Nutrition and the development of developmental orthopedic disorders

In studies of large and giant breed dogs excess energy consumption 
along with excess 
calcium intake has been found to be correlated with developmental 
orthopedic disorders 
(DODs). There are several risk factors associated with development 
of DODs.  These 
include:
1. genetic predisposition
2. excessive caloric consumption
3. excessive calcium intake 

The 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. There has 
been no correlation between high protein intake and 
DODs.  The risk for DODs increases significantly in dogs allowed 
free choice feed. 

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). Subtle trauma, (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.  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). 
 
Proposed etiologies for the development of nutritionally induced 
DODs include:

1. Excess energy stimulates growth hormone and IGF-1 to be released, 
which, in turn,stimulates the proliferation of bone.  Dogs that have 
had free choice access to food have higher levels of T3/T4 which is 
indicative of metabolic activity.  Cartilage lesions develop 
secondary to excessive biomechanical stresses. 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. 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. 

2. Abnormalities of the cartilage canal vessels and chondrocyte 
necrosis are thought to precede degenerative changes in the 
articular cartilage matrix. Focal lesions of dead 
and nectrotic chondrocytes develop, and subsequently, biomechanical 
stresses disrupt the lesion

Rapid growth in large and giant-breed dogs increases the risk of 
skeletal disease. 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. Because fat has twice 
the caloric density of protein or carbohydrate, 
dietary fat is the primary contributor to excess energy intake. 

The absolute level of calcium in the diet, rather than an imbalance 
in the calcium/phosphorus ratio, influences skeletal development. 
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. Feeding treats containing calcium and/or providing 
calcium supplements further 
increases daily calcium intake. 

The balance of anions and cations in the food (specifically sodium, 
potassium, and chloride) may 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. The changes in osmolality and fluid 
volume could be a result rather than a cause of CHD. 

Sources: Small Animal Clinical Nutrition, Veterinary Clinical 
Nutrition notes, Canine Hip Dysplasia: A Symposium Held at Western 
Veterinary Conference, February 1995.