Elbow dysplasia is a general term used to identify inherited
polygenic diseases of the elbow in dogs.
Three specific etiologies make up this disease and they can occur independently
or in conjunction with one another.
These etiologies include:
1. Fragmented medial coronoid process of the ulna
2. Osteochondritis of the medial humeral condyle
3. Ununited anconeal process
The clinical signs involve lameness which may remain subtle for long periods
of time. No one can predict at what age lameness will occur due to a large
number of genetic and environmental factors such as degree of severity of changes,
rate of weight gain, degree of exercise, etc. Affected dogs may not show obvious
lameness and may only have an abnormal gait. Range of motion in the elbow
is also usually decreased. Frequently, there is bilateral disease but unilateral
elbow dysplasia is not uncommon.
Once it is diagnosed, conservative
therapy can be an option for dogs affected by intermittent and/or mild degrees of
lameness. The use of pain relievers/anti-inflammatory agents such as Aspirin,
EtoGesic or Rimadyl can be used during bouts of lameness especially an hour or so
before known periods of exercise. Various osteoarthritis modifying agents
and nutraceuticals now on the market would be another option such as Adequan, Cosequin,
SynoviCre, Glycoflex, Arthramine, and MaxFlex Pet. The use of these
drugs should be tailored for the individual dogs improvement note. If side-effects
occur or there is persistence of obvious lameness, change the therapy to a different
drug from the above choices. You may notice obvious improvements this way.
With oral nutraceuticals, the dog may have to have taken the medication for an extended
period of time before benefits are noted. It is important to keep your dog
as lean as possible to reduce concussive mechanical forces across the diseased joints.
Also, to maintain the range of joint motion, strengthen surrounding muscles to improve
joint stability and improve the health of the joint fluid, non-weight bearing forms
of exercise such as swimming or low weight bearing exercise with leash walking should
be done on a regular basis.
If the dog is showing a continuous
and severe pattern of lameness, arthroscopic or surgical exploration of the joint
is recommended because usually in these cases, significant pathology is more likely
to be found and there is also more of a possibility for postoperative improvement.
Surgically, to remove joint fragments, the best treatment option would be arthroscopic
surgery however, this is not readily available except at some veterinary teaching
colleges and private practice surgical referral hospitals.
Arthrotomy where an actual
incision is made into the joint capsule is the most common surgery performed however
it is more invasive. Studies comparing surgical arthrotomy treatment with
non-surgical treatment have repeatedly shown that the incidence of lameness is the
same in both groups. Some studies have shown that the severity of lameness
is reduced in surgically treated dogs, but radiographic progression of osteoarthritis
occurs irrespective of the treatment given. Future studies will most likely
show a much more favorable outcome with the use of arthroscopic surgery. A
more rapid return to normal joint function has been clinically reported by most
owners.
The outcome or prognosis elbow
dysplasia depends on the degree of severity of elbow dysplasia and the degree of
severity of secondary degenerative joint disease (osteoarthritis). Dogs with
severe degenerative joint disease are more likely to have occasional bouts of lameness
even after surgery. Overall, the outcome for full return to normal is guarded.
Clinically, prognosis has been better in dogs that have had arthroscopic surgery
performed early in the course of the disease. With regular surgery where the
joint is opened with an lygenic variation is determined by the addition or combination
of factors. In additive heredity, traits become more evident according to
the number of genes present. Non-additive heredity does not depend some much
on the number of genes but rather their combination. The results which have
been obtained through selection against hip dysplasia and elbow dysplasia point
to the important role played by additive gene inheritance.
The phenotype of an animal is its physical appearance. The phenotype with
regard to the traits of hip and elbow development is found in dogs and cats by radiographing
the hips and elbows and evaluating the type of conformation present. With
basic genetics regarding any polygenetic trait, it is important to know the equation:
P (phenotype) = G (genetics)+ E(environment).
This equation expresses that
the variation in hip and elbow conformation phenotype (represented by excellent
to severely dysplastic from the OFA hip scoring method and normal to grade 1, grade
2 or grade 3 elbow dysplasia) comes about from the complex interaction of the animal's
own inherited genotype with the environment to which it has been exposed.
Quantitative hereditary characteristic traits for hip and elbow dysplasia are influenced
in various degrees by environmental factors. Overweight, excess of protein
and energy rich food, rapid growth rate, excess exercise or lack of excercise, high
calcium intake and other dietary influences have been suggested. Without
genetic pre-disposition however, environmental influences alone will not create
hip or elbow dysplasia (this goes back to the P=G+E equation).
In order to achieve rapid
genetic progress with the use of hip and elbow conformation phenotypes, heritability
estimates can be calculated. Heritability estimates are statistically determined
(usually through mid-parent offspring analysis statistical methods) and express
the reliability of the phenotypic value (radiographs) as a guide to the breeding
value of the animal. Heritability measures the relative . This also
increases the accuracy in predicting the animal's breeding value and identifies
carrier animals.
If the heritability estimate
is between 0.4 and 1.0, it is generally considered high and the animal's phenotype
is a good predictor of its genetic makeup and rapid results are obtained with genetic
selection for or against any trait.
This information can be complex to understand without detailed training in genetics.
