Double Barrel Bulldogs

French Bulldogs

NCL: The Disease-Description, Symptoms, and it's Affects

 Ceroid lipofuscinosis is a broad term describing a group of incompletely
understood diseases caused by an abnormal accumulation of metabolic
by-products within cellular lysosomes of neural and visceral organs. The
disease is reported as an inherited cause of progressive nervous system
dysfunction in humans, nonhuman primates, dogs, cats, cattle, sheep, and

goats.1–11 Clinical signs of disease include impairment of motor function,
conscious proprioceptive deficits, ataxia, progressive blindness, behavior
changes, hypersensitivity to stimuli, and seizures. The disease is variable
in rate of progression, irreversible, and fatal. The report link below is 

graphic and contains a case history, including autopsy  details of the case study.

This report describes the
clinical, computed tomographic, biochemical, microscopic, and ultrastructural
features of ceroid lipofuscinosis in a dog.

Many vets, just seeing the dog in the early stages, will guess that it has hip dysplasia.  While others havn't a clue what infact NCL is.  Within the next 1 to 3 years, the dog won’t even be able to keep from falling.. when walking the dog will tend to stagger and move randomly, especially down a flight of stairs or over uneven ground. When running, the rear will show very little control.  Normally, by the time the dog is 5 years old, the dog will be euthanized....just standing will be very difficult, much less trying to walk. With hip dysplasia, on average a dog can live a reasonably normal life, even if it has to be on pain killers. Also, except for severely dysplastic dogs, most dogs won’t even show signs of a problem until later in life.

 
NCL Description for American Bulldogs
Age of onset of clinical signs: 0.9 to 3 years
Age of death or euthanasia: 3.5 to 5.5 years
Abnormalities often observed by the owner:
Mental changes: Physical symptoms may appear to worsen during times of stress.
Affected dogs do not indicate they are in any pain as coordination decreases.
Changes in gait and posture: Initially, uncoordinated movement in the rear is noted. As
the disease progresses, affected dogs develop a wide-based stance in the rear, and
eventually involving all four legs. Affected dogs may exhibit muscle twitching, especially
when sleeping. The dogs remain well-muscled through the course of the disease.
Visual abnormalities: None reported
Seizures/convulsions: None reported
Other changes: None reported

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NCL The Three Possibilities and Risks

CLEAR                 CARRIER            AFFECTED

 

Basically a clear dog bred to a carrier will, on average, produce 50% clear pups and 50% carriers, with no affected pups. 2 carriers bred together will produce 50% carriers, 25% affected and 25% clear pups, on average.  With a little thought you can see how just a few breedings, even of carrier to clear, will produce a lot of potential problems for the breed, especially since symptoms may not manifest until the dog is up to 3 years of age. Breeding an affected dog with a carrier, produces 50% carrier, 50% affected.

 

TESTING 

A collaboration of scientists from the Veterinary Neurological Center in Los Vegas, the
University of Missouri-Columbia (UMC), the University of California-San Diego, and
Cornell University in Ithaca has recently described a new form of NCL in American
Bulldogs. At UMC we have been studying DNA from affected American Bulldogs and
their relatives, and have discovered the mutation causing NCL in this breed. A DNA test
(blood sample testing) is  available which will definitively identify clear, carrier, and affected dogs. The
charge for this test is $40 (plus the cost of overnight shipping of the chilled sample) per dog through the University of Missouri, payable to "University of Missouri". For instructionsand forms, see the SAMPLE SUBMISSION section of the NCL portion ofwww.CanineGeneticDiseases.net .
  OFA now offers DNA testing by swabbing the dogs mouth and transferring DNA to a card. The cost for this test is $65.00. See the website for details: OFA DNA Disease Testing
 

Known Carriers of NCL

 In Matt Boyd’s line Moleque and High Jumping Mikie were the most influential dogs that were carriers, even Greg Souza has said that Koa and Matias are both carriers.  But anything from Moleque Country Boy x Snowbird, Cross Eyed Mary, Outback's Diesel, or anything that originated with Hines should be tested.  Its also be known that some Johnson lines have been found to be carriers of the disease too.

One of the littermates of Rob Boyd’s “Hammer” was a carrier so he and any of his littermates have a 50% chance of being carriers. All dogs with any of these dogs in their pedigree need to be tested before breeding!!
This does not mean that a carrier cannot be bred, it must not be bred to another carrier, and that if bred to a clear dog, the disease can be easily controlled with careful breeding. And the breeder has a responsibility to test the puppies to determine which are carriers and which are clear before placing or selling them.

 

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      ICHTHYOSIS

Ichthyosis is a terrible genetic skin disorder. Pups are affected very soon after birth in the American Bulldog breed. Dogs/pups can be carriers with no signs of the disease. A DNA test must be performed in order to determine if a dog is a carrier, or normal. It is a recessive gene mutation and occurs when two dogs are bred that both carry the recessive gene. Here is a forum that talks about the different affects it has on their dogs and the difficulty of treating it. Even causes blindness.
http://www.ichthyosis.com/ubb/Forum1/HTML/000870.html


You cant miss it if a pup is affected. They stand out like a sore thumb.

Their skin thickens, wrinkles and may develop scales much like an our skin does as it ages, and gets worse each day. The pads of their feet look like little clubs the skin gets so thick. Starts off like wet matted fur at about 5-7 days old (I bathed them thinking mom wasnt keeping them clean) and within a couple days of that the skin starts changing. Gets worse every day. By day 9 or 10 it's almost tight and leathery-still have their fur but wrinkled like a shar pei on their legs, and they quickly get a "dirty look" that wont wash off (I tried bathing a second time a couple days later thinking mom was again neglecting bathing duties) and they didnt grow at the same rate as the other pups. They slowed down and stayed smaller-all three about the same size, noticably smaller by 2wks old than the other pups and they were all the same size a week before.

 

Canine Models of Ichthyosis. M. L. Casal1, E. A. Mauldin2 1) Sect Medical Genetics, Univ Pennsylvania, Philadelphia, PA; 2) Dept Pathobiology, Univ Pennsylvania, Philadelphia PA.

Ichthyoses are characterized by faulty formation of the outer layer of the epidermis, the stratum corneum, with resultant scaling and include a heterogeneous group of hereditary and congenital diseases in humans. In dogs, relatively few ichthyosiform disorders have been documented and most are reported as single cases. Here we present two forms of non-epidermolytic ichthyosis in the golden retriever and the American bulldog. The golden retriever disease is characterized by mild to moderate, generalized, nonpruritic scaling (large, loosely-adherent, soft, white to gray scales) with clinical lesions becoming apparent between 8 weeks and 2 years of age. American bulldogs typically have a more severe phenotype with lesions evident at birth or shortly thereafter. The scaling is generalized with large, light brown, plate-like, adherent scale on the ventral thorax and abdomen. The puppies may develop chronic pruritus that coincides with the onset of secondary malassezial infections. Histopathologic findings are similar in both disorders: laminar orthokeratotic hyperkeratosis with an absence of epidermal hyperplasia and dermal inflammation. Ultrastructural analysis using a ruthenium tetroxide fixation method revealed retained and convoluted membranes with crystalline structures in the stratum corneum in both breeds of dogs. Scattered keratinocytes in the granular cell layer had prominent, clear, membrane bound, cytoplasmic vacuoles. Pedigree analyses in both breeds are highly suggestive of an autosomal recessive trait. Molecular characterization is underway for both forms. In humans, many forms of ichthyosis can be debilitating and require lifelong treatment which is only symptomatic. Here we offer a large animal model for treatment trials that will hopefully lead to curative therapies for humans affected with ichthyosis.


ICHTHYOSIS TESTING IS 100% ACCURATE NOW!

How do I test my dog? It's right below! Read further below for online submission instructions!! 

The letter below was sent to me in an effort to share the updated testing news  from The University of Pennsylvania with breeders and owners who are interested in testing :

American Bulldog Ichthyosis

Over the years, breeders and veterinary dermatologists had reported sporadic cases of a skin disease characterized by generalized non-pruritic (non-itchy) scaling in young American bulldogs.  The observant breeder recognizes the disease, termed ichthyosis or fish scale disease, shortly after birth but the scaling becomes quite apparent when the puppy is about 2 weeks of age.  Their belly skin looks dirty and scaly, but the “dirt” cannot be washed off because it is abnormal skin. The disease manifests itself mainly on the trunk, footpads and ears with large plate-like scales, and reddening of the skin. With time, the skin will loose its protective barrier and affected dogs will have decreased resistance to infectious diseases and develop secondary skin infections and yeast dermatitis.  Currently, there is no curative treatment for ichthyosis.  Because of the severity of the disease, most affected dogs are euthanized before 12 weeks of age.

Several years ago, we set out to determine the cause of this disease.  Many of you had sent in samples to help develop a DNA test and many of you are still waiting for results.  We are happy to inform you that we now have a test available to all American bulldog breeders and owners. We would like to thank all of the breeders who have helped make this test a reality; we couldn’t have done it without you!

Margret Casal, Dr med vet, PhD

Medical Genetics/

 

PLEASE BE AWARE-THE TESING FOR THE ICTHYOSIS LINKED MARKER IN THE AMERICAN BULLDOG IS NO LONGER OFFERED THROUGH THIS TESTING LABORATORY>PLEASE REVIEW THE NEW TESTING LABORATORY INFORMATION IN ORDER TO AVOID DELAY IN TEST RESULTS AND PROCESSING OF YOUR SAMPLES

 

These test are now offered by the *PennGen Laboratories* and are all priced at $75 each. PennGen does not accept any of our manually filled submission forms, so please make sure that you go to the PennGen website http://research.vet.upenn.edu/PennGen acreate an account for yourself, login into your account, fill in the animal details, select the appropriate test to obtain a Submission ID for each animal and then print it out and mail it along with the sample.  You may visit the PennGen website for more information on submission and payment procedures.  Please be patient with us during this time of transition! 



 

Here is a website with some great pictures:

http://www.amerikaanse-bulldog.com/index.html/pagina46a.html


 

Here is a copy of my public service announcement on 06/29/2010 to the bulldog community. It sums up pretty well my perspective based in the information available at the time. As I learn or more information is presented, it may change, but for now....

 We all have to deal with the bad and the good when it comes to decisions regarding these dogs. Some are sad, but necessary. Since no dogs are perfect, and few breeders provide full honest disclosure it's accepted as the "nature of the beast".

Medical Science has made a multitude of tests and screening available for us to assist in breeding better dogs, enabling us to make better breeding decisions. The lack of disclosure is IMO a large factor that assists in hurting the breed. That doesnt always have to be the case. Some of it is lack of knowledge, some is a personal preference on what faults are unacceptable or important, and some is simple deception for fear it will interfere with their dog sales.


I recently had to put down 3 pups for Ichthyosis and sent biopsies from each one to the University of Pennsylvania. I know some treat it as one of the poisons that come with the breed, and others blow it out of proportion as if it's the plague. I can understand why, since it doesnt rear it's ugly head until two carriers are bred together. Until recently, no testing to screen carriers vs normal has been available so I can see why to some it's better as an invisible plague and not discussed. Why worry someone buying a pup if you cant confirm it's a carrier? What are the chances of them breeding a carrier to a carrier?

Based on my experience, it is 1 in 3 however the final test results are not in so that is a tentative claim.

Brooster has produced 3 litters, and one has produced pups with Ichthyosis-however I am testing each and every one of my adult/young dogs so I know who is and who isnt a carrier. I'm not going by the assumption that just because some litters didnt produce affected pups, it excludes the dams from being carriers. We all know how crazy genetics can fall.


Sometimes the full disclosure is something we all battle with. Too much information can cause worry that you cant do anything about anyway, but it dang sure helps alleviate the SURPRISE factor LOL. In my dealings with the University of Pennsylvania, I've learned they are now able to identify affected vs normal and are still working on the obstacle of identifying carrier vs affected. From a breeders standpoint, that's BATTING 1000! Hell, what more are they waiting for???? It's pretty undeniable and hard to miss when a pup/dog is affected. From the University's Research Lab's standpoint, it must be precise before it is marketed as legitimate testing so it is still not publicly offered. I've contacted most of the people with dogs down from Brooster and will be sending them a test kit, as well to any breeders that I do breedings with. I
do know from here on out, there is no reason to buy or breed a dog with uncertainty or fear of this genetic skin disorder as it is now possible to know what you are buying, or breeding. I've added the Ichthyosis screening as necessary health testing for all foundation and litters sired by affected dogs. Most breeders are afraid of lowering the worth or breed-ability of their stock..as far as I'm concerned it's less grief to be honest and eventually the dogs speak for themselves, however I've learned that even that can be twisted around LOL. NOBODY can produce ALL show quality or ALL breed worthy offspring, and on the flipside it isnt always the best decision to take a dog out of the genetic pool because it possesses a fault. Choosing your poison is the term I've become most familiar with and since few can agree on the degree of seriousness, or in many cases what a fault actually is in these dogs then its probably a mute point anyway. I'm not here to judge what is right, or wrong but improving the breed and self accomplishment is what it's all about, not our pockets or ego. Done with my rant, take what you can use and throw the rest away. Doesnt matter if you agree, or disagree-any INTELLIGENT input is always useful. If you have dogs or pups that are affected and are interested in getting involved in the Ichthyosis Study to help expedite public testing availability, contact Margaret Casal at the University of Pennsylvania. She is in the directory. Happy Bulldoggin, and I hope this helps the ones that care, and to heck with the ones that dont
There's testing on the way, so it can still be dealt with, regardless

 

Some will feel strongly that carriers should not be bred to eradicate the disease., however in the bigger picture of things, here is something to ponder:
Boyd's has produced some fantastic dogs and some have a history of NCL carriers-but his decisions are knowingly what is what. I am afraid if we took all the dogs out that carry Ich, or NCL,it would also remove some valuable attributes to the breed. Making good decisions is what will eventually eradicate the problem and keep the desired strengths IMO. Funny thing is, nature often plays tricks on us with the package deal theory-What if it came down to all Ich or NCL carriers were proven to be the cleanest breathers, or the best hips, or some other consistent attribute that would improve AB's? It is a possibility as some genetic/breeding case studies have proven color, structure and several other things appear to be a package deal with temperament and or other attributes in different canine related species (reference: The Genetics of The Dog)

 

 

Nutrition and Dog Food

 We feed Victor Dog Food daily supplemented with Food Grade Diamataceous Earth (for parasite control) Kelp, Green Phyto Food, Kefir Yogurt, and Raw Chicken Leg Quarters once or twice a week.

 

 

GRADE YOUR DOG FOOD

 If you dont have excel, follow the below instructions

Start with a grade of 100:

         
                 
1) For every listing of "by-product", subtract 10 points      
2) For every non-specific animal source ("meat" or "poultry", meat meal    
or fat) reference, subtract 10 points          
3) If the food contains BHA, BHT, or ethoxyquin, subtract 10 points    
4) For every grain "mill run" or non-specific grain source, subtract 5    
points                
5) If the same grain ingredient is used two or more times in the first    
five ingredients (i.e. "ground brown rice", "brewer's rice", "rice flour"      
are all the same grain), subtract 5 points          
6) If the protein sources are not meat meal and there are less than two    
meats in the top three ingredients, subtract 3 points        
7) If it contains any artificial colorants, subtract 3 points      
8) If it contains ground corn or whole grain corn, subtract 3 points    
9) If corn is listed in the top five ingredients, subtract 2 more points    
10) If the food contains any animal fat other than fish oil, subtract 2    
points                
11) If lamb is the only animal protein source (unless your dog is allergic    
to other protein sources), subtract 2 points          
12) If it contains soy or soybeans, subtract 2 points        
13) If it contains wheat (unless you know that your dog isn't allergic to    
wheat), subtract 2 points            
14) If it contains beef (unless you know that your dog isn't allergic to    
beef), subtract 1 point            
15) If it contains salt, subtract 1 point          
                       
                 
Extra Credit:              
                 
1) If any of the meat sources are organic, add 5 points      
2) If the food is endorsed by any major breed group or nutritionist, add 5    
points                
3) If the food is baked not extruded, add 5 points        
4) If the food contains probiotics, add 3 points        
5) If the food contains fruit, add 3 points          
6) If the food contains vegetables (NOT corn or other grains), add 3    
points                
7) If the animal sources are hormone-free and antibiotic-free, add 2 points  
8 ) If the food contains barley, add 2 points        
9) If the food contains flax seed oil (not just the seeds), add 2 points    
10) If the food contains oats or oatmeal, add 1 point      
11) If the food contains sunflower oil, add 1 point        
12) For every different specific animal protein source (other than the    
first one, count "chicken" and "chicken meal" as only one protein source, but    
"chicken" and "" as 2 different sources), add 1 point        
13) If it contains glucosamine and chondroitin, add 1 point      
14) If the vegetables have been tested for pesticides and are      
pesticide-free, add 1 point            
                 
Scores:            
94-100+ = A  BEST!              
86-93 = B      STILL GOOD.            
78-85 = C      May need to change or add additives.        
70-77 = D      Need to think about changing.        
69 = F           AWFUL! CHANGE!          
                 
Here are some foods that have already been scored.         
                 
Scored Dog Foods:            
                 
Arkat VF Large Breed Puppy Score 103 A+     103 A+  
Diamond Large Breed 60+ Formula / Score 99 A   99 A  
Sensible Choice Chicken and Rice / Score 97 A   97 A  
Wolfking Adult Dog (bison) by Solid Gold / Score 97 A   97 A  
Authority Harvest Baked / Score 116 A+     116 A+  
Canidae / Score 112 A+       112 A+  
Chicken Soup Senior / Score 115 A+     115 A+  
Dick Van Patten's Natural Balance Ultra Premium / Score 122 A+ 122 A+  
Dick Van Patten's Duck and Potato / Score 106 A+   106 A+  
Foundations / Score 106 A+       106 A+  
Innova Dog / Score 114 A+       114 A+  
Innova Evo / Score114 A+       114 A+  
Kirkland Signature Chicken, Rice, and Vegetables / Score 110 A+ 110 A+  
ProPlan Natural Turkey & Barley / Score 103 A+   103 A+  
Royal Canin Bulldog / Score 100 A+     100 A+  
Royal Canin Natural Blend Adult / Score 106 A+   106 A+  
Wellness Super 5 Mix Chicken / Score 110 A+   110 A+  
Diamond Lamb Meal & Rice / Score 92 B     92 B  
Nutrisource Lamb and Rice / Score 87 B     87 B  
Nutro Natural Choice Large Breed Puppy / Score 87 B   87 B  
Hund-n-Flocken Adult Dog (lamb) by Solid Gold / Score 73 D 73 D  
Iams Lamb Meal & Rice Formula Premium / Score 73 D 73 D  
Bil-Jac Select / Score 68 F       68 F  
Diamond Maintenance / Score 64 F     64 F  
Pet Gold Adult with Lamb & Rice / Score 23 F   23 F  
Purina Beneful / Score 17 F       17 F  
Purina Dog / Score 62 F       62 F  
Purina Come-n-Get It / Score 16 F     16 F  
Science Diet Advanced Protein Senior 7+ / Score 63 F   63 F  
Science Diet for Large Breed Puppies / Score 69 F   69 F  
 
 

Natural Treatment VS Pharmecutical

There are many skin and health issues that can be resolved by change of diet or supplementing to replace the deficiancy that has created the symptoms/issue. The most common is allergy symptoms. You can spend a ton of money at the vet and be prescribed  medications that are actually harmful and detrimental to your dogs well being. Over abundance of yeast in a dogs system in my opinion is the most common issue confused with allergies. The dog scratches, has a rash or redness of skin, rust colored areas under the tail, front legs next to the chest  same as in people, it can manifest into a variety of symptoms different in each dog. Antibiotics and or prednisone treatment resolve the issue temporarily only to return in full force shortly after the treatment is stopped. These medications actually help the yeast grow by killing the good bacteria necessary to keep things in balance. If it is yeast related there is a simple way to stop the problems and avoid recurrence with very little trouble. Follow the basics and I promise you and your pet will be happier for it. The dogs system gets out of balance and allows the yeast to overproduce. Yeast is present in everyone. When it overproduces, it causes a variety of problems internal and external. It can even affect internal organs. Changing the ph in the dogs digestive tract and over all system will inhibit over production putting the dog back in balance resolving the issue. It takes several weeks to see improvement and a few months to get completely under control. Persistence is the key, and it does work.

Feed food with NO corn. Avoid food with wheat or soy and use rice or sorghum based dog food ingredients.

Feeding a probiotic supplement may be another alternative that produces results. In theory it should be a quicker way to get there, however I dont have any experience there fore unable to provide an opinion.

Add a few tablespoons of dried cilantro to the dogs food each day. This absorbs the trace metals in the digestive system. An over abundance can be present in tap water, ground water etc. Yeast needs this so removing it controls the yeast.

Feed 1/3 to 1/2 cup of plain yogurt or plain Kefir milk (found in some grocers dairy/organic dairy section) every day. This helps put good bacteria back in the dogs digestive system and helps control the yeast that has taken over. It's also a natural way to protect a puppy against parvo-scientific fact that parvo needs certain bacteria to do its damage.  Crowds out the bad bacteria and promotes the good enabling the dogs immune system to be the best it can be.

Add  a few tablespoons of ACV (apple cider vinegar)  for each gallon to your dogs watering dish, bucket etc. Replace the ACV each time you change. This will also control tear stains, which is yeast growing in the dogs fur.

Here is a link that has a TON of information and other ways to approach the resolution of yeast. What ever method you decide to use..keep after it for several months. It takes that long to eradicate it from the dogs digestive system as it may even be living in the dogs internal organs, i.e.it must be treated from the inside out in addition to any topical solutions you apply for temporary relief.

 http://www.earthclinic.com/Pets/yeast_infections_dogs_questions.html#Question_2033

 

I highly recommend only giving your dog filtered water if your water quality is sub par in general. We actually installed a filtering system and swear by the results.

