Nutrition during growth and skeletal development in the dog

Nutrition plays a vital role during growth and skeletal development and according to some studies it could also have an impact on the onset of certain diseases or be used to support orthopaedic treatment. The percentage of dogs with orthopaedic problems is of around 10%, with a higher prevalence of certain specific diseases in large breed dogs (Lafond et al., 2002).

MACROELEMENTS

CARBOHYDRATES. Carbohydrates have been described as essential for growth (Meyer, 1983), but no studies exist establishing a correlation between carbohydrate deficiency and the development of orthopaedic diseases.

PROTEIN. A low-protein diet correlates with growth retardation and in severe cases with growth arrest and weight loss. A low intake of energy and protein causes a decreased hepatic production of IGF-I and hence a decrease in skeletal growth (Sheffy et al., 1979). In contrast, studies on large breed dogs fed a high protein diet (30% DMB) have not shown any difference in the incidence or severity of osteochondrosis compared to dogs fed with a normal or decreased protein content (Nap et al., 1991).

ENERGY. Studies have shown that energy excess may favour a more rapid growth of long bones and accelerate weight gain, which overloads the skeletal system. An ad libitum diet may favour the onset of the following orthopaedic diseases: osteochondrosis, radius curvus syndrome, hip conformation alterations and wobbler syndrome (Hedhamman et al., 1974) (Figs. 1a and 1b). Converseenergy deficiency may be the cause of delayed growth, but with the return to a correct diet the dog then grows faster and for a longer period of time.

MICROELEMENTS

CALCIUM DEFICIENCY. Calcium necessary for growth is usually between 0.8%-1.2% DMB. In fast growing animals, such as in large breed dogs, the recommended calcium intake is higher than in slow growing animals, i.e. small breed dogs.

Chronic calcium deficiency (0.55% DMB) does not hamper growth but results in decreased plasma levels of calcium, with consequent secondary nutritional hyperparathyroidism. Such condition is characterized by an increased bone resorption of calcium by osteoclasts and osteocytes. Parathyroid hormone (PTH) increases plasma levels of Vitamin D3, thus allowing the differential diagnosis between secondary nutritional hyperparathyroidism and hypovitaminosis D. Secondary to this nutritional deficiency there may be a chronic progressive demyelination of skeletal bones with consequent pathologic or compression fractures.

CALCIUM EXCESS. A common mistake made by owners is to supplement calcium in large breed dogs already taking a balanced diet, with the intent of preventing the occurrence of orthopaedic diseases. In reality, a high calcium intake in the diet has been shown to cause hyperplasia of CT cells, which produce calcitonin, with consequent depression in the activity of osteoclasts and a reduction of bone remodeling. Great Dane puppies fed between 3-6 weeks of life with a high calcium diet (3.3% DMB) exhibited an increased response of CT cells and an increased plasma calcium concentration until the 17th week of life; eosinophilic panosteitis was diagnosed radiographically in all the puppies (Schoenmakers et al., 2000).

In addition, the chronic administration of a calcium-rich diet may be the cause of decreased enlargement of the vertebral foramina for blood vessels and for the spinal cord. A study on Great Danes fed with a calcium content of approximately 3.3% DMB (Hazewinkel et al., 1985) has in fact reported a higher incidence of Wobbler Syndrome.

Excessive calcium intake has also been associated with other skeletal growth disorders, such as osteochondrosis, radius curvus and elbow incongruity (Hazewinkel et al., 1991: a diet with 3.3% of Ca DMB resulted in the development of severe osteochondrosis, radius curvus syndrome and wobbler syndrome; Schoenmakers et al., 2000: a diet with 3.3% of Ca DMB administered for 3-6 weeks resulted in the development of panosteitis at 4 months, severe osteochondrosis and radius curvus at 6-26 weeks).

PHOSPHORUS DEFICIENCY. Phosphorus deficiency in the diet is rare, with calcium excess in the diet being much more frequent, which causes hypercalcaemia with negative feedback on PTH synthesis and consequent decreased synthesis of Vitamin D. The association of hypophosphataemia and decreased Vitamin D synthesis may be the cause of altered skeletal mineralization. Radiographically, a characteristic manifestation is hypophosphataemic rickets (Schoenmakers etal., 2000).

VITAMIND DEFICIENCY. In dogs and cats, unlike in reptiles, amphibians, herbivores, and omnivorous birds, the only source of Vitamin D is food. Animal fats are rich in Vitamin D, while vegetarian foods and white meat foods have low levels of Vitamin D.

The main player inbone mineralization is 1,25(OH)2-vitamin D3, a metabolite of vitamin D3 metabolized within the body and absorbed at gastrointestinal level.

A very low plasma concentration of metabolites 25(OH)VitD3 and 23,25(OH)2VitD3, with 1,25(OH)2VitD3 in the normal range, is indicative of hypovitaminosis D. Hypovitaminosis D may be the cause of rickets, bowedlimbs and pathologic fractures.

VITAMIN D EXCESS. Vitamin D excess (100 times the recommended intake of 500 IU/kg of food) at the age of six weeks triggers an adaptive mechanism in which the Vitamin D excess is hydroxylated into 25(OH)VitD and 1,25(OH)2VitD, with no increase in the absorption of calcium, phosphorus or of pathologic mineralization characteristic of vitamin D intoxication. This adaptation mechanism causes an increase in plasma 23,25(OH)2VitD and a decrease of 1,25(OH)2VitD with severe alterations in endochondral ossification, known as osteochondrosis, which can lead to the radius curvus syndrome at the age of 15 weeks. In a study performed on dogs fed with an excess of Vitamin D capable of causing Vitamin D intoxication, the diet caused a significant PTH decrease and an increase in the proliferation of calcitonin (CT) producing cells, mimicking the scenario resulting from calcium excess (Tryfonidou et al., 2002).

VITAMIN A EXCESS. Vitamin A is essential for bone metabolism and influences the proliferation of chondrocytes and the activity of osteoclasts/osteoblasts. Vitamin A is found in animal fat and can, in dogs but not in cats, be synthesized from beta-carotene (in the intestine or liver). In the cat, the requirement of vitamin A is therefore significantly higher than in dogs. Another difference between the two species is that the dog can inactivate vitamin A and eliminate up to 15-60% of it in the urine, while the cat tends to sequester it in the liver, with no apparent adverse effects.

In puppies and kittens, protracted vitamin A overdose may result in hypervitaminosis A. These puppies will manifest reduced growth and osteoporosis of the long bones. In the dog, hypervitaminosis A is also the cause of anorexia, weight loss, narrowing of the growth plates and thinning of the cortex. In the cat, hypervitaminosis A is more commonly described in adult subjects on a raw fish or liver diet and is the cause of stiffness and pain in the neck and forelimbs (Hazewinkel et al., 1994).

References

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