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Metabolic bone disease

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Synonym(s): MBD, Nutritional secondary hyperparathyroidism (NSHP), Hypocalcemic metabolic bone disease


  • Cause: lack of dietary calcium and/or vitamin D3 usually in conjunction with inadequate UVB light provision.
  • Signs: failure to grow, generalized weakness, anorexia, soft/pliable mandible, swollen/thickened bones, fractures, tremors/muscle fasciculations.
  • Diagnosis: blood chemistry and radiographs.
  • Treatment: oral calcium glubionate; calcium gluconate SC, IM or IC for hypocalcemic patients.
  • Prognosis: fair to grave depending on stage when diagnosed.
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Presenting signs

  • Failure to grow.
  • Generalized weakness.
  • Anorexia.
  • Soft or pliable mandible on palpation.
  • Tongue disfunction, especially chameleons.
  • Palpably swollen or thickened long bone(s).
  • Fractures of long bones.
  • Angular limb deformities due to previous fractures.
  • Tremors or fine muscle fasciculations.
  • Opisthotonos and seizures.

Acute presentation

  • Animals may present collapsed or moribund.

Age predisposition

  • Young growing lizards and chelonia.

Breed/Species predisposition

  • Seen in all lizards and chelonian species.
  • Extremely common and often very severe in captive chameleons.

Cost considerations

  • If treatment is carried out, it may be prolonged and involve intensive care and veterinary involvement.
  • In addition, a significant outlay will be required to buy the correct heating and lighting equipment to fix the husbandry deficits that have caused the problem.

Special risks

  • Hypocalcemia may make anesthesia more risky.
  • These animals may be dehydrated and significantly comprised.
  • Manipulation of the jaw for feeding or medication may result in pathological fractures and dramatically worsen prognosis.



  • Suboptimal supplementation of vitamin D3 and insufficient UVB light provision.
  • Growing animals and reproductively active young females with high calcium requirements are more markedly affected.
  • Turtles fed liver, heart or muscle meat will often develop metabolic bone disease (MBD).

Predisposing factors

Poor diet

  • Vitamin D3 is not present in any plants, fruit, vegetables or insects and for species that do not eat whole vertebrate prey as the main part of their diet, must be obtained from exposure to heat and UVB light.
  • In the wild, most species eat a seasonal and varied diet specific to their natural range that cannot be reproduced in captivity.
  • Common commercially cultured insects such as crickets, locusts, mealworm and wax moth larvae are limited in variety and are not only low in calcium but have a negative calcium:phosphorous ratio further inhibiting calcium uptake (ideal Ca:P ratio is 1-2:1.
  • Vegetation fed to herbivorous animals may also be limited compared to natural diets and may not contain sufficient calcium.

Poor or no calcium and vitamin D3 supplementation

  • Owners may not be using any supplementation.
  • A common mistake is to supplement only calcium which without a source of vitamin D3 cannot be absorbed.
  • Supplements may be poorly bioavailable and not of a reputable brand.
  • Supplements may be incorrectly stored.
Vitamin containing supplements should be stored in a cool, dark, dry place and used within 6 months of the container being opened.

Poor or no UVB provision

  • UV light is most easily measured as the Ultra Violet Index (UVI).
  • Owners may not be providing any UVB.
  • Owners may be using a lamp that does not produce the correct level of UVB for the species.
  • If the lamp is placed behind glass or most commercial acrylic/perspex, no UVB light will penetrate.
  • Fine mesh may reduce UVB output by 50%.
  • UVI may be insufficient because the lamp is placed too high above the animal.
  • Lamps are designed to be used with reflectors. Not using a reflector dramatically decreases UVB output.
  • UVI decreases over time and if the lamp has not been replaced according to the manufacturer's instructions (usually around 12 months), it can be producing visible light but no UVB Poor or no heat provision.
  • The reaction to convert provitamin D to calcediol is temperature dependent.
  • If the reptile is not kept at its preferred optimal temperature, even with UVB provision, it cannot produce vitamin D3.


  • With the exception of species that eat only whole vertebrate prey, all reptiles require exposure to sunlight in order to manufacture vitamin D3.
  • 7-dehydrocholesterol (Provitamin D) is converted to previtamin D3 and then to calcediol.
  • UVB light of around 295 nm is required alongside sufficient environmental temperatures. This reaction is temperature dependent and the reptile must be at its preferred optimal temperature.
  • Calcediol (25-hydroxy-vitamin D3) is converted to Calcetriol (1,25-dihydroxyvitamin D3) which controls the uptake of calcium from the intestines, its reabsorption from the renal tubules and its release from bone.
  • Chronic low blood calcium leads to increased secretion of parathyroid hormone (PTH) from the parathyroid gland.
  • This results in reabsorption of calcium from bone.
  • Because calcium is involved in contraction of cardiac, smooth and skeletal muscle, neurotransmission, bone mineralization and egg production, hypocalcemia leads to suboptimal mineralization of bone, pathological fractures , gut stasis, tremors, seizures, anorexia, lethargy, pre- and post-ovulatory stasis, inability to eat and death.
  • Cloacal prolapses and intestinal impactions may be secondary to direct effects of hypocalcemia or through behavioral pica (often with sand substrates).


  • This is a chronic disease, but clinical signs are usually not noticed until later in the course of disease.



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