However, the concept is important with regard to providing an indication
to an animal's potential reproductive potency based off the heritability estimate
of hip dyplasia and elbow dysplasia usually being in the moderate to high range.
An important question that
usually arises with regard to genetics of hip conformation is which mate has the
most influence on the offsping's hip conformation the sire or dam? Studies
looking at progeny hip scores for both the sire and dam show there is approximately
the same equal effect. A worse offspring hip conformation will occur as the
hip conformation of the dam and the sire worsen. Overall, the transmission
of hip dysplasia to the offspring depends on the dam as well as the sire.
This would also apply to elbow dysplasia. On the other hand, sire's with many
high awards obviously have a far greater influence on the breed than dams and selection
of an appropriate sire is more critical because they have the potential for more
offspring, therefore more impact on the phenotypic measurement of hip conformation
and frequency of elbow dysplasia than a dam.
With regard to genetics of
hip and elbow in a breeding program, dogs without canine hip dysplasia and without
elbow dysplasia are more likely to be born to parents without hip or elbow dysplasia.
It is generally accepted that if two litter mates with similar genetics from a strong
pedigree are used in a breeding program and one is rated excellent and the other
rated fair, the parent will commonly produce the majority of offspring with hip
conformation's similar to their own hip conformation. A small percentage of
the offspring may have less superior hip conformation than the parents and another
small percentage will have superior hip conformation than the parents. This
is expected with any polygenetic trait whether it be hips, size, speed, movement
etc. Likewise, numerous reports show that many offspring from parents with
hip or elbow dysplasia also become dysplastic, often several or all siblings in
a litter are dysplastic. Research performed by Willis summarized results of
a number of breeding programs and concluded that in various dog populations, between
64 to 81% of the progeny of normal dogs (as determined on the basis of standard
hip conformation scoring) would also be normal and between 19 and 36% would be dysplastic.
On the other hand, between 17 and 37% of the progeny of dysplastic dogs would be
normal and between 63 to 93 % would be dysplastic. Even with using a dysplastic
dog that has a strong pedigree for normal hips, over the course of a few generations,
there are higher percentages of dysplastic dogs. Even if the first generation
offspring is phenotypically normal from this type of mating, there is increased
frequency of dysplastics in subsequent generations due to an increase in the number
of carriers in the litter that when breed, go on and pass undesirable traits for
hip dysplasia onto their offspring. This is why the OFA does not recommend
the use of dysplastic animals in any breeding program no matter what type of pedigree
they come from.
The most important information
to answer in any breeding program is what is an animal's predictive breeding value?
This value can usually be ascertained by the available information present on hip
and elbow status of the individual dog, the dog's parents and the dog's littermates.
All three of these questions are important with the heritability of canine hip dysplasia
and elbow dysplasia being in the moderate range in most dog populations. Unfortunately,
all of this information is usually not available since most animals in a litter
are not radiographed for hip or elbow conformation. When looking at the order
of importance of hip and elbow information on a pedigree analysis and ranking them
with regard to placing a predictive breeding value for an individual dog, the dog's
parents hip and elbow information is very important followed by the dogs own individual
hip and elbow conformation then followed by litter mate information. With
most breeders making their predictive breeding value decisions on individual hip
and elbow phenotype scores, a decreased frequency of dysplasia will be substantial
but slow. Information on parents and siblings makes it more feasible for the
breeder to apply greater selection pressure against dysplastic traits and achieve
more rapid reductions in the frequency of canine hip dysplasia and elbow dysplasia
in their lines. An example would be looking at two potential new sires from
different pedigrees to use in a breeding program. Each sire has similar
desirable traits that are above average when compared to other members of the breed.
The only difference is one sire has excellent hips but has only one parent
with an OFA hip number of good (the other did not have an OFA number) and no siblings
with OFA hip numbers and one known dysplastic sibling. The other sire has
fair hip conformation out of two OFA good parents and 2 OFA good and 2 OFA excellent
littermates. The probability for normal hips would most likely be with the
use of the fair sire especially when bred to an excellent or good mate that has
a similar strong pedigree for hip conformations. When the breeder has all
of the information to work with, a higher success rate for hip and elbow conformation
is achieved more rapidly.
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REFERENCES:
1. Brass, W. Hip dysplasia in dogs. J Sm An Prac, 1989, vol. 30, pp.166-170.
2. Riser WH. Canine Hip Dysplasia: Cause and Control. JAVMA, Vol. 165, No. 4, 1974,
pp. 360-362
3. Leighton EA. Genetics of canine hip dysplasia. JAVMA, Vol. 210, No. 10, 1997,
pp. 1474-1479.
4. Mackenzie SA. Why heritibility estimates differ. Can Prac, Vol. 12, No. 2, 1985,
pp. 1922.
5. Lust G. Overview of the pathogenesis of canine hip dysplasia. JAVMA, Vol. 210,
No. 10, 1997, pp. 1443-1445.
6. Padgett GA, et al. The inheritance of osteochondritis dissecans and fragmented
coronoid process in the elbow joint in Labrador Retrievers. JAAHA, Vol 31,
1995, pp. 327-330.
*Reprinted with permission
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