Hip Dysplasia - Inviting discussions

[gemy]

Here is an old article I found on my computer. I've not found updated research material at this point in time.
Whilst I know that HD in Yorkies is not as common as in the large breeds, sadly Leggs Perthes and HD seem to be on the increase in the Yorkie breed.

If you know of more recent articles/research I'd love to have them posted here on this thread.

Managing Polygenic Disease:
Canine Hip Dysplasia as an Example

Jerold S Bell, DVM
Tufts University School of Veterinary Medicine, N. Grafton, MA

Polygenic disorders have been difficult for breeders to control. Examples are hip dysplasia, congenital heart defects, and epilepsy. Controlling polygenically inherited disorders involves; 1) identifying traits that more closely represent genes being selected against, 2) the standardization of nuisance factors (such as environment) that can limit your selective pressure against the genes and 3) selecting for breadth of pedigree as well as depth of pedigree.

Hip dysplasia is a classic example of a polygenically controlled hereditary disease. Due to genetically controlled defects in anatomy and/or joint laxity, affected dogs can become lame, and eventually crippled due to secondary osteoarthritis. The genetic test used to control hip dysplasia is the pelvic radiograph (x-ray).

To control polygenic disorders, they must be considered as threshold traits. A number of genes must combine to cross a threshold producing an affected individual. Genes that combine in an additive manner are considered quantitative genes. If we theoretically state that five quantitative genes contributing to hip dysplasia can produce a dysplastic dog, then dogs receiving less than five genes from their parents would have normal hips. If phenotypically normal parents produce affected offspring, both should be considered to carry a genetic load that combined to cause the disorder.

Many polygenic disorders have a major recessive or dominant trigger gene that must be present to produce an affected individual. Genes that act in a dominant or recessive manner are considered qualitative genes. If qualitative genes play a role in hip dysplasia, then it is possible that dogs with more than the threshold of quantitative genes could be phenotypically normal if they do not carry a qualitative trigger gene. They would pass on a high liability for dysplasia through their contributing high numbers of the additive genes.

A trigger gene in one breed or family may be different from the gene in others. Consequently, if a test for a trigger gene is developed in one breed or family, it may not provide useful information for all breeds or families. Molecular genetic research to identify major qualitative disease causing genes can allow better control of polygenic disorders such as hip dysplasia, epilepsy, and cataracts.

Breeders must break down hip phenotypes into traits that more directly represent the genes that control them.

One reason we have not had great progress with hip dysplasia control is that it is being treated as a single gene disease, with a test for carriers. There is no excellent hip gene, although that is what most breeders are selecting for. In polygenic disorders, the phenotype of the individual does not directly represent its genotype. Breeders must break down affected phenotypes into traits that more directly represent the genes that control them. These include clinical signs of lameness (especially during the critical period of bony ossification between six and eighteen months of age), palpable laxity under anesthesia, deep acetabula, rounded femoral heads, the absence of remodeling, deeply seated hips on an extended leg view, and radiographic distractibility.

We know that the environment has a role in the expression of hip dysplasia. Overnutrition and excessive environmental trauma during the critical growth periods prior to skeletal maturation will promote later dysplastic development. While limiting these environmental stresses is prudent in pet dogs, it is recommended that breeders do not overly protect or overly stress prospective breeding dog’s development. You do not want to mask the expression of dysplasia causing genes in breeding stock. Breeders should evaluate prospective breeding dogs raised under fairly uniform conditions, which neither promote, nor overly protect against hip dysplasia.


The genetic cause of hip dysplasia between these two dogs is different.

All dogs do not have hip dysplasia due to the same gene combinations. A dog with laxity and subluxation but normal anatomy has hip dysplasia caused by different genes than a dog with no subluxation but malformed sockets. Selection against the components of the syndrome may provide better control. If a quality dog is to be bred, but has shallow hip sockets, it should be bred to a dog with deep hip sockets. Two dogs with fair hips can be bred together and produce much worse hips if they share detrimental traits, or could improve on each other if they compliment each other’s good traits. You need to select for enough genes influencing normal development, to get above the threshold where dysplasia develops. Not all of these aspects will insure a genetically normal dog, but the chances increase with the more that are present.

Phenotypic Tests for Hip Dysplasia Control

The Orthopedic Foundation for Animals (OFA) has a longstanding hip dysplasia registry to attempt to control the disorder based on an extended-hip radiograph. OFA ratings are based on hip joint conformation (anatomy), joint laxity, and remodeling (arthritic changes). The Institute for Genetic Disease Control (GDC) also maintains a registry for hip dysplasia based on the extended leg view.

The PennHip method of evaluating hip status is based on a measurement of joint laxity different from that recorded on the extended leg radiograph. The PennHip method utilizes a radiograph taken while applying a uniform force on the hips of an anesthetized dog to measure the maximum distractibility of the hips. By computing a breed average of distractibility, and selecting for tighter hips than the breed average, it is believed that the incidence of hip dysplasia should decrease over time.

