Diseases Related to Calcium Metabolism in Rabbits
World Small Animal Veterinary Association World Congress Proceedings, 2010
Frances Harcourt-Brown, BVSc, DECZM (Small mammal), FRCVS, RCVS Specialist in Rabbit Medicine and Surgery
Harrogate, UK

Calcium Metabolism in Rabbits

Calcium is an important mineral in all vertebrate animals. It is a major constituent of bone and teeth and, although the fundamental principles of calcium metabolism are the same for all animals, the regulatory mechanisms are variable between species and even subspecies, depending on their way of life. In species, such as rabbits, with teeth that continually erupt and grow, a constant supply of calcium for the continual formation of new dental tissue is required. Rabbits can also have a high demand for calcium for pregnancy and lactation as they have such a high reproductive rate.

In all species, calcium can be absorbed from the intestine by two processes1: 1) passive paracellular diffusion that depends on the concentration gradient between the intestinal lumen and blood and 2) active vitamin D dependent transcellular transport that is dependent on blood calcium levels. In rabbits, passive absorption is the main mechanism of intestinal calcium uptake.2 It is efficient, so if intestinal concentrations of calcium are adequate or high, the amount of calcium that is absorbed from the gut is proportional to the amount of calcium that is present.3 However, if intestinal calcium levels are low, vitamin D is required to boost absorption in order to maintain blood calcium levels.4 This efficient passive absorption of calcium from the gut is a way of meeting rabbit's high calcium demand and also recycles calcium because, as the teeth wear away, calcium is released into the gut only to be absorbed again to lay down new dental tissue. Because of efficient passive calcium absorption, blood calcium levels can reflect dietary calcium intake. Total serum calcium concentrations of rabbits are 30-50% higher than other domestic mammals and vary over a wide range. These naturally high blood calcium levels might explain the rabbit's propensity for rapid dystrophic calcification in areas of devitalised tissue.

Although calcium uptake from the gut is not well regulated in rabbits, excretion of calcium through the kidney is well regulated. The kidney can increase or reduce excretion of calcium into the urine considerably5,6 and efficient intestinal calcium absorption means that large amounts may need to be excreted. Excess calcium that is excreted by the kidney forms calcium carbonate sediment, which is normal, although the amount depends on 1) the rabbit's demand for calcium, 2) the amount of calcium in the diet, 3) renal function, and 4) urine pH, volume and concentration. Rabbits that are growing, pregnant or lactating excrete clear urine. So do rabbits with chronic renal disease or those on a calcium deficient diet. Rabbits on a high calcium diet have more sediment in their urine3, which complicates urinary tract problems although it does not cause urinary tract disease. Reducing dietary calcium is an important part of treatment of urinary tract problems.

Calcium Requirement of Rabbits

The dietary requirement of calcium for rabbits has been determined because rabbits are used as laboratory models of osteoporosis, which is induced by feeding a calcium deficient diet. Bone density studies using dual energy X-ray absorptiometry (DXA) scanning show that demineralisation of the vertebrae occurs can easily be induced by feeding a low calcium diet. These studies show that a dietary level of 0.6-1% calcium is required for optimum bone calcification.7 The calcium content of the diet of many pet rabbits is well below this level. Mixed, muesli type mixtures are a popular, cheap, convenient way of feeding pet rabbits and are available in most countries. Many components of these mixtures contain much less calcium than the 0.6-1% that is required for bone calcification. For example, peas contain 0.14% calcium and 0.46% phosphorus. The calcium content of maize is 0.04%. Analysis of these muesli type diets may show adequate levels of calcium but this is only achieved by adding a vitamin or mineral supplement. This is usually incorporated into pellets that are added to the mixture but most rabbits do not like the pellets and select other ingredients.8 A hay and vegetable diet can also be deficient in calcium. The calcium content of fruit and root vegetables is often low and the calcium content of hay depends on the species of grass that it was made from and the part of the plant that is analysed. Hay stems may have as little as 0.15% calcium. Low or marginal dietary calcium levels can be tolerated by rabbits with adequate vitamin D levels, because passive intestinal absorption can be boosted by active vitamin D activated absorption but many pet rabbits are probably vitamin D deficient. They are housed in hutches, sheds or houses and not exposed to sunlight, which is necessary to synthesise vitamin D. If they are fed on mixed rations, they probably do not eat the vitamin D supplemented pellets in their diet. Vitamin D is not present in fresh vegetables or plants although it might be present in sun dried hay. However, because of unreliable weather conditions, there is a growing trend to dry hay artificially. Undetectable vitamin D levels have been recorded in pet rabbits.9

