I t may interest breeders and fanciers of the larger breeds of
dogs, 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
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 sutdy 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
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
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 orginated from biochemist at medical teaching
institutions and other research facilities other than veterinary
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."