Metabolic Bone Diseases in Reptiles and Amphibians Christina Miller Last update: Sunday, May 18, 2008.

Metabolic bone diseases ("MBD") are probably one of the most common groups of illnesses affecting captive herps. "Metabolic bone disease" is actually a blanket term for a variety of symptoms that may have different pathologies (causes). There are different types of metabolism-related diseases that can affect the form and function of the skeleton, two general categorizations are nutritional metabolic bone disease and renal metabolic bone disease.

These illnesses are almost completely unique to captive animals (it would be exceptional to see this occur in a wild animal), and can be traced back to inadequate or poor husbandry. The most common metabolic bone disease in captive herps is nutritional secondary hyperparathyroidism (NSHP). This is the "classic" MBD that is caused by a calcium-poor diet, insufficient exposure to ultraviolet lighting, or a combination of the two. (Mader 2006)

Considering MBD is such a broad term, the symptoms it refers to include (but are not limited to):

 

• Osteomalacia: Softening of the bones.
• Fibrous osteodystrophy: The body lays down fibrous deposits across decalcified bones.
• Hypocalcaemia: Low blood calcium
• Rickets: Somewhat of a lay term for the body's inability to put sufficient calcium into the bones, due to a lack of vitamin D3, typically resulting in skeletal deformities (bowing of the long bones, like the humerus and femur, is the most common). Note that rickets does not actually occur in reptiles, it is a mammalian disease.

A quick physiology lession

The body needs vitamin D3 so that it can use calcium. Vitamin D3 can be obtained from the diet, but many animals rely heavily (or completely) on sunlight so that their own bodies can make it. It is suspected that some species cannot absorb vitamin D3 effectively from their diet, and absolutely require ultraviolet-B light (found in sunlight) to make their own D3.

Sunlight consists of a very broad spectrum of different wavelengths of light, visible light that we can see is only a part of the spectrum. Ultraviolet-B radiation (wavelength between 270-300 nm) reacts with compounds in the animal's skin to produce vitamin D3, also called cholecalciferol. See Understanding Ultraviolet and Calcium for more information.

Vitamin D3/Cholecalciferol is transported to the liver, where it is transfmored into calcidiol and stored until needed. When needed, calcidiol is sent to the kidneys, where it is transformed into calcitriol. Calcitriol is the active form of vitamin D3, and acts like a hormone. This hormone increases the levels of blood calcium in three ways:

• It increases absorption of calcium and phosphate (two major bone compounds) from the digestive tract.
• It increases calcium and phosphate reabsorption in the kidneys (excess would noramlly be passed in the urine or urates).
• It inhibits the release of parathyroid hormone (PTH), we will revisit this hormone later.

The body needs calcium to build and maintain bones and teeth, but also for muscular function. Calcium is being "used up" by the body every day, and the body is constantly building up and breaking down hard bone tissue rich in calcium and phosphorus. Bones are not just there for support and protection, but they also act as storehouses of calcium and phosphorus for the body, two vital nutrients.

If blood calcium levels fall drastically low, nerve signals to the muscles cannot be transmitted effectively, and the animal can go into hypocalcaemic tetany and die. Tetany (not to be confused with tetanus) is involuntary muscle contractions, when the condition is severe, the muscles stay contracted and cannot relax. No muscle action means the heart and muscles powering the lungs stop working, which, needless to say, will be fatal without intervention!

So, the body will try to correct low blood calcium, or hypocalcaemia, when it occurs. When blood calcium levels start to drop, the parathyroid gland (located in the neck region) produces parathyroid hormone (PTH) to increase blood calcium. It does this in three ways:

• It indirecty increases calcium absorption in the intestine, by increasing calcitriol production in the kidneys (remember that calcitriol is the active form of vitamin D3, and it increases blood calcium levels through three paths listed above)
• It increases calcium reabsorption in the kidneys, so less is excreted in the urine or urates
• It signals to osteoclasts, the cells that are responsible for disassembling or "breaking down" hard bone tissue, to disassemble more hard bone to send calcium into the blood

The big difference between calcitriol and PTH is that PTH tells the body to start breaking down bone tissue to increase the amount of calcium in the blood. Parathyroid hormone is naturally self-limiting, as it tells the body to start producing calcitriol, which tells the body to stop producing PTH!


Linking physiology to disease

The above process may seem somewhat complicated, and difficult to grasp. We will break down some common scenarios that occur in captivity, and relate them to what the physiology tells us.

There is not enough available calcium in the diet. This occurs either when the animal's diet simply contains insufficient amounts of calcium, or when there are too many calcium antagonists in the diet. (Calcium antagonists are naturally-occurring chemicals found in many common fruits and vegetables. They bind to calcium in the digestive tract, and stop it from being absorbed by the body.) Either way, there is just not enough calcium present in the digestive tract. The body uses the calcium available, but will run short, and will resort to depleting more and more calcium from the bone "storehouse." This eventually results in a notable loss of bone density.

