Daniel C. Richardson1
Phillip W. Toll1
disease is common in large and giant-breed puppies. One manifestation, hip dysplasia, affects millions of dogs. Genetics,
environment, and nutrition all contribute to developmental skeletal disease. Of the nutritional components, rate of growth,
specific nutrients, food amounts consumed, and feeding methods influence skeletal disease. Excess energy and calcium are known
risk factors; therefore, the level of these nutrients in the food should be near the Association of American Feed Control
Officials minimum requirement. Puppies should be fed a growth-type food using a food-limiting technique. All puppies should
be weighed and evaluated at least every two weeks. Amounts fed should be increased or decreased based on weight and body condition
Words: Developmental skeletal disease, calcium, energy, hip dysplasia, electrolyte balance, osteochondrosis, body condition,
The musculoskeletal system
changes constantly throughout life. These changes are most rapid during the first few months of life and slow with skeletal
maturity (about 12 months for most breeds). The skeletal system is most susceptible to physical and metabolic insult during
the first 12 months of life because of the heightened metabolic activity. The physical manifestation of these results can
be lameness and/or altered growth. Both can affect locomotion and/or soundness of adult dogs.
skeletal disease is a multifactorial process that has genetic, environmental, and nutritional components. These skeletal abnormalities
primarily affect fast growing, large-breed dogs. Lack of careful genetic monitoring can introduce and propagate disorders
(e.g., hip dysplasia, osteochondrosis) that are difficult to eliminate. Trauma, whether obvious (e.g., hit by a car) or subtle
(e.g., excessive weight) can adversely affect relatively weak growth centers and cause skeletal disease (e.g., angular limb
deformities). Nutrient excesses (e.g., excess calcium supplementation) often exacerbate musculoskeletal disorders.1-4
This article reviews the role of nutrition in developmental skeletal disease in young dogs.
Nutrition and Skeletal Disease
role of nutrition in developmental skeletal disease is complex. Rate of growth, specific nutrients, food consumption, and
feeding methods have all been shown to influence skeletal disease. Large and giant breeds are most susceptible to developmental
skeletal disease, presumably because of their accelerated growth rate.4,5 Dietary deficiencies are rare in young,
growing dogs fed commercial growth foods.6 Problems associated with dietary excess are far more likely, especially
if a high quality growth food is supplemented with minerals, vitamins, and energy.6 The following review discusses
some of the more critical nutrients in developmental skeletal disease.
The energy needed for
any individual depends on breed, age, neuter status, and activity levels. In general, growing puppies require twice as much
dietary energy as adults for body maintenance, activity, and growth. The need is greatest right after birth and decreases
as the dog grows and matures. Rapid growth in large and giant-breed dogs increases the risk of skeletal disease.4,5
Excessive dietary energy may support a growth rate that is too fast for proper skeletal development and results in a higher
frequency of skeletal abnormalities in large and giant-breed dogs.7 Because fat has twice the caloric density of
protein or carbohydrate, dietary fat is the primary contributor to excess energy intake.
energy leads to rapid growth. Dietary energy in excess of a puppy's needs will be stored as body fat. Body condition scoring
evaluates body fat stores and therefore correctness of energy intake. Maintaining appropriate body condition during growth
not only avoids excess body fat storage, but also helps control excess growth rate. Limiting intake to maintain a lean body
condition will not impede a dog's ultimate genetic potential. It will only reduce food intake, fecal production, obesity,
and lessen the risk of skeletal disease.8 Energy or food-dose calculations can only be used as general guidelines
or starting points that must be modified based on frequent clinical evaluation of each puppy because individual needs can
vary widely. (Fig. 1). Physical evaluation or body condition scoring should be done at least every two weeks (See Evaluation
of Feeding Methods and Scoring to follow).
other species, protein excess has not been demonstrated to negatively affect calcium metabolism or skeletal development in
dogs. Protein deficiency, however, has more impact on the developing skeleton. In Great Dane puppies, a protein level of 14.6%
(dry matter basis) with 13% of the dietary energy derived from protein can result in significant decreases in bodyweight and
plasma albumin and urea concentrations.9,10 The minimum adequate level of dietary protein depends on digestibility,
amino acids, and their availability from protein sources. A growth food should contain > 22% protein (dry matter basis)
of high biologic value (Table 1).11 The dietary protein requirements of normal dogs decrease with age.
