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Overview of Dystrophies Associated with Calcium, Phosphorus, and Vitamin D


Walter Grünberg

, DrMedVet, MS, PhD, DECAR, DECBHM, University of Veterinary Medicine Hannover, Foundation

Last full review/revision Apr 2014 | Content last modified May 2014

The principal causes of osteodystrophies are deficiencies or imbalances of dietary calcium, phosphorus, and vitamin D, as well as dysregulation of parathyroid hormone (PTH) activity. Their interrelationships are complex and not easily defined.

The primary source of calcium and phosphorus is the diet. These elements are absorbed in amounts depending on the source of the minerals, intestinal pH, and dietary levels of vitamin D, calcium, phosphorus, iron, and fat. If vitamin D or its activity is decreased, calcium and phosphorus absorption are reduced. Vitamin D is obtained either through the diet or by production when the skin is exposed to sunlight (ultraviolet radiation). Before vitamin D can be used, it must be processed into its metabolically active form in two consecutive hydroxylation steps by the liver and kidney. Vitamin D3 (cholecalciferol) acts primarily on the GI tract to increase absorption but also affects the bone, thereby increasing availability of elemental calcium. Through a negative feedback loop, it also contributes to the regulation of PTH secretion.

PTH secretion occurs in response to a low circulating calcium ion concentration and depends on the availability of magnesium. The target organs of PTH are the kidneys, bones, and intestines. In the kidneys, PTH promotes renal tubular absorption of calcium while enhancing the renal excretion of phosphorus, as well as the activity of 1α-hydroxylase, the enzyme responsible for activation of vitamin D3 in the kidney. In the intestine, PTH promotes absorption of calcium. PTH also facilitates mobilization of calcium and phosphorus from bone by allowing utilization of calcium from the osteoid matrix. In ruminants, PTH increases the salivary excretion of phosphorus in exchange for bicarbonate.

Specific bony lesions are associated with abnormalities in absolute or relative amounts of vitamin D, calcium, phosphorus, and PTH. Often, in addition to the deficiency or excess in one element, this also causes a secondary pathology due to feedback mechanisms, altered ratios, or concomitant metabolic deficiencies. Specific disease syndromes can be classified as nutritional, metabolic, or genetic in nature. Classic examples of nutritional osteodystrophies are rickets, osteomalacia, enzootic calcinosis, or hypervitaminosis D. Fibrous osteodystrophy and hyperparathyroidism are common metabolic osteodystrophies. Genetic osteodystrophies can be caused by defects in phosphate transporters or genetic abnormalities in the hormonal regulation of phosphorus homeostasis. Examples of genetic defects associated with osteodystrophies include X-linked hypophosphatemia and hereditary hypophosphatemic rickets.

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