So when there is too little blood calcium available, parathyroid glands ‘choose’ the brain over the bones. The result is a reptile or amphibian with all of their wits about them, but suffering from NSHP.
Nutritional Secondary Hyperparathyroidism
NSHP can occur in all kinds of reptiles and amphibians but is most commonly seen in lizards, turtles and tortoises. A disproportionately high percentage of veterinary cases are seen among juveniles of these species due to their higher need for calcium for bone growth, and in pregnant female animals due to their increased demand for calcium during gestation. The reptiles and amphibians that suffer from NSHP the most often are herbivores and insect-eating species:
- bearded dragons
- water dragons
- leopard geckos
Symptoms of Insufficient Calcium Intake
When these creatures do not have enough absorbable calcium in their diet, spines and limbs deform, and shells and jaws loose rigidity, which is why in some circles the disease is called rubber jaw.
Other symptoms can include:
- Swollen hind legs (look muscular and are suddenly too hard to the touch).
- Broken bones.
- Misshaped shells in turtles and tortoises (often it appears as if the shell is either too small for the animal, or is curved).
- Spinal deviations (kinking, curving, developing lumps).
- Problems lifting the body and/or tail off the ground when walking.
- Jerky movements of the limbs and head (tremors and seizures) especially during handling.
- Swollen or rubbery jaw and droopy lips that expose the gums.
- In chameleons, a tongue that hangs from the mouth.
- difficulty with egg-laying
- prolapses (organs protruding from the anus).
If you observe any of these symptoms, you may instinctually want to offer calcium right away, hoping to cure these sufferable problems. However, that won't be enough for the animal at this point.
Don't forget the Phosphorus
NHSP and other forms of MBD can develop as a result of an improper ratio of calcium to phosphorous in the reptile’s diet. So although phosphorus is also important, it is the ratio that determines a reptile’s (or even a human’s) health. Although animal bones may seem solid and unchanging, the process of bone formation is very dynamic.
Calcium and phosphorus are continually being added to bones and then reabsorbed back into the body. For instance, when the level of blood phosphorous becomes too high relative to calcium, it favors the formation of calcium phosphate in the gut, which is difficult for the animal’s body to handle, since in this form it becomes an insoluble salt, thereby sequestering the ingested calcium and making it unavailable to the animal’s metabolic needs. So even a pet with plenty of calcium in the diet can still experience a deficiency if too much dietary phosphorus is present as well.
The Normal Calcium : Phosphorus Range
A normal range for the calcium to phosphorous ratio necessary for health is 1.5:1 to 2:1, with 2:1 being best. If the ratio drops much below this, hyperphosphataemia can result, and it is this which stimulates the parathyroid glands to secrete parathyroid hormone (PTH).
In addition, there needs to be an adequate amount of Vitamin D3 to help the body absorb and use the calcium. Imbalances that may lead to metabolic bone disease can occur as a result of:
- Overabundance of certain substances in the diet that negatively affect calcium absorption (oxalates, fats)
- Inadequate amounts of protein in the diet
- Insufficient exposure to ultraviolet A (UVA) and ultraviolet B (UVB,) resulting in inadequate D3
- Diseases of other organs that affect the metabolism of calcium, phosphorus and/or vitamin D3 (kidneys, small intestine, parathyroid gland, liver) and cause MBD as a secondary complication
- Poor environmental conditions, such as overly cool temperatures, which impair digestion and calcium absorption
Ultraviolet Light to create Vitamin D3
Metabolic bone disease is frequently seen in reptiles that require ultraviolet light (sunlight) for the production of vitamin D3. These include diurnal lizards, especially iguanas, and turtles. It is rare in snakes, who do not require ultraviolet light for the synthesis of vitamin D3, and also because they generally eat whole mammalian prey, which provides the proper balance of calcium and phosphorus.
The herbivorous and insectivorous diurnal lizards and chelonians should be exposed to 12 hours of UVB light each day. Natural sunlight is best, but UVB rays cannot penetrate plastic or glass effectively, so mesh screening is required for light penetration and for ventilation. Certainly do NOT expose any reptile to direct sunlight through a poorly ventilated glass enclosure, as overheating can quickly develop due to the greenhouse effect.
If safe exposure to sunlight is not an option, fluorescent lighting will work. Use only full spectrum-with UVB bulbs designed for herps that have the UVB in the range of 290-320 nanometers.
Reversing Mild MBD with Lighting
If you think your beloved pet is suffering from MBD, find the closest vet near you. In very mild cases of MBD, alterations of lighting regime and dietary supplementation may be sufficient to reverse the deterioration. In more severe cases, oral or injectable calcium supplements such as calcium glubionate (NeoCalglucon), calcium lactate (Calphosan) or calcium gluconate are indicated.
In addition, after the serum calcium level is normal, calcitonin may be prescribed for a while. Calcitonin is a hormone that assists in the regulation of calcium by opposing PTH, in other words it acts to increase bone calcium content and decrease the blood calcium level when it rises above normal while at the same time lowering blood phosphorus levels when necessary.
Softshell Syndrome in Turtles
Chelonians are affected by the NSHP form of MBD just as often as diurnal lizards. ‘Softshell syndrome’ is a major killer of young turtles, especially aquatics. If the shell yields to the touch, it means that the bony structure which holds the keratin shields (outer shell) rigidly in place is already badly compromised. This should not be confused with causes of discoloration of the outer laminae, which indicates an infection of some sort and not MBD.
However, since both MBD and shell infections (often called shell rot) are commonly caused by husbandry errors, the two diseases often appear together in the same animal. It takes a long time in very poor conditions for the most serious symptoms of advanced MBD to appear, but once it does and the shell is noticeably soft, treatment can be difficult.
Prevention can be as simple as providing a cuttlebone. They are sold in most grocery stores in the pet aisle. They are used by bird owners, but turtle owners also find them indispensable. Many experienced keepers scrape off the brittle backing and float a piece of the cuttlebone in the water. Hopefully, the turtle will eat it periodically. If not, food must be dusted with the correct supplement. However, these measures are not sufficient when the disease is so advanced that the shell already feels soft. Injected calcium and veterinary care will be required.
This is definitely a case where an ounce of prevention is worth a pound of cure. Severe cases of MBD may leave disfigurations to the pet’s bones and/or shells for the rest of their lives, long after the animal has made an apparently full recovery (which can take many weeks). A deep understanding of this illness, and the means of prevention, will save hours of labor and vet bills and ensure that your pet lives a long life free of disfigurement.