The absolute level of
calcium in the diet, rather than an imbalance in the calcium/phosphorus ratio, influences skeletal development.2
Young, giant-breed dogs fed a food containing excess calcium (3.3% dry matter basis) with either normal phosphorus(0.9% dry
matter basis) or high phosphorus(3% dry matter basis, to maintain a normal calcium/phosphorus ratio) had significantly increased
incidence of developmental bone disease.2 These puppies apparently were unable to protect themselves against the
negative effects of chronic calcium excess.3 Further, chronic high calcium intake increased the frequency and severity
Often puppies are switched
from growth to maintenance-type foods to avoid calcium excess and skeletal disease. However, because some maintenance foods
have much lower energy density than growth foods, the puppy must consume more dry matter volume to meet its energy requirement.
If the calcium levels are similar (dry matter basis) between the two foods, the puppy will actually consume more calcium when
fed the maintenance food. This point is exemplified in the case of switching a 15-week-old, 15-kg male Rottweiler puppy from
a growth food containing, on an as fed basis, 4.0 kcal/g metabolizable energy and 1.35% calcium (1.5% on a dry matter basis)
to a maintenance food containing the same amount of calcium but at a lower, 3.2 kcal/g energy density. The puppy would require
approximately 1,600 kcal/day. In order to meet this energy need the puppy would consume approximately 400g of the growth food
(containing 5.4g of calcium) vs. 500g of the maintenance food (containing approximately 6.7g of calcium).
Feeding treats containing
calcium and/or providing calcium supplements further increases daily calcium intake. Two level teaspoons of a typical calcium
supplement (calcium carbonate) added to the growth food of the 15-week-old, 15-kg Rottweiler puppy would more than double
its daily calcium intake. This calcium intake is well beyond the levels shown to increase the risk for developmental bone
disease. A recent review article best sums up the need for calcium supplements: "Because virtually all dog foods contain more
calcium than is needed to meet the requirement, the use of a calcium supplement certainly is unnecessary. Now that the deleterious
effects of excess dietary calcium have been delineated, we can say that the feeding of calcium supplements not only is unnecessary,
but, in fact, contraindicated!"8
these studies demonstrate the safety and adequacy of 1.1% calcium (dry matter basis) and the Association of American Feed
Control Officials (AAFCO) minimum recommendation is 1% (dry matter basis, Table 1), we recommend that calcium levels for a
growth food be within this range for at risk puppies, with no supplementation.
L-ascorbic acid (Vitamin
C) is necessary for hydroxylation of proline and lysine during biosynthesis of collagen, a major component of ligaments and
bones. Food devoid of Vitamin C fed to puppies for 147 to 154 days neither affected growth nor caused skeletal lesions.12
There are no known dietary requirements for Vitamin C in the dog.11
Vitamin C supplementation
in pigs elevates plasma levels of Vitamin C without changing articular concentrations of hydroxyproline.13 Similar
studies in dogs demonstrated transient elevation of plasma Vitamin C concentrations; however, long-term supplementation did
not increase concentrations much above normal.14 Even though Vitamin C has been recommended, the relationship between
Vitamin C and developmental skeletal disorders in dogs such as osteochondrosis and hip dysplasia is unproven.15
Vitamin D metabolites
regulate calcium metabolism and therefore skeletal development in dogs. These metabolites aid in the absorption of calcium
and phosphorus from the gut, increase bone cell activity, and influence endochondral ossification and calcium excretion.16
Unlike other omnivores, the dog seems dependent on dietary Vitamin D sources from plants (Vitamin D2) or animals
(Vitamin D3). Commercial pet foods contain from two to 10 times the AAFCO recommended amounts of Vitamin D.6
Diagnosis of Vitamin D deficiency can be made by measuring circulating levels of Vitamin D metabolites and by measuring growth
plate width. Clinical cases of Vitamin D deficiency (rickets) are extremely rare in animals eating commercial foods.6
Increased growth plate width is not associated with low calcium/high phosphorus foods but is a strong indicator of rickets.16
Excess Vitamin D can cause hypercalcemia, hyperphosphatemia, anorexia, polydipsia, polyuria, vomiting, muscle weakness, generalized
soft tissue mineralization, and lameness. In growing dogs, supplementation with Vitamin D can markedly disturb normal skeletal
development due to increased calcium and phosphorus absorption.16
The trace minerals copper
and zinc are involved in normal skeletal development. Supplementing a mare's dietary copper intake during the late stages
of pregnancy, and supplementing the foal's diet from 90 to 180 days of age has been shown to reduce the prevalence and severity
of developmental cartilage lesions.17 Copper deficiency in dogs has been associated with hair depigmentation, hyperextension
of the distal phalanges, and decreased copper levels in the hair, liver, kidney, and heart muscle.18 However, bone
copper concentration was not influenced by dietary treatment and developmental skeletal abnormalities associated with a deficiency
of dietary copper were not described. Similarly, long-term studies of dietary zinc on canine growth and reproduction showed
no significant clinical influence on the skeletal development.19 The role of these two nutrients in the development
of skeletal disease in the dog remains unclear at this time.
of the most common skeletal diseases of growing dogs are hip dysplasia and osteochondrosis. The balance of this section will
review the relationship between these diseases and critical nutrients.
