From: djg@cray.com (Dennis Guldan)
Subject: The Long awaited OFA Pamphlet on Hip Dysplasia
Keywords: OFA Pamphlet
Date: 15 Sep 92 09:52:38 CDT



  ALRIGHT YOU HIP DYSPLASIA DEBATE FANS.

  Below if the first 9 pages of the 28 page pamphlet I got from OFA.
 The rest will be sent in a few days.


General:

  Canine hip dysplasia (CHD) was first reported in 1935 by Dr. G.B. Schnelle.
Little to no further information was added to his report over the following
decade, due primarily to limited availability of radiographic equipment and
radiographic knowledge in the veterinary profession.


  Popularity of the working dog, particularly the German Shepherd Dog,
increased greatly in the late 1940s and the importance of CHD became evident to
the breeder, dog owner, and veterinary profession. Unrelated, but concurrently,
veterinary education underwent an explosion in numbers of veterinary colleges
and in quality of education. The discipline of radiology emerged and became a
recognized specialty in 1966.


  Hip dysplasia has been reported in man and in most domestic species of
animals. In some breeds of dogs, it is the most common cause of osteoarthritis or
degenerative joint disease. Hip dysplasia in man resulted in increased availabili-
ty of research funds using CHD as the model to study the disease process. Thus,
man and dog benefited from the research.


      We now know that CHD is a more complex disease
      than was first thought. Thereare no simple answers
      or solutions to the problem.


  Research efforts have experienced "peaks and valleys" depending on avail-
ability of research funds and the demand for answers to questions raised by
observations-made by those involved in breeding of dogs and those in the
practice of veterinary medicine. We now know that CHD is a more complex
disease than was first thought. There are no simple answers or solutions
to the problem.           


   The complexity of the problem is expected to and has produced research
findings that appear to be contradictory. These research reports, plus anecdotal
writings that continually appear in the popular press, contribute to feelings of
confusion and frustration in breeders and veterinarians not familiar with the
scientific literature. Thus, few diseases in the dog have resulted in such extreme
emotional reactions, controversy, or monetary expense as CHD.


   However, each research study has added to our knowledge and understand-
ing of the problem, as many aspects of the disease have been repeatedly and
independently documented. These aspects are generally accepted by the scientif-
ic community. Three examples that are important to the breeder are:


1) Canine hip dysplasia  is currently accepted to be an inherited disease
   caused by the interaction of many genes (polygenic). No environmental
   cause has been found, but environmental factors may influence the
   degree of expression of the genes within an individual.


2) The only current means for reducing the genetic frequency of CHD is by
   selectively breeding for normal hips.


3) Radiography is currently the accepted means for evaluating the hip status.
   It is expected that these currently accepted aspects will be refined by future
   research studies. Advances in molecular genetics may replace radiography as
   the primary diagnostic tool or an environmental factor, i.e. medical or 
   nutritional, may be found that will overcome the genetic expression of CHD
   in an individual dog.


  There are many esoteric debates surrounding the myriad of possible factors
that may influence or initiate one or more aspect-of CHD. While interesting,
the breeder and veterinarian must pursue their primary goal using today's
knowledge without becoming mired in the debate. The responsible breeder
attempts to produce the best possible representatives of the breed. The
veterinarian assists the breeder in accomplishing this objective by education
of the breeder, maintaining the general health of the dogs, and providing
the best possible treatment when appropriate.


  The purposes of this paper are to assist the breeder, dog owner, and
veterinarian in accomplishing their goals by providing a summary of informa-
tion on CHD, its diagnosis, a reference source for further study, and an
explanation of the Orthopedic Foundation for Animals (OFA).


