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Relationship between Nutrition and Bone Growth in Large and Giant Dogs1

Klaus Dämmrich2

Institute of Veterinary Pathology, Free University of Berlin, Berlin, Germany

The pathogenesis of the osteochondrosis syndrome was studied in large and giant breeds of dogs. Spontaneous cases of osteochondrosis were examined in large breed dogs, and experimental disease was investigated in Great Dane puppies fed ad libitum or restricted diets until 6 mo of age. This investigation concluded that the primary lesion occurring in osteochondrosis of dogs from the large and giant breeds is an acquired pattern of osteopenic and biomechanically weak subchondral spongiosa that cannot provide adequate bony support for the articular cartilage of joints. Excessive biomechanical loading of the inadequately supported epiphyseal articular cartilage leads to secondary disturbances in the nutrition, metabolism, function and viability of the chondrocytes in the developing joint surface. The primary lesion in the subchondral spongiosa develops when overnutrition (ad libitum feeding) overstimulates skeletal growth and cancellous bone remodeling mechanisms in those breeds of dogs who already have an inherent capacity for rapid skeletal growth. The epiphyseal spongiosa of rapidly growing dogs of the larger breeds is inherently less dense and less strong per unit area than epiphyseal spongiosa of dogs from the smaller breeds. Overnutrition in dogs from the larger breeds exaggerates this tendency to create osteopenia by increasing the rates of skeletal growth and remodeling of the newly formed cancellous bone. Accelerated rates of bone growth and bone remodeling act in concert to produce a pattern of epiphyseal spongiosa that is composed of fine trabecular systems that are spaced relatively far apart and that are ultimately less strong per unit area than in small breeds of dogs. Overnutrition also predisposes to development of lesions of osteochondrosis by promoting increases in muscle mass and body weight that further overload inadequately supported joint surfaces.


KEY WORDS: • symposium • dogs • osteochondrosis syndrome • bone growth

1 Presented as part of the Waltham International Symposium on Nutrition of Small Companion Animals, at University of California, Davis, CA 95616, on September 4–8, 1990. Guest editors for the symposium were James G. Morris, D'Ann C. Finley and Quinton R. Rogers.

2 To whom correspondence should be addressed: Institut für Veterinär-Pathologie, Freie Universität Berlin, Straße 518 Nr. 15, D 1000 Berlin 37, Germany.




This article has been cited by other articles:


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Vet PatholHome page
B. Ytrehus, C. S. Carlson, and S. Ekman
Etiology and Pathogenesis of Osteochondrosis
Vet. Pathol., July 1, 2007; 44(4): 429 - 448.
[Abstract] [Full Text] [PDF]




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