Excess energy intake during growth commonly occurs as a result of feeding a high-quality, growth diet to a young dog on a free-choice basis or feeding excess quantities of food on a portion-controlled basis. Some owners believe that puppies should be kept “plump” in appearance, and that a rotund puppy is a healthy puppy. However, when puppies are fed excessive amounts of a balanced diet, growth rate is maximized before excess weight in the form of fat is gained. As a result, a growing dog that appears to be slightly overweight is usually growing at a maximal rate. Studies with dogs, humans, and other species have shown that the consumption of excess calories resulting in a maximal or an above-average growth rate is not compatible with optimal and healthy skeletal development. ^{17. and 18.}

The first study to demonstrate the relationship between overnutrition, rapid growth, and developmental skeletal disease was conducted with growing Great Danes. ¹⁹ Two groups of growing puppies were fed a highly palatable, energy-dense food throughout growth. The first group was fed free-choice, and the second group was fed amounts of food that were restricted to two thirds of the intake of the first group. The dogs that were fed free-choice grew significantly faster than did the dogs fed restricted amounts of food, and bone tissue was significantly affected by the rapid growth rate. A variety of skeletal abnormalities were observed in the dogs that were fed free-choice, including enlargement of the costochondral junctions and the epiphyseal-metaphyseal regions of long bones, hyperextension of the carpus, and sinking of the metacarpophalangeal and metatarsophalangeal joints. These changes were associated with pain and varying degrees of lameness. It was concluded that generalized overnutrition, in the form of excess energy, protein, calcium, and phosphorus, caused increased growth rate in these dogs that contributed to abnormal skeletal development.

Subsequently, other studies were conducted with growing dogs of several large breeds, including German Shepherd Dogs, Golden Retrievers, and Labrador Retrievers. In one study, a group of puppies that had high parental frequencies of CHD were examined. The incidence and severity of dysplasia was greater in puppies that had rapid growth rates as a result of increased caloric intake, when compared with puppies that were fed restricted amounts of food. ²⁰ Similarly, when a group of puppies was hand-reared at a reduced rate of growth, they developed a very low incidence of hip dysplasia. ^{21. and 22.} In contrast, a control group that was fed to allow a much higher growth rate showed a very high incidence of hip dysplasia.

A well-controlled longitudinal study with a group of 48 Labrador Retrievers found that dogs fed 25% less food than dogs fed free-choice, starting after weaning and continuing throughout life, had significantly less hip joint laxity at 30 weeks of age and a significantly lower incidence of CHD. ^{18. and 23.} Of the dogs in the free-choice group, 16 of 24 developed CHD by 2 years of age, compared with 7 of the 24 dogs in the limited-feeding group. OA was observed in the hips of 7 of the 24 free-choice dogs by the time they were 1 year old, while none of the limited-feeding dogs showed OA at 1 year. ²⁴ By 5 years of age, 12 of the 23 remaining free-choice dogs (52%) and only 3 of the 23 limited-feeding dogs (13%) had radiographic signs of hip OA, and the degree of OA was more severe in free-choice dogs than in the restricted-feeding dogs. Additional evaluations showed that arthritic changes to hips and shoulders increased linearly (rather than bimodally) throughout life, and these changes were more frequent, occurred earlier, and were more severe in dogs fed free-choice compared with dogs fed restricted amounts of food. ^{25. and 26.} Finally, the dogs fed free-choice weighed more and had higher body condition score values during growth and throughout life; a significant and positive correlation was found between body weight and the presence and severity of OA. ²⁴

The skeletal system of dogs is most susceptible to physical and metabolic stressors during the first 12 months of life. It is theorized that abnormal skeletal development during periods of rapid growth results from overloading the growing skeleton with prematurely increased muscle mass and body weight. ²⁷ This theory is supported by the fact that rapidly growing male dogs of the large and giant breeds are more frequently affected than are smaller females. ²⁸ There also appears to be a correlation between increasing body size and the occurrence of the lesions associated with osteochondrosis. ²⁹ A comparison between the bones of large and small breeds of dogs during periods of rapid growth shows that the bones of large breeds are relatively less dense than are the bones of small breeds at similar stages of development. Bones of large breeds have a thinner cortex, larger medullary cavity, and a less dense spongiosa. ^{29. and 30.} It is possible that the bones of large dogs during growth are not as strong as those of smaller dogs during the same period. This may be the basis for the genetic predispositions toward skeletal abnormalities in the large and giant breeds. Recent evidence suggests that mechanical stress on the joints caused by excessive weight during growth and throughout life also contributes to the development of OA. ²⁴