Development of the Hip Joint:

   After conception, the embryonic hip joint and its supporting structures
begin to develop from an undifferentiated mass of embryonic tissue.
Differentiation of this tissue into the distinct parts of the hip joint
is predetermined by a genetic code. A cartilage mold for the unique parts
of this ball and socket joint is formed. The socket is the acetabulum and
the ball is the head of the femur. The muscles, a special connective tissue
that encases the joint (the joint capsule), and ligaments of the joint are
formed from the embryonic tissue, but in a different manner. The structures
continue to grow and differentiate as the embryo matures. Ossification
(bone formation) begins at approximately 49 days of pregnancy. The degree
of skeletal maturity at birth appears to be breed dependent. That is,
ossification in some breeds is more advanced than in others which accounts
for the continued difference in rates of skeletal growth after birth.


   The surfaces of the femoral head and acetabulum are covered with smooth
articular cartilage. A thin layer of fluid (synovial fluid) which serves as a
lubricant for the joint and nourishment for the articular cartilage separates the
opposing surfaces. The head of the femur is attached to the depth of the
acetabulum by a ligament (round ligament).


   The joint capsule encases the joint by attaching the neck of the femur to the
rim of the acetabulum. It contains a specialized tissue, the synovial membrane,
which produces the synovial fluid. Muscles encase the entire hip structure and
serve to stabilize and move the joint. The major pelvic muscles exert a forward
and upward pressure on the femoral head during movement.


  The head of the femur is held in the acetabulum by the pelvic muscles, joint
capsule, surface tension, and the round ligament. Proper development of the
joint depends on the head of the femur being held firmly within the acetabulum
until all parts are mature.



   Hip Dysplasia.

   Dysplasia literally means bad development. The hip joint of the dog is
reported to be normal at birth.  After birth, something initiates a bad fit or

                 It is likely that multiple initiating factors
                 are involved and they may differ between
                 genetic lines, as CHD is caused by interaction 
                 of many genes (polygenic).



function of one or more of the parts of the hip joint. What the initiating
factors may be is unknown. It is likely that multiple initiating factors are
involved and they may differ between genetic lines, as CHD is caused by
interaction of many genes (polygenic). Currently, any attempt to define the
process in an exact sequence of events is speculative.

    Regardless of what the initiating factor or factors may be, abnormal loose-
ness (joint laxity), occurring sometime after 2 weeks of age, appears to be the
event most commonly reported to result in the pathologic changes of dysplasia
However, some dogs with tight hips have also been reported to develop
dysplastic changes.


  Many of the early pathologic changes (2-14 weeks) are not readily detectable
by clinical or radiographic examination. They include: swelling, fraying, and
possible rupture of the round ligament, inflammation of the synovial membrane
(synovitis) resulting  synovial fluid changes, stretching of the joint capsule,
and damage to the cartilage mold of the acetabulum and femoral head. These
structural alterations result in joint instability and subluxation which is followed
by erosion of the articular cartilage, changes in the bone beneath the articular
cartilage, microfractures of the dorsal acetabular rim, filling in of the acetabulum,
remodeling (change in size, shape or architecture) of the femoral head, neck
and acetabular rims, and production of osteophytes (bone spurs) around the
joint.


  Depending on the individual dog and the initiating factor/s of the joint
instability, the changes occur at varying rates and to differing degrees. Severe
cases can be detected radiographically as early as 7 weeks of age, while others
may not be evident until later in life (greater than 2 years of age).


Cause of Hip Dysplasia:

  Hip dysplasia is an inherited trait and it is controlled by the genetic makeup
(genotype) of the individual dog. The genotype is determined by the genes
received from the parents; one-half from the sire and one-half from the dam.
From the first to the last published scientific report, veterinary scientists have
agreed that there is a genetic basis for hip dysplasia. The literature contains
differences in concepts of the mode of inheritance. There dre also reports on
how the genes may bring about the dysplastic changes -estrogen metabolism,
muscle mass, pectineus musde spasm, synovial volume, etc. Unfortunately,
some investigators have mislabeled these as the possible cause/s of dysplasia.
Thus, some breeders and veterinarian mistakenly look to these factors rather
than the genetic factors to avoid the rigors of selective breeding.



       Regardless of changes in the concepts of
       the mode of inheritance, or how the genes
       exert their influence, scientists have re-
       peatedly demonstrated that hip dysplasia
       is controllable by selective breeding.