Diseases Related to Calcium Deficiency

Osteoporosis is common in rabbits kept as pets and is manifested by decreased radiopacity of vertebral bone and visible osteopaenia of prepared skulls. Osteopaenia of the skull is evident in rabbits with dental disease. There are many causes of dental abnormalities in rabbits including congenital prognathic abnormalities, trauma, neoplasia or incorrect diet. In general practice, the majority of dental problems in pet rabbits are part of a 'progressive syndrome of acquired dental disease' (PSADD) that affects the shape, position and structure of the teeth.10 Although this syndrome is often attributed to lack of dental wear, the author believes it is due to calcium and/or vitamin D deficiency. The syndrome can be staged.

1.  Root elongation and enamel hypoplasia. Loss of alveolar bone supporting the apices of the teeth results in root elongation. This precedes any crown abnormalities. Owners are usually unaware of any dental abnormalities, although they may have noticed that their rabbit will not eat hay or other hard foods, which is probably due to elongated roots pressing on the sensory nerve supply as it enters the tooth at its apex. Eventually the roots are so long that they can be palpated along the ventral border of the mandible. Another noticeable sign of root elongation is epiphora due to pressure on the nasolacrimal duct by elongated roots of the upper first incisors. Demineralisation of dental tissue is manifested by enamel loss, which can be seen as ribbing in the enamel on the labial aspect of the incisors and loss of the enamel ridges on the cheek teeth, which leads to uneven wear.

2.  Acquired malocclusion. Loss of supporting alveolar bone also allows curvature of the teeth in response to forces generated during chewing and biting. It also results in widening of the periodontal spaces and, in some cases, rotation of the teeth within the socket. Wide periodontal spaces and tissue necrosis at the apices of the teeth predispose to abscess formation. As the shape and position of the teeth change, they do not meet and wear correctly and cause malocclusion. Malocclusion of the cheek teeth can lead to the development of sharp spurs that lacerate the tongue or cheek, which is distressing for the rabbit and affects eating, swallowing and grooming. Facial abscesses and chronic dacryocystitis are common complications and are seen more frequently as dental disease progresses.

3.  Cessation of tooth growth. Eventually the changes that are taking place in the apices of the teeth destroy the germinal tissue so the teeth stop growing. This may be mistakenly interpreted as a successful response to treatment instead of the passage of time and progression of the disease. The pathological changes do not take place simultaneously so some teeth still grow while others have stopped. At this stage, most of the teeth appear uneven, misshapen or discoloured although some can retain their normal structure and shape and continue to grow. Others remain as non-growing stumps.

4.  Erosion, fracture and root resorption of the teeth occur as a result of continued demineralisation. Some crowns break off altogether, usually just below the gingival margin and the gum heals over the site where the crowns should be. Eventually the rabbit has few or no crowns left on the teeth. Some cases develop dystrophic calcification of the skull and degenerating teeth. Others do not. Infection and the calcium/vitamin D status of the rabbit might influence the advanced changes that take place.

Prevention of PSADD (Progressive Syndrome of Acquired Dental Disease)

There are two main hypotheses for the cause of PSADD: lack of dental wear and underlying metabolic bone disease. The advice on prevention of PSADD is the same for both hypotheses. Exclusion of muesli mixes and the provision of a high fibre diet in the form of hay, grass, leafy green plants and vegetables and a small amount of extruded food should provide adequate dental wear as well as optimum calcium and vitamin D levels, especially if the rabbit is allowed outside to be exposed to natural sunlight.