 Please feel free to call and ask any questions you may have. It is difficult to cover everything and it may be something new to you that is common knowledge to most so I dont think to post it. Visit the CONTACT US portion of the website. I am always happy to talk dogs and do my best to answer any questions you may have.

 

DJD: The Disease-Description, Symptoms, and it's Affects

Hip Dysplasia is a terrible genetic disease because of the various degrees of arthritis (also called degenerative joint disease, arthrosis, osteoarthrosis) it can eventually produce, leading to pain and debilitation.

The very first step in the development of arthritis is articular cartilage (the type of cartilage lining the joint) damage due to the inherited bad biomechanics of an abnormally developed hip joint. Traumatic articular fracture through the joint surface is another way cartilage is damaged. With cartilage damage, lots of degradative enzymes are released into the joint. These enzymes degrade and decrease the synthesis of important constituent molecules that form hyaline cartilage called proteoglycans. This causes the cartilage to lose its thickness and elasticity, which are important in absorbing mechanical loads placed across the joint during movement. Eventually, more debris and enzymes spill into the joint fluid and destroy molecules called glycosaminoglycan and hyaluronate which are important precursors that form the cartilage proteoglycans. The joint's lubrication and ability to block inflammatory cells are lost and the debris-tainted joint fluid loses its ability to properly nourish the cartilage through impairment of nutrient-waste exchange across the joint cartilage cells. The damage then spreads to the synovial membrane lining the joint capsule and more degradative enzymes and inflammatory cells stream into the joint. Full thickness loss of cartilage allows the synovial fluid to contact nerve endings in the subchondral bone, resulting in pain. In an attempt to stabilize the joint to decrease the pain, the animal's body produces new bone at the edges of the joint surface, joint capsule, ligament and muscle attachments (bone spurs). The joint capsule also eventually thickens and the joint's range of motion decreases.

BREEDING PROSPECT vs EVALUATION RESULTS

Do not ignore the dog with a fair hip evaluation. The dog is still within normal limits. For example; a dog with fair hips but with a strong hip background and over 75% of its brothers and sisters being normal is a good breeding prospect. A dog with excellent hips, but with a weak family background and less than 75% of its brothers and sisters being normal is a poor breeding prospect.

Although there is a genetic disposition for this disease, the variables as described on the OFA and Penn Hip websites clearly summarize that research should be done prior to breeding to avoid producing dysplastic offspring. Since it is rare that  every dog in any given pedigree  has been screened, there is a chance regardless. The more consistent background a puppy has regarding hip scores, the better . The OFA has a data base you can look up any dog that has been read and obtain the results of their hip evaluation. The University of Pennsylvania (Penn Hip) is in the process of doing the same.  Below is information regarding the difference between Penn Hip, and OFA hip evaluations.

THE BOTTOM LINE 

 There is much controversy over which method more accurately predicts the possibility of Dysplastic Joints, the reason being; One measures laxity and the other at hip conformation so techically you can have a dog that is OFA good with deep sockets, smooth lines and nice looking hips but questionable degree of laxity which means that may not stay good into adulthood because there is more room for movement, bone damage etc. Hopefully this helps you understand why both are often deemed necessary to determine the breeding worthiness of the dog.

No one can predict when or even if a dysplastic dog will start showing clinical signs of lameness due to pain. There are multiple environmental factors such as caloric intake, level of exercise, muscle structure and weather that can affect the severity of clinical signs and phenotypic expression (radiographic changes). There is no rhyme or reason to the severity of radiographic changes correlated with the clinical findings. There are a number of dysplastic dogs with severe arthritis that run, jump, and play as if nothing is wrong and some dogs with barely any arthritic radiographic changes that are severely lame.

 SUMMARY

The Penn Hip can be done as early as 6 months of age where as OFA  requires the animal to be at least 24 months old. The laxity does not change, however the bones can.  A dog should have minimal laxity-the closer to 0.30 the better, and the closer you get to 0.70 raises the probability of problems regardless of the socket depth and shape of the bones. 

Deep socket covering 50% or more of the femur head in conjunction with round femur head (and low laxity) results in a lesser probability. Shallow sockets, and a less round femur head  CAN  be a higher probability IF the degree of laxity is 0.60 or higher. The most accurate probability is to have an evaluation using both methods utilize the information using common sense.

 home

 

"In Australia and the United Kingdom, a numerical hip score is awarded to each dog based on the sum of points given for nine different areas of the hip joint. The scores for each hip are then added together giving a possible best score of zero and a worst of 106. This data is then collected by the national veterinary association and the national kennel council or club to compile breed averages. Breeding is generally not recommended for any dogs at or above the breed average hip score. Ideally, only dogs well below the breed average with relatives also below the average should breed. Of course this mean score will only be a true reflection of the problem in the breed if enough dogs have been tested. In the UK, hip scores are published by the Kennel Club and are also available in the dog's pedigree record and that of its progeny. In Australia, hip score results are not published but the owner of the dog will receive papers showing the hip evaluation. " 

 

 

DEFINITION
 OFA FCI GERMANY NETHERLANDSSWEDEN
 SWITZERLAND UK-AUSTRALIA BVA
 No Signs of Hip Dysplasia

 Excellent

Good

 (1)

  A

 (2)

 (a) Normal

 Negatief geheel

gaaf (1) (-)

Negatief neit geheel

gaaf (2) (-)

 Utmarkt

U.A.

 Frei

 0-4 (no>3hip)

5-10 (no>6/hip)

 Near Normal Hip Joints

 Fair

Borderline

 (1)

  B

 (2)

(a) Fast Normal

 Transitional

Changes (TC)

I I

 11-18

 19-25

 Mild Hip Dysplasia Mild

 (1)

  C

 (2)

 (a) Leichte HD

 Licht positief

(3) (LP/+-)

 II 26-35
 Moderate Hip Dysplasia Moderate

 (1)

  D

 (2)

 Mittlere HD
 Positief (3.5) (P/+)
 II II 36-50
 Severe Hip Dysplasia Severe

 (1)

  E

 (2)

 Schwere HD

 

Positief (4) (P/++)

Positief optima

forma (5) (P/++++)

 III

 IV

 III

IV

 51-106

 

Additional articles and information

The published article included below is in my opinion one of the most complete and informative available online.

Canine Hip Dysplasia Part I 

To understand this genetically transmitted disease, we must first understand the workings of the normal canine hip.

By John C. Cargill, MA MBA, MS and Susan Thorpe-Vargas, MS

 This is the first in a series of articles addressing canine hip dysplasia. What follows is written from the perspective that the readers of the series are conscientious breeders who are the guardians of the genetic pools that constitute their breeds. While this series of articles will not replace a stack of veterinary medical texts, it is a relatively in-depth look at the whole problem of canine hip dysplasia. Furthermore, the series is designed to be retained as a reference. When you finish reading it you will have a sufficient background to make rational breeding choices and will be able to discuss the subject from an informed basis with your veterinarian. You may not like what you read, but you will be more competent to deal with the problem.

Hip dysplasia is one of the most controversial and widespread problems in the dog fancy. So many old-wives tales, anecdotes, misconceptions and even lies abound that one of the goals of this series of articles must be to lay things out to the reader as they are, supported with some scientific basis.

Let's start with a hypothetical scenario, but one which too many of us have faced:

He's major-pointed; he moves like a dream; that head piece may just be the best you have ever bred. In short, this boy typifies everything that is good about your breed and is the culmination of many years of hard work, hopes, tears, frustration and all the ups and downs, joys and heartaches common to the fancy. Now it is time to X-ray his hips so that you can not only use him in your breeding program, but advertise him at stud. This is one boy that is going to make it, and we are talking national specialty here.

Problem - the radiographic results come back with a diagnosis of canine hip dysplasia-severe. What should you do?

More among us than will admit have had this experience, and most of those who haven't have seen it happen to other breeders concentrating on similar bloodlines. Now back to our hypothetical scenario:

You never suspected a thing. The dog never appeared to be in pain and his gait was what won him his major points. You have invested time, money and your hopes on this animal, and it all has been for naught! Now is the time for hysteria and self-blame:

  • What went wrong?
  • Could this have been prevented?
  • Was he not fed correctly?
  • Was he kept on an improper surface while growing?
  • What is this disease that keeps reappearing in the most conscientious of breeding programs, and which frustrates our attempts to eradicate it?

The first step in understanding canine hip dysplasia is to recognize it as not just one disease but many diseases, which together result in degenerative effects on the hip joint. An extremely complex disorder, hip dysplasia is now thought by some to be the most noticeable manifestation of a systemic condition that can affect not only the hip joints but also those of the elbow, shoulder and event the joints between the vertebrae1. Whatever else might result from the systemic conditions of this polygenic and multifactorial disease, hip dysplasia remains a common, usually painful and often debilitating disease. "Efforts by dog breeders and veterinarians to reduce the prevalence of the disorder have proven marginally effective." 2

While there is much that we do not know we do know that canine hip dysplasia is a genetically transmitted disease. If you need to, or if you disagree at this point, please re-read that statement. We will be repeating it throughout this series of articles, and this concept is the basis for determination of fitness for breeding. The genetic concept of heritability is a complicating factor and is one reason why hip dysplasia remains so controversial. So often when you breed you get more than you see. Without resorting to too much math, heritability is equal to the statistical variance due to genetic influence divided by the sum of the statistical variance due to the genetic influence plus the variance due to the environmental influence. It is easier to comprehend the mathematical notation than the statement of the equation:

 

H2 = heritability index
Vgenetics = variance due to genetics
Venvironment = variance due to environmental influences

 

Thus, heritability is defined as an estimate of how much environmental factors play in the expression of the inherited genes. A high heritability index means that environmental considerations are not as important as genetic elements. The numerical value or heritability index is a function not only of breed type but of the population from which the data is extracted. "Studies of hip dysplasia genetics have indicated that the disease is polygenic and multifactorial, with estimates of heritability index in the range of 0.2 to 0.3"3

For instance, in a 1986 Swedish study, the heritability of hip dysplasia in German Shepherds was 0.40 in Sweden, but only 0.25 in the British Isles during the same time period. The difference between breeds may also reflect their levels of inbreeding. The more inbreeding, the lower the heritability index because inbreeding reduces the total genetic variability-that is, the gene pool is smaller. Inbreeding is not a bad word. It only becomes problematic when undesirable genetic traits are concentrated within the gene pool. By definition, every purebred dog of any given breed is highly inbred, or else it would look like a feral dog. We frequently hear that the problem with the American Kennel Club purebred dogs is that they are inbred. We should hope so, otherwise we could never fix type to the point where there were discernible differences between breeds. On the other hand, we would hope that the concentrated gene pools for the various breeds would have been concentrated from stock exhibiting only desirable genetic traits. We would hope that our field, bench and obedience champions would be fit to contribute to the gene pool. Of course, we know that is not true, or there would be no purpose in writing this article. 4,5,6

(diagram based on reprint from the Journal of the American Veterinary Association, Vol.196, No.1,pp.59-70. "New concepts of coxofemoral joint stability and the development of a clinical stress-radiographic method for quantitating hip joint laxity in the dog," by Gail K. Smith, V.M.D., Ph.D.; Darryl N. Biery, D.V.M.; and Thomas P. Gregor, B.S.)

To further complicate matters is the fact that the pattern of inheritance indicates that more than one gene is involved. Hip dysplasia is polygenic (involves many different genes) and multifactorial (influenced by many non-genetic factors). This makes sense when you think of the complexity of the various structures involved. Every cell in the body, except for sex cells, carries two copies of each gene and each gene codes for a specific characteristic. One very simple example is eye color:

If the cell's two sets of genes for a specific characteristic are exactly alike, then the animal is homozygous for that characteristic.

If the two genes are different, i.e., heterozygous, then one copy of the genes could code for blue eyes and the other could code for brown eyes.

Let's complicate the matter even further. If the animal carries two different copies of the same gene for eye color, only one copy can be expressed in any given eye. Closer to home, in humans for example, a child born to parents heterozygous for eye color (both parents have a blue-eyed gene and brown-eyed gene) will have a one-in-four chance of having blue eyes. This is because the gene for blue eyes is recessive and both copies for that code for blue eyes must be present before that characteristic can be expressed. On the other hand, if the child has brown eyes, we don't know what type of genes for eye color he or she has. This is because the gene for brown eyes is dominant and is able to "mask" the physical expression of the blue-eyed gene. Alternatively, the child could have only the genes that code for brown eyes. It is beyond the scope of this article to address the various "odd" eye color combinations, but co-dominance and variable penetrance may be what we are dealing with in canine hip dysplasia.

What you have just read is an example of phenotype vs. Genotype. Phenotype is the physical expression of a genetic characteristic. Genotype is genetic composition of the organism. Using our eye-color example, the child with two different copies of the gene will express the brown-eyed phenotype, but his or her genotype will be heterozygous.

Let's add to the complexity once again. Co-dominance of genes is a situation where neither gene is dominant. A clear example illustrating the concept of genetic co-dominance is flower color. A snap dragon homozygous (both copies of color genes exactly alike) for white petals crossed with a snap dragon homozygous for red petals will produce a flower with pink petals, not a flower with either white or red petals or a mixture of red and white petals. Many researchers feel that hip dysplasia may be a mixture of dominant, recessive and co-dominant genes. Quite probably, this is one of the reasons why isolation of the causative genetic factors of canine hip dysplasia has been so elusive.

The concepts that you need to be clear on as we leave this mini-course on genetics are: heritability index; genetic and environmental variability; dominant vs. Recessive genes; homozygous vs. heterozygous; genetic co-dominance; and most importantly that hip dysplasia is genetically inheritable and is polygenic and multifactorial. In short, you can get it in your breeding program when you bred from animals that did not show it.

Before we can discuss an abnormal process (disease), we need to first understand the normal process. In this case, we must be able to answer the question, "What is a normal hip, what makes it normal, and how does it get that way?"

First, what is the hip? The hip joint is a main weight-bearing joint consisting principally of a ball and socket. This joint connects the pelvis to the lower extremities. The ball is on the end of the femur (thigh bone) and the socket (acetabulum) is part of the pelvis. Note from figure 1 how the femoral head fits into the acetabulum in the normal hip joint. This will be key to all our discussions from this point forth. A true ball-and-socket joint has three degrees of freedom, that is, it supports rotation about three different axes. The canine hip joint is unusual as a ball-and-socket joint in that it has a fourth degree of freedom. The femoral head may be displaced laterally from the acetabulum. While this is the genius of this joint, allowing the attached appendage a full range of motion, it can also create a problem if there becomes too much laxity in the joint. Note the fourth degree of freedom in Figure 2, which provides for the femoral head (ball) to move directly away from the acetabulum (socket). From Figures 1 and 2, it should be obvious that much lateral displacement of the femoral head from its seat in the acetabulum will produce high joint stresses during weight bearing. This joint laxity will be a major consideration for the changes it causes in the joint mechanics as we progress through this series of articles.

The acetabulum is formed from the embryonic process of fusion of the ilium (top of the hip), the ischium (lowest part of the hip) and the pubis (below the ilium but above the pubis) and the acetabular bone. Most researchers feel that normal development requires close conformity (close, tight fit) between the acetabulum and the femoral head throughout their growth period. In other words, the joint must fit tightly, deeply and snugly. This is how a puppy's hip starts out-dysplastic and non-dysplastic puppies' hips are indistinguishable. The first six months of life seem to be the most critical growth period when the depth of the socket must be maintained. It is believed that the depth of the socket in the growing puppy may be in part a function of the amount of stress the femoral head can produce on the immature acetabulum. Think of it as a thumb pushing into a ball of clay. The harder the thumb pushes, the deeper the indentation in the clay. Much as a knife edge concentrates force onto a relatively small surafce area (and a pin of a diameter equal to the width of the knife edge even more), the two phenotypic traits that maximize the forces between these two developing bony structures are a small femoral head and a long femoral neck. Note, however, that the normal acetabulum is well-formed in utero, thus the stress may only serve to maintain that socket depth.

To cushion the force between these two bony surfaces, there is a truly remarkable substance called articular cartilage. This cartilage is similar to a hard sponge with a slick hard surface facing the interior of the joint. In the normal joint, articular cartilage is able to change its shape slightly when force is applied to it, thus spreading and distributing force more evenly into the subchrondal bone directly beneath the articular cartilage. This is of major importance to the long-term integrity of the joint.

Holding everything in place is another structure that does more than just enhance the stability of the joint. The joint capsule is a fibrous structure filled with synovial fluid that surrounds, isolates and protects the joint. This joint capsule is essential to proper development and functioning of the joint. This structure is similar to the rubber grease bladder around a ball joint in the front suspension of your car. The cushioning effect of the grease with the fluid pressure of the grease and the elasticity of the bladder helps to stabilize the joint. The bladder helps keep out contaminants. This function becomes even more important as the joint ages and surfaces become worn. The joint capsule contains the all-important synovial fluid, the most important ingredients of which are nutrients, which diffuse into the joint from the blood supply, and hyaluronic acid (HA). The tissues within the joint extract nutrients from the synovial fluid in which they are bathed.

Hyaluronic acid has a critical function: to provide lubrication. This slippery and viscous substance prevents rapid erosion of the articular cartilage and the surfaces of the femoral head and the acetabulum. A membrane called the synovial membrane lines the inside of the joint capsule, providing further isolation of the joint space. Should the synovial membrane become injured or ruptured, white blood cells release enzymes and oxygen radials (free radicals) that attack and destroy hyaluronic acid. When this occurs, the loss of HA reduces the lubrication that prevents friction and limits erosion of the articular cartilage. Even worse, loss of HA allows the enzymes from white blood cells to join forces with oxygen free radicals and attack the articular cartilage. Free radicals play a major role in degenerative arthritis.

The ball-and-socket (coxofemoral) joints of an affected puppy radiographically appear to be structurally and functionally normal at birth. The hips of an affected puppy are indistinguishable from a normal puppy at birth. This is an important point to remember. As an affected puppy grows, the hip joint undergoes severe structural alterations. The changes result from joint laxity and adulteration/destruction of the constituents of the synovial fluid and subsequent loss of lubrication and nourishment, which serve to reduce the regenerative and elastic (force-absorbing and distributing) properties of the articular cartilage. The normal joint retains its tightness and close fit. Whereas in the genetically dysplastic-to-be puppy, the acetabular rim and femoral head become eroded.

Remember that the acetabular depth is partially a function of the small "footprint" of the femoral head which concentrates force into a small surface area. As the femoral head is flattened, the coxofemoral joint no longer fits snugly. Excessive force is applied unevenly, especially at the edges of the flattened femoral head. Visualize this joint looseness as the difference between the impact of a boxer's fist when the punch is thrown with the glove already in contact with the opponent's jaw as contrasted with an initial stand-off distance of say 20 inches. In the first case, little impact force is transmitted and no damage is done; in the second, there may be a knock-out. In the joint, the increase in stress results not only in abnormal wear of the articular cartilage, but causes tiny micro-stress fractures to appear in the subchondral bone. The body attempts to heal these fissures, causing the acetabulum to become filled in, i.e., made shallower. It is this cycle of damage and repair (osteophyte formation) that leads to deformation of the joint, and degenerative hip disease.

Conclusions: Hip dysplasia is not something a dog acquires; a dog either is genetically dysplastic or it is not. Initially, the hips of affected and normal puppies are indistinguishable. Later in life, an affected animal can exhibit a wide range of phenotypes, all the way from normal to severely dysplastic and functionally crippled. You should take away from this article the idea that hip dysplasia is genetically inherited. Never believe a fellow breeder or fancier who claims there is no hip dysplasia in his or her line. Never believe breeders who claim that if their breeding lines carried the genes for hip dysplasia they would be able to see it in their animals' gaits. This just is not true.

Although work has been started to find the genetic markers for the disease, we have as yet no method of genetic analysis that can tell breeders whether their dogs are dysplastic or not. We only have physical expression of the disease, and an effort to "back door" into clear stock for breeding purposes. Breeders must come to understand that the only way to reduce the incidence of hip dysplasia is by trying to breed from as few animals that have progenitors, siblings, get, or get of siblings that had clinical manifestations of hip dysplasia. Obviously, a great amount of information is lacking to make a rational breeding choice. These are hard words to have read, but much of our problem has come from thousands of years of less than natural selection resulting from the domestication of the dog.

In our second article in this series we will address in greater detail the parts nutritional, environmental and other factors play in mitigating or increasing the physical expression of canine hip dysplasia.

CREDITS

 References

  1.  Olsewski J.M., Lust G., Rendano B.T., et al. "Degenerative joint disease: Multiple joint involvement in young and mature dogs." Am J Vet Res. 1983; vol 44:1300-1308.

  2.  Smith G.K., Biery D.N. "New concepts of coxofemoral joint stability and the development of a clinical stress-radiographic method for quantitating hip joint laxity in the dog." J Am Vet Med Assoc. 1990;196:59-70. Ibid., p. 59.

  3. Cargill J. "Truth in advertising: breeder self-regulation I." Dog World. 1990(Jul);75 No.7:38-82.

  4. Cargill J. "Truth in advertising: breeder self-regulation II." Dog World. 1990(Aug);75 No.8:111-116.

  5. Cargill J. "What should 'champion' mean?" Dog World. 1993(Feb);78 No.2:34-35. 

Canine Hip Dysplasia Part II - Causative Factors of Canine Hip DysplasiaCanine Hip Dysplasia Part II

Causative Factors of Canine Hip Dysplasia

 Owners must separate fact from myth when examining theories on genetic, nutritional and environmental factors that influence CHD. By John C. Cargill, MA MBA, MS and Susan Thorpe-Vargas, MS

 This is the second part in a series on canine hip dysplasia. What follows is written from the perspective that the readers of the series are conscientious breeders who are the guardians of the genetic pools that constitute their breeds. While this series of articles will not replace a stack of veterinary medical texts, it is a relatively in-depth look at the whole problem of a canine hip dysplasia. Furthermore, the series is designed to be retained as a reference. When you finish reading it you will have a sufficient background to make rational breeding choices and will be able to discuss the subject from an informed basis with your veterinarian. You may not like what you read, but you will be more competent to deal with the problem.