Canine Hip Dysplasia (CHD)
Canine hip dysplasia
(CHD) is the most frequently encountered orthopedic disease in veterinary medicine (Fig. 2). The actual number of cases is
estimated to be in the millions.20 This extremely common heritable disorder of large and giant-breed dogs can be
influenced by nutrition during growth. Early developmental findings of CHD, including joint laxity and coxofemoral anatomical
changes, have been documented within 2 weeks of birth. Rapid weight gain in German Shepherd dogs during the first 60 days
after birth has been associated with CHD at a later age. The importance of this early influential time period was demonstrated
in a study comparing cesarean-section, hand reared puppies to vaginal birth, bitch-fed puppies. Cesarean section and hand
rearing markedly reduced growth and the incidence of CHD in these puppies. Vaginally born, bitch-fed puppies that grew "optimally"
or somewhat "suboptimally" had a higher incidence of CHD.21 The period from 3 to 8 months of age is important in
the development of CHD, with the first 6 months generally regarded as the most critical. Frequency and severity of CHD was
influenced by weight gain in growing dogs that were offspring of parents with CHD or parents with a high incidence of CHD
in their offspring. Dogs with weight gain that exceeded breed standards had a higher frequency and more severe CHD than dogs
with weight gain below breed standards.22
In one colony of fast
growing Labrador Retriever dogs, the triradiate growth plates of the acetabula fused at 5 months as determined by conventional
radiography. These growth plates normally close at 6 months in puppies growing at conventional rates. The investigators speculated
that early fusion in the acetabulum may result in bone/cartilage disparities in the future and predispose to dysplastic changes.23
Limiting food intake in growing Labrador Retriever puppies has been associated with less subluxation of the femoral head and
fewer signs of hip dysplasia.24
Palpation of the hip
is of little to no value in predicting development of hip joints. However, the combination of physical and radiographic examination
are important diagnostic methods for evaluating the hips (Orthopedic Foundation for Animals, Columbus, MO; Penn HIP, Malvern,
PA). A recent review of nutritional influences on CHD contains more information and a more complete reference list.25
Electrolyte Balance and
of dietary electrolytes has been proposed as a preventative for CHD.26 Investigators have associated the dietary
anion gap (DAG) with the radiographic changes of subluxation in the coxofemoral joints in several canine breeds. A food with
a DAG (Na+ + K+ - Cl-) < 23 mEq/100g of food was fed to large-breed puppies and resulted
in less femoral head subluxation, on average, at 6 months of age. The slowed progression of subluxation was also observed
in dogs fed a food with a reduced DAG from 35 to 45 weeks of age.28 Hip joint laxity was determined using the Norberg
hip score computed from radiographs. Significant correlation between radiographic findings (e.g., Norberg hip scores)and progression
of CHD, either radiographic or clinical was not proven. The authors propose the balance of anions and cations in the food
(specifically sodium, potassium, and chloride) influence the electrolytes and osmolality in joint fluid. The joint fluid of
dysplastic dogs has higher osmolality and is increased in volume when compared to that of disease-free hips from dogs of the
same breed.29 The changes in osmolality and fluid volume could be a result rather than a cause of CHD. Changes
in synovial fluid osmolality and electrolyte concentrations were not reported. These studies suggest an association between
DAG and joint laxity without proving a mechanism of action.