  The current concept is: hip dysplasia is an inherited polygenic trait. That is,
many genes affect the trait of dysplasia. This concept was presented in the late
1960s, and has been supported by independent research efforts throughout the
1970s and 1980s. One report, in 1974, refined the concept to suggest that at least
one pair of the genes is recessive and the remaining genes serve to modify the
effect. Further refinements can be expected as new knowledge becomes
available.


   Regardless of changes in the concepts of the mode of inheritance, or how
the genes exert their influence, scientists have repeatedly demonstrated that hip
dysplasia is controllable by selective breeding.



Rationale for Selective Breeding:


  Most inherited traits in animals are polygenic. Some examples, other than
hip dysplasia, are: conformation, type, size, longevity, disease resistance,
temperament, elbow dysplasia, speed, milk and egg production, growth rate,
maturation rate and sexual maturity rate.


   Intuitively, it is recognized that these traits do not follow patterns based on
Mendelian genetics. Mendelian genetics usually use one pair of genes to explain
basic genetic principles. For example, assume that: 1) The color black is
dominant to brown, 2) The black gene is represented by B and the brown gene
by b, and 3) We mate a homozygous black (BB) with a brown (bb). All of the
offspring will be black but of the Bb genotype (heterozygous). If we mate two
heterozygous blacks (Bb), then the offspring are expected to be 3 blacks (lBB
and 2Bb) and 1 brown (bb). The ratio of 1:2:1 for the genotypes is based on
probability. If only a small number of offspring are available from this type of
mating, they may all be of the same genotype, but larger numbers will give the
expected ratio. The finding of 1 brown offspring from the mating of black
parents means that both parents are carriers (heterozygous) of the recessive
brown gene. Also, 2 out of 3 black litter mates are camers but until bred we 
can't state which are the carriers. Thus, by examination of the progeny the
probable genotype, of the parents can be determined.


    Polygenic traits are affected by many genes. An oversimplified example is
two genes affecting the same trait. Assume the mating of two dogs with
genotypes, for a trait, of AaBb. The expected genotypic outcome is 9 different
genotypes with the following frequencies:


Genotypes- AABB  AABb  AAbb  AaBB  AaBb  Aabb  aaBB  aabb  aabb
Frequency- 1/16  2/16  1/16  2/16  4/16  2/16  1/16  2/16  1/16


   Only 25% of the progeny from this mating are expected to have the same
genotype for a trait as the parents. Some of the remaining progeny will have a
more desirable genotype while others will have a less desarable genotype for the
trait. As the number of involved genes are increased the possibilities sosr. The
problem is further magnified if each gene pair exerts a different degree of
influence on a trait. The number of genes affecting hip dysplasia, or any other
polygenic trait, is unknown. Predictions of a specific outcome from a particular
mating, involving polygenic traits, is currently impossible.


   Animal geneticists have developed breeding programs to improve milk
production in cows, egg production in hens, speed in horses, growth rate in
food animals, etc. They use basic genetic principles that have been demonstrated 
effective in the dog. Some of the following aspects of polygenic traits considered 
in arriving at these principles include:


1. Polygenic traits have a range of findings from the most desirable to the least
   desirable characteristic being considered.

   For example, mating two dogs of ideal conformation can be expected to
result in a larger number of offspring with ideal conformation when compared
with offspring of a mating where one or both parents have less than ideal
conformation. However, both litters will present a range of conformational
findings.


     Hip dysplasia follows the same pattern. Normals mated with normals
produce more normals than matings of two dysplastics or a normal with a 
dysplastic. The appearance (phenotype) of the hips ranges from excellent to
severely dysplastic with all degrees between the extremes.


2. Polygenic traits are influenced by the environment, as environmental factors
   may minimize or maximize genetic potential.

For example, a horse with a respiratory infection will not be able to achieve
its genetic speed capability, or a cow on a starvation diet will not produce milk to
its full genetic potential.


    The manifestation of hip dysplasia follows the same pattern. The most
studied environmental influence is caloric intake. A