Conclusions from Part I: Genetics is the foremost causative factor of canine hip dysplasia. Without the genes necessary to transmit this degenerative disease, there is no disease. Hip dysplasia is not something a dog gets; it either is dysplastic or it is not. An affected animal can exhibit a wide range of phenotypes, all the way from normal to severely dysplastic and functionally crippled. Hip dysplasia is genetically inherited.

In this article we will address the issue of genetic, nutritional and environmental factors. We hope to debunk some of the myths and introduce some recently developed theories.

Other diseases, infections or trauma can produce clinical signs suggestive of canine hip dysplasia. In some breeds the animals learn to live with pain and are stoic about letting anyone know of their pain. This stoicism seems to be especially prevalent in terriers and northern breeds and is the case - not the exception - in the fighting breeds. Those fanciers who participate in pulling, freighting, carting or sledding events with their dogs should always be aware that tendonitis or pulled muscles can cause a gait change reminiscent of hip dysplasia. Anyone involved in lure chasing or coursing for real needs to understand that on occasion, an animal will twist or turn the wrong way while in full chase. In the older dog, trauma from younger years may manifest itself as arthritic deterioration. A little bit more unusual is to have viral penetration of the joint capsule with resultant damage to articular cartilage, or the epiphyseal surfaces of the femur. Absent such unusual occurrences, the reality of hip dysplasia is that it is a genetically linked condition--always was, always will be.

The role of growth

In the first article we said that the first six months of a puppy's life seem to be a critical time of development. The rate of growth can be astonishing. When one thinks of the number of things that could go wrong as an Akita puppy, for instance, goes from a birth weight of slightly more than 1 pound to 60 to 70 pounds in six months and then adds another 30 to 40 pounds by year end, it is amazing that most dogs mature without serious problems. It is during this period that dogs are most active. There is evidence to suggest that exercise is necessary to retain the depth of the acetabulum. How much exercise and of what type is unknown.

One Norwegian anecdotal study published in England in 1991 concluded that German Wirehaired Pointer, English Setter, Irish Setter, Gordon Setter and Labrador Retriever puppies growing up during the spring and summer had a lower incidence rate of hip dysplasia than puppies growing up during autumn and winter. Oddly enough, Golden Retrievers and German Shepherd Dogs did not manifest the same seasonal pattern of incidence of hip dysplasia. 1

While this study may lack strict experimental protocol, it raises many questions. The first question is whether there was an exercise differential between the dogs due to weather in Norway. The second question was whether there was different availability of sunlight necessary for vitamin D production and utilization. The list of questions could go on, but this study is brought up to show that there may be exercise and diet factors at play, and that various breeds may respond to these factors in different ways. It would be reasonable to conclude that there is probably an amount of exercise during a genotypically dysplastic puppy's rapid growth period where phenotypic expression is mitigated, delayed, or both. Without taking the time, cost and effort to conduct a rigorous scientific study, it is still sometimes possible to glean valuable information from existing, i.e., available data. Therefore, do not shy away from creating working hypotheses from anecdotal studies; conversely, do not lock their findings in concrete as inviolate fact.

With respect to the published scientific literature, we found nothing in Medline (an online listing of medical and biological articles) referencing any journal article addressing the subject of surfaces and their effects on the incidence of hip dysplasia. While we know of breeders who write into their sales contracts that animals must be kept on a specific surface and fed a specific feed, these demands seem to be without scientific basis.

There is some evidence that preventing rapid growth reduces the extent to which the adult dog will manifest hip dysplasia. Decreasing the dog's food consumption during its growth period seems to correlate well with normal hips. 2 The Kealy study published in 1992 was based upon 48 8-week-old Labrador Retriever puppies. These puppies were sex-matched littermates randomly assigned to two groups: the first group was fed ad libitum (as much as they wanted, when they wanted to eat); the second group was fed the same feed until they were 2 years old, but in amounts of only 75 percent of what the first group consumed ad libitum. Thus for every puppy fed ad libitum, there was a same-sex littermate on a restricted diet. This rigid protocol gives this study great respectability and credence. The accompanying chart gives the findings in tabular form. Note the tremendous increase in normal animals at two years of age when kept on a restricted diet for those two years. This ought to more than suggest that overweight animals are at risk for phenotypic expression of canine hip dysplasia.

Radiographic
Evaluation
Method

Group 1
Ad Libitum Feeding

Group 2
75% of Ad Libitum Feeding

Dysplasic

Normal

% Normal

Dysplasic

Normal

% Normal

OFA
Swedish

16
18

8
6

33%
25%

7
5

17
19

71%
79%

Many researchers conclude that early fusion may lead to bone and cartilage deviations which then could predispose the animal to future dysplasia. An important point that these studies illustrate is that it is possible to improve the individual phenotype of dogs whose parents carried the gene for hip dysplasia (genotypically dysplastic).

In the first article we alluded to joint laxity as being present whenever there is canine hip dysplasia. Given that joint laxity is at least one of the factors governing the onset of hip dysplasia, then any process that retards this condition could possibly minimize the severity of the disease. It also is conceivable that retardation of joint laxity could delay the onset of the physical appearance of the disease.

Feed for health

A recent study (1993) showed that coxofemoral joint stability was improved in dogs that were fed increased levels of chloride and decreased levels of sodium and potassium. 3 In the eight-part "Feed That Dog!" series (Dog World, July 1993 through February 1994) we emphasized repeatedly the importance of the ratio of sodium and chlorine, with a ratio of 1.5 sodium to chlorine being accepted as the dietary requirement. 4 We noted also that "sodium chloride deficiency is manifested by fatigue, decreased utilization of protein, decreased water intake, inability to maintain water balance, retarded growth, dryness of skin and loss of hair." 5 Potassium deficiency " results in poor growth, restlessness, muscular paralysis, a tendency toward dehydration, and lesions of the heart and kidney." 6 We cautioned that "prednisone, a steroid commonly prescribed for various skin allergies, causes a loss of potassium and retention of sodium, and retention of sodium can cause further loss of potassium." 7

Calcium (Ca), sodium (Na), and potassium (K) are the electrolytes considered most important, as they are necessary to many biological functions. Electrolytes are atoms or molecules that carry either a negative or a positive charge. Anions have an extra electron, and thus carry a negative charge. Cations are missing an electron, thus they carry a positive charge. In the study cited, Kealy et. Al. Introduced the theory of "dietary anion gap" or DAG. 8 The researchers explained DAG as the amount of chloride ion subtracted from the sum of sodium ion and potassium ions:

DAG = [(K+ + Na+) - Cl-]

This experiment, consisting of the raising of 167 puppies, included puppies from five different breeds. They were placed on three different diets tat varied only in their DAG content. Examples of low DAG ingredients are rice with a DAG of 6 and corn gluten meal with a DAG of 5. The result of this experiment showed that except for some breed-specific exceptions, those dogs that were fed a lower DAG diet had better hips at 30 weeks than those fed a diet with a higher DAG content. Differences in DAG balance did not result in different rates of weight gain. This is important, for it allowed elimination of weight gain as a causative factor in the study. Hips were evaluated by their degree of subluxation as measured by the Norberg angle. The Norberg angle is the "angle included between a line connecting the femoral head centers and a line from the femoral head center to the crainiodorsal acetabular rim." 9 The greater the Norberg angle, the less the subluxation. Norberg angles are commonly measured as <90 degrees for loose hips and>105 degrees for tight hips. Those dogs with better hips at 30 weeks also had good hips at 2 years of age.

Unfortunately, the researchers were unable to explain the mechanism or the "why" of how they got the results they did. One of the theories proposed was that a lower DAG somehow affected the pH or "acidity" of the synovial fluid. This in turn affected the osmolality or "thickness" of the synovial fluid. The osmolality of a fluid depends upon the number of dissolved particles in it, and is the measure of the osmotic pressure. In previous studies, a higher osmolality was associated with the greater synovial fluid volume found in dysplastic dogs. Note, of course, that there is a normal range of DAG values in a balanced diet. Leaving that range while formulating a dog food, for example, could cause serious problems.

Calcium

The question of calcium supplementation while controversial among breeders, is fairly easy to answer: don't do it. It is not necessary to add extra calcium to your dog's diet. Not only is calcium an essential skeletal component, it is also necessary for blood coagulation, hormonal release and muscle contraction. The three biological systems involved in controlling the amount of calcium in the blood are bones, kidneys, and the intestine.

Calcium is constantly being recycled in and out of living bone. In the adult dog, under balanced conditions, both accretion (calcium uptake) and resorption (calcium loss from bone) values vary from 0.1 to 0.2 mmol per kilogram of body weight per day. [A millimole is a minute measure of molecular weight.] For the rapidly growing puppy these values are at least 100 times higher. 10 Another difference between an adult dog and a puppy is their relative abilities to absorb calcium from the food they ingest. In the adult dog, the percentage of calcium assimilated from food varies from 0 to 90 percent, depending upon the composition of the food and its calcium content. 11

A 1985 study which examined the physical, biochemical and calcium metabolic changes in growing Great Danes, showed that young puppies do not have a mechanism to protect themselves against excessive calcium feeding. Under the influence of certain hormones, the calcium excess is routed to the bones. This results in severe pathological consequences for the patterning for the growing skeleton and the subsequent impairment of gait. Strongly correlated with high calcium intake is disturbed enchrondral ossification (growth plate anomalies) causing the clinical appearance of radius curvus syndrome and osteochondrosis (a disturbance of bone formation within the cartilage, occurring during periods of maximum growth). 12 Chronic, high calcium intake in large breed dogs has also been associated with hypercalcemia, elevation of the liver enzyme alkaline phosphatase, retardation of bone maturation, an increase in bone volume, a decrease in the number of bone resorption cells, and delayed maturation of cartilage. 13 We can safely conclude that calcium plays a significant role in skeletal disease. The giant breed dogs, because of their rapid and intense growth, are sentinels for nutritionally influenced diseases. These changes, while exaggerated in the giant breeds, are just as real-though they may be slower to surface and not as easily identified-in the smaller breeds.

Vitamin C

Vitamin C (L-ascorbic acid) has frequently made it into the literature along with calcium. At one time or another vitamin C has been touted by somebody as a cure-all for virtually any malady known to man and beast. This is not discount the requirements for vitamin C, for it is absolutely necessary. Fortunately for dogs, they produce an enzyme called L-gulonolactone oxidase, which allows them to synthesize vitamin C from glucose without having access to a dietary form of vitamin C. (A deficiency could only be the result of either a problem with absorption or an increased need.) Interestingly, canines produce only 40mg of ascorbate per kilogram of body weight, which is far less than other mammals with the ability to synthesize their own vitamin C. There is no established minimum daily requirement for vitamin C in canine nutrition. That said, let's look at the function of the vitamin C the dog manufactures.

Vitamin C figures prominently in the biosynthesis of collagen. 14 Collagen is an important structural protein in the body. There are different types of collagen, but it is Type I collagen that appears most often in connective tissue, particularly in bone and ligaments. Vitamin C adds an -OH group to the two amino acids proline and lysine. Without this functional group there is a decrease in the number of cross-links in collagen. Without this cross-linking, the melting temperature of the protein is reduced from about 39 degrees to 23 degrees centigrade. In other words, without the cross-links this protein can be denatured at body temperatures.

There is experimental evidence that vitamin C may play a role in bone mineralization by stimulating bone resorption. What has been shown by one researcher to be efficacious in treating the physical manifestations of canine hip dysplasia (CHD) is a form of vitamin C called polyascorbate. 15 Calcium ascorbate, used in conjunction with vitamin E, also is considered helpful in reducing the inflammatory processes that accompany the disease. In this form, vitamin C is taken up by the bone along with calcium, and this acts like a time release factor that keeps the blood plasma concentration high and the cells constantly "bathed" with vitamin C.

With all the continuing fuss about vitamin C in the fad literature, it was inevitable that it would be tried for treatment of hip dysplasia. Belfield (1976) conducted a somewhat anecdotal study on eight German Shepherd Dog litters of puppies from dysplastic parents or parents known to have produced dysplastic puppies. 16 Megadoses of ascorbate were given to dams (2 to 4 grams of sodium ascorbate crystals per day) and to the pups (birth to 3 weeks-calcium and vitamin E supplement; 3 weeks to 4 months-500 grams ascorbate per day; 4 months to 1.5 to 2.0 years-1 to 2 grams ascorbate per day). Belfield claimed that none of the pups developed hip dysplasia, and breeders involved with the research were so convinced that they guaranteed dysplasia-free puppies if the ascorbate therapy was followed by the new owner. It is significant to note that no follow-up studies were published. While this is interesting, there is little accepted hard evidence to suggest that supplementation with ascorbate can prevent or ameliorate canine hip dysplasia. Readers are cautioned that large doses of vitamin C are not considered mainstream prophylaxis or therapy. The truth of the matter is that it is in the genes, not the diet, though diet may play a minor part.

A recent study (1993) observed that synovial fluid volume as related to osmolality correlated highly with the incidence of hip dysplasia. 17 This suggested that the swelling of the joint capsule from excess fluid pressure might be forcing the femoral head out of position in the acetabulum.

Tissue changes

Before any radiographic indications appear, there are structural changes at the tissue level of muscles, ligaments and cartilage. Cellular changes and molecular changes occur both in the joint capsule and in the synovial fluid. One study suggested that one of the first observable changes of the disease process is hypertrophy or swelling of the pectineus muscle fibers. 18 This hypertrophy is thought to be a compensatory adaptation to extreme contractile tensions and may be the result of the muscle mass trying to hold the acetabulum and the femoral head in the proper position.

Another study showed that the composition of the pectineus muscle was significantly different between 2-month-old puppies that eventually developed normal hips, and those that were dysplastic by 24 months. 19 The two groups differed by the size of the muscle fibers, but this time, the dysplastic animals had smaller than normal muscle fibers (hypotrophy) and the ratio between contractile tissue and non-contractile tissue was lower. Thus, not only did the affected animals have diminished capacity to contract their muscles, their muscles were also less elastic. This study begs the question of joint laxity: Once stretched, would the muscles tend to remain stretched, thus resulting in a looser hip joint? Unfortunately, it cannot be said with any certainty whether these differences are causal or correlative.

It is certain, however, that hip dysplasia is characterized by joint laxity. 20,21,22,23,24 Whether such laxity is the result of the pathological processes involved in the disease, or whether the laxity is the cause of the disease, cannot be determined. Remember, however, that loose joints and hip dysplasia are found together. We will be coming back to this point in later articles. There is a little twist to what we find: All dogs that have hip dysplasia have loose hips, but not all dogs with loose hips have hip dysplasia. It is not known which comes first: remodeling of the bony surfaces leading to abnormal wear of articular surfaces and joint instability or vice versa. It may very well be that both processes are concurrent and/or iterative processes.

Other changes that can precede either clinical signs, like pain and gait abnormalities, or radiographic evidence of hip dysplasia include thickening of the joint capsule and swelling of the round ligament. Subtle and early changes in articular cartilage structure also precede clinical signs. Specifically, in affected animals, the ratio between Type A cells and Type B cells differs from the norm. Type A cells are macrophages, i.e., large mononuclear cells produced by the immune system which ingest damaged cells and blood tissue. Type B cells are fibroblasts which are precursors of connective tissue. In one study, the population of Type A cells increased. 25 Conceptually this makes sense, as the function of macrophages is to scavenge damaged cells, which would be the case if articular cartilage is being damaged. Note that these changes can only be observed after dissection and examination under an electron microscope. While diagnostic and predictive, such examination is without use to the clinician who is trying to diagnose the disorder. What is important to remember is that these changes are found in dogs whose x-rays showed them to be perfectly normal at the time of radiographic study. As a concerned breeder or fancier of dogs, this should alarm you. Do not be too alarmed, however, because there is hope for predictive techniques. These will be covered in later articles in this series.

Significant studies

The major study demonstrating the polygenic and multifactorial aspects of canine hip dysplasia is probably the 1991 German study an German Shepherd Dogs. 26 Unfortunately this article is in German and we know of no translations available. While this poses no problem for co-author Thorpe-Vargas, as she used to be at the Max Planck Institute in Germany, it is a real problem for co-author Cargill, as he has to take her word for it, supported only by Medline abstracts in English! The importance of this study is that it covered 10,595 dogs. Furthermore, this study attempted to quantify both environmental influences and genetic influences on the frequency of hip dysplasia. Models were developed using the following variables-independent random variables: age at X-raying, birth year, season, litter size, percent of X-rayed dogs in each litter and sex ratio of litter; independent fixed variables: sire and dam.

Through multiple linear and non-linear regression methods it was shown that sire, dam, sex and age at X-raying all showed statistically significant influence on the occurrence of hip dysplasia. The heritability indices (H2) were-Relationship: full siblings, H2 = 0.30; maternal half-siblings, H2 = 0.48; and paternal half-siblings, H2 = 0.11.

The researchers' caveat at the end of the study was that only the paternal half siblings' heritability index should be accepted because kennel and breeder effects are confounded with the dam effect. Their overall conclusion was that the frequency of hip dysplasia could be reduced if selection for breeding based upon the estimation of breeding values (H2) with respect to the frequency of hip dysplasia in allrelatives was implemented.

Many of the world's militaries are good sources of information on German Shepherd Dogs. The goals of such organizations have been to improve behavioral traits and to reduce the frequency of CHD. One of the more interesting studies in the literature is the one based uopn information provided by the US Army's division of Biosensor Research on the German Shepherd Dogs bred between 1968 and 1976.27 Detailed records were available for 575 animals representing 4 years, 18 sires, 71 dams and 48 human handlers. Variance component estimates were made, which allowed estimates of the heritabilities for both temperament and CHD scores to be made. The heritability index (H2) for temperament was 0.51 and for CHD was 0.26. Interestingly, in this population the genetic correlation between good temperament and bad hips was -0.33. Given the selection process of the U.S. Army, it was not surprising to find that dogs with good temperaments also had good hips. Because of the extremely high heritability index for temperament, records of the animal being evaluated can be used for repeat breeding selection rather than the records of the progeny.

A 1993 Austrian dissertation looked at a population of 10,750 Hovawarts from 1962 to 1988, out of which CHD findings were available for 4,387 dogs. 28 The goal of the dissertation was to statistically calculate two parameters. The first was a prediction coefficient based upon the CHD findings of all the ancestors of a specific animal. The second was a "taint" coefficient calculated on the basis of the CHD findings of all ancestors as well as of the individual CHD finding as well as those of any offspring already checked for CHD. The conclusions of this dissertation were that both the "prediction" and "taint" coefficients were useful in calculating the relative CHD risk of the prospective offspring when selecting breeding partners. A connection was found between the CHD findings and the inbreeding level of an animal as calculated from the "ancestor loss coefficient" and Malecots "coefficient de parente." Thus, increasing levels of inbreeding increase the risk of CHD. There was no difference between males and females for risk of CHD. Detailed coverage of the various genetic coefficients is beyond the scope of this article. Readers are directed to modern comprehensive texts, dissertation abstracts and the like in genetics should more than a passing familiarity with the intricacies of these coefficients be required.

Conclusions: While environmental effects, to include nutrition and exercise, may play a part in mitigating or delaying the onset of clinical signs and clinical symptoms hip dysplasia remains a genetically transmitted disease. Only by rigorous genetic selection will the incidence rate be reduced. In the meantime, it makes sense to have lean puppies that are exercised regularly and to avoid breeding any animals from litters that showed signs of hip dysplasia. It is probable that even normal exercise levels may increase the phenotypic expression of CHD of a genetically predisposed dog. Stay away from calcium supplementation of any kind; all it can do is hurt. There is no conclusive evidence tat vitamin C can prevent hip dysplasia, but there is some evidence that vitamin C may be useful in reducing pain and inflammation in the dysplastic dog. Let your conscience and your veterinarian be your guides in supplementing with vitamin C. Fortunately, large doses of vitamin C are readily excreted, but it is still possible to cause untoward side effects with megadoses.

The next article in the series will address the abnormal hip, to include differential diagnosis, observation, palpation fluid sampling and sedated and unsedated radiographic studies.

CREDITS

 

1.      References

  1. Hanssen I. "Hip Dysplasia in dogs in relation to their month of birth." Vet Rec. 1991 May 4;128(18):425-6.

  2. Kealy R.D., Olsson S.E., Monti K.L., Lawler D.F., Biery D.N., Helms R.W., Lust G., Smith G.K. "Effects of limited food consumption on the incidence of hip dysplasia in growing dogs." J Am Vet Med Assoc. 1992 September 15;201(6):857-63.

  3.  Kealy R.D., Olsson S.E., Monti K.L., Lawler D.F., Biery D.N., Helms R.W., Lust G., Smith G.K. "Effects of dietary electrolyte balance on subluxation of the femoral head in growing dogs." Am J Vet Res. 1993 April:54(4):555-62.

  4.  Cargill J.C. "Feed That Dog! Part II." Dog World. 1993 August;75(8):12.

  5.  "Effects of dietary electrolyte balance." Pp. 555-62.

  6.  Smith G.K., Gregor T.P., Rhodes W.H. Biery D.N. "Coxofemoral joint laxity from distration radiography and its contemporaneous and prospective correlation with laxity, subjective score, and evidence of degenerative joint disease from conventional hip-extended radiography in dogs."" Am J Vet Res. 1993 July;54(7):1023.

  7.  Hedhammer A., Wu F.M., Krook L., Schryver H.F., de Lahunta A., Wahlen J.P., Kallfelz F.A., Nunez E.A., Hintz H.F., Sheffy B.E., Ryan G.D. " Overnutrition and skeletal disease. An experimental study in growing Great Dane dogs." Cornell Veterinarian 1974;64 supp15:11-160.

