By Dr. Wendell O. Belfield
It may interest breeders and fanciers of the larger breeds of dogs,that the winds of time are changing the concept of canine hip dysplasia (CHD). In the May, 1997 issue of the Journal of the American Veterinary Medical Association, were two papers discussing a new outlook on CHD.
The first paper, “Onset of epiphyseal mineralization and growth plate closure in radiographically normal and dysplastic Labrador Retrievers,” was a collaboration of seven researchers/educators at the veterinary schoool at Cornell University. The results of this study is as follows:
There were 26 radiographically normal left and right hip joints. Onset of mineralization of the proximal femoral epipysis and of the right proximal tibial epiphysis was significantly later in dysplastic than in radiographically normal puppies. The left femoral capital growth plates closed significantly later in dysplastic than radiographically normal joints, but other differences in growth plate closure were not detected.”Clinical Implications — Endochondral ossification may be abnormal in dogs with CHD. The disease appears to affect multiple joints, even though it is most evident clinically in the hip joint.”
The second paper was presented by Jens Sejer Madsen, Ph.D., D.V.M. from the Small Animal Hospital, Department of Clinical Studies, Royal Veterinary and Agricultural University, Frederiksberg C, Denmark.
“Mechanical strength of the joint capsule is related to its collagen content and composition. In children with congenital hip joint dislocation, the collagen composition of the joint capsule has been shown to be abnormal. Thus, it is reasonable to hypothesize that laxity of the hip joint in dogs may be related to the collagen composition of the capsule. To test this hypothesis, a study was performed on 19 mature dogs (14 with radiographic evidence of CHD) and 10 Greyhounds (9 with radiographically normal hip joint conformation). Joint capsules were harvested from all dogs, and the ration of type-III:I collagen in each capsule was calculated. The mean ratio was significantly higher in dogs from breeds with a high prevalence of hip dysplasia (1:0.161) than in Greyhounds (1:0.100; P=0.005); however, within each group of dogs, there was no difference in ratio between dogs with normal and dysplastic hips. A high collagen type-III:I ratio indicates a weak joint capsule, because strength requires type-I collagen. Therefore, results of the study support the hypothesis that a change in collagen composition may contribute to hip joint laxity in dogs with a predisposition to CHD.”
For over twenty years I have asked the “experts” to describe the lesion of the dysplastic hip joint; at the cell level; the pathology involved, if you will. I was delighted to read these reports because they give hope that this disease can be prevented be it genetic or nutritional.
In October, 1976 I published a paper, “Chronic Subclinical Scurvy and Canine Hip Dysplasia” published in Veterinary Medicine/Small Animal Clinician.” My conclusion was as follows:
“In large breeds of dogs, hip dysplasia, long considered an inherited birth defect, may be an easily controlled biochemical condition. The lesion in hip dysplasia appears to be merely poor-quality, low-strength collagen in the affected ligaments, caused by too little ascorbate for proper synthesis and maintenance of collagen. In eight litters from dysplastic German Shepard parents or parents that had produced dysplastic offsprings, there were no signs of hip dysplasia when the bitches were given mega doses of ascorbate during pregnancy and the pups were kept on a similar regimen until they reached young adulthood.”
Though my observation was made more than twenty years ago, it was rejected by most researchers and educators. As the analogy made by Dr. Madsen in children with congenital hip joint dislocation, my analogy was drawn from a book by John Lind describing the pathology in the hip joints of scarbutic cadavers, the book was “A Treatise on Scurvy” published in 1753.
My elation over these publications was short lived as I began to recall the numbers of beautiful canines that had been euthanized over the past two decades. The number of breed-lines that are now extinct. This was a canine genocide. It has taken more than fifty years, after CHD was first reported, for the “experts” to describe the lesion of the disease; how long will it take them to offer a solution, another half century?
Now that CHD is a systemic condition we can get on with the business of saving these canines from this crippling disease. Lets begin eliminating some myths that have prevailed over the past fifty years. Unilateral CHD, does not exist. One normal hip and the other subluxted is not CHD this is simply an injury. Since the experts recognize that all joints can be involved in slow mineralization why then one hip will remain normal. Since collagen synthesis is involved in CHD, another systemic problem, why will one hip and not the other be involved. CHD must be in both hip joints. The next issue, is CHD an inherited disease? I have never been a proponent of this concept. To me, it has always been a biochemical problem. Regardless if CHD is genetic or not, it does have systemic implications which means it can be prevented and controlled; I have had success in this area for more than twenty years.
The 1990’s have brought forth scores of research publications from around the world on the subject of collagen synthesis and its relationship to nutrition and nutritional supplementation. These publications are not by veterinarians and do not appear in veterinary journals. It does require those who are seeking broader knowledge go beyond the limits of veterinary medicine. As a contributing author to a recent textbook, “Complementary and Alternative Veterinary Medicine: Principles and Practice” all of my literature research into collagen synthesis originated from biochemist at medical teaching institutions and other research facilities other than veterinary research facilities.
Much to my surprise, many veterinary practioners are not aware of these recent publications on these new observations of CHD. Does this mean that some canines are still being euthanized? We have known about CHD since 1945, and the “experts” have failed to solve this problem. To fail only gives rise to a new beginning and a fresh approach to new concepts. belfield.com
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