The dietary ratio of calcium to phosphorus (Ca:P) is incorrect. Reptiles and amphibians generally need a dietary Ca:P of at least 1.5:1.0 (one-and-a-half times as much calcium as there is phosphorus), and a target of 2.0:1.0 (twice as much calcium compared to phosphorus) is reccommended for many species, including Green Iguanas. The body needs both calcium and phosphorus to function, but the digestive tract is much better at absoring phosphorus as it is at absorbing calcium. The digestive tract is usually not very efficient, a lot of nutrients go to waste in the feces because there is only so much time to absorb nutrients from the food that is passing through. High levels of phosphorus compared to calcium in the diet can result in very little calcium actually being absorbed. With not enough calcium being absorbed from the diet, the body needs to take calcium from the bones, etc...

The animal is not exposed to sufficient amounts of UV-B lighting. Many species of reptile and amphibian rely heavily on sunlight to produce their own vitamin D3, rather than obtain all of their needed D3 from their diet. No UV-B means no vitamin D3 production, resulting inlow blood calcium because not enough is absorbed from the digestive tract, whether there is enough in the diet or not.

Now we can look at why nutritional secondary hyperparathyroidism (NSHP) is the most common "form" of MBD in captive reptiles and amphibians. When blood calcium falls because there is not enough calcium being absorbed from the diet, or there is not enough vitamin D3 to allow dietary calcium to be absorbed, the parathyroid gland becomes "hyperactive" and continuously produces PTH to use the skeleton's calcium stores. In a sense, the body would "rather" have weak bones, than to die of hypocalcaemia. (Note that a lack of UV-B causing a vitamin D3 deficiency is classified as a nutritional factor.) We call this disease NSHP because the parathyroid gland is hyperactive, occurring secondary to nutritional causes.

Renal MBD can occur when the animal is in kidney failure. The kidneys can be so damaged that they do not excrete enough phosphorus, leading to excessive levels of phosphorus in the blood (hyperphosphataemia) and proportionately less calcium in the blood. Also, less calcitriol will be synthesized by the damaged kidneys. Because less calcitriol is produced, PTH production is encouraged by low blood calcium and not inhibited by calcitriol, so the result is a renal secondary hyperparathyroidism.


Detection and treatment

Metabolic bone diseases are easy to detect if you know what to look for. Examining the animal in question's husbandry history is vital to determine if proper environmental conditions and nutrition have been provided. Radiographs (x-rays) will reveal a poor bone density, and fibrous deposits around the long bones if fibrous osteodystrophy is occurring (these deposits can often be palpated, as well).

Consult your veterinarian for a proper diagnosis and to discuss a treatment regimen. MBD is treated depending on how far the disease has progressed, below is a guideline of physical characteristics of different "stages" of the disease, and recommended treatment for nutrtional MBD. Renal MBD treatment will incorporate therapy for kidney disease. Metabolic bone diseases are fatal if left untreated.

This Leopard Gecko (Eublepharis macularius) presented symptoms of early NSHP: Kinked tail, slightly receded lower jaw, and difficulty lifting the torso off of the floor.	Another view, emphasizing the receded mandible.
Fractures due to reduced bone density are extremely common in MBD patients. This Asian Water Dragon (Physignathus cocincinus) suffered fractures in both forearms, that healed crooked without treatment. Note the stress colouration.	The same water dragon presents swollen thighs, typical of fibrous osteodystrophy- the femurs and other long bones have bulky fibrous deposits for reinforcement.
This Green Iguana (Iguana iguana) had NSHP at a very young age, resulting in a severe spinal deformity, rhoecosis. Although stunted and somewhat deformed, this animal is now healthy and lives a relatively normal life, only having a bit of difficulty to climb.	The same iguana. Note that despite the obvious skeletal deformities, this animal has excellent bone density, having recovered well.
This Bluetongued Skink (Tiliqua sp.) presents a drastic spinal deformity, rhoecosis, as a result of NSHP. Photo courtesy of Vanier College Animal Health Technology.	Another water dragon, presenting a severe spinal deformity. Note the fractured forearm, and mandibular warping. The lizard is also extremely dehydrated. This animal was for sale in a pet shop, for full price. It was brought back by a customer, who wanted a replacement...

Prevention

Inarguably, the best treatment is prevention. MBD is well-known to be extremely common in captive herps, but it is one of the most preventable captive diseases. Ensuring your are providing suitable husbandry is really all that is necessary: A suitable temperature gradient with room to thermoregulate, access to ultraviolet B lighting if the species needs it, and a suitable diet for the species you are keeping.

Sources:

Further Reading:

• Herptiles.net:
  • Light Quality
  • Understanding Ultraviolet and Calcium
• External:
  • ARAV: Association of Reptile and Amphibian Veterinarians