In addition to weight-related mechanical stressors, overnutrition has direct effects that negatively influence skeletal development. Studies with Great Danes have shown that overnutrition stimulates accelerated skeletal growth. ²⁹ Great Dane puppies were fed a diet formulated for growth from weaning to 6 months of age. Puppies in one group were fed free-choice (ad libitum), and puppies in the second group were restricted to 70% to 80% of the amount consumed by the first group. As in previous studies, dogs fed ad libitum weighed significantly more than the restricted group at 6 months of age. Bone measurement data showed that accelerated skeletal growth, in the form of increased size and volume of bone, contributed significantly to the increased weight. The male dogs that experienced overnutrition also showed an increased rate of bone remodeling, resulting in enlarged bones with relatively low densities and low resistance to the greater weight they were required to bear. It appears that if a large dog is allowed to attain its maximal growth rate by consuming excess amounts of a balanced diet, the accelerated growth rate creates a rapidly growing skeleton that is less strong and less able to withstand the biomechanical stresses of the greater muscle mass and body weight that are put on it. Not only do these dogs weigh more, but their bones are less able to handle the added weight. The end result is the development of aberrations in ossification, damage to developing cartilage and growth plates, and premature closure of growth plates. Most often this manifests as osteochondrosis, but these changes may also be involved in the onset of several other developmental skeletal diseases.

Calcium is a nutrient that is commonly supplemented to the diets of dogs and, less commonly, to the diets of cats. The reason most often cited for calcium supplementation relates to its essential role in normal skeletal growth and development. Supplements such as dicalcium phosphate and bone meal are added to a growing dog’s diet during growth spurts or when problems such as hyperextension of the carpus or sinking of the metacarpophalangeal joints occur. Some breeders encourage all of their puppy buyers to routinely supplement their puppy’s diet with calcium during the entire first year of life as a prophylactic measure. Some believe that calcium supplementation is not only necessary for proper bone development but that it also prevents the development of certain skeletal disorders. Regardless of the good intentions, there are potential risks when excessively high levels of calcium are either included in the diet itself or added to an adequate and balanced diet.

Research has shown that normal growth in puppies can be supported by a calcium intake of 0.37% available calcium or 0.6% total calcium. ³⁴ The Association of American Feed Control Officials’ (AAFCO’s) Nutrient Profiles for dog foods sets minimum levels for calcium of 0.8% for growth and reproduction and 0.5% for adult maintenance. The profile also mandates a maximum level of 2.5% calcium in all dog foods. This maximum level was included because published data show that excess calcium during growth may contribute to abnormal skeletal development and increase a dog’s risk of skeletal disease.

A series of studies were conducted in the 1980s to determine the effect of varying levels of dietary calcium upon the occurrence of developmental skeletal disease in growing Great Danes. ^{35. and 36.} An experimental diet was formulated that met the recommendations of the 1974 National Research Council’s (NRC’s) Nutrient Requirements for Dogs. Both the control group and the experimental group of dogs received this food throughout growth. In addition, the experimental group received calcium carbonate supplementation to achieve a level of 3.3% in the diet, three times the amount recommended by the NRC at that time. ^{37. and 38.} Dogs that were fed excessive calcium during growth developed chronic hypercalcemia and hypophosphatemia. Skeletal differences between the control and experimental dogs included a higher percentage of total bone volume, retarded bone maturation, retarded bone remodeling, and a decreased number of osteoclasts (bone resorption cells) in the dogs receiving calcium supplementation. This group also showed a higher incidence and severity of cartilage irregularities associated with osteochondrosis at the distal and proximal humeral cartilages. Clinically, calcium-supplemented dogs exhibited retained cartilage cones, severe lateral deviation of the feet, and radius curvus syndrome.

