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Osteochondrodysplasias Leg Deformities and Dwarfism - in the Canine
by Fred Lanting
Copyright July, 2008 -
There has been renewed interest in the subject of "abnormal" bone lengths, joints, angles between limbs, and related phenotypic variations from what I have called "the ancestral type". We need to establish some definitions of terms before entering into a discussion of the subject. The "ancestral" phenotype in my arbitrary definition (which, however, is in line with the views of many or most professionals in animal science) is one that comes to mind when one thinks of the Jackal, Northern Wolf, and descendants of the extinct Pale-footed Wolf (such as sighthounds). The head is neither brachycephalic (pushed-in/shortened) nor exaggeratedly long and narrow (the dolichocephalic Borzoi, etc.), the leg length is such that the total height at withers is roughly twice the distance from elbow or chest to the ground, and limbs give an impression of being straight. Typical examples of ancestral types are the German Shepherd Dog, Saluki, various Spitz breeds, and many pariah breeds such as found in every corner of the world.
"Abnormal" phenotypes (and this will rouse the ire of many people who love their dogs and think of them as being "normal") include breeds specifically bred to produce the characteristics that would be agreed on as being "faults" in the ancestral types. Think of the ("English") Bulldog, Pekingese, Corgis, Dachshunds/Teckels, and others. I have long maintained that there is a genetic defect affecting primarily the hypophysis or pituitary gland, the "master gland" that so greatly influences the functions of the others as well as developmental processes.
Some variation within normal parameters results from the tremendous plasticity of the canine genotype, but here we are more interested in the departure from those limits of normality. Whatever the combinations of defective DNA nucleotide pairs (adenine-thymine, cytosine-guanine, etc.), and which glands or organs they initiate the changes in, many of the irregularities we are discussing here manifest themselves in the cartilage that is on the ends of bones and "bone centers". Bone centers are those hard, mineralized portions of a growing bone that become enlarged (almost entirely on their long-axis surfaces) and fused together to form the eventual limb, and the cartilage between most bone centers is called a "growth plate" or physis. It gradually "calcifies" into bone tissue, thus uniting epiphysis (called a cap or head, usually) and metaphysis (shaft); it disappears during maturation. But if there is an abnormal coding of the nucleotide pairs, there is an abnormal calcification process, a "growth-plate disturbance".
If one bone in a two-bone limb segment (such as the tibia/fibula or ulna/radius combinations) has more of a disturbance than the other, or if one end of the growing bone's cartilage is disrupted during remodeling into bone tissue, there are unequal rates of growth and consequent bowing of that limb, with one part wanting to be longer than the other part does. In some dogs, disruption of normal cartilage-bone turnover at the ends can keep a single bone from growing in length, or if the disruption is laterally asymmetrical, the femur or humerus may also become slightly bowed. The pull of muscles and ligaments on different parts of such bones also has some effect on shape.
The general definition of "dysplasia" is poor or abnormal (dys-) shape or form (-plasia). Here, we are talking mostly about bone (osteo-) and cartilage (chondro-), and mostly about those tissues in joints. But just as the poet says, "no man is an island", and genes that cause one thing can sometimes also cause something else. Some times it is a very obvious double influence, such as the gene that causes both deafness and white coat phenotypes in some breeds, or dwarfism and blood disorder in the Malamute. Most of the time, the influence of one gene or set of nucleotides is less obvious.
A couple more definitions would be helpful at this point, although you should realize that there are sometimes loose adherence to strict interpretation of such definitions:
• chondrodysplasia: any growth plate (cartilage) disturbance resulting in canine dwarfism; in human pathology, it has a different meaning: enchondromatosis, a rare disorder marked by enlarged cartilage and tumors in joints.
• chondrodystrophic: semantically similar to the above, but while –plasia refers to changeable shape, –trophic refers to growth. Thus, an abnormal cartilage growth pattern.
• achondroplasia: that type which results in an individual with extremities shorter than the trunk. Examples in dogs include Basset Hound, Shih-Tsu?, and others mentioned elsewhere. In humans, it usually is marked by stubby hands, large head with sunken nasal bridge and, frequently, spinal column deformities.
CHONDRODYSTROPHY
Several breeds are of a body type we call chondrodystrophic, such as the Dachshund and Corgi. They have shorter legs (often bowed) and other dwarf characteristics in parts of the body. Frequently, these breeds also have a shorter vertebral arch that tends to produce a smaller vertebral canal. The vertebral body centers of ossification unite with the arch prematurely, with the same type of dystrophic bone growth pattern that causes shorter "long bones" in those breeds. See Chapter 16 in my 2004 orthopedics book for more illustrations and discussion on dwarfism. In some chondrodystrophoid breeds such as the Basset, a premature closure of the distal metaphyseal plate of the ulna (near the wrist) was thought by Herron, Grüll, Henschel, and von Hitz to cause fracture of an already closed anconeal process at the other end of that limb. Kasström and colleagues (and later, Wind) thought that this condition in certain dwarfed breeds "was the result of an abnormal pressure on the anconeal process... by the shortened ulna." This anomaly in the anconeal process is not the same as the failure to unite, and obviously has a different genetic origin. Dr. Wind, the eminent expert on elbows, has observed that many cases of elbow dysplasias include subluxations associated with dwarfism.
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Editor’s Note: A well-respected and frequent GSD specialty and all-breed judge for many clubs around the world, with KC and other-country credentials, Mr. Lanting since 1966 has lectured on Gait-and-Structure, Canine Orthopedic Disorders, and other topics, and has judged in about 30 countries, including the prestigious FCI Asian Shows hosted by Japan Kennel Club and the KC of India, the Scottish Kennel Club, and many National Specialties in the USA and elsewhere. He has been described by a former OFA director as the world’s leading non-veterinarian authority on hip dysplasia. A dog breeder since 1945, a GSD owner since 1947, and a show judge since 1979, he has lectured at numerous veterinary schools in the USA and abroad. He is the author of “must read” books for the dog owner (see below for ordering info). Curriculum Vitae available upon request.
Announcing the new “Canine HD and Other Orthopedics Disorders” book: The expanded revision is a comprehensive (nearly 600-page), amply illustrated, annotated, monumental work that is suitable as a coffee-table book, a reference work for breeders and veterinarians, and a study adjunct for veterinary students. It is equally valuable for the owner of any breed. It covers every aspect of HD and other orthopedic, bone, or spinal disorders, and includes genetics, diagnostic methods, treatment options, and the role of environment. Your autographed copy will be mailed from the USA as soon as the appropriate amount is received and is processed. Pricing: US $68, plus $5 postage in the U.S., or ask about mail overseas. Combine orders with “The Total German Shepherd Dog” by the same author ($50 plus postage). 17 of the 20 chapters are suitable for owners of any breed.
