Canine Hip Dysplasia (CHD)

Hip Dysplasia in Dogs

” Canine hip dysplasia is on the rise”: Clinicians brief by Wendell O. Belfield, D.V.M. (2011)

As early as 1945, there were publications in the Journal of the North American Veterinarian, describing Canine Hip Dysplasia(CHD). It was at this time, Dr. G.B. Schnelle wrote of his observations, the condition was “predominantly in wire-haired terriers and English setters, to be most frequently affected,” and in 1947, Dr. W.N. Konde wrote of his observations of CHD in German Shepherds. Dr. Schnelle theorized the condition to be caused by a recessive gene and recommended that “the young of both sexes in affective families be castrated to prevent further inherent transmission.” Dr. Schnelle, a radiologist was considered an authority, had the attention of the profession though other observers did not have the same heredity conclusion. Though there was no scientific evidence of heredity by Dr. Schnelle, only a theory, those following his concept adhered to his heredity dialog. It became the accepted practice, by the profession and breeders, those dogs with the condition, as recommended by Dr. Schnelle, were neutered some euthanized. Unlike Dr. Schnelle, Dr. Konde offered no predisposing conditions for the cause of CHD.

“Signs of the Times”

To Better understand the present “Heredity Concept,” it is most important to regress in time when veterinary medicine, at best, would have been considered primitive in comparison to today’s veterinary standards.

During the first half of the twentieth century, the focus in veterinary medicine was in large animal medicine, farm and food producing stock. Also during this period, the advances in veterinary medicine were limited to Western Europe where American veterinary educators and researchers embarked for additional and advanced training. Many of the textbooks employed into the curricula of the then ten veterinary teaching institutions, in the US, originated in Europe and translated into English from those non English speaking countries. These textbooks and overseas training of our educators helped advance our methods for approaching new and different treatments protocols.

Veterinary research, in the US, did not exist and the one veterinary journal (The North American Veterinarian) contained papers, presented, for publication, were predominately, from veterinary practitioners discussing their practice experiences. These published practitioners were often looked upon as “authorities” in their subject matter and often depended upon for information to be shared. So as it was with Dr. Schnelle with his observations into canine hip dysplasia. Dr. Schnelle’s area of interest and expertise was radiology, in fact wrote one of the first veterinary textbooks on the subject. His observations and heredity conclusions, though never proven, were included in the first edition of Canine Medicine which became the primary textbook in veterinary teaching curricula and is continued in textbooks, now, in the twenty-first century.

The True Cause of CHD

For more than two decades, the heredity theory went unchallenged though the heredity concept along with selective breeding had no effect on the prevention of CHD. In March, 1968 two veterinary practitioners, Drs. John W. Bordens and Herbert Hardwick, published their clinical studies with conclusive scientific evidence to prove their findings, “New Observations on the Diagnosis and Cause of Hip Dysplasia” published in Veterinary Medicine & Small Animal Clinician. These clinicians developed a method for palpating the hip joints of four week old pups to determine those pups with the potential for developing canine hip dysplasia. To prove their findings, the petineus tendon at the femoral attachment on one leg was surgically excised the other remained intact. When radiographed, months later, the coxofemoral joint of the severed tendon was normal, the tendon not severed on the other joint, the head of the femur was subluxated indicating CHD had occurred. The recorded pathological findings were “loose-fitting joints, articular surface wear, increased joint fluid containing increased neutrophils, and increased tension of the pectineus muscle in relation to the other muscles of the hip” which indicated the pectineus muscle was directly involved in CHD “It was determined via necropsy (autopsy) on 154 dogs which palpation had indicated were afflicted with hip dysplasia”. To determine the exact pathology of the pectineus muscle, biopsies from the effected dogs were forwarded for histopathological examination by George H. Cardinet III, D.V.M., PhD., Kansas State University School of Veterinary Medicine who’s findings included Myopathy (atrophy) due to spinal or renal disease. Because the pectineus muscle extends from the anterior border of the pubis to the middle of the medial border of the femur and does not develop proportionately to the growth of the femur resulting in the femoral head separating from the acetabulum, a subluxation. Their findings indicated hip dysplasia to be of both hips. This has been the only definitive evidence of the true cause for CHD. These findings by Bordens and Hardwick is the only scientific clinical observation until the present, unfortunately this study has never been discussed or debated. Presently, the veterinary educators and researchers mandate that prior to accepting a concept or protocol there must be scientific proof, then why has this scientific evidence been rejected in preference to the erroneous hereditary theory an archaic theory of the 1940’s? It seems “When a failed theory is repeated often enough, it is accepted as truth.”