When plasma calcium levels increase, the hormone calcitonin is secreted from the thyroid gland. Calcitonin functions to lower plasma calcium to normal levels; it exerts this effect by decreasing the activity of osteoclasts, which leads to decreased bone resorption and slowed cartilage maturation. ^{19. and 35.} This is a normal hormonal response to both eating and calcium influx, and calcitonin functions along with parathyroid hormone (PTH) to closely regulate calcium homeostasis. However, the chronic elevation of calcitonin suppresses bone resorption for an abnormal period of time, resulting in a gradual thickening and increased density of cortical bone. For example, when growing Beagles were supplemented with 2.3 g of calcium per day for 2 months, the thyroid glands of supplemented dogs contained significantly increased proportions of calcitonin-producing C cells and decreased proportions of thyroid follicles, when compared with those of the control dogs. ³⁹ High dietary calcium intake caused thyroid C-cell hyperplasia, which would suggest the occurrence of chronic hypercalcitoninism in these dogs. Additionally, electron microscopy of the thyroid C cells of dogs fed excess calories, protein, and calcium showed that these cells were releasing larger amounts of calcitonin than were the C cells of dogs fed restricted diets. In growing dogs, these changes interfere with normal bone remodeling and development. The deposition of excessive subperiosteal bone that results may cause the clinical signs of HOD and Wobbler syndrome, and the chronic effects of calcitonin on cartilage maturation may result in the eventual detachment of the articular cartilage that is seen in osteochondrosis.

A more recent study, again with Great Danes, fed the same diets described previously plus a third experimental diet that contained additional phosphorus to provide a balanced calcium-to-phosphorus ratio. ⁴⁰ Puppies in this study were fed the high calcium diets during the period of most rapid growth, between 6 and 17 weeks of age. At 17 weeks, all of the puppies were switched to the control diet, which contained normal calcium and phosphorus levels (1.04% and 0.82%, respectively). Puppies fed the high calcium-only diet developed hypercalcemia and hypophosphatemia that persisted throughout the experimental diet feeding period. Puppies fed the food containing elevated calcium and phosphorus had normal serum calcium values during this period and slightly lowered plasma phosphorus levels. Although both groups of puppies that were fed excessive calcium showed skeletal disturbances during the feeding period, changes were more severe in puppies fed excessive calcium without phosphorus. This difference was attributed to the hypercalcemia and subsequent reduction in PTH secretion, leading to hypophosphatemia. This study also found that normalizing dietary calcium levels after 17 weeks of age corrected some skeletal abnormalities, but joint changes that were consistent with osteochondrosis still developed in the puppies that were fed the diet containing high calcium without added phosphorus.

To further examine the effects of elevated calcium when a normal calcium to phosphorus ratio is maintained, Great Dane puppies were fed diets containing three levels of calcium (0.48%, 0.8%, and 2.7%). ⁴¹ Each diet contained sufficient phosphorus to provide a consistent calcium-to-phosphorus ratio of 1.2:1.0. To control for other factors that can affect skeletal development, the experimental diets had reduced caloric density and contained 26% protein and 14% fat. Puppies were assigned to the three diets at the age of weaning, and they were fed the experimental diets for 18 months. Even when balanced with phosphorus, increasing dietary calcium had a rapid and direct effect on the amount of mineral deposited in maturing bones. Bone mineral content and bone density were positively correlated with dietary calcium and phosphorus beginning almost immediately after weaning and continuing until the dogs were 6 months old. Six of the 15 dogs that were fed the highest level of calcium (2.7%) showed clinical signs of lameness during the first 6 months of the study, and three of these dogs showed clinical signs of HOD. After 6 months, the bone density differences seen between the high-, medium-, and low-calcium groups gradually diminished and were not apparent by the time that the dogs were 12 months old (Table 37-1). Similar to the results of Schoenmakers et al., ⁴⁰ dogs fed high amounts of calcium that were balanced with phosphorus did not develop hypercalcemia. Conversely, dogs fed the highest calcium diet had low total and ionized serum calcium values when they were between 4 and 7 months of age. This decrease was not observed in dogs fed the low- and medium-level calcium diets. It is likely that these values are a result of increased deposition of circulating calcium into developing bone, possibly in response to chronically increased calcitonin levels. The normalization of bone composition between the three groups after 6 months of age may reflect the natural maturation of the dogs’ regulatory mechanisms that control calcium absorption and excretion (see below).