Treatment of PSADD

Although the advice for prevention of PSADD may be the same for both hypothetical causes of PSADD, the approach to treatment, especially of cheek tooth malocclusion and spurs, is very different. If PSADD is due to insufficient chewing rather than metabolic bone disease, reducing the height of the crowns and attempting to restore normal occlusion is a logical approach. Burring the exposed crowns of the teeth down to gum level is often suggested as appropriate treatment for cheek teeth malocclusion. Some authors even recommend electively performing this procedure every 4-6 weeks with the advice that the rabbit's diet should include more hay and fibrous food. In this author's opinion, this approach is unnecessary, inappropriate and counterproductive. Rabbits need exposed crowns on their teeth to eat hay. Also, it is not possible to restore normal occlusion, no matter how extensive the dental procedure is. The alternative approach is to only remove the spurs and crowns that are causing discomfort. Eventually, the teeth stop growing.

Excessive Dietary Calcium as a Cause of Urinary Tract Disease

The concept that rabbits could suffer from calcium deficiency is a difficult one for many people because of the belief that excessive amounts of dietary calcium cause urinary tract disease and soft tissue mineralisation in rabbits. Examples include sludgy urine, urolithiasis or mineralisation of the aorta and kidneys. Although this is plausible, it is not so straightforward. Rabbits have evolved to excrete sediment in the urine. Sediment is normal. The potential to absorb large amounts of calcium is a way of meeting rabbits' high demand for calcium for the continual formation of new dental tissue and their high rate of reproduction. The amount of sediment varies with calcium intake, calcium demand, urine pH, and renal function. Excessive amounts of sediment ('sludgy urine') develop in rabbits that cannot or do not urinate properly because of neurological deficits, bladder atony, urethritis, arthritis or spinal disorders that result in incomplete emptying of the bladder so sediment accumulates in the retained urine. Although sediment is present, it is not the initiating cause of the problem although it will compound it. When a lot of sediment is present in the bladder, it becomes impossible for the rabbit to void it. The presence of calcium carbonate sediment in urine also increases the likelihood of stone formation. In rabbits, the protozoon parasite Encephalitozoon cuniculi causes kidney disease with areas of focal inflammation and fibrosis. It is common in the pet rabbit population and could predispose them to the formation of kidney stones because the inflammatory lesions within the kidney would obstruct urine flow and inflammatory cells would also act as nidi for stone formation. Because the kidney is so important in calcium regulation, kidney disease has a major effect on calcium regulation. Renal disease impairs calcium excretion while passive calcium absorption from the gut continues. A feature of chronic renal failure in some rabbits is an increase in bone density and soft tissue mineralisation, especially if blood phosphate levels are high. The bones of affected rabbits are heavy, white with a roughened surface. Despite their dense appearance the bones are brittle and prone to fracture.

References

1.  Breslau NA. (1996) In Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism. pp.49-56

2.  Bourdeau JE, et al (1986) Min Electr Metab;12:176-185

3.  Kamphues, et al (1986) J An Physiol Nutr; 50;191-208

4.  Buss SL, et al (1984) Min Electr Metab;10; 127-132

5.  Bourdeau JE, et al. (1988) Miner Electr Metab;14;150-157

6.  Whiting SJ, et al (1984). Min Electr Metab;10:217-221

7.  Norris SA, et al (2001). Bone; 29; 62-69

8.  Harcourt-Brown FM (1996) Vet Rec;139: 567-571

9.  Fairham J, et al (1999).Vet Rec;145:452-454

10. Harcourt-Brown FM. (2009) In Practice;31; 370-379

 

Speaker Information
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Frances Harcourt-Brown, BVSc, DECZM (Small Mammal), FRCVS, RCVS (Specialist in Rabbit Medicine and Surgery)
Harrogate, UK


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