  8.  Hedhammer A., Krook L., Schryver H.F., Kallfelz F. " Calcium balance in the dog." In "Nutrition of the Dog and Cat" ed. Anderson R.S.; Pergamon Press, Oxford 1980:119-27.

  9.  Hazewinkle H.A.W. "Influence of different calcium intakes on calcium metabolism and skeletal development in young Great Danes." PhD Thesis Utrecht State University 1985.

  10.  Hazewinkle H.A.W., Goedegbuure S.A. Poulos P.W., Wolvekamp W.ThC. "Influences of chronic calcium excess of the skeletal development of growing Great Danes." J Am An Hosp Assoc. 1985;21:377-91.

  11.  Berg R.A., Prockop B.J. "The thermal transition of a non-hydroxilated form of colagen: Evidence for a role for hydroxiproline in stabilizing the triple helix of collagen." Bio Chem Bio Phys Res Commun. 1973; Vol. 52:115-129.

  12.  Berge, G.E. "Polyascorbat, et behandlings-alternativ ved kroniske forandringer I stotte og bevegelsesapparetet hos hund" ("Polyascorbate, an interesting alternative by problems in the support and movement apparatus in dogs.") Norsk Veterinaertidsskrift (Norwegian Vet J), August/September 1990;102:581-582.

  13.  Belfield, W.O. "Chronic subclinical survey in canine hip dysplasia." Vet Med Sm An Clin. 1976; Vol. 71:1399-1403.

  14.  Lust G., Beilman W.T., Rendanom V.t. "A relationship between degree of laxity and synovial fluid volume in coxofemoral joints of dogs predisposed for hip dysplasia." Am J Vet Res. 1980,41:55-60.

  15.  Cardinet, G.H. III, Wallace L.J., Fedde M.R. "Developmental myopathy in the canine." Arch Neurol. 1969, 21:620-630.

  16.  Lust G., Craig P.H., Ross G.E. "Studies on pectineal muscles in canine hip dysplasia." Cornell Vet. 1972, 62:628-645.

  17.  Henricscon B., Norberg I., Olsson S.E. "On the etiology and pathogenesis of hip dysplasia: a comparative review." J Small Anim Pract. 1966;7:673-687.

  18.  Smith G.K., Biery D.N., Gregor T.P. "New concepts of coxofemoral joint stability and the development of a clinical stress radiographic method for quantitating hip joint laxity in the dog." <em em assoc.< med vet am j>1990 January 1;196(1):59-70.

  19.  "Coxofemoral joint laxity." Pp.1021-1042.

  20.  Morgan S.J. "The pathology of canine hip dysplasia." Vet Clin N.Am Sm Anim Pract. 1992 May;22(3):541-50.

  21.  Alexander J.W. "The pathogenesis of canine hip dysplasia." Vet Clin N.Am Sm Anim Pract. 1992 May;22(3):503-11.

  22.  Greisen H.A., Summers B.A., Lust, G. "Ultra Structure of the Articular Cartilage and Syunovium in the Early Stages of Degenerative Joint Disease in Canine Hip Joints." Am J Vet Res. 1982; 43:pp. 1963-1971.

  23.  Distl O., Grussler W., Schwarz J., Karusslich H. "Analyse umweltbedingter un genetischer Einflusse auf die Haufigkeit von Huftgelenksdysplasie beim Deutschen Shaferhund." ("Analysis of environmentally conditioned and genetic influences on the frequency of hip joint dysplasia in German Shepherd Dogs"). Zentralbl Veterinarmed A. 1991 Jul;38(6):460-71.

  24.  Mackenzie S.A. "Inheritance of temperament and hip dysplasia scores in German Shepherd Dogs." 1984 March; Dissertation Abstracts International-B 44/09, p.2652.

  25.  Potscher L.A. "Selektion gengen hueftgelenksdysplasies (HD) in einer Hovawart population" ("Selection criteria concerning hip dysplasia (HD) in a Hovawart population.") 1993 Winter; Dissertation Abstracts International-C 54/04, p.1069.

 Canine Hip Dysplasia Part III

The authors assess the pros and cons of standard diagnostic methods for hip dysplasia
By John C. Cargill, MA MBA, MS and Susan Thorpe-Vargas, MS

 

This article is the third in an eight-part series on canine hip dysplasia (CHD). What follows is written from the perspective that the readers of the series are conscientious breeders who are the guardians of the genetic pools that constitute their breeds. While this series of articles will not replace a stack of veterinary medical texts, it is a relatively in-depth look at the whole problem of canine hip dysplasia. Furthermore, the series is designed to be retained as a reference. When you finish reading it you will have a sufficient background to make rational breeding choices and will be able to discuss the subject from an informed basis with your veterinarian. You may not like what you read, but you will be more competent to deal with the problem.

Conclusions from Part I:

Genetics is the foremost causative factor of canine hip dysplasia. Without the genes necessary to transmit this degenerative disease, there is no disease. Hip dysplasia is not something a dog gets; it either is dysplastic or it is not. An affected animal can exhibit a wide range of phenotypes, all the way from normal to severely dysplastic and functionally crippled. Hip dysplasia is genetically inherited.

Conclusions from part II:

 While environmental effects, to include nutrition and exercise, may play a part in mitigating or delaying the onset of clinical signs and clinical symptoms, hip dysplasia remains a genetically transmitted disease. Only by rigorous genetic selection will the incidence rate be reduced. In the meantime, it makes sense to have lean puppies and to avoid breeding animals from litters that showed signs of hip dysplasia. It is probable that even normal exercise levels may increase the phenotypic expression of CHD of a genetically predisposed dog. Stay away from calcium supplementation of any kind; all it can do is hurt. There is no conclusive evidence that vitamin C can prevent hip dysplasia, but there is some evidence that vitamin C may be useful in reducing pain and inflammation in the dysplastic dog.

Part III:

This third article deals with the abnormal hip and how to diagnose it. Though CHD can afflict all breeds, it is more common in the large and giant breeds. There is far more to a proper diagnosis than first meets the eye. Anecdotal evidence has shown that canine hip dysplasia is one of the most over-diagnosed and misdiagnosed problems afflicting dogs. Many clinicians may depend too often on only subjective radiographic interpretation in the diagnosis of CHD. Physical examination techniques are helpful, and one can often pick up on concurrent conditions that could be otherwise overlooked. Initially, this article will focus on the clinical signs of hip dysplasia, the specific methods used by the experienced practitioner to make the diagnosis and the problems associated with the classic hips-extended, Orthopedic Foundation for Animals-approved X-ray positioning for radiographic study. The latter part of the article will be devoted to important new developments that hold promise for predicting the probability of phenotypic expression of CHD.

In the second article in the series, we said that canine hip dysplasia can be conveniently categorized into two major types. The first is severe and is seen early in the afflicted dog�s life. The second, and far more common type, is the insidious chronic form that develops over a period of time. It is therefore useful to separate dogs by age classification when describing the clinical signs of hip dysplasia. A reasonable classification that takes into account maturity, puberty and attaining adult height, if not near adult weight, would be dogs less than one year in age and those more than one year in age. This gives time for atrophy and extraordinary musculature to develop as clinically recognizable signs. In the young dog, the first symptoms appear to be decreased activity, sometimes accompanied by joint pain. 1 If a young dog is found to have a swaying or unsteady gait, or runs with both hind legs moving together - often referred to by breeders as the "bunny hop" - it is worth further investigation. Acute episodes of lameness with both or only one side affected can also occur after exercise or minor trauma. These signs can also be the result of infections in joints, lack of synovial fluid or the result of trauma. As CHD progresses, the dog may also have difficulty rising from a lying or sitting position and will frequently balk at going up or down stairs.

TYPE OF MOVEMENT

RANGE IN DEGREES

Flexion

From Neutral to 70 to 80

Extension

From Neutral to 80 to 90

Adduction

From Neutral to 30 to 40

Abduction

From Neutral to 70 to 80

Internal Rotation

From Neutral to 50 to 60

Internal to External

From Neutral to 80 to 90

Two clinical signs that most often appear together in the older dog are well-developed muscles in the forelimbs and shoulders due to shifting weight forward. As the disease progresses, hypertrophy (over-development) of the front end is accompanied by symmetrical or non-symmetrical atrophy of the pelvic muscles. Such animals appear weak in the pelvic region, are reluctant to exercise, generally prefer sitting to standing and exhibit extreme discomfort when their forelimbs are lifted off the ground.

RADIOGRAPHIC
METHOD

SCORES

TYPE OF
SCORING

TYPE OF
SCALE

7 Point Scale(OFA)

Excellent

Good

Fair

Borderline

Mild-HD

Severe-HD

Subjective

Oridinal

3 Point Scale

Normal

Borderline

Dysplastic

Subjective

Oridinal

Norberg Angle (NA)

Tight hip > 105 degrees

Loose Hip <90 degrees

Quantitative

Interval

DJD Score

DJD Absent

NA

DJD Present

Subjective

Oridinal

Distraction Index

Index = 0 Tight Hip

NA

Index = 1 Loose Hip

Quantitative

Interval

         

Remember also that the affected dog may exhibit none of these symptoms. A substantial number of dogs with radiographic signs of hip dysplasia show no clinical signs of the disease. Explanations of this phenomenon are as varied as they are controversial. Quite a few practitioners believe that a dog radiographically positive for hip dysplasia but clinically negative for signs is just a dog in an intermediate stage of the disease progression. This period may last for months, even years, until the onset of substantial degenerative joint disease. It is not uncommon for an afflicted (genetically predisposed) dog to die of old age before any non-radiographic signs develop.

We repeat again the warning issued in the preceding articles: You cannot tell if a dog is genetically predisposed to hip dysplasia by its movement. Reject the false wisdom of the old-time breeder who emphatically states that if his or her dogs had hip dysplasia he or she would be able to see it. Hip dysplasia is a polygenic, multifactorial disease.

Before a definitive diagnosis of CHD can be made, other problems must be ruled out. 3 Thorough medical, orthopedic and neurological examinations must be made in order to rule out other disorders of the hip and spine. Multiple joint involvement may be the case. The following is a condensed list of some of the more common conditions that mimic or may be concurrent with canine hip dysplasia:

  • Physical disorders of the stifle-ruptured or torn cranial cruciate ligaments; luxating patellae; meniscus tears in the knee.
  • Diseases of the joints-rheumatoid arthritis; metabolic bone disease; polyarthritis from Lyme and other infectious disease; panosteitis (bone inflammation).
  • Nutritional bone disease-chronic subclinical scurvy.
  • Spinal disorders-ruptured vertebral disease; degenerative spinal disease; lumbosacral instability.
  • Neurological conditions-trauma; poisoning (lead, etc.);infections; neural lesions; proprioception (posture sense).

An example of another condition masquerading as hip dysplasia is the all-too-common spinal degenerative myelopathy in German Shepherd Dogs. After reading the preceding list, you should realize that CHD is not an easy condition to diagnose with great surety unless a full examination is conducted. If you do not find radiographic signs, that still does not preclude some of the problems mentioned above.

Dr. William Inman a clinician in Washington state feels that canine hip dysplasia is the most over-diagnosed and misdiagnosed condition in the veterinary medical practice. 4 While he feels that hip dysplasia is genetically predisposed, he remains puzzled by finding in his practice clinically dysplastic dogs with radiographically normal hips and symptom-free dogs with coxofemoral joints that look "like a bomb went off in them." Inman states, "Curiously, in all the young dogs we see with hip dysplasia signs in the 5 to 18-month range, we always find a subluxation at T8-T10 [dislocation of the Thoracic vertebra 8 through Thoracic vertebra 10]." This is a potentially important finding because the T8 to T10 area "innervates the peraspinal muscles and the iliopsas muscle, which attaches to the femoral head and pulls it forward. Subluxation leads to muscle spasming, which causes continued anterior traction of the femur on the hip socket, flattening the joint�reduction of this subluxation reverses the progression of hip dysplasia by curing the musculo-skeletal dysfunction." Inman has relieved the symptoms of more than 3,500 dogs with his procedure.

The conclusion that Inman has drawn from his practice is that the T8-T10 subluxation is a physical condition that, unless dealt with immediately, will progress to the joint capsular fibrosis and muscle stricture associated with decreased range of motion. The subsequent skeletal changes that follow can only be addressed surgically. He recommends early intervention in dogs thus afflicted to halt this insidious process.

Inman�s theory appears radical, but it is not contrary to the concepts previously presented. He does not maintain that a genetic disease is not associated with hip dysplasia, only that a misdiagnosed physical condition mimics the disease process. Thus, the incidence of CHD may be lower than previously thought by other researchers.

Given that many other processes may be at play, the following are some of the physical techniques used in the diagnosis of CHD. While a tentative diagnosis can be made on the basis of history, clinical signs and the various palpation methods, standard veterinary practice requires radiographic signs of CHD. Diagnostic methods fall into two general categories: subjective and quantitative. We have found no method, subjective or quantitative, that is without its detractors or without serious controversy.

Subjective Methods of Diagnosis

Observation. The first step in the diagnosis of a suspected case of CHD is orthopedic examination, which should include observation of the dog at rest, walking, running and a re-examination of the dog the day following vigorous exercise.5, 6 Observation and neurologic examination should be conducted before administering any drugs, and especially before sedation or general anesthesia, which can significantly alter the dog�s neurologic status.

Range of motion. In an anesthetized dog, the coxofemoral joint�s range of motion is approximately 110 degrees. 7 With pathology, this range of motion can be reduced to as little as 45 degrees. When following a chronic patient, the clinician uses changes in the range of motion to quantify the progress of the disease and as an aide when determining treatment options. Figure 1 is a table of the clinical categories by range of motion.

Changes in gait patterns. A shortened length of stride is associated with a loss in range of motion. There is a considerable variance among animals, but as a general rule, shortened stride length does not appear until fully extended movement is painful for the dog. This is the case with severe degenerative joint disease. Similarly, this type of gait abnormality can occur if the joint capsule has become fibrous. The many shapes and sizes of dogs make it impossible to describe all the potential gait changes. However, the bunny hop, left to right shift of the pelvis or an elliptical swing of the leg and hip are common gait problems encountered.

Forced extension. Affected dogs will not only exhibit discomfort with forced extension of the hip, but will try to return the limb to a more relaxed position. Depending on the temperament of these animals, they may also vocalize or exhibit aggressive behavior in response to pain. Be aware that the fighting dogs and the Northern breeds tend to have high pain tolerance levels and are generally stoic with respect to pain.

Downward pressure on the rear limb. When force is applied to the hips of a standing animal, the affected animal will show little or no resistance to the pressure, and will assume a sitting position. Several factors may simultaneously be involved and interrelated, such as pain, muscle weakness or atrophy.

Palpation. In humans, the most popular and reliable palpation maneuver used to identify congenital dislocation of the hip determines the presence or absence of the Ortolani sign. "A positive Ortolani sign confirms the diagnosis of coxofemoral subluxation in newborns prior to development of clinical signs or radiographic changes." 8 Many veterinarians feel that the techniques have too much subjectivity and variance to be of much use. Nonetheless, the Ortolani sign still figures prominently in the literature. 9-14 Animals to be examined must be anesthetized past the point where there is still a palpable response. Two basic approaches are used: dorsal recumbency and lateral recumbency, with dorsal recumbency being preferred for large dogs. Downward pressure is applied down the axis of the femur until the femoral head subluxates. The leg is slowly abducted while holding the stifle firmly. If the joint is loose, a distinct clicking may be felt and in some cases will be audible.

Other palpation methods have been proposed by Barlow and Bardens. 15,16 Barlow�s Sign is essentially the first half of the Ortolani Test. Downward axial pressure is applied on the femur without abducting the leg. The Bardens� Test places the dog on its side, and the leg is held perpendicular to the spine. Lifting pressure is applied to the femoral shaft without abduction. The examiner�s finger is placed on the greater trochanter. Any movement of the finger by more than one-fourth inch is considered a positive sign for a loose joint. Palpation has shown diagnostic use in human neonates, but is controversial and may have little diagnostic or prognostic utility in the dog. A caution: In human infants, it has been suggested that repetitive Barlow tests, and presumably Ortolani and Bardens as well, are capable of making infant hips unstable, thus giving a false-positive result. 17

The Neurologic exam. During a normal physical examination, the clinician will observe both the posture and movement of the dog. Of the two observations (gait and posture), how the animal stands or its ability to return to a normal stance tells more about the neurological status. Some breeds have been selectively bred for a characteristic gait. Thus gaits may vary tremendously among breeds. A Borzoi moving as a Bulldog would be one sick Borzoi. A poor postural response may indicate a proprioceptive deficit.

Proprioception, or posture sense, is the ability to recognize the location of limbs in relation to the rest of the body without visual clues. An abnormally wide stance is one indication of a possible problem. The simplest method of evaluation is to bend the paw so the back of the foot is bearing the dog�s weight. The normal response is to immediately reposition the paw correctly. A problem in proprioception positioning is often an early indication of neurological problems, and most often precedes motor dysfunction (gait anomalies).

When evaluating the dog specifically for hip dysplasia, one needs to rule out deficits in the spinal-reflex arc. An example of the spinal-reflex arc where the neural response is not transmitted to the brain but returned (arcs back) is the familiar tap on the knee with a rubber hammer. (The neural response travels from the muscle to the spine and returns to the muscle, without traveling to the brain.) The absence of an involuntary response or an exaggerated response are indications of neurologic problems. Some variance among breeds is noted, as large dog responses tend to be less rapid than those in smaller breeds.

Routinely, the "knee jerk" (quadricep reflex) is tested first with the normal reaction being a single quick extension of the stifle. Next, the flexor reflex is evaluated by gently pinching the toes. The normal dog should pull the entire limb (hip, stifle and hock) up toward the belly. Although not strictly analogous, the extension toe reflex has been compared to the Babinski reflex in humans. The examiner will hold the hock and gently stroke the back surface from the hock down toward the pad. The normal animal will either exhibit no response or a slight flexion of the toes. The abnormal reaction is the extension and spreading of the toes. These tests, by no means comprehensive or exhaustive, constitute the minimal examination to rule out spinal problems in a dog being evaluated for hip dysplasia. 18

Subjective Diagnostic Radiographic Methods

Hip-extended radiographic method. This traditional X-ray position has been the standard position, which has the dog sedated, on its back, with legs fully extended and patella facing upward, became the standard of the American Veterinary Medical Association Panel on Hip Dysplasia in 1961, and was adopted by the Orthopedic Foundation for Animals in 1966. University of Pennsylvania studies have been conducted that show interpretations are not highly consistent among radiologists, and are not highly consistent when the same radiologist reads the same deck of X-rays in shuffled order.19 OFA scores (excellent, good, fair, borderline, mild, moderate and severe) have wide acceptance but as subjective interpretations not readily repeatable with the same animal , nor likely to be interpreted consistently by different radiologists. At first it appeared that the seven-point scale was more discrete than diagnostic protocol warranted. When the seven-point scale was collapsed to a three-point scale (normal, borderline, dysplastic) agreement improved. The hips-extended positioning has come under criticism because it masks joint laxity. This positioning masks joint laxity in two ways both involving the joint capsule. With the hip extended, the fibers of the joint capsule tighten in such a way as to push the femoral head into the acetabulum. This position also leads to a lowering of the intra-articular pressure, which combined with the fixed synovial fluid volume causes invagination of the joint capsule. These two conditions limit the amount of sideways movement of the femoral head. Similarly, unsedated positioning may further mask joint laxity.

Norberg Angle method. The Norberg Angle radiographic method of determining joint laxity (subluxation) has been used more in Europe than in the United States. The standard OFA hip-extended radiographic projection is used (see figure 3). Norberg angles typically range from 55 degrees to 115 degrees, with the smaller numbers representing looser hips. Unfortunately, there is no common agreement as to what constitutes a normal angle, though 105 degrees may be used as a point estimate for normal joint laxity. Correlation with OFA interpretations is poor, which is one reason the Norberg Angle method is not well accepted as a diagnostic tool and is considered subjective at this time.

Quantitative Diagnostic Radiographic Method

Compression/Distraction method. This new stress radiographic method originated at the University of Pennsylvania School of Veterinary Medicine and is currently marketed by PennHIP�. What started as a look at the role of passive hip laxity in CHD has become a quantitative diagnostic protocol referenced to an extensive data base. In recent years joint laxity has been established in the literature as prognostic for degenerative joint disease. Initially, however little statistical evidence supported this contention. Now that a major data base has been developed for purposes of comparison and for determining probabilities, joint laxity can be used as an indirect variable with which to predict the probability of eventual phenotypic expression of CHD.

Unfortunately for breeders, deep sedation is required in the compression/distraction method. The traditional OFA positioning was found inadequate. In the stress radiographic method, the dog is laid on its back with its hips at a neutral flexion/extension angle. A compression view is taken with the femoral heads seated tightly in the acetabula congruency between the two joint surfaces. A second, or distraction, view is taken showing the maximum separation distance of the femoral head center from the acetabular center A special device is used to force the femoral head away from the acetabulum for the distraction view. This protocol has been shown at University of Pennsylvania to reveal 2.5 times more joint laxity than the standard hip-extended radiograph.

The power of this method lies both in the new positions and in the statistical significance of the compression index (CI) and the distraction index (DI) as supported by a data base. 20 The indices range from 0 to 1, with "0 being a fully congruent hip (as seen in the compression radiographic view) and 1 representing the most extreme joint laxity as might be seen in the distraction view of hips that are virtually luxated." 21 The OFA scoring method is an ordinal scale, the Norberg Angle method is an interval scale and the DI is a ration scale. Thus the DI is intuitive in its meaning: A hip with a DI of 0.5 has twice the laxity of a hip with a DI of 0.25. Similarly a DI of 0.5 can be thought of as a hip 50 percent luxated. The DI ratio scale is far more useful a rating than the Norberg Angle. See figure 2 for a comparison of scales.

