Metabolic Bone Disease
Large quotes taken from the writings of Dr. Fredrick L. Frye DMV are contained within this document. Please be sure to read Calcium Deficiency in herbivore and omnivorous reptiles as well as this article.
Fredrick L. Frye DMV states in his book "Metabolic bone disease is, perhaps the most common nutritional deficiency affecting captive reptiles. It is usually the direct results of diets whose overall calcium to phosphorus ratio is seriously skewed toward an overabundance of phosphorus. It is far beyond the scope of this chapter to discuss this important group of disorders fully, therefore attention will be focused upon fibrous osteodystrophy the most frequently encountered of the metabolic bone diseases within the complex. "
Variously called secondary nutritional hyperparathyroidism, osteomalacia, renal rickets, osteogenesis imperfecta, cage paralysis, osteodystrophia fibrosa cystica, etc., this author prefers the specific term fibrous osteodystrophy for it most properly denotes the pathological lesions exhibited in affected individuals.
The etiology may involve disorders originating in the parathyroid glands, intestine, kidneys, liver, thyroid, and bone. Realizing fully that many more factors may enter the equation yielding the final answer. For the purpose of exposition, comments will be confined to that form of fibrous osteodystophy which results from dietary imbalances in calcium and phosphorus.
Since the ion product(s) of total skeletal calcium and phosphorus in most vertebrate species are in a ratio of approximately 2:1 it would appear reasonable that the available dietary ratio of these elements also should be in a range of 1:1 to 2:1. Simple stoichiometric chemistry predicts that an excess of either calcium or phosphorus will create an imbalance. In clinical practice, one usually finds diets containing gross excesses of phosphorus ion products. Muscle meats and many vegetables contain extremely low quantities of available calcium but are well endowed with excessive phosphorus.
When gross imbalances in the calcium: phosphorus ratio exist, the relatively insoluble salt, calcium phosphate (which is minimally absorbed from the gut), is favoured within the intestine. Excess phosphate ion can be absorbed thus resulting in hyperphosphatemia. The parathyroid glands are stimulated to secrete parathormone, thus inducing the leaching of calcium from the hydroxyapatite crystals in the mature bone matrix. As reabsorption continues, the bone is weakened and, concomitantly, is partially replaced by fibrocollagenous connective tissue. Affected bones tend to be larger in diameter with irregular outlines and a characteristically spongy consistency. Radiographs demonstrate normal medullary cavities surrounded by massively expanded cortical bone of greatly diminished radiodensity. These bones are deformed easily, and pathological fractures of weight-bearing long bones and vertebrae are common sequelae to this disorder. Ingestion of excessive dietary calcium ion products (with respect to phosphorus) is possible, but very unusual. When it does occur, the parafollicular cells or "C" cells of the thyroid gland(s) and ultimobranchial bodies are stimulated to secrete a hormone like substance, calcitonin, which acts to inhibit calcium ion resorption from hyroxyapatite, ie., it is antagonistic to the action of parathormone and, thus, reduces plasma calcium levels.
The plasma calcium concentration usually is elevated in fibrous osteodystrophy until late in the course of the disease, at which time it may be so low that hypocalcemic muscle tremors, tetany or asthenia occur. Death from cardiac failure usually ensues when the plasma calcium reaches such precipitous levels. Even the novice herpetologist usually would have noted the gross abnormal skeletal lesions by this time.
Interestingly, even advanced cases of fibrous osteodystrophy often yield to therapy. Crocodilians and lizards, particularly herbivorous iguanas, respond well to oral and injectable calcium salts such as calcium lactate and calcium gluconate. Oral calcium carbonate is useful also. Vitamin D3 also should be provided to ensure adequate uptake from the intestinal mucosa. The diet must be corrected to restore the intake of available calcium and phosphorus to an appropriate physiological ratio."
In other words I think Dr. F. L. Frye is saying that MBD is made up of a number of disorders. One of the most common of these disorders is an improper balance of calcium and phosphorus in the diet resulting in hyper or hypo calcemia. MBD can affect the internal organs as well as the bones.
When there is an imbalance of calcium in the diet (hypocalcemia or hypercalcemia) bones become weak and spongy. The affected bones will also enlarge, and have irregular outlines ie bumps and swellings. These bones will deform easily and may also fracture easily. As the calcium levels in the blood drop muscle tremors, tetany, and or asthenia occur. When the calcium level becomes critically low death from cardiac failure may occur.
Excerpt From "Reptile Rehabilitation", In, The Biology, Husbandry and Health Care of Reptiles and Amphibians, Vol. I., Reptiles. Lowell Ackerman (ed.) In press. (c) 1995 Melissa Kaplan
MBD and calcium metabolism are discussed in great detail in many texts and so will not be elaborated upon here. Quite simply stated, vitamin D3 (dietary or derived from exposure to ultraviolet B), calcium (dietary and matter recycled from the bone matrix) and phosphorus (dietary) interact together to perform a number of functions besides bone growth and maintenance, including muscle contractions and blood coagulation (Wright, 1993). The result is a well-functioning system, with calcium restored to and, in the case of growing animals, added to the bone matrix. Too much phosphorus can throw this process off, as can too much or too little vitamin D3 or too little access to ultraviolet B wavelengths. As the dangers of calcium deficiency become more widely known, there is increased risk that pet owners may add too much calcium to their reptile's diet. This results in hypercalcemia, a condition as fraught with peril as is hypocalcemia.
Signs of metabolic bone disease include hard knobs in the long bones of the legs, bumps along the vertebral column of the back and tail, softening or hard swelling of the jaw, and softening of the plastron or carapace. All of these signs may be felt before they can be seen, making a careful physical exam important. Visible signs of moderate to severe MBD include jerky gait when walking, tremors and twitches in the limbs and muscles of the legs and toes when at rest, and shakiness when being held. Advanced cases of MBD include all the above signs plus anorexia and fractured bones. Severely deficient reptiles tend to be lethargic and may only be able to drag themselves along the ground. Arboreal lizards spend all of their time on the ground as they lack the strength to grip and climb.
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April, 10, 2012
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