By addressing the problem of pectineal atrophy, the author has had success in the prevention of CHD via a biochemical protocol discussed in his paper “Chronic Subclinical Scurvy and Canine Hip Dysplasia” Belfield,W.O., Veterinary Medicine/Small Animal Clinician, p. 1339-1400-1401-1403, 1976) a nutritional supplemental protocol initiated at birth for optimization of collagen synthesis. As a result of the Bordens and Hardwick clinical study, the author applied the surgical procedure to adolescent and adult CHD canines with extreme success. Excision of the pectineus tendon prior to its attachment to the femur afforded instant relief from the symptoms associated with CHD. Belfield, W.O.,“The Dysplastic Dog Can Be Helped,” Veterinary Medicine/Small Animal Clinician, p. 883-884-885-886 , September, 1971.

Preventing Canine Hip Dysplasia (CHD) begins with supplementing the pregnant female with MEGA C PLUS and is continued in the newborn two hours after birth with MEGA C DROPS. Mega C Plus is a crystalline form which is easily incorporated into a wet ration.

Conclusion

The Results of the heredity theory has been one of despair, frustration, and heartbreak for dog owners dealing with CHD, breeders having to discontinue breeding, and many dogs having to pay with their lives via euthanasia. Dr. Schnelle has made a significant contribution to the canine world by his observations into CHD sixty-six years ago, but, because of the 1940’s time frame, he had limited information about biochemistry, pectineus atrophy, collagen and glucosamine synthesis, oxidation, free radicals and antioxidants which limited his scope for a more definitive conclusion to the cause of the condition. With all due respect, Dr. Schnelle was not a small animal practitioner nor was he an orthopedist or pathologist which added to his limitations. Drs. Bordens and Hardwick obviously recognized, as practitioners, they were limited as pathologist and took the clinical study to the next level by enlisting the help from who was an authority in the field of macro and micro pathology.

Drs. Bordens and Hardwick, in their clinical study, met all of the criteria essential for a successful scientific research:

  1. Developed a positive diagnostic procedure for CHD
  2. Study included 154 subjects
  3. Determined CHD to be bilateral
  4. Identified the involvement of the pectineus muscle
  5. Histopathology: atrophy of the pectineus muscle
  6. Described macroscopically and microscopically the pathology of the dysplastic hips
  7. Each subject had its own controls, the severed pectineus versus the intact pectineus

Dr. Schnelle, nor the present proponents of his theory, have explained the action of the alleged gene/genes, how and when it affects the coxofemoral joint. The clinical studies of Drs. Bordens and Hardwick with 154 subjects, controls and histopathological evidence have proven, without any doubt, that canine hip dysplasia is a biochemical phenomenon that can be prevented. More than a decade has been completed in this new millennium and the CHD problem has yet to be solved by the “veterinary experts” who are clinging to the erroneous archaic heredity theory. Each year hundreds of veterinary graduates are departing their respective teaching institutions where they were “spoon fed” a failed theory which they, in turn, will spread to others. Ignoring proven scientific evidence, the “Heredity Theory” will be “frozen in time” from the last millennium, the last century, the 1940’s.

Since there have not been reductions in instances of CHD via “selective breeding and OFA confirmations, it is obvious this procedure has failed for the past sixty plus years. There has been positive results, in preventing CHD, by incorporating nutritional dietary protocols into daily rations that proves the condition to be biochemical, not hereditary.

This publication has been presented to offer additional information, to the general public, in order to have enough knowledge of the history and circumstances of canine hip dysplasia and to open a dialog for discussions and debates with the veterinary educators and researchers about changing the present course for solving this crippling disease.

In these times when genes are being isolated and identified, it should be a simple matter of applying this technology to determine the presence of those alleged genes causing CHD.