There are pros and cons to both the OFA and PennHip radiographic methods of hip dysplasia control. The OFA radiograph documents anatomical abnormalities (shallow sockets, early bony changes), but only natural laxity in a hip extended view. The PennHip radiograph documents maximum distractibility, but many dogs with a high distraction index do not develop hip dysplasia. It is shown that both techniques have false positive and false negative results. For both methods, radiographic findings at an early age are highly correlated to dysplasia at a later age. OFA does not give permanent certification until two years of age, but offers preliminary evaluations at any age.

While PennHip identifies maximal laxity, and OFA identifies hip conformation, neither radiographic method accounts for the breadth of pedigree. For selective pressure against hip dysplasia, these tests must be used in conjunction with knowledge of the hip status of the littermates.

Selection for Breadth vs. Depth of Pedigree

Another reason for diminished progress against hip dysplasia and other polygenic disorders is that breeders have been selecting for generations of phenotypically normal parents and grandparents (depth of pedigree). In polygenic disorders the phenotype of the full brothers and sisters more directly represent the range of genes present in the breeding individual. In other words, the breadth of the pedigree is as important, if not more important than the depth of the pedigree in polygenic disease control. If a dog with normal hips comes from a litter with a high incidence of hip dysplasia, you would expect it to carry a higher than normal genetic load of genes for hip dysplasia. By selecting for breadth of phenotypically normal littermates of breeding dogs, and of parents of breeding dogs, all breeds should realize a decrease in hip dysplasia. In addition, the offspring of breeding dogs should be monitored to see which are passing the disorder with higher frequency.

[gemy]

A number of environmental factors can affect the incidence of hip dysplasia in dogs The link to the article below.


A Number of Environmental Factors Can Affect the Incidence of Hip Dysplasia in Dogs
Mar. 26, 2012 — Hip dysplasia (HD) in dogs is affected to a larger degree than previously believed by the environment in which puppies grow up. It is particularly during the period from birth to three months that various environmental factors appear to influence the development of this disease. During the puppy stage, preventive measures can therefore be recommended with a view to giving dogs disposed to the condition a better quality of life.
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Randi I. Krontveit's doctoral research has studied the incidence of HD in four breeds of dog in Norway and examined factors in the environment where the dogs grew up that can have an affect on the number of cases. HD is a genetic disease which also occurs in several other species. Dogs are not born with HD, but genetically disposed puppies can develop varying degrees of HD. The degree of HD has an affect on when the dogs show symptoms and on how long they live.
Five hundred privately owned dogs participated in the study and the four breeds investigated were the Newfoundland, the Labrador Retriever, the Leonberger and the Irish Wolfhound. The environment in which the dogs were born and grew up was registered by means of questionnaires filled out by the breeder and the new owner, and by examinations carried out by veterinary surgeons.
Findings from previous experiments and studies from other countries have indicated that rapid growth and a high body weight are factors that increase the likelihood of developing HD. Randi I. Krontveit's research has shown that rapid growth and high body weight in the first year of the puppies' life did not result in an increased risk of HD. On the contrary, she found that the breed that had the slowest growth rate -- the Newfoundland -- had the highest incidence of HD (36%). The Irish Wolfhound had the lowest incidence of HD (10%), yet had the fastest rate of growth.
Puppies usually live with their mother at the breeder's for the first eight weeks of their life. Several factors related to the living conditions at the breeder's were shown to have an influence on the incidence of HD. Puppies born in the spring or summer and at breeders who lived on a farm or small holding, had a lower risk of developing HD. After about eight weeks, the puppies began life with their new owner. The opportunity to exercise daily in parks up until the age of three months reduced the risk of HD, whereas the daily use of steps during the same period increased the risk. Overall, it would appear that daily exercise out in gently undulating terrain up until the age of three months gives a good prognosis when it comes to preventing HD.
The dogs in this study were followed up until they reached 10 years of age by means of annual questionnaires filled out by the owner. Dogs seriously affected by HD were put down earlier than dogs with a milder form of the disease. This was particularly the case for Newfoundlands and Leonbergers. HD did not have such a large affect on the longevity of Labrador Retrievers or Irish Wolfhounds. Serious and moderate degrees of HD increased the risk of symptoms such as limping and hip pain and these symptoms occurred earliest in Newfoundlands. The Labrador Retriever was the breed in which symptoms appeared latest in life. Varied exercise had a positive effect and dogs that exercised on a daily basis on a lead and running free in different types of terrain were free of symptoms longer than dogs that were less active.
Based on the findings of this doctoral research, preventive measures related to early canine life can be recommended. If HD in its most serious forms can be prevented, the life quality of dogs will be improved.
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Norwegian School of Veterinary Science (2012, March 26). A number of environmental factors can affect the incidence of hip dysplasia in dogs. ScienceDaily. Retrieved December 13, 2012, from http://www.sciencedaily.com* /releases/2012/03/120326112842.htm
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Dogs playing. (Credit: Image courtesy of Norwegian School of Veterinary Science)
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[gemy]

Canine hip dysplasia genes identified

[lisaly]

This is wonderful news. Thank you for sharing this.

[gemy]

With two breeds identified with the HD genetic markers, a similar methodology employed should help them identify more breeds faster!