Osteochondrosis is a
focal disruption in endochondral ossification. OCD is manifested clinically by pain and lameness. Physical examination results
can be confirmed radiographically. Figure 3 shows a classic inoperative lesion on the proximal humerus. Acute inflammatory
joint disease begins when the subchondral bone is exposed to synovial fluid. Inflammatory mediators and cartilage fragments
are released into the joint and perpetuate the cycle of degenerative joint disease.27 OCD occurs in the physis
and/or epiphysis of growth cartilage, and is a generalized or systemic disease. When OCD affects the physis, it may cause
growth abnormalities in long bones. OCD is wide-spread among young, rapidly growing, warm-blooded, domesticated species and
humans. In all species, the etiology is considered multifactorial. In dogs, risk factors for OCD are age, gender, breed, rapid
growth and nutrient excesses (primarily calcium).1,5,25,29
All large and giant-breed
dogs are at increased risk for OCD. Great Dane, Labrador Retriever, Newfoundland, and Rottweiler breeds are at highest risk.29
Males have an increased risk of OCD in the proximal humerus but gender relationships are not found with OCD involving other
At least two schools
of thought exist concerning the pathogenesis of OCD. In the first, cartilage lesions develop secondary to excessive biomechanical
stresses. This may be termed an "outside-in" development. Over-nutrition, such as ad libitum feeding, stimulates skeletal
growth, cancellous bone remodeling, and weight gain in breeds already having inherent capacity for rapid growth.5
Rapid growth combined with remodeling results in weakened subchondral regions to support the cartilage surface. If osteopenic
and biomechanically weak subchondral spongiosa develops, there is inadequate bony support to the articular cartilage. The
increasing body mass exerts excessive biomechanical forces on the cartilage and secondarily disturbs chondrocyte nutrition,
metabolism, function, and viability. An outside-in development suggests OCD results when nutritional effects initiate a biomechanical
An "inside-out" pathogenesis
has also been proposed. Here, abnormalities of the cartilage canal vessels and chondrocyte necrosis are thought to precede
degenerative changes in the articular cartilage matrix.30 Focal lesions of dead and nectrotic chondrocytes develop,
and subsequently, biomechanical stresses disrupt the lesion. Osteochondrosis lesions are routinely found in pigs as young
as 25 days of age, when rapid growth and weight gain are much less of a factor. These findings support a localized, primary
effect on the chondrocyte rather than secondary effects of biomechanical force.
Regardless of the pathogenesis
of OCD, nutrition is still an underlying factor. In growing puppies, overnutrition can result in a mismatch between body weight
and skeletal growth, which can overload skeletal structures.7 Nutrition of the mother may also play a role in the
development of OCD in the offspring.
The nutrient profile
of the food and how it is fed control nutritional risk factors for developmental skeletal disease. There are three basic methods
of feeding growing dogs: free-choice (ad libitum), time-limited, or food-limited.
Free-choice feeding is
relatively effortless and may reduce abnormal behavior such as barking at feeding time. Frequent trips to the food bowl help
reduce boredom, timid or unthrifty animals have less competition when eating, coprophagy may be decreased, and frequent small
meals may result in a more constant blood level of nutrients and hormones. Disadvantages of ad libitum feeding include food
wastage, only dry forms of pet food can be fed, and competition or boredom may stimulate overeating. The most serious disadvantage
is increased risk of developmental bone disease because of overconsumption in the large and giant breeds.1-4,24
In general, free-choice feeding in contraindicated in "at risk" dogs until they have reached skeletal maturity (about 12 months
of age or at least 80 to 90% adult weight).
can be used for most large and giant breeds. Making food available for a set period of time, two to three times per day, may
help control intake and help in discipline and housetraining young puppies. The owner interacts with the puppy during this
time and is able to observe general condition and behavior. This may lead to earlier detection of health problems. A routine
of feeding a puppy then taking it outdoors can enforce housetrainng by taking advantage of the gastrocolic reflex.
Some researchers have
proposed that puppies fed on a time-limited basis consumed less food, had slightly reduced growth rates, but achieved similar
adult size and lean body mass when compared to puppies eating free-choice.8 Other studies have shown that feeding
15 minutes twice a day did not result in decreased food intake between ad libitum and time-restricted groups.31
Many variables (e.g., breed, temperament, housing, etc.) influence these results and account for the varied findings. If time-restricted
feeding is used, 5 to 10 minute feeding periods (3x per day for the first month after weaning, then 2x per day) may be required
to decrease food intake in some puppies.
The method of choice
for feeding puppies is limiting food intake to maintain growth rate and body condition. Food-limited feeding requires feeding
a measured amount of food based on calculated energy requirement or as recommended by the manufacturer. Energy requirement
is most easily calculated by using resting energy requirement (RER) as a base on which to build. RER can be calculated using
either of the following two equations:
(kcal/day) - 70 (Wtkg)0.75
(kcal/day) = 30 (Wtkg) + 70
As a starting point use
3x RER for the first 4 months of life and 2x RER from 4 months of age to skeletal maturity (about 12 months for most breeds).
Most large and giant-breed dogs will continue to increase bodyweight and muscle mass after 12 months, but the growth rate
is reduced and most if not all growth plates are closed. At 12 months they can be fed as adults (1.6x RER).
