The principal causes of osteodystrophies are deficiencies or imbalances of dietary calcium, phosphorus, and vitamin D. Their interrelationships are not easily defined, and their interrelationship with the parathyroid gland must also be considered. Deficiencies of any of the 3 may be absolute or relative and must be assessed in relation to availability and growth rate.
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 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 feed back loop, it inhibits parathyroid hormone (PTH) secretion.
PTH is secreted in response to a low circulating calcium ion concentration. In general, it plays a role in increasing available calcium. The 3 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 or metabolic in nature.
Abnormal levels of calcium and phosphorus may also cause secondary disease. In general, diseases to which dogs are genetically predisposed can be increased in incidence by oversupplementation of calcium and phosphorus. Specifically, osteochondritis dissecans and hypertrophic osteodystrophy are more frequent in giant-breed dogs fed excess calcium.
Last full review/revision March 2012 by Walter Gruenberg, DrMedVet, MS, PhD, DECAR, DECBHM