HD in Yorkies according to the offa data base is as follows: Note that only 103 evaluations were done as compared to 561 on Patellas and LCP fewer still at 93. Also please note that these evaluations represent only those breeders who agree to post the results. Note the ranking for LP at No2. Not surprising at all they are ranked No 2 against all breeds for this condition - Pomerians beat them for the No 1 spot. Oh and btw you don't want to be at the top of the list here when we are talking about diseases. The accumulated numbers run from 1974 to December 2013. Very few evaluations done and submitted given the popularity of this breed!


Evaluations through December 2013RegistryRankEvaluationsPercent
AbnormalPercent
NormalPercent
CarrierPercent
EquivocalCARDIAC93242.0100.0.0.0ELBOWN/A5.0100.0.0.0EYES27641.698.4.0.0HIPS1261036.892.2. 0.0LEGG-CALVE-PERTHES2933.296.8.0.0PATELLA256124.475.6.0.0THYROI D10355.085.5.014.5

[gemy]

Sorry the beautifull chart did not copy right.


Here is the link: Orthopedic Foundation for Animals

[Mike1975]

Gemy here is a very interesting article for Legg-Calve-Perthes Disease.

http://www.akcchf.org/news-events/li...update0110.pdf



Since a recessive gene may be involved, it is impossible to know if a clear dog (with no clinical signs) is a carrier. There is no method for detecting carriers of the disease.

Assuming that it is recessive, the presence of even one puppy with LCPD, shows that BOTH parents are carrying the recessive LCPD gene.
So both the sire and the dam should be excluded as carriers. This also shows that the whole litter may carry the recessive gene.

Anyway... Lets hope in our lifetime that there will be a genetic test for LCPD

[gemy]

Originally Posted by Mike1975

Gemy here is a very interesting article for Legg-Calve-Perthes Disease.

http://www.akcchf.org/news-events/li...update0110.pdf



Since a recessive gene may be involved, it is impossible to know if a clear dog (with no clinical signs) is a carrier. There is no method for detecting carriers of the disease.

Assuming that it is recessive, the presence of even one puppy with LCPD, shows that BOTH parents are carrying the recessive LCPD gene.
So both the sire and the dam should be excluded as carriers. This also shows that the whole litter may carry the recessive gene.

Anyway... Lets hope in our lifetime that there will be a genetic test for LCPD

I second the hope of a genetic test for LCP in our lifetime. I suspect that it is not just one recessive gene but several genes - which makes it even more difficult to find. And makes it a *crap* shoot to understand who in any puppy litter might be carrying the recessives.


I also wonder if it is actually associated with a boney disorder instead of a failure of the arterial walls to develop normally. This is of course will make a difference on where in the genome researchers target their research. If it is an arterial wall problem why only on the femoral artery supply? Why aren't other arteries affected? Perhaps it is a local blood pressure regulation problem? Just thinking aloud.


I also find it curious that it seems to be limited to small breed dogs - why?


In the same way HD is much more prevalent in larger breed dogs - why?


Mike I don't know if you have PennHIP qualified vets in Greece, but look up PennHip, it is an early diagnostic tool for HD, and many breeders here are going with this method. I have not researched yet if PENNHIP methodology would also catch early signs of LCP but it would be good to find out. You can test as early as 3months old.


Before breeding any YOrkie I believe they all should have offa certifications on hips, this way you do know if you have a breeding dog affected. How-ever LCP should start to show up around 7-8months old but that is no guarantee, as some dogs only exhibit clinical signs at over one year old and older dependent upon the progression of the disease. The clinical signs start off subtly, mild limping etc.


If you do Xrays at around one year old, even if there are no overt clinical signs, there should be evidence of the disease........ This way before you breed at least you know your dog is clear of LCP, but of course that doesn't mean they don't carry the recessive gene(s).

[gemy]

http://breedingbetterdogs.com/pdfFil...ne_12_2013.pdf


Please note she describes LCPD as a polygenetic one.

[gemy]

Here is Part 1 http://breedingbetterdogs.com/pdfFil...il_20_2013.pdf

[Mike1975]

Thanks Gemy for the links and all the info.
All these are very interesting.

I haven't found PennHIP qualified vets here yet, but since I am not a breeder I haven't done much research on the subject. Of course it would be useful to have this information all the same.

Its nice to know that there are people who care about our breed.

[gemy]

Your very welcome. Health is one topic I am pretty passionate about

[Lorraine]

This site is interesting. It lists the breeds that LCP seems to be a bit of a problem however as it does state, I have known before it can occur in children. Orthopedic Foundation for Animals: Legg-Calve-Perthes
Another interesting article. Legg-Calvé-Perthes syndrome in dogs

[gemy]

Basic site, not showing the research they base their article on, nor in any, how to catch this early, before symptoms are visible.


If the first the very first sign of lameness means the femoral head has not de-constructed and then re modelled, that would be very good for pet owners to know, not to DELAY in getting their dogs X-rayed to see what is going on.


I remain with my recommendations, that all Yorkies should have OFFA on the hips done, before breeding! This should help to insure Leggs Calves Perthes dogs are not bred. And of course the YTCA AND THE CYTA, to fund research into this disease.!