Once daily caloric requirement
has been calculated (kcal/day), divide this number by the energy density of the food (kcal/cup or kcal/can) to determine the
number of cups or cans to feed per day. Remember, these calculations and manufacturers' recommendations are only starting
points. Clinical evaluation of the growing puppy and adjustment of food offered is crucial. Rapidly growing, large and giant-breed
dogs have a very steep growth curve and their intake requirements can change dramatically over short time periods. These puppies
should be weighed, evaluated, and their daily feeding amount adjusted at least once every 2 weeks (Fig. 1). Most of the studies
that have demonstrated the beneficial effects of limiting food intake of puppies have fed the limited group 25 to 30% less
food then their counterparts ate when fed free-choice. Unfortunately, this is not a practical approach to feeding most puppies
in a home environment.
Evaluation of feeding
methods and body condition scoring
Regardless of a food's
nutrient profile and how it is fed, the ultimate measurement of appropriate intake is the physical condition of the puppy.
The only way to reduce potentially harmful nutritional risk factors that may affect skeletal development is to assess body
condition and adjust the amount fed to ensure lean, healthy growth. We recommend that at risk puppies be evaluated at least
every 2 weeks. Figure 4 reviews body condition scoring and physical findings. A more in-depth discussion follows.32
A body condition score
of 1 is characterized as very thin. The ribs are easily palpable with no fat cover. The tailbase has a prominent raised bony
structure with no tissues between the skin and the bone. The bony prominences are easily felt with no overlying fat. In animals
over 6 months, there is a severe abdominal tuck when viewed from above.
An underweight condition
is categorized as a 2 in the scoring system. The ribs are easily palpable with minimal fat cover. The tailbase has a raised
bony structure with little tissues between the skin and the bone. The bony prominences are easily felt with minimal overlying
fat. In animals over 6 months, there is an abdominal tuck when viewed from the side and a marked hourglass shape when viewed
The ideal body condition
of a puppy is represented by a score of 3. The ribs are palpable with a thin layer of fat between the skin and the bone. The
bony prominences are easily felt with a significant amount of overlying fat. In animals over 6 months, there is an abdominal
tuck when viewed from the side and a well proportional lumbar waist when viewed from above.
A score of 4 is defined
as overweight. The ribs are difficult to feel with moderate fat cover. The tailbase has some thickening with moderate amounts
of tissue between the skin and the bone. The bony structures can still be felt. The bony prominences are covered by a moderate
layer of fat. In animals over 6 month, there is little or no abdominal tuck of the waist when viewed from the side. The back
is slightly broadened when viewed from above.
An obese condition is
represented as a 5 on the scale. The ribs are very difficult to feel under a thick fat cover. The tailbase appears thickened
and is difficult to feel under a prominent layer of fat. The bony prominences are covered by a moderate to thick layer of
fat. In animals over 6 months, there is a pendulous ventral bulge and no waist when viewed from the side. The back is markedly
broadened when viewed from above.
Large and giant-breed
dogs are the most susceptible to developmental skeletal disease. Genetics, environment, and nutrition play key roles. Nutritionally,
rate of growth, food consumption, specific nutrients, and feeding methods influence our ability to optimize skeletal development
and minimize skeletal disease. Maximizing the growth rate in young, growing puppies does not correlate to maximal adult size.
It does, however, increase the risk of skeletal disease. The growth phase of 3 to 8 months, and possibly the phases before
weaning, are vital to ultimate skeletal integrity. The large and giant breeds may be limited in their ability to cope with
excesses of minerals such as calcium.
Overnutrition from overconsumption
and oversupplementation increases the frequency of developmental bone disease in large and giant-breed dogs. Energy and calcium
are the nutrients of greatest concern. Often, owners feeding highly palatable, energy-dense growth foods switch to maintenance
type foods in an attempt to reduce developmental disorders. As shown earlier, this practice may worsen total calcium intake.
It is not only important to feed the appropriate food, but to feed the food appropriately.
Table 1 lists the minimum
requirement of some nutrients of concern for growing puppies. These values represent the minimum and in some cases the maximum
AAFCO recommendations for these nutrients. Foods for large and giant-breed puppies should meet these recommendations. Because
energy (primarily from fat) and calcium are nutrients known to be risk factors for developmental skeletal disease, the level
of these nutrients should be near the minimum requirement. Meeting but not exceeding the requirement for these nutrients ensures
proper growth while minimizing risk factors for skeletal disease.
alone will not completely control developmental bone diseases. Skeletal diseases can be influenced during growth by feeding
technique and nutrient profile. Dietary deficiencies are minimal concern in this age of commercial foods specifically prepared
for young, growing dogs. The potential for harm is in overnutrition from excess consumption and oversupplementation.