Breeders are always looking for earlier detection of CHD, the earlier the better for determining which animals to keep and classify as show and breeding hopefuls. Compression and distraction evaluations have been done on a sample of 8-week-old German Shepherd Dog puppies without the results being conclusive. At 16 weeks, this method becomes useful. Dr. Gale Smith, et. al., at the University of Pennsylvania Hip Improvement Program (PennHIP) recommended that dogs not be evaluated before 16 weeks and that follow-up radiography should be done at 6months or 1 year of age. 22 In later articles in this series we will address the utility of the PennHIP protocol for prognosis.

Genetic (blood-based) diagnostic test. At this time, no biomechanical or metabolic differences have been identified in the dysplastic dog. Extensive work continues for an early blood marker for the condition. Finding such a marker would be ideal, as it would both allow the breeder to definitively screen breeding stock, and help the clinician identify appropriate treatment protocols. Parallel work is being done in determining genetic factors in humans for rheumatoid arthritis and osteoarthritis. Restriction Fragment Length Polymorphism (RFLP) linkage analysis has been used to identify genes associated with those diseases. Since there appears to be a strong genetic base for CHD, restriction fragments in the white blood cell DNA should correspond to the dysplastic phenotype. 23, 24

Conclusions: Canine Hip Dysplasia can be difficult to diagnose. Other orthopedic, neurological, autoimmune/infection and metabolic problems may mimic CHD or may be concurrent with CHD. Numerous palpation techniques (Ortolani, Bardens, Barlow) have been proposed; however, they remain subjective nonquantitative methods that rely heavily on the skill of the clinician. The standard in current veterinary practice is to confirm CHD radiographically. The traditional American Veterinary Medical Association and Orthopedic Foundation for Animals hip-extended radiographic view distorts the amount of joint laxity present by forcing the femoral head deeper into the acetabular cup, thus understating the amount of laxity present. University of Pennsylvania (PennHIP) protocols for stress radiography are coming to the forefront as a more definitive way of visualizing hip joint laxity. Canine hip dysplasia remains a polygenic, multifactorial disease.

The next article in this series will discuss the various hip dysplasia registries, their approaches to the problems of canine hip dysplasia and the importance of having a "tamper-proof" identification system.

CREDITS

 References

1.        Bardens JW Hardwick H. "New Observations on the diagnosis and cause of hip dysplasia." Vet Med Small Anim Clin,63:238, 1968.
2. Bar ARS, Denny HR, Gibbs C. "Clinical hip dysplasia in growing dogs: The longterm results of conservative management." J Sm Anim Pract,28:243, 1987.
3. Brinker WO, Peirmattei DL, Flo GL. "Physical examination of lameness." In Handbook of Small Animal Orthopedics and Fracture Treatment, ed 2. Philadelphia, WB Saunders, 1990, p. 267.
4. Personal communication with Dr. William Inman, Lake City Animal Hospital, 13045 Lake City Way N.E., Seattle, WA 98125; (206)362-0909.
5. Brinker WO, Peirmattei DL, Flo GL. "Physical examination of lameness." In Handbook of Small Animal Orthopedics and Fracture Treatment, ed 2. Philadelphia, WB Saunders, 1990, p. 341.
6. Lust G, Rendano VT, Summers BA. "Canine hip dysplasia: Concepts and diagnosis." J Am Vet Med Assoc, 187:638, 1985.
7. Riser WH, Newton CD. "Canine hip dysplasia as a disease." In Bojrab MJ (ed). Pathophysiology in Small Animal Surgery.Philadelphia, Lea & Febiger, 1981, p. 618.
8. Chalman JA, Butler HC. "Coxofemoral joint laxity ant the Ortolani sign." J Am Animal Hosp Assoc, 21:671, 1985.
9. Fry TR, Clark DM. "In canine hip dysplasia: Clinical signs and physical diagnosis." Vet Clinics No Am Sm Anim Prac, Vol 2, No. 3, pp., 554-557, 1992.
10. Ibid.
11. Ortolani M. "The Classic: Congenital hip dysplasia in the light of early and very early diagnosis." Clin Orthop, 119;6-10, 1976.
12. Bardens JW. "Palpation for the detection of dysplasia and wedge technique for pelvic radiography." In proceedings, 39th Annual Meet Am Anim Hosp Assoc 1972;468-471.
13.Wright PJ Mason TA. "The usefulness of palpation of joint laxity in puppies as a predictor of hip dysplasia in a guide dog breeding programme." J Smal Anim Prac, 1077;18:5513-5522.
14. Dixon RT. "Some experimental observations of the detection and demonstration of coxofemoral subluxation in the dog." Aust Vet Prac, 1975;55:220-226.
15. Bardens JW Hardwick H. "Observations on the diagnosis and cause of hip dysplasia." Vet Med Small Anim Clin,63:238-245, 1968.
16. Barlow TG. "Early Diagnosis and treatment of congenital dislocation of the hips." J. Bon Joint Surg, 44-B:292-301 1968.
17. Fry TR, Clark DM. "In canine hip dysplasia: Clinical signs and physical diagnosis." Vet Clinics No Am Sm Anim Prac, Vol 2, No. 3, pp., 554-557, 1992.
18. Oliver JD, Lorenz MD. Handbook of Veterinary Neurology. 1993,W.B. Saunders, pp. 3-45.
19. Smith GK, Gregor TP Biery DN et al. "Hip dysplasia diagnosis: a comparison of diagnostic methods and diagnosticians." Proceedings of the 1992 Annual Scientific Meeting of the Veterinary Orthopedic Society, Keystone, CO, 1992, p.20.
20. Smith GK Biery DN Gregor TP. "New concepts of coxofemoral joint stability and the development of a clinical stress-radiographic method for quantitating hip joint laxity in the dog." i>J Am Vet Med Assoc, 1990; 196:59-70.
21. Smith GK. "Diagnosis of Canine Hip Dysplasia." Adapted from Smith GK: Current Concepts in the Diagnosis of Canine Hip Dysplasia, in Bonagura JD (ed): Kirk�s Current Veterinary Therapy XII: Small Animal Practice. Philadelphia, W.B. Saunders, 1995, p. 16.
22. Ibid, p.18.
23. Sinha AA Lopez MT, McDevitt HO. "Autoimmune diseases: The failure of self tolerance." Science, Vol. 248, June 15, 1990, pp. 1380-1387.
24. Tod JA, Acha-Orbea H, Bell, Chao N, Froneck Z, Jacob CO, McDermott M Sinha AA, Timmerman L, Steinman L, McDevitt HO. "A molecular basis for MHC Class II-Associated Autoimmunity." Science, Vol. 240, May 20, 1988, pp. 1003-1009. 

Canine Hip Dysplasia Part IV

 The Role of Orthopedic Registries in Fighting Canine Hip Dysplasia; Registries, although essential in documenting CHD, have not been used to their full potential. By John C. Cargill, MA MBA, MS and Susan Thorpe-Vargas, MS

 This article is the fourth in an eight-part series on canine hip dysplasia (CHD). What follows is written from the perspective that the readers are serious and conscientious breeders who are the guardians of the genetic pools that constitute their breeds. While this series of articles will not replace a stack of veterinary and medical texts, it is a relatively in-depth look at the whole problem of canine hip dysplasia. Furthermore, the series is designed to be retained as a reference. When you finish reading this series, you will have a sufficient background to make rational breeding choices and will be able to discuss the subject from an informed basis with your veterinarian. You may not like what you read, but you will be more competent to deal with the problem.

Conclusions from part I:

Genetics is the foremost causative factor of canine hip dysplasia. Without the genes necessary to transmit this degenerative disease, there is no disease. Hip dysplasia is not something a dog gets; it is either genetically dysplastic or it is not. An affected animal can exhibit a wide range of phenotypes, all the way from normal to severely dysplastic and functionally crippled. Hip dysplasia is genetically inherited.

Conclusions from part II:

While environmental effects, to include nutrition and exercise, may play a part in mitigating or delaying the onset of clinical signs and clinical symptoms, hip dysplasia remains a genetically transmitted disease. Only by rigorous genetic selection will the incidence rate be reduced. In the meantime, it makes sense to have lean puppies and to avoid breeding animals from litters that showed signs of hip dysplasia. It is probable that even normal exercise levels may increase the phenotypic expression of CHD of a genetically predisposed dog. Stay away from calcium supplementation of any kind; all it can do is hurt. There is no conclusive evidence that vitamin C can prevent hip dysplasia, but there is some evidence that vitamin C may be useful in reducing pain and inflammation in the dysplastic dog.

Conclusions from part III:

Canine hip dysplasia can be difficult to diagnose, as a number of other orthopedic neurological, autoimmune and metabolic problems may mimic it. Controversy surrounds the question of positioning for hip X-rays and what part joint laxity plays in hip dysplasia. Hip dysplasia may be more common in large and giant breeds and is one of the most over-diagnosed and misdiagnosed conditions.

Part IV:

In this article we address the issue of orthopedic registries. Given the widespread incidence of canine hip dysplasia, registries are not just nice to have; they are essential until we have a DNA or other genetic test available for screening and breeding.

The name of this article might well have been titled "Hip Dysplasia: The Controversy." We find that the various registries and the various diagnostic bodies have their own separate agendas, much of which seem to be mutually exclusive. The reader must understand that there are few definitive answers concerning hip dysplasia, and those that are more definitive than others are so only through the power of statistics and at the expense of the other theories. Generally accepted practices, and widespread acceptance of many popular beliefs and status of a given registry, seem to have little scientific basis.

The reality is this: Canine hip dysplasia is a polygenic and multifactorial disease that is closely associated with selection for breeding. There is a host of entrepreneurs ready in the wings, or already established, with many a system of registry or diagnostic and identification method to purvey to the dog breeder. The chaff greatly outnumbers the wheat. The focus of this article is to examine several registries, their practices, their strong points and their shortfalls. In so doing, we recognize we will be speaking unfavorably about some well-established "cash cows" from which many draw their livelihood. We recognize that along with "God, Country and Corps" there is the American Kennel Club, the Orthopedic Foundation for Animals and each of the breed clubs. In this article we will be taking several sacred institutions to task.

The AKC�s Stance

The traditional stand of the AKC is that it is a registry for purebred dogs of breeds that have petitioned through their breed clubs to have their stud books accepted. The AKC has resisted requests to perform the wider task of registering the results of genetic screening, leaving that matter up to the breed clubs. A bench championship means no more than your dog amassed the necessary 15 points with two majors in shows sanctioned by the AKC. The "you breed them, we register them" mentality means that there is no warranty, expressed or implied, that such animals are fit for any task, function or for breeding. It is possible to register an animal that is a carrier or which is phenotypic for any genetically transmittable disease. So if the AKC in the United States is not going to stand for genetic screening, who is? The AKC has suggested that since the breed clubs set their rules and standards, they should also set the rules for their breeds genetic screening. This is what is done in Germany, for example. As of this writing, our attempts to discuss this stance with the AKC have gone unanswered.

The Role of OFA

The grandfather of orthopedic registries in the United States is the powerful and prominent Orthopedic Foundation for Animals. Beyond a shadow of a doubt, the OFA is the world�s largest all-breed orthopedic registry with more than 475,000 cases from 221 breeds on file evaluated between January 1, 1974 and January 1, 1995. 1

Your vet anesthetizes your dog, shoots the X-rays in the hip-extended, American Veterinary Medical Association-approved position, and the film is sent to OFA for evaluation by three veterinary radiologists. These OFA-licensed veterinary radiologists evaluate the film based upon the hip-extended position. Your vet collects a fee; OFA collects a fee; if the hips pass, you get a number. This is the number much like an AKC registration number. The AKC number has so little value that the Canadian government does not currently allow importation of commercially bred dogs under the age of ten months if the dubious claim is made that because they are AKC-registered they are purebred. AKC registration is based on the honor system, and not all breeders or puppy mills have been honorable. The AKC is a cash cow catering to the puppy mills and breeders from which they draw significant revenue. The AKC has announced it is putting OFA numbers on registrations. Thus, for a little bit-or not so little bit-of money you can have two numbers of dubious value associated with your dog. This is only where the hip dysplasia controversy begins, not where it ends.

The problem with many closed(confidential) orthopedic registries is that they can become self-serving, self-selecting and, if they pass the test of time, self-perpetuating. While we authors have both separately done preliminary X-rays on young dogs, and later sent in X-rays for formal evaluation by a registry both in the United States and in Europe, we also have not bothered to spend money for formal evaluation when the local preliminary evaluation was "junk." We suspect that this is more common than not. We suspect that more dysplastic dogs are not evaluated by a registry than those that are. As we shoed in the earlier articles in this series, when a disease is polygenic and multifactorial, the best possible prediction is made by knowing about parents, siblings and progeny. 2 Here is where most registries fall down. There is no requirement for filing of pedigrees and having all get in a litter evaluated. The OFA position is that the frequency of hip dysplasia in the general population is not that essential to know, but the frequency in the breeding population is. 3 The premise is that:

  1. Occurrence of HD in the progeny is significantly less when both parents are considered phenotypically normal. The reduction in occurrence of HD is even greater if there is pedigree depth and breadth for normal animals.
  2. Occurrence of HD in the progeny significantly increases when normals are mated with dysplastics and increases even more when dysplastics are mated with dysplastics.4

Taking a priori (beforehand-speculation) approach, one would predict that if a fledgling registry became established and self-perpetuating, it would be used for demonstrating that a given animal was in fact sound at the time of evaluation. Thus, the self-selection process would predominate, the percentage of animals with "excellent" hips would increase over time and the percentage of dysplastic animals would decrease. This has been the case with the OFA registry.5 All it means is that the registry is now catering to owners who wish to demonstrate the soundness of some of their dogs. Before OFA, there was no good public vehicle for doing this. Unfortunately, soundness of an individual animal means little genetically. One needs to know the soundness of siblings, parents and siblings of the parents. Unfortunately, hips which are sound at 24 months of age may be dysplastic later in life. The chronic (most common) form of hip dysplasia is insidious and may not show up radiographically for some time; however, radiographic signs are usually in evidence by 12 months of age.

Has OFA Reduced Dysplasia?

Perspective in understanding this phenomenon is necessary if one is to draw appropriate conclusions about correlation and causation. The question before the dog fancy is whether OFA has in any meaningful manner contributed to the reduction of hip dysplasia. The answer is a resounding "No." Each year more than 2 million new dogs are registered with AKC. Over the period January 1974 to January 1995, this amounts to 40 million dogs. OFA evaluated only 475,000 dogs. This amounts to about 1 percent of the new dogs registered. The modest decrease in the self-selected dysplastic evaluations is but a drop in the bucket compared with the number of new AKC registrations. Thus the impact of the registry on hip dysplasia has been negligible.

A quick survey of various breed publications reveals that some breed followers are very much into thyroid and von Willebrand�s tests and OFA and Canine Eye Registration Foundation (CERF) registry of hips and eyes, respectively. On the other hand, followers of other breeds are reluctant to advertise such results. Hip dysplasia is with us now as it was before. What we have been doing is not the answer. Until the time that provisional non-breeding registrations are given, and until proof is presented of the animal being clear of hip dysplasia, it is doubtful that the situation will much change. There have been limited efforts by breed clubs to reduce problems, but the examples are few and far between. Two stand out immediately for their success: When achondrodyplasia (dwarfism) was recognized in the Newfoundland, the parent club took immediate steps to require test breedings based upon pedigree research and virtually eliminated the problem within a few generations. 6 Similarly, the Malamute club is having success in ferreting out dwarfism and eliminating it from the gene pool. Without grassroots action by parent clubs supported by policies of the main registry (AKC), little can be expected. 7-14

Dysplasia Testing Abroad

In Germany, as in Japan, the breed clubs are very powerful and dictate to their members pretty much how things are going to be. Using Rottweilers in Germany as an example, pups are tattooed in their right ears at 8 weeks by a "breed warden." At 18 months of age they are X-rayed by a veterinarian licensed by the breed club, and the X-rays are interpreted by veterinary radiologists at the university clinic at Gottingen, also licensed by the breed club. The breed club then maintains a registry of the results. Currently, three ratings are given: HD free, HD+/-, and HD+, with the Norberg Angle used in making the determination. Progeny can only be registered from animals rated HD free or HD+/-.

By way of contrast, the Hovawart breed club follows a similar process of using club-licensed veterinarians to take the X-rays and to interpret them. However, only progeny from HD free parents are admitted to the registry. Remember, the subjectivity of legs-extended X-ray determinations and the lack of correlation between OFA and the Norberg Angle. 15

Persons we have interviewed report there have been instances where animals that scored well in Germany did less well under OFA scoring and vice versa. In the United Kingdom, the British Veterinary Association got together with the Kennel Club. English breed clubs were encouraged to establish standards for their own breeds and several have. However, in the absence of such a breed standard (and most clubs have not established a standard), the system is this: The lower the score, the less the degree of hip dysplasia. The minimum score for each hip is 0 and the total score of 0-4 with not more than 3 for one hip may be regarded to the "pass certificate" of old. A score of not more than 6 for one hip equates to a "breeder�s letter" under the old system. 16

The scores are derived by deducting points corresponding to faults differing from a concept of perfect hips. From the limited experience author Cargill has had with only one dog (Ch. Kobu�s K.O.) having been evaluated under both the OFA and BVA/KC systems, and they appear to be comparable. An OFA "excellent" or "good" should still show up as a score less than 8 in England, consistent with the subjectivity of interpretation discussed in the third article in this series. The British Veterinary Association informs the Kennel Club periodically of registered dogs that have obtained a score of 8 or less, with not more than 6 on one hip, and their names are published in the Kennel Gazette, the official publication of the Kennel Club.

The Question of Joint Laxity

Time for more controversy: joint laxity. The findings of research reported in the first three articles of this series indicate that hip dysplasia may be predicted by joint laxity determined through stress radiography. 17-23 The OFA rejects this hypothesis on the basis of "lack of standard pressure for the fulcrum and lack of pathologic evidence of secondary changes." 24 Thus the conclusion drawn concerning the efficacy of joint laxity measurements made from stress radiography (as being propounded by Penn-HIP/ICG) being prognostic indicators of future phenotypic expression of canine hip dysplasia are rejected out of hand by OFA. Both OFA and Penn-HIP/ICG claim the other�s methods are subjective and not reliable as predictors of future phenotypic expression of hip dysplasia.

Conclusions: Sadly, no breed registry body in the United States requires genetic screening of parents as a prerequisite for litter registration, or even offers a "fitness for breeding" certification. The current registries for hip dysplasia (and other genetically transmitted problems) cover so little of the AKC-registered dog population that their impact so far has been minimal. The tools we need are there. Joint responsibility for failing to use the tools at hand lies with the AKC, United Kennel Club, parent clubs and individual breeders. Until this is done, we, the dog fancy, are wasting our time, and any breed registry body such as the AKC, must be known as a "registry of sick dogs."

The next article in the series will cover the OFA vs. PennHIP controversy, and the requirement and desirability of an evaluation method that is not only diagnostic but also prognostic with an ability to predict the probability of phenotypic expression of hip dysplasia. Hand in hand with these methods goes the requirement for positive identification rather than the honor system currently in place and the concept of "open" genetic registries.

CREDITS

 

References

1.        Corley, E.A., Keller, G.G. "Hip Dysplasia: A progress report and update." 1993 Supplement. Orthopedic Foundation for Animals. p.1.
2. Cargill, J.C., Thorpe-Vargas, S. "Canine Hip Dysplasia Parts I & II." DOG WORLD. May and June 1995.
3. Corley, E.A., Keller, G.G. "Hip Dysplasia: A progress report and update." 1993 Supplement. Orthopedic Foundation for Animals.
4. Ibid.,p.2.
5. Ibid.,p.6.
6. Cargill, J.C. "What should �champion� mean?" DOG WORLD. February 1993. Vol. 78, No. 2, p. 34.
7. Cargill, J.C. "Truth in advertising: breeder self-regulation Part I." DOG WORLD. July 1990. Vol. 75, No.7.
8. Cargill, J.C. "Truth in advertising: breeder self-regulation Part II." DOG WORLD. August 1990. Vol. 75, No.8.
9. Cargill, J.C. "Genetic Screening Essential." Pure-Bred Dogs/Am Kennel Gazette. January 1991, pp.68-72.
10. Jolly, R.D., Dodds, W.J., Ruth, G.R., Trauner, D.B. "Screening for genetic diseases: principles and practice." Adv. Vet. Sci. Comp. Med. 25:245-276, 1981.
11. Dodds, W.J. "Protect the health and longevity of purebred dogs through genetic screening for blood and thyroid diseases." Teaching syllabus. 1988.
12. Dodds, W.J. "Detection of genetic defect by screening programs." Pure-Bred Dogs/Am Kennel Gazette. June 1982. Pp.56-60.
13. Dodds, W.J. "An effective mass screening program for animal models of the inherited bleeding disorders." Prog. Clin. Biol. Res. 94:117-132. 1982
14. Dodds, W.J. "Genetic screening for inherited bleeding disorders. " Kal-Kan Forum. 1:52-28. 1982.
15. Smith, G.K., Gregor, T.P., Biery, D.N., et. al. "Hip dysplasia diagnosis: A comparison of diagnostic methods and diagnosticians." Proceedings of the 1992 Annual Scientific Meeting of the Veterinary Orthopedic Society, Keystone, Colorado, 1992. P.20.
16. British Veterinary Association. New BVA/KC Hip Dysplasia Scoring Scheme. February 1988.
17. Lust, G., Beilman, W.T., Rendanom, V.T. "A relationship between degree of laxity and synovial fluid volume in coxofemoral joints of dogs predisposed for hip dysplasia." Am J Vet Res.1980, 41:55-60.
18. Henricscon, B., Norberg, I., Olsson, S.E. "On the etiology and pathogenesis of hip dysplasia: a comparative review." J Small Anim Pract. 1966;7:673-687.
19. Smith, G.K., Biery, D.N., Gregor, T.P. "New concepts of coxofemoral joint stability and the development of a clinical stress-radiographic method for quantitating hip joint laxity in the dog." J Am Vet Med Assoc. 1990 Jan 1;196(1):59-70.
20. Smith, G.K., Gregor, T.P., Rhodes, W.H., Biery, D.N. "Coxofemoral joint laxity from distraction radiography and its contemporaneous and prospective correlation with laxity, subjective score and evidence of degenerative joint disease from conventional hip-extended radiography in dogs." Am J Vet Res. 1993 Jul; 54(7).pp.1021-1042.
21. Morgan, S.J. "The pathology of canine hip dysplasia." Vet Clin N Am Sm Anim Prac. 1992 May;22(3):541-50.
22. Alexander, J.W. "The pathogenesis of canine hip dysplasia." Vet Clin N Am Sm Anim Prac. 1992 May;22(3):503-11.
23. Potscher, L.A. "Selktion gengen hueftgelenksdysplasies (HD) in einer Hovawart popuulation" [Selection criteria concerning hip dysplasia (HD) in a Hovawart population]. 1993 Winter; Dissertation Abstracts International-C 54/04, p.1069.
24. Corley, E.A., Keller, G.G. "Hip dysplasia: A progress report and update." 1993 Supplement. Orthopedic Foundation for Animals. p.17. 

Canine Hip Dysplasia Part V 

Predicting the Abnormal Hip

An evaluation method is needed that is not only diagnostic but which can predict the probability of canine hip dysplasia. By John C. Cargill, MA, MBA, MS and Susan Thorpe-Vargas, MS

 This article is the fifth in an eight-part series on canine hip dysplasia (CHD). What follows is written from the perspective that the readers are serious and conscientious breeders who are the guardians of the genetic pools that constitute their breeds. While this series of articles will not replace a stack of veterinary and medical texts, it is a relatively in-depth look at the whole problem of canine hip dysplasia. Furthermore, the series is designed to be retained as a reference. When you finish reading this series, you will have a sufficient background to make rational breeding choices and will be able to discuss the subject from an informed basis with your veterinarian. You may not like what you read, but you will be more competent to deal with the problem.

Conclusions from part I:

Genetics is the foremost causative factor of canine hip dysplasia. Without the genes necessary to transmit this degenerative disease, there is no disease. Hip dysplasia is not something a dog gets; it is either genetically dysplastic or it is not. An affected animal can exhibit a wide range of phenotypes, all the way from normal to severely dysplastic and functionally crippled. Hip dysplasia is genetically inherited.

Conclusions from part II:

While environmental effects, to include nutrition and exercise, may play a part in mitigating or delaying the onset of clinical signs and clinical symptoms, hip dysplasia remains a genetically transmitted disease. Only by rigorous genetic selection will the incidence rate be reduced. In the meantime, it makes sense to have lean puppies and to avoid breeding animals from litters that showed signs of hip dysplasia. It is probable that even normal exercise levels may increase the phenotypic expression of CHD of a genetically predisposed dog. Stay away from calcium supplementation of any kind; all it can do is hurt. There is no conclusive evidence that vitamin C can prevent hip dysplasia, but there is some evidence that vitamin C may be useful in reducing pain and inflammation in the dysplastic dog. Fortunately, large doses of vitamin C are readily excreted, but it is still possible to cause untoward side effects with megadoses.

Conclusions from part III:

Canine hip dysplasia can be difficult to diagnose, as a number of other orthopedic neurological, autoimmune and metabolic problems may mimic it. Controversy surrounds the question of positioning for hip X-rays and what part joint laxity plays in hip dysplasia. Hip dysplasia may be more common in large and giant breeds and is one of the most over-diagnosed and misdiagnosed conditions.

Conclusions from part IV:

Sadly, no breed registry body in the United States requires genetic screening of parents as a prerequisite for litter registration or even offers a "fitness for breeding" certification. The current registries for hip dysplasia (and other genetically transmitted problems) cover so little of the American Kennel Club-registered dog population that their impact so far has been minimal. The tools we need are there. Joint responsibility for failing to use the tools at hand lies with the AKC, United Kennel Club, parent clubs and individual breeders.

Part V:

This article will cover the Orthopedic Foundation for Animals vs. PennHIP controversy, the requirement and desirability of an evaluation method that is not only diagnostic but also prognostic with an ability to predict the probability of phenotypic expression of hip dysplasia. Hand in hand with these methods goes the requirement for positive identification rather than the honor system currently in place and the concept of "open" genetic registries in order that genetic pedigree research can be done.

The first four articles in this series have generated many letters. In response, we restate that dogs of any recognizable breed, i.e., non-feral dogs, are inbred on a relatively small number of genes. Each breeding to members of the same breed constitutes continued inbreeding and thus further reduces the gene pool (genetic depletion), thus giving increased probability that recessive traits-desirable and undesirable-will match from each donor and will be expressed phenotypically in their get. We restate that it is desirable to inbreed (and line-breeding is inbreeding) to maintain breed characteristics. Unfortunately, over time this will cause more problems than it will solve, as virtually every dog (and human) carries several defective genes.

Preventing genetic depletion

A basic fundamental fact of genetics is that genetic health decreases with every generation of breeding within a breed. This point must be made very clear. Only 10 to 30 genes distinguish one breed from the next, yet in the dog thousands of recessive and co-dominant genes also become fixed in the genetic makeup of a breed. The only way to prevent genetic depletion and its resultant inbreeding depression is to outcross for hybrid vigor.

The various registries will have to understand the genetics of the situation: To maintain genetic vigor, breeds will have to outcross. In the near term this heretical necessity can be temporarily staved off through restricting stud use, as is being done in some European breed clubs. AKC, in recent years, literally saved the Dalmatian from extinction (nobody wanted a breed of deaf dogs, regardless of other characteristics) by allowing breeding to non-Dalmatians. Similarly in Europe, Dutch Shepherd Dogs were outcrossed with the Belgian Tervuren, and Bernese Mountain Dogs were crossed with Newfoundlands. Some will decry this practice, calling it the blackest of heresy; others will rejoice in the genetic salvation. In the meantime, genetic screening and open registries of genetic traits could allow the identification and breeding to the least genetically related animals in a breed�s gene pool.

"therefore, the breeder controls the occurrence of hip dysplasia in his/her breed."1

This is a quote from a recent memorandum from the OFA to the breed club representatives. So once again breeders must take the blame, yet how many of you have bred an OFA "normal" to another OFA "normal" and still produced dysplastic puppies? Some unscrupulous breeders commit fraud and offer a dog for OFA certification using the papers of another animal,, but most of us are conscientious breeders. We love our dogs and our breed and really want to eradicate this insidious disease.

Orthopedic registries: Hip or hype?

Could something be wrong with the current method of evaluating an animal for hip dysplasia? Where are the scientific papers that prove the efficacy of the OFA diagnostic method? Where are the peer reviews of these papers? From what population data do they base their conclusions?

What is population data? It is a term that statisticians use. It isn�t feasible to check every single dog for a particular condition so one simply checks a sample population. However, to be accurate that sample must truly represent the entire population. It is our contention that the OFA is basing its conclusions on self-selected and therefore biased, data. The OFA does not require of veterinarians that all radiographs of client dogs taken for initial evaluation be submitted to OFA. Each breeder must answer this question: Do you send X-rays to the OFA that your own vet feels are from a dysplastic animal? We thought not. So, if the OFA is mostly seeing "normal" hips, on what does it base its claim that the incidence of the disease is decreasing in some breeds? It also claims to have evaluated a significant percentage of those breeds most likely to be affected. 2 In the last 20 years, less than one percent of all the dogs registered by the AKC have been evaluated by OFA, so what does OFA consider significant?

Predicting genotype

Let us now consider the diagnostic method used by the OFA and its ability to predict genotype based on phenotype. In other words, does the physical appearance of the dog tell us what genes he is carrying? This is not the case, unfortunately, because the appearance of the animal shows only the genes he is expressing. The hip-extended view used by the OFA is good for evaluating an existing problem with degenerative hip disease when that diagnosis is based upon the specific radiographic signs of osteophyte formation, subchondral sclerosis and joint remodeling, and not subluxation. In a previous article in this series, it was demonstrated that the hip-extended radiographic view actually masked joint laxity or "looseness."3 The hip-extended position actually "screws" the femoral head into closer congruity with the acetabular cup.

If there is also a correlation between joint laxity and the subsequent development of degenerative joint disease (and we feel that this already has been demonstrated), then a diagnostic method that conceals this fault may negate its predictive value. 4,5 We should also examine two other factors that can influence the effectiveness of a diagnostic method. These factors are the scoring procedure and the reproducibility of the scoring technique. The OFA uses a seven-point, subjective hip-scoring scheme that has an inherent flaw.6 When evaluating a radiograph using this method it is possible to choose between Borderline and Mild Hip Dysplasia. Because of the problems associated with wide variation in interpretation among radiologists and even the agreement of an examiner with himself or herself, this scoring technique can introduce a false-negative into the breeding pool. For our purposes as breeders, this means that a dog that should not be used for breeding is allowed to propagate, further delaying the elimination of deleterious genes.

Since the first article in this series, we have been taken to task by a number of veterinarians, anatomists and radiologists who feel that the variance in structure between breeds requires different definitions of normal hips. For example, the angle of the pelvis, flexion and elasticity of the spine and differing gaits among breeds all contribute to a separate definition of what should clinically constitute a good set of hips for a given breed. For example: the German Shepherd Dog, with its feet out somewhere in the lower 40 acres, experiences a lever and fulcrum action that exerts more force on the hip joint than if the legs were underneath the dog. It may well be-and is according to some of the veterinarians and breeders who have written in response to the earlier articles in this series-that the German Shepherd Dog must have tighter hips with deeper acetabular cups than other breeds if its hips are to be considered normal. These are issues that bring into question the practice of relying solely on radiographic evidence of hip dysplasia when there are no other clinical signs. He�s 10 years old, moves like a dream,, but�bad hips by radiograph. Is this a dog that has bad hips, or is there some problem with the definition of good hips?

The role of hip laxity

In 1982, a group of researchers and clinicians at the University of Pennsylvania School of Veterinary Medicine, who were concerned that the incidence of canine hip dysplasia did not seem to be decreasing began to investigate the role of passive hip laxity in the development of degenerative hip disease. Using mass-selection techniques, i.e., breeding "normal" to "normal," was still producing a greater incidence of CHD than would be expected. Since a genetic screening test for this disease is not available, the problem these researchers faced was to select a phenotypic trait that was most likely to reflect the dog�s genotype with respect to CHD, one that would be the least effected by environmental factors. They concluded that functional hip laxity was the most likely condition that predisposed an animal to future degenerative joint disease due to biomechanical stress on the joint and the subsequent cartilage damage. 7 Herein lies the prediction capacity of the PennHIP system. Since it is impossible to measure functional hip laxity directly they proposed that passive hip laxity was a prerequisite for functional hip laxity, though not itself a causal event. "Some dogs, in fact, have a greater tolerance for passive laxity. That a well-muscled breed may have marked passive laxity yet be naturally protected from functional hip laxity by prominent hind limb musculature." Examples of exceptionally muscled dogs are the fighting, carting and freighting dogs.

What this means is that the biomechanical stresses on the joint due to the lateral displacement of the femoral head while the dog is standing in a normal stance are different from the supine animal, yet there remains a correlation. This correlation has been tested extensively for statistical significance.

"Passive hip laxity, then, may be considered a risk factor or perhaps loosely defined, a carrier state for HD in dogs"8

The OFA maintains that the issue of joint laxity as a predictor of CHD is neither new nor revolutionary.

"The [1972, author�s note] symposium concluded and published that there was no scientific evidence to support the clinical application of palpation and/or stress radiography."9 The methodology and the scoring techniques for these early diagnostic techniques were highly subjective and depended largely on the skill and experience of the individual examiner. To address these concerns, the University of Pennsylvania researchers first determined what the normal range was for the degrees of freedom in the coxofemoral joint, where passive laxity is maximized.10 This work was necessary in order to design a precise and accurate clinical stress-radiographic method that would hold up statistically.

The canine hip has four degree of freedom. Flexion/extension is when the leg moves forward toward the belly or back away from the body-what a breeder/exhibitor would call the "side gait." Abduction/adduction is when the dog moves the leg sideways away from the body or inward toward the belly. Internal/external rotation is the twisting motion the femur can make within the acetabulum until restrained by the round ligament and the joint capsule. Lateral translation is the sideways displacement or passive laxity. Maximal passive laxity, which approximates the neutral weight-bearing stance, was obtained at 10 degrees extension, 20 degrees of abduction and 10 degrees of external rotation.11

This early study also revealed the limitations of the hip-extended radiographic view. The magnitude of lateral displacement of the femur is concealed by this view, not only because of resultant forces on the joint capsule, but there appears to be a hydrostatic effect also. The hip-extended view lowers the pressure within the joint capsule, which causes it to invaginate. A sort of vacuum or "suction" effect occurs that when combined with the fixed synovial fluid volume limits the sideways movement of the femoral head.

Developing better diagnostic methods

Using this information, the University of Pennsylvania researchers were able to design a radiographic protocol based on quantitative parameters.12 The distraction index or DI is based on a compression radiographic view that determines where the center of the femoral head and the center of the acetabulum coincide. The distraction view then measures how far the femoral head can be moved away from the center. This view requires the use of a special device called a distractor. The proper positioning of a distractor and the amount of force is crucial. Clinicians wishing to become certified in the PennHIP method are required to attend a one-day training session. Prior to certification, in order to ensure consistency and repeatability they are also required to submit radiographs that demonstrate their proficiency to Dr. Gail Smith and his colleagues. This certification process is designed to enhance quality control and protects the all-important integrity of the PennHIP data base. Once the two views are taken, it is possible to derive a unitless variable by dividing the amount of sideways displacement from the center by the radius of the femoral head.

This variable or distraction index ranges from 0 to 1 and a later study indicated that dogs with a DI of 0.3 or lower were truly negative for CHD. Those animals with a DI of 0.7 or greater were associated with a high probability for developing dysplastic joints. A variety of statistical methods, including those that evaluate qualitative parameters, were used to evaluate their data.

The DI range between 0.3 and 0.7 is still a gray area and is most dependent on specific breed variability. In a recent publication the DI was shown to be the only statistically significant predictor of the risk of developing degenerative joint disease in Rottweilers.13 When German Shepherd Dogs were included, the results indicated they had a greater susceptibility to the disease. It is clear that further research must focus on elucidating the specific breed differences when correlating passive joint laxity and susceptibility to degenerative joint disease. As more dogs are added to the data base, it will be easier to quantify the specific DI range for each breed that indicates the disease-free phenotype. It is for this reason that every radiograph taken by a PennHIP-certified veterinarian will be submitted to PennHIP for evaluation. Breeders will not have a choice of whether to submit the radiographs or not, as is the case with veterinarians taking preliminary radiographs prior to submitting the case to OFA for interpretation and scoring. Not having this choice will make some breeders uncomfortable, but responsible breeders will be pleased to know they have contributed to the betterment of their breeds. Breeders can expect that some of their dogs that have "passed" OFA certification will not be deemed suitable for breeding using the PennHIP method.

The question needs to be answered whether it is less deleterious to breed to a dog that is genotypically positive for canine hip dysplasia than it is to lose the opportunity to breed an animal because it was a "false-positive" for canine hip dysplasia. At first such a question sounds a bit philosophical, but in practice where it hits the breeder, it has an operational answer. There will always be other dogs, other champions to be made and other suitable brood bitches and studs tat can produce fine litters. It makes no sense whatsoever to risk doubling up on defective genes whether for hip dysplasia or any other known genetically transmittable disease. Once you introduce undesirable genes into your pedigree, you will have great difficulty getting them out-and it may take several human lifetimes to do so.

As we have seen previously the honor system in registries does not work. In fact it works so poorly in the AKC�s registration of puppy mill animals that the Canadian government will not allow importation of AKC-registered animals if the claim is made that they are purebred. That is called fraud. It works so poorly that the U.S. Department of Agriculture found in 1992 that 70 percent of the licensed commercial dog breeders inspected did not track pedigrees accurately.14 It works so poorly that in 1987 Mark Hyland, an AKC attorney, represented to a federal judge in Kansas City that the AKC does not revoke fraudulent dog registrations because of the "infinite back up" of such registrations.15 How bad is the AKC situation?

Identification methods

No one outside of AKC really knows how bad the pedigree situation is, but Alan Stern a former AKC vice president, is on record with a 1990 statement to the Sacramento Bee that fraud happens on half of AKC�s registrations.16 Other registries have a similar problem with dishonesty as do Greyhound and thoroughbred racetracks. What is needed is a foolproof method for identifying a particular animal. While several identification systems are available, the Destron-Fearing microchip, now distributed by Schering-Plough, and the Avid microchip are the two contenders for the market.

Much ado has been made about the AKC wanting action on genetic problems, but until the simple matter of pedigree is cleaned up, do not look to the AKC to solve genetic problems. In author Cargill�s breed, Akitas, it has only been in the past few years that AKC has allowed the breeding to Akitas imported from Japan because three separate breed registries were there. No great intellect is required to ascertain that the gene pool was artificially restricted by the AKC and that many genetic problems experienced now and that will surface in phenotype in the future will have resulted from a restricted gene pool.

Computer chip "passive responders" have been injected in dogs, cats, birds, horses fish, reptiles and exotic and endangered species since 1991. More than 2 million identification chips have been sold. These rice-size chips are injected without requiring anesthesia. They consist of a coil and a small circuit board with a one time programmable memory. The data programmed into the Avid chip�s memory is encrypted, and thus not susceptible to tampering. A reader is a transceiver that transmits a radio frequency pulse (125KHz), which energizes the coil in the implanted chip, enabling it to transmit a message back to the reader.17

Although the implanted chips can be detected by X-ray, they have proven to be extremely difficult to remove, other than through advanced surgical techniques. There is one report that a staff of veterinarians were able to remove an injected chip in a horse using dual plane radiographic surgical techniques; however such imaging equipment is well beyond the reach of all but the most well-equipped veterinary centers. None of this wonderful technology has potential if costs are high, but they are not. A survey of veterinarians indicates that injection price (including the chip) is $25 to $50. Readers are available to veterinarians for less than $300. "We have the technology."

The next step in the battle against CHD is to marry up PennHIP, OFA and other evaluations with an "open" genetic registry such as the one maintained by the Institute for Genetic Disease Control in Animals (GDC).18 Unfortunately, OFA�s registry is closed to outsiders, and does not require the submission of X-rays and pedigree data of all animals radiographed. PennHIP is also a closed registry, but does require submission of the cases of all animals radiographed. The authors feel so strongly about the requirement to collect and make available the phenotypical data on parents, siblings, progeny and other progeny of parents and siblings in a cross-referenced data base that they challenge both OFA and PennHIP to make their data available to some central genetic registry. The only one available and capable at present is the GDC.

Conclusions:

The two major methods of diagnosing canine hip dysplasia available to the fancy in the United States are those followed by OFA and those followed by PennHIP. Both are diagnostic; however, the hip-extended protocol followed by OFA may produce false-negative results. The protocol followed by PennHIP has a prognostic or predictive capacity through the use of statistics and a carefully guarded data base that allows a prediction to be made with respect to the probability of phenotypic expression of canine hip dysplasia. No one has a clear quantification of the gray area between obviously clear and obviously dysplastic hips. Controversy still rages. Until there are open genetic registries, mandatory evaluation of all dogs registered and some assurance of pedigree validity, canine hip dysplasia will remain a common affliction of the domestic dog, especially of purebred dogs.

References

  1. Corley, E.A. Year-end data update. Memorandum from E.A. Corley, D.V.M., Ph.D., Orthopedic Foundation for Animals, to OFA Breed Club Representatives in Samoyed Club of America Bulletin, March 1995, p.15.
  2. Ibid., p.15.
  3. Cargill, J.C., Thorpe-Vargas, S. "Methods for Diagnosing the Abnormal Hip." DOG WORLD. July 1995.
  4. Lust, G.; Williams, A.J.; Burton-Wurster, N.; Pijanowski, G.T.; Bech K.; Rubin, G.; Smith, G.K. "Joint laxity and its association with hip dysplasia in Labrador Retrievers." Am J Vet Res. Vol. 54. No. 12. Pp. 1990-1999.
  5. Smith, G.K.; Gregor, T.P.; Rhodes, W.H.; Biery, D.N. "Coxofemoral joint laxity from distraction radiography and its contemporaneous and prospective correlation with laxity, subjective score, and evidence of degenerative joint disease from conventional hip-extended radiography in dogs." Am J Vet Res. 1993 Vol. 54. No. 7. Pp. 1021-1042.
  6. Corley, E.A., Keller, G.G. "Hip Dysplasia: A guide for dog breeders and owners." 2nd ed. Columbia, MO.: Orthopedic Foundation for Animals, 1989; pp. 1-27.
  7. Smith, G.K.; Biery, D.N.; Gregor, T.P. "New concepts of coxofemoral joint stability and development of a clinical stress-radiographic method for quantifying hip joint laxity in the dog." J Am Vet Med Assoc. 1990; Vol. 196, No. 1, pp. 59-70.
  8. Smith, Gregor, Rhodes and Biery. Pp. 1021-1042.
  9. Corley, E.A.; Keller, G. OFA Memorandum. Feb. 2, 1994.
  10. Heyman, S.J.; Smith, G.K.; Cofone, M.A. "Biomechanical study of the effect of coxofemoral positioning on passive hip joint laxity in dogs." Am J Vet Res. 1993;54:210-215.
  11. Smith, G.K.; Popovitch, C.A.; Gregor, T.P. "Evaluation of risk factor for degenerative joint disease associated with hip dysplasia in dogs." J Am Vet Med Assoc. 1995;206:642-647.
  12. PennHip seminar San Francisco. April 8, 1995.
  13. Smith, Popovitch and Gregor.
  14. Shook, L. "Cop tails AKC: Feds should investigate." The Spokesman-Review, Spokane, WA, December 11, 1994.
  15. Ibid.
  16. Ibid.
  17. Product data sheets. AVID, Inc., 3179 Hammer Ave. Norco, CA 91760.
  18. Institute for Genetic Disease Control in Animals (GDC), Box 222, Davis, CA 95617; (916)756-6773.

Canine Hip Dysplasia Part VI 

Treatment of this disease must be tailored specifically to the needs of your pet, whether using conventional or alternative medicine

By John C. Cargill, MA, MBA, MS and Susan Thorpe-Vargas, MS

 This article is the sixth in an eight-part series on canine hip dysplasia (CHD). What follows is written from the perspective that the readers are serious and conscientious breeders who are the guardians of the genetic pools that constitute their breeds. While this series of articles will not replace a stack of veterinary and medical texts, it is a relatively in-depth look at the whole problem of canine hip dysplasia. Furthermore, the series is designed to be retained as a reference. When you finish reading this series, you will have a sufficient background to make rational breeding choices and will be able to discuss the subject from an informed basis with your veterinarian. You may not like what you read, but you will be more competent to deal with the problem.

Conclusions from part I:

Genetics is the foremost causative factor of canine hip dysplasia. Without the genes necessary to transmit this degenerative disease, there is no disease. Hip dysplasia is not something a dog gets; it is either genetically dysplastic or it is not. An affected animal can exhibit a wide range of phenotypes, all the way from normal to severely dysplastic and functionally crippled. Hip dysplasia is genetically inherited.

Conclusions from part II:

While environmental effects, to include nutrition and exercise, may play a part in mitigating or delaying the onset of clinical signs and clinical symptoms, hip dysplasia remains a genetically transmitted disease. Only by rigorous genetic selection will the incidence rate be reduced. In the meantime, it makes sense to have lean puppies and to avoid breeding animals from litters that showed signs of hip dysplasia. It is probable that even normal exercise levels may increase the phenotypic expression of CHD of a genetically predisposed dog. Stay away from calcium supplementation of any kind; all it can do is hurt. There is no conclusive evidence that vitamin C can prevent hip dysplasia, but there is some evidence that vitamin C may be useful in reducing pain and inflammation in the dysplastic dog. Fortunately, large doses of vitamin C are readily excreted, but it is still possible to cause untoward side effects with megadoses.

Conclusions from part III:

Canine hip dysplasia can be difficult to diagnose, as a number of other orthopedic neurological, autoimmune and metabolic problems may mimic it. Controversy surrounds the question of positioning for hip X-rays and what part joint laxity plays in hip dysplasia. Hip dysplasia may be more common in large and giant breeds and is one of the most over-diagnosed and misdiagnosed conditions.

Conclusions from part IV:

Sadly, no breed registry body in the United States requires genetic screening of parents as a prerequisite for litter registration or even offers a "fitness for breeding" certification. The current registries for hip dysplasia (and other genetically transmitted problems) cover so little of the American Kennel Club-registered dog population that their impact so far has been minimal. The tools we need are there. Joint responsibility for failing to use the tools at hand lies with the AKC, United Kennel Club, parent clubs and individual breeders. 

Conclusions from part V:

The two major methods of diagnosing canine hip dysplasia available to the fancy in the United States are those followed by OFA and those followed by PennHIP. Both are diagnostic; however, the hip-extended protocol followed by OFA may produce false-negative results. The protocol followed by PennHIP has a prognostic or predictive capacity through the use of statistics and a carefully guarded data base that allows a prediction to be made with respect to the probability of phenotypic expression of canine hip dysplasia. No one has a clear quantification of the gray area between obviously clear and obviously dysplastic hips.

Part IV:

This article will address the long-term medical management of canine hip dysplasia, the goals of which are to relieve pain, restore function and hopefully mitigate or delay the progression of the disease. There are philosophical choices to be made based on the psyche and the general approach to life of the individual animal. Some breeds are noted stoics, able to tolerate what would appear to be a great deal of pain. For such animals, restoration of function is the greatest gift. For other animals more susceptible to pain, relief of that pain may be the greatest gift. Much of the philosophy of medical management of canine hip dysplasia must come from the animals themselves. The authors both are more experienced with Northern breeds (Akitas and Samoyeds), which tolerate pain well; however, our experience covers other breeds as well. The philosophy of treatment must come from multiple sources: from traditional medicine, holistic medicine, acupuncture and even chiropractic.

Caveat: Before starting medical treatment, surgical procedures may be necessary to correct anatomical malformations. Such surgical procedures will be addressed in the seventh and eighth articles in this series.

Chiropractic

William Inman, D.V.M., a clinician working in the Seattle area, is the reason we have included chiropractic. Inman�s research, presented in the third article in this series suggests that spinal conditions, especially subluxation of between the eighth and tenth thoracic vertebrae, can cause a neurological condition that mimics the symptoms and signs of canine hip dysplasia. Inman�s treatment method includes the traditional chiropractic "spinal adjustment," but with a twist. He has had numerous successes with a device called the "Activator." This instrument applies a small force very quickly on the affected spinal segment. Inman calls this technique "Veterinary Orthopedic Manipulation" and maintains that with this device he can "reactivate" the neurological pathway that has been compromised. The problem with discounting this whole process as being just a little too "New Age" lies in the number of apparent successes he has had.

Ask the owner of a paralyzed Dachshund and the 30 or more other people (including respected dog breeders, veterinarians and chiropractors) who saw the Dachshund start walking after only one such treatment. This little dog had been through the veterinary process and its owner was preparing to put it down after traditional veterinary medicine had failed to relieve the pain or restore the function. In a last-ditch effort to help her dog the owner brought her to a seminar hosted by the Wenatchee (Wash.) Kennel Club on April 22. The results were those described above. The case is definitely anecdotal; however, Inman has too many such cases to be dismissed out of hand, even by those in the mainstream of veterinary medicine.

With a background in genetics, neuroanatomy and neuropathology, Inman still questions the mechanism of how his technique works. What is it that may be happening at the cellular level that promotes healing? Why is it that an animal has to be "readjusted" periodically on a specific schedule for the results to stick? "Once the body has been returned to normal neurologic function via adjustment, it stays in adjustment for about three days. Months to years of functioning out of adjustment impinge on this newly rehabilitated neurologic ability, and the spine slips back to its previous out-of-adjustment condition. This is why further adjustments are necessary . At three, seven, 14, 21, 42 and 70, the body falls out of adjustment�."1 From the authors� perspective further research is clearly indicated, but meanwhile, this option of chiropractic is available to that segment of the dog population not suffering with the genetic disease of hip dysplasia, but from subluxation of the spine between the eighth and tenth vertebrae.

Acupuncture

While relatively few Western veterinarians are using acupuncture, Western medicine is beginning to respect its potential and to practice it. As with many things in life a full understanding of the process is unnecessary for employing it. In physics, for example, light and electricity are poorly understood, yet the modern way of life is predicated on the use of both light and electricity. Acupuncture survives from a time before modern science and physical mechanisms were described in philosophical terms that do not hold up to strict scientific examination, yet the phenomena exists. This appears to be the state of acupuncture in medicine and in veterinary medicine. A great body of anecdotal evidence exists to suggest that acupuncture has potential for at least temporarily reducing pain and promoting natural healing. Acupuncture has a following among not only dog people but horse people, and many are the accounts of lame animals being restored to full function. As with Inman�s chiropractic example, acupuncture has too many apparent successes to be discounted without further study.

Drug Therapy

Because Hip Dysplasia results in abnormal forces being applied to the coxofemoral joint one of the most effective treatments is control of the dog�s weight. If indicated, even small amounts of weight loss are productive. Restricted activity also should be considered not only to avoid excessive wear on the affected joint, but to control transient inflammation. Even so, most of the pharmacological treatment alternatives function by reducing the inflammatory response. These drugs can be divided into corticosteroids, which can include but are not limited to methylprednisolone, dexamethasone and prednisone and a variety of NSAIDs (non-steroidal anti-inflammatory drugs). Although useful in the acute stage, the corticosteroids are inappropriate for long-term treatment modalities due to their multiple undesirable side effects. Besides suppression of the immune system and loss of adrenal function, the use of corticosteroids can cause increased appetite increased thirst and gastrointestinal ulceration. Other research also indicates that corticosteroids can disrupt the articular cartilage matrix by inhibiting proteoglycan synthesis. 2,3 Proteoglycan is necessary for stiffness and compressibility of the matrix. Fortunately, this effect is reversible within two or three weeks. Experimenting to determine the right interval between injections may be necessary.

NSAIDs are not without their drawbacks, either. Common aspirin (acetylsalicyclic acid) can cause vomiting and bloody stools; bleeding times may be extended due to irreversible inhibition of platelet function, and severe overdose can lead to an abnormally high fever, electrolyte imbalance, renal hemorrhage, convulsions and coma. Clotting time returns to normal within several days, however, as a result of normal platelet turnover. There is some indication that though aspirin is often the drug of choice, it may possibly accelerate the degeneration of articular cartilage.

Another drug used to relieve the symptoms associated with hip dysplasia is phenylbutazone. This drug4 has a potentially serious side effect in that it depresses bone marrow formation. Bone marrow is the site of red blood cell maturation. Not yet approved for dogs by the Food and Drug Administration is the promising anti-inflammatory drug carprofen. Clinical trials have shown it is a more effective anti-inflammatory than both aspirin and phenylbutazone, and when compared to placebo it is 24.8 times more efficacious. In a double-blind study of 209 dogs, it was therapeutic in relieving pain, lameness and contralateral (opposite-side) weight-bearing.5 The drug also increased range of motion and reduced crepitus (the dry crackly sound when two dry articular surfaces rub together). An added benefit is that carprofen also seems to have a reduced potential for inducing gastrointestinal problems.

Caution: Of these drugs, only aspirin and phenylbutazone are FDA-approved for use in dogs.sup>6/sup>

"However, few NSAIDs are approved by the U.S. Food and Drug Administration for use in dogs, which has resulted in the empirical use of those approved in humans with sometimes disastrous results." In 1987 NSAID exposures comprised 8 percent of all human and veterinary medication calls to the Illinois Animal Poison Information Center.

"Many of these newer NSAIDs have a small margin of safety, due to long half lives and low rates of elimination."7

A few years ago dimethyl sulfoxide(DMSO), an industrial solvent, became a popular, though unapproved and unproven, treatment for arthritic joints. DMSO is a free-radical scavenger and is reported in the popular press to produce favorable results. Caution is advised.

Nutritional Therapy

The common mechanism for most of the anti-inflammatory drugs is inhibition of prostaglandin E2 synthesis. Also referred to as the arachadonic "cascade," these drugs function by blocking the activity of the enzyme cyclooxygenase. What most people do not realize is that the antioxidant vitamins, d-alpha-tocopherals (the most biologically available form of vitamin E) and calcium ascorbate (a more effective form of vitamin C), also modulate PGE2 synthesis by inhibiting cyclooxygenase and stabilizing the cell membrane. Even though dogs manufacture their own vitamin C, to be therapeutically effective the blood plasma concentrations of these two vitamins must be maintained at a higher than normal value. Therefor, the form of the vitamin is important, and the amount ingested is higher than that suggested by the Association of American Feed Control Officials. These nutritional supplements are not useful for acute symptoms, but if taken daily and consistently, they can be reduce inflammation without any detrimental side effects.

An added benefit of these two vitamins is that they scavenge free-radicals (highly reactive and unstable compounds generated in mammalian cells as a result of cellular metabolism and cell damage), and when taken together vitamin C can regenerate the "reduced" form of vitamin E so that it can be recycled by the cell. Free-radicals are formed also in the inflammation process and when the animal is exposed to various environmental pollutants, including ultraviolet light. Besides being implicated in arthritic disease process, free-radicals are associated with the onset of cancer, aging, cataracts, neurologic disorders and a reduced immune function. Edward A. Moser, M.S., V.M.D., suggests in his article in the November/December 1994 issue of Veterinary Technician, "For a thirty pound dog, giving approximately 80 I.U. of vitamin E [and] 50 mg of Vitamin C�can safely be recommended. Smaller dogs need proportionately less, larger dogs proportionately more."8 Other sources would consider this a very conservative dosage. In a Norwegian study, 30 mgs/kg of body weight of polyascorbate was given three times a day for six months.9 (A kilogram is 2.2 pounds)

Approximately 77 percent of the dogs treated showed marked improvement after six months, and 32 dogs out of the 45 diagnosed with hip dysplasia were symptom-free after only one week. Polyascorbate is a mineralized form of vitamin C that aids in the absorption and retention in the body�s tissues, and because it has a neutral pH it does not cause gastric upset. Ascorbic acid, the vitamin C we are most familiar with, is too rapidly excreted to be effective, can irritate the lining of the digestive tract, and at the higher dosage recommended will cause the formation of crystals in the urinary tract.

GAGS

The drugs and nutritional supplements mentioned so far either retard the breakdown of joint components or reduce pain and inflammation, thus improving the quality of life for the dog. None of them, except calcium ascorbate, are able to repair cartilage that has been compromised. While vitamin C is necessary for maintenance of collagen, it is also a carrier of activated sulfates needed for the synthesis of glycosaminoglycans (GAGS). An injectable form of polysulfated glycosaminoglycan called Adequan is in the process of being approved for dogs by the FDA. Considered a chondro-protective drug, it is already available in Canada for dogs and licensed for horses here in the United States. Previous laboratory trials (in-vitro cell-line experiments) demonstrated its effectiveness in promoting the synthesis of cartilage matrix components. It also slows down the destruction of these cartilage components, decreases joint inflammation, restores the normal hyaluronic acid content in the synovial fluid (increases viscosity) and relieves pain.10,11 Another study conducted at Cornell University has shown that PSGAG (polysulfated glycosaminoglycans), given prophylactically, are able to improve coxofemoral joint congruity in puppies prone to hip dysplasia.12

To understand how this product works, let us review a few pertinent facts about joint structure and the articular cartilage. Stress due to the abnormal biochemical forces in the dysplastic joint causes injury to the chondrocytes and the release of various destructive enzymes. Chondrocytes are responsible for the synthesis of collagen and proteoglycans, which constitute the ground substance (matrix) of articular cartilage. Acting somewhat like "glue," the matrix proteoglycans play an important role in the structural integrity of cartilage. A number of destructive enzymes have been isolated that break down joint matrix components; among these are the metalloproteinases. These enzymes break down proteins and depend upon the metal ions CA++ (calcium) and Zn++ (zinc) for their activity. Adequan is thought to function by inhibiting the activity of these metalloproteinases and other degenerative mechanisms, but a dual role has been suggested in that it may also act by stimulating the synthesis of proteoglycans and collagen by the chondrocytes.13

Both the femoral head and the acetabulum are covered with articular cartilage. The entire surface area is lubricated by synovial fluid, which is composed of and ultrafiltrate of plasma and glycosaminoglycan hyaluronic acid. Viscosity is the result of hyaluronic acid concentration, so anything that affects the concentration of HA also affects the lubricating potential of the synovial fluid. Synovial fluid, the source of nutrition for the articular cartilage, functions by eliminating metabolic waste products, and is contained by a fibrous structure called the joint capsule. The joint capsule itself is composed of an inner layer called the synovial membrane and another consisting of a fibrous outer covering. Thus most of the pathologic changes associated with hip dysplasia and subsequent degenerative joint disease can be attributed to the various chemical changes in the synovial fluid and the articular cartilage.

No toxic effects from the use of polysulfated glycosaminoglycans in dogs have been reported in the literature, but caution should be taken for use in those breeds with known blood coagulation problems such as von Willebrand�s disease (vWD) or hemophilia.14 Furthermore, this drug should not be used in conjunction with other drugs that interfere with normal blood clotting mechanisms. Other studies have shown that it can inhibit the complement cascade (part of the secondary immune response), and suppress neutrophil activity.15 Neutrophils are white blood cells that surround and digest foreign substances, including bacteria and viruses. So its use would be proscribed if the dog had an active infection, especially joint sepsis.

Two nutritional products are now being suggested for management of degenerative joint disease as possible alternatives or adjuncts to the drug Adequan, Glyco-Flex and Cosequin. These two products have the advantage of being administered orally, and so far the data supports their manufacturers� claim that absorption readily occurs from the gastrointestinal tract. 16

Glyco-Flex is a freeze-dried preparation of the New Zealand green-lipped mussel, Perna canaliculus, to which brewer�s yeast and alfalfa have been added to reduce the marine odor and increase palatibility. The end result is a complex mixture of proteins, mixed glycosaminoglycans, amino acids, chelated minerals, enzymes and vitamins. The activity of the Perna mussel is probably the effect of several ingredients working in combination.

Cosequin 17,18 is a patented nutraceutical sold only to vets which has numerous clinical studies currently under way at veterinary universities. The active ingredients in Cosequin are glucosamine HCL (hydrochloride), purified chondroitin sulfate and manganese ascorbate. Currently this product is being evaluated by veterinary orthopedic surgeons for use in dogs and the results are encouraging. Other studies are looking at Cosequin�s ability to stabilize articular surfaces of the joint and improve the joints� overall function.19

Physical Therapy and Exercise

Owner-conducted physical therapy is an indispensable component of treatment. Heat, followed by range of motion exercises, may provide temporary relief. Often favorable results are obtained by gently moving the affected joint through a full range of motion several times daily. This may prevent capsular contraction and its increased pressured on the articular cartilage. A variety of forms of heat are available., ranging from the unsophisticated heating pad to ultrasound and diathermy. Simplicity, availability and cost are considerations. A heating pad under the bedding is often appreciated as may be seen by the dog resting with the most affected hip placed over the heating pad. Where possible, refraining from weight-bearing on affected joints may help. Similarly, vertical load reduction on joints may help. Thus in some cases of CHD, the dog should be prevented from going up or down stairs, from jumping up or jumping down from a height.

Muscle atrophy can cause increased stress on the affected joint. Graduated exercise may be effective to correct this muscle imbalance so characteristic of CHD (overdeveloped shoulder girdle; weak hips). In any case, weight loss, even if it means a "lean and hungry" look in old age, often pays large dividends in quality of life for the animal. Simple measures such as bedding changes can make a difference. Many an older dog, which in younger days would refuse a bed, preferring instead hard concrete or linoleum floors, may accept and be helped by a piece of plush pile carpet or a pad of some kind.

Warning: medical management of a degenerative joint disease, such as canine hip dysplasia, is simply management, not cure. Both you and your animal have to learn to live with the condition and to adjust your lifestyles accordingly. In mild cases, especially of the insidious form of CHD, little adjustment may be required, other than to precede bouts of increased activity with a "pre-dose" of aspirin. Be very careful that you do not fall in the trap that many human patients and their dogs fall into: When the pain is gone and the inflammation is reduced there is an extreme tendency to overdo it. The pain will come back to visit if the animal gives in to temptation to romp until it drops.

Conclusions: For many animals, canine hip dysplasia is a manageable condition, and they can lead relatively normal and active lives given that caution is exercised. Every dog is different in its response to pain, and the treatment protocol needs to be tailored specifically to the particular animal. Only aspirin and phenylbutazone ("bute") are FDA-approved drugs for use in dogs, and they are not without serious side effects. Corticosteroids are dangerous and may require experimenting to find proper dosage levels and intervals. Favorable results have been reported from chiropractic, physical, drug and nutritional therapy.

The final two articles in this series will cover surgical intervention in the management of canine hip dysplasia. Surgical measures are measures of last choice. We hope however, to make the case that surgery may be a viable choice, and even an economically sensible choice, especially for companion dogs for the elderly, assistance, drug-sniffing, search-and-rescue and other specially trained dogs where costs and time associated with training and replacement are high.

References

  1. Personal Communication with Dr. William Inman, Lake City Animal Hospital, 13045 Lake City Way N.E. Seattle, WA. 98125; (206)362-0909.
  2. Peltier, J.P.; Peltier, J.M. "Protective effects of corticosteroids on cartilage lesions and osteophyte formation in the Pond-Nuki model of dog osteoarthritis." ArthritisRheum. 32:181-193, 1989.
  3. McIllwraith, C.W. "Current concepts in equine degenerative joint disease." J Am Vet Med Assoc. 180:239-250. 1982.
  4. Pederson, N.C.; Wind, A.; Morgan, J.P.; Pool, R.R. "Joint diseases of dogs and cats." in Textbook of Veterinary Internal Medicine, Ed. 2, Vol. 2 (Ettinger, S.J.-ed.). Philadelphia: WB Saunders Co. 1989.
  5. Holtzsinger, R.H.; Parker, R.B.; Deale, B.S.; Friedman, R.I. "The Therapeutic efficacy of carprofen (Rimadyl-VTM) in 209 clinical cases of canine degenerative joint disease." VCOT. 1992. Vol. 5, pp. 140-144.
  6. Boulay, J.; DeAngelis, M.; Kincaid, S.; Leeds, E.; Prostredny, J.; Todhunter, R. "Medical Therapy of Osteoarthritis in Dogs." Veterinary Exchange. Veterinary Learning Systems Co. 1995.
  7. Holtzsinger, R.H.; Parker, R.B.; Deale, B.S.; Friedman, R.I.
  8. Moser, E.A. "Antioxidant vitamins in canine nutrition." Veterinary Technician. Nov./Dec. 1994, pp.587-589.
  9. Berge, G.E. "Polyascorbat, et behandlings-alternativ ved kroniske forandringer I stotte og bevegelsesapparetet hos hund." ("Polyascorbate, an interesting alternative by problems in the support and movement apparatus in dogs.") Norsk Veterinaertidsskrift (Norwegian Vet J), August/September 1990;102:581-582.
  10. Altman, R.D.; Dean, D.D.; Muniz, O.E.; Howell, D.S. "Therapeutic treatment of canine osteoarthritis with glucosaminoglycan polysulfuric acid ester." Arthritis and Rheum. Vol. 32, No. 10, Oct. 1989.
  11. Clark, D.M. "Current concepts in the treatment of degenerative joint disease." Compen Cont Educ Prat Vet. 13(9):1991, pp. 1439-1447.
  12. Lust, G.; Williams, A.J.; Burton-Wurster, N.; Beck, K.A.; Rubin, G. "Effects of intramuscular administration of glycosaminoglycan sulfates on signs of incipient hip dysplasia in growing pups." Am J Vet Res. Vol. 53, No. 10, pp. 1836-1843.
  13. Altman, R.D.; Dean, D.D.; Muniz, O.E.; Howell, D.S.
  14. Beale, B.S.; Goring, R.L.; Clemmons, R.M.; Altman D. "Effect of semi- synthetic polysulfated glycosaminoglycan on the hemostatic mechanism in the dog." Pro ACVS. 25:430, 1990.
  15. Gustafson, S.B.; McIlwraith, C.W.; Jones, R.I. "Comparison of the effect of polysulfated glycosaminoglycan, corticosteroids, and sodium hyalurnate in the potentiation of a subinfective dose of Staphlococcus aureus in the midcarpal joint of horses." Am J Vet Res. 50(12): pp. 2014-2017. 1989.
  16. Veterinary Exchange.
  17. Setnicker, I.; Giachetti, C.; Zanolo, G. "Pharmacokinetics of Glucosamine in the dog and man." Artneimittleforschung. 39(2):pp. 729-736. 1986.
  18. Tesoriere, G.; Dones, F.; Magestro, D.; Castagetti, I. "Intestinal absorption of glycosamine and N-acetylglycosamine." Experimentia. Vol. 28, pp. 770-71. 1972.
  19. Veterinary Exchange.

Canine Hip Dysplasia Part VII

Surgical Management of Canine Hip Dysplasia 

Surgery may be recommended for suitable candidates, taking into account expected activity level, longevity and use and value of the dog.

By John C. Cargill, MA, MBA, MS and Susan Thorpe-Vargas, MS

This article is the seventh in an eight-part series on canine hip dysplasia (CHD). What follows is written from the perspective that the readers are serious and conscientious breeders who are the guardians of the genetic pools that constitute their breeds. While this series of articles will not replace a stack of veterinary and medical texts, it is a relatively in-depth look at the whole problem of canine hip dysplasia. Furthermore, the series is designed to be retained as a reference. When you finish reading this series, you will have a sufficient background to make rational breeding choices and will be able to discuss the subject from an informed basis with your veterinarian. You may not like what you read, but you will be more competent to deal with the problem.

Conclusions from part I:

Genetics is the foremost causative factor of canine hip dysplasia. Without the genes necessary to transmit this degenerative disease, there is no disease. Hip dysplasia is not something a dog gets; it is either genetically dysplastic or it is not. An affected animal can exhibit a wide range of phenotypes, all the way from normal to severely dysplastic and functionally crippled. Hip dysplasia is genetically inherited.

Conclusions from part II:

While environmental effects, to include nutrition and exercise, may play a part in mitigating or delaying the onset of clinical signs and clinical symptoms, hip dysplasia remains a genetically transmitted disease. Only by rigorous genetic selection will the incidence rate be reduced. In the meantime, it makes sense to have lean puppies and to avoid breeding animals from litters that showed signs of hip dysplasia. It is probable that even normal exercise levels may increase the phenotypic expression of CHD of a genetically predisposed dog. Stay away from calcium supplementation of any kind; all it can do is hurt. There is no conclusive evidence that vitamin C can prevent hip dysplasia, but there is some evidence that vitamin C may be useful in reducing pain and inflammation in the dysplastic dog. Fortunately, large doses of vitamin C are readily excreted, but it is still possible to cause untoward side effects with megadoses.

Conclusions from part III:

Canine hip dysplasia can be difficult to diagnose, as a number of other orthopedic neurological, autoimmune and metabolic problems may mimic it. Controversy surrounds the question of positioning for hip X-rays and what part joint laxity plays in hip dysplasia. Hip dysplasia may be more common in large and giant breeds and is one of the most over-diagnosed and misdiagnosed conditions.

Conclusions from part IV:

Sadly, no breed registry body in the United States requires genetic screening of parents as a prerequisite for litter registration or even offers a "fitness for breeding" certification. The current registries for hip dysplasia (and other genetically transmitted problems) cover so little of the American Kennel Club-registered dog population that their impact so far has been minimal. The tools we need are there. Joint responsibility for failing to use the tools at hand lies with the AKC, United Kennel Club, parent clubs and individual breeders.

Conclusions from part V:

The two major methods of diagnosing canine hip dysplasia available to the fancy in the United States are those followed by OFA and those followed by PennHIP. Both are diagnostic; however, the hip-extended protocol followed by OFA may produce false-negative results. The protocol followed by PennHIP has a prognostic or predictive capacity through the use of statistics and a carefully guarded data base that allows a prediction to be made with respect to the probability of phenotypic expression of canine hip dysplasia. No one has a clear quantification of the gray area between obviously clear and obviously dysplastic hips.

Conclusions from part VI:

For many animals, canine hip dysplasia is a manageable condition, and they can lead relatively normal and active lives given that caution is exercised. Every dog is different in its response to pain and the treatment protocol needs to be tailored specifically to the particular animal. Only aspirin and phenylbutazone ("bute") are FDA-approved drugs for use in dogs, but they are not without serious side effects. Corticosteroids are dangerous and may require experimenting to find proper dosage levels and intervals. Favorable results have been reported from chiropractic, physical drug and nutritional therapy.

Part VII:

It is no accident that this discussion of surgical interventions should appear at the end of this series on hip dysplasia, as it is not only the viewpoint of the authors but also many veterinarians that these procedures are measures of last resort. On the other hand there are very clear indications for surgery.
Surgery is indicated when:

  • medical management has resulted in unacceptable side effects;
  • medical management has not been effective in restoring function and eliminating pain;
  • surgery will correct current problems;
  • surgery will preclude or ameliorate future problems.

It is important to remember from the earlier articles in this series that canine hip dysplasia, as a degenerative joint disease, is a process, and that different interventions may be required at different stages in the process.

Many animals lead a non-working pet life and have a level of activity that would not be expected to accelerate the degenerative process. Thus they might not require surgery in order to sustain that level of activity for their remaining life spans. Working and other high-activity-level dogs are another issue entirely, as are dogs used for special purposes. Some of these procedures are also recommended when there exists a genetic or traumatic orthopedic condition that must be corrected in order to begin long-term medical treatment modalities.

We should also note that surgery is used jointly with adjunct therapies.1 Weight control, or where indicated weight loss, along with appropriate exercise restrictions, also apply. Careful consideration must be taken to limit the post-surgical canine patient to those exercises and exercise levels that do not accelerate the degenerative process. Water exercise is ideal as a non-weight-bearing activity that prevents atrophy of those muscle masses that support the hip, burns calories and maintains cardiovascular fitness. For those dogs for whom water activities are not available, or who do not enjoy the water or retrieving, the choice of exercise surface should be considered. Hard-packed sand along the water�s edge, soft grass or dirt roads and trails are much preferred over concrete or asphalt. Appropriate drug and nutritional support are also indicated.2

Surgical procedures for the management of canine hip dysplasia tend to be controversial. Each procedure has its pros and cons, and therefore, not surprisingly, there are veterinary orthopedic surgeons who for a given patient would choose different procedures, much as in human medicine. This leads the authors to conclude that there is no one ideal procedure that is suitable for all stages of the disease process. Each dog presenting with hip dysplasia may be more or less a candidate for one or more of the procedures described here. There are, however, clear indications for the type of procedures that might be most beneficial at different stages of the disease process.

 

Femoral neck lengthening

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The goal of this article is to acquaint the reader with the options available, and to provide a depth of understanding sufficient that the reader may participate in the choice of techniques chosen or rejected by the attending veterinary orthopedic surgeon. Caveat: Many orthopedic surgeons become so skilled in one method that their success is greater with that procedure than with another that theoretically might be better suited for the candidate animal. The authors suggest finding a surgeon comfortable with a particular procedure that would seem to fit the case, and whose patients have done well. Be aware that no one procedure is suitable for all candidates for surgery and that some level of argument may be made for and against any given procedure for any given candidate. The best choice, when factoring cost, age value of the animal, use of the animal, stage in the disease process, etc., may not always be clear.  

 

 

Before the development of advanced degenerative joint disease, surgical options include:

  • pectineal myotomy-cutting or dissection of the pectineous muscles;
  • pectineal myectomy-excision of a portion of the pectineous muscles;
  • three-plane intertrochanteric osteotomy-changing the angle of the femoral head;
  • triple pelvic osteotomy-cutting the pelvis into three pieces then putting it back together with more favorable acetabular angles.

After the development of advanced degenerative joint disease, surgical options include:

  • excision of the femoral head and neck;
  • shelf arthroplasty;
  • total hip replacement.

The excision of the femoral head and neck is often selected for those animals in the end stage of the disease. For advanced cases, where the value of the animal warrants the expense, often the procedure of choice is total hip replacement. For those dogs that are too far advanced into degenerative joint disease for a reconstructive procedure such as triple pelvic osteotomy to be effective, and yet not bad enough to warrant total hip replacement, there is a new "shelf" procedure in development that uses a bone graft technique to extend the acetabular rim and improve femoral head coverage. Due to their complexity and cost, we will reserve our treatment of femoral neck and head excision and THA (total hip arthroplasty) to the eighth and final part of this series.

Pectineal Myotomy/Myectomy

Originally developed by J. Barden, Larry J. Wallace, D.V.M., M.S., modified the procedure in 1967 to include the tenectomy (cutting out a portion of the tendon) or tenotomy (cutting of the tendon) of the pectineus tendon of insertion (that part of the muscle that goes into and attaches to the bone). Pectineal myotomy/myectomy was first used to treat canine hip dysplasia in clinically affected dogs.3 Wallace�s procedure is by no means a cure for CHD, but has been described as somewhat effective in temporarily relieving pain and restoring function. One of the adductors of the hip, the pectineal muscle brings the hind leg in toward the mid-line of the dog. The rationale for this procedure is to relieve the tension on the joint capsule, caused by the upward force on the coxofemoral joint from a contracted pectineus muscle. It is also thought that improved weight loading of the femoral head within the acetabulum may result from the increased range of abduction. Note the difference between "adduction" (moving toward the center line) and "abduction" (moving away from the center line). This type of surgery should be considered strictly therapeutic in nature and does little or nothing to stabilize the dysplastic hip. Therefore, the owner of an affected animal can expect the degenerative changes due to osteoarthritis to continue.

Figure 3 (left) shows before and Figure 4 (right) shows after triple pelvic osteotomy and femoral neck lengthening. Figures 1-4 courtesy of Dr. Barclay Slocum, Slocum Veterinary Clinic.

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Complications attributed to this surgical option include fibrotic reattachment of the muscle or tendon and seroma formation. Seroma are tumor-like collections of blood and serum in the muscle tissue. A modification of the earlier procedure, which allows suturing the tendon of insertion to the "belly" of the pectineus muscle, has been suggested to address both of these post-surgical consequences.

Published data showing the efficacy of this surgical treatment include several studies where dogs that had had pectineus surgery at 4 to 12 weeks of age demonstrated no beneficial effects from this procedure when evaluated again at 12 to 47 months.4,5 However, this surgery is used in clinical practice when an owner cannot afford one of the more sophisticated surgical procedures, or to restore function to a working animal when the dog needs to be used in the near future. Activity is restricted for only two weeks after this type of surgery.

Shelf Arthroplasty

The purpose of shelf arthroplasty is to form an extension over a shallow acetabulum to improve joint stability. Diminished depth of the acetabulum is most often the result of osteophyte formation. This procedure is supposed to improve coverage of the femoral head, prevent stretching of the joint capsule and thus eliminate and reduce pain. But as yet, there is no evidence that this surgery alters the progression of CHD in young dogs.

Because of the controversy surrounding the BOP (biocompatible osteoconductive polymer) shelf arthroplasty, which questions both the efficacy of the procedure itself and the safety of the material used, the authors choose not to recommend this surgical option. "I have reservations about the procedure," says Dr. Marvin Olmstead, professor of small animal orthopedics at the Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Ohio State University. "When one critically looks at the postoperative radiographs provided by the BOP manufacturer, it is apparent that the arthritis continues. I know of several cases in which there was development of foreign body reactions and draining tracts from this substance." [Authors� emphasis.]6 Dr. Barclay Slocum of the Slocum Clinic (Eugene, OR) also concurs with this opinion and adds, " It just doesn�t do what it claims to do."7 Minor complications can include broken screws and seroma formation. There are a number of researchers developing bone graft shelf arthroplasty techniques to extend the acetabular rim to provide greater coverage of the femoral head. Shelf arthroplasty is not a true arthroplasty as it does not change the existing joint surfaces, it only extends their rim.

Intertrochanteric Osteotomy

Prior to improvements in the method for performing triple pelvic osteotomy, the intertrochanteric osteotomy was commonly used if there was adequate depth in the acetabulum socket, and if the dorsal rim was normal, i.e., osteophyte formation had not begun.8 This surgery reduces the angle of the femoral neck, which improves congruity between the femoral head and the acetabulum, resulting in an improved fit. Because it corrects conformational and structural problems of the femoral head, this procedure must be performed before any major remodeling of the acetabulum has occurred. Nevertheless, pain and radiographic subluxation must be clinically evident prior to any reconstructive surgery in order to justify the pain, effort and expense. The average angle of inclination of the femoral neck in the dog is 149 degrees(normal range 141 to 157 degrees). The intertrochanteric osteotomy over-corrects this angle to approximately 135 degrees by removing a wedge of bone. See Figure 5 and Figure 6 for before and after images. This is thought to increase the surface area over which the pressure or "load" is spread. The greater the surface area, the less the pressure per unit of area there is on the coxofemoral joint in any one place.

Figure 5 (left) shows before and Figure 6 (right) shows after double intertrochanteric osteotomy. Note the improved congruity between the femoral head and acetabulum. Photos courtesy of Braden, T.D.; Prieur, W.D. "Three plane intertrochanteric osteotomy for treatment of early stage hip dysplasia." Vet Cl N Am Sm Anim Prac. Vol.22 No.3 May 1992. pp.624-643.

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Two studies have been done to evaluate the effectiveness of this surgical procedure. The first one was published in 1987 and assessed 183 dogs from one to seven years after the surgery was performed.9 The results of this study demonstrated an 89.6 percent "excellent" or "good" return to motor activity. "Excellent" was reserved for those dogs that exhibited a normal gait and no pain when exercised over long distances. "Good" was defined as a slight limp appearing after exercise, but exhibiting a normal gait while walking or running. Better results were attained if the dogs were operated on prior to the appearance of degenerative joint disease. Only 12.1 percent of the dogs with severe osteoarthritis had excellent results as opposed to 51.4 percent of those dogs without any osteoarthritis before surgery and 45 percent of those dogs with mild degenerative joint disease. A later study covered the seven-year period between 1980 and 1987. Published in 1990, this article evaluated 37 dogs with a total of 43 hip surgeries.10 The evaluation procedure consisted of a questionnaire and/or an orthopedic examination. Also included was a report from the owners via telephone. A rating of "excellent" in this second study was defined as normal function, whereas "good" was characterized as normal weight-bearing with joint stiffness after strenuous exercise or a long rest. Follow-up consisted of:

  • owners� phone reports-68 percent "excellent" or "good" at 11 months;
  • a questionnaire that evaluated dogs at one year-70 percent "excellent" or "good";
  • an orthopedic exam at 15 months-80 percent "excellent" or "good."

The stated goal of this procedure is to relieve pain. In humans, the surgery provides relief for an average of five to six years.11 It has been assumed that the results are somewhat similar in dogs, but the actual expected duration of improvement has not yet been determined.

Triple Pelvic Osteotomy

The TPO may be considered the exception to the view that these surgeries are "salvage" in nature. For this procedure to be effective, this surgery must be performed before major remodeling of the femoral head and the acetabular rim has occurred. That means that the primary abnormality should be radiographic indications of subluxation of the affected hip.

Slocum believes there are two forms of canine hip dysplasia.12 One condition exhibits either a shortened femoral neck or an improper angle between the femoral head and the long axis of the femur. This problem can be corrected by lengthening the femoral neck (Figure 1). The femur is split down the long axis and a polymer wedge is placed proximal (toward the center) to the femoral head. The bone is then wired together and the new bone fills in the gap. Some controversy exists with this procedure, however. "I view the femoral neck lengthening procedure with extreme caution," says Dr. Gail Smith of Penn State. "Although I have not performed mechanical testing on femurs treated with this method I estimate the reduction in femoral torsional strength [resistance to twisting] to be at least 70 percent, leaving the femur susceptible to fracture. This procedure has a theoretical basis only, and I am unaware of scientific proof supporting its clinical efficacy."13 In answer to this criticism, Slocum adds, "Although drilling a hole or cutting a bone as in any surgical technique will make a bone weak to torsional stresses, the healed bone is strong, durable and functional. After healing has been completed in the femoral head lengthening, no clinical experiences of this bone fracturing has been reported by other doctors using this technique or experienced by me in my clinical practice."14

By far the most common form of CHD that Slocum sees in his clinical practice is acetabular hip dysplasia.15 This type is characterized by having an excessive slope to the dorsal rim of the acetabulum. When the dog is standing, it is this portion of the pelvis that supports the animal�s weight. Slocum believes excessive slope of the acetabulum is the primary cause of the sideways displacement or subluxation of the femoral head. This leads to stretching of the round ligament, which in turn can cause the joint capsule to stretch, thus producing the hip laxity that commonly characterizes CHD.

Slocum believes that the best candidate for this type of surgery should have a combined dorsal acetabular rim (DAR) slope of more than 15 degrees. The determining factors for suitability of triple pelvic osteotomy are: DAR angle, angle of reduction and angle of subluxation. His past candidates have been from 4 months to 8 years of age. The surgical procedure consists of cutting the pelvis at three different points (Figure 2). This allows the acetabulum to be tilted until it is perpendicular to the femoral head. With the force generated at a 90-degree angle the femoral head is kept within the socket by the weight of the animal. This procedure also relies on muscular contraction to keep the femoral head seated within the socket, so any neurological deficit or muscular problems would necessarily disqualify a dog for this type of surgery. Various methods are used by the surgeons to determine the angle at which to tilt the pelvis. Slocum uses the DAR projection and draws a line parallel to the top of the femur. This indicates the required angle when this line intersects the dorsal slope.

Note that the intertrochanteric osteotomy and the triple pelvic osteotomy are in essence two approaches to the same overall goal: that of aligning the acetabulum and the femoral head for the greatest congruity. The intertrochanteric osteotomy attacks the problem from the pelvis. If done well, indications are that the results are beneficial and similar. Indications for a triple pelvic osteotomy combined with a femoral neck lengthening are: the dorsal acetabular rim is damaged, the acetabulum is not filled with osteophytes and the joint capsule is stretched. Figure 3 and Figure 4 show before and after imaging of femoral neck lengthening and pelvic osteotomy procedures done on the same animal. Note the great improvement in the femoral head to acetabular cup fit in the after view.

Conclusions:

Surgery is a viable option given the suitability of the candidate animal, the financial resources available, the expected activity level, longevity and the use and value of the animal. Choice of intervention, medical, surgical or activity level is process-dependent. Problems with certain procedures may be associated with improper patient selection relative to the stage of the disease. To be fair, patient compliance, i.e., owner post-operative management, may also be a significant factor.

The next and final article in this eight-part series will cover total hip replacement. Exciting new advances have been made and are currently supported by manufacturers. The costs remain high, but then so are the benefits to be gained in a suitable candidate.

References

  1. Goring, Robert. "Surgical and medical management of canine hip dysplasia." Hoffman-LaRoche Symposium on Degenerative Joint Disease. Orlando, FL January 12, 1992. Pp.7-15.
  2. Cargill, J.C.; Thorpe-Vargas, S. "Medical management of canine hip dysplasia." Dog World. October 1995. Pp.24-28.
  3. Wallace, L.J. "Pectineous tenectomy or tenotomy for treating clinical canine hip dysplasia." Vet Clin N Am. 1971. Vol. 1. Pp.455-465.
  4. Bowen, J.M.; Luis, R.E.; Kneller, S.K., et al. "Progression of hip dysplasia in German Shepherd Dogs after unilateral pectineal myotomy." J Am Vet Med Assoc. 1972. 161:899-904.
  5. Lust, G.; Craig, P.H.; Ross, G.E.; et al. "Studies on pectineous muscles in canine hip dysplasia." Cornell Vet. 1972. Vol. 62. Pp. 628-645.
  6. Smith, Carin. "Treatments for hip dysplasia spark controversy." J Am Vet Med Assoc. Vol. 201. No. 2. July 15, 1992.
  7. Personal communication with Dr. Barclay Slocum, Slocum Clinic, (503) 689-9393. August 17, 1995.
  8. Prieur, W.D. "Intertrochanteric osteotomy in the dog: Theoretical considerations and operative techniques." J Sm Anim Pract. 28:3-20, 1987.
  9. Walker, T.; Prieur, W.D. "Intertrochanteric femoral osteotomy." Seminar Vet Med Surg (Small Animal). 2:117-130, 1987.
  10. Braden, T.D.; Prieur, W.D.; Kaneene, J.B. "Clinical evaluation of intertrochanteric osteotomy for treatment of dogs with early-stage hip dysplasia: 37 cases (1987-1989)." J Am Vet Med Assoc. 196:337-341, 1990.
  11. Reigstad, A.; Gronmark, T. "Osteoarthritis of the hip treated by intertrochanteric osteotomy." J Bone Joint Surg Am. Vol. 66. Pp. 1-6. 1984.
  12. Slocum, B.; Slocum, T.D. "Pelvic osteotomy for axial rotation of the actabular segment." Vet Clin N Am. Vol. 22. No. 3. Pp. 645-682. May 1992.
  13. Smith.
  14. Personal communication with Dr. Barclay Slocum, Slocum Clinic, (503)689-9393. August 22, 1995.
  15. Slocum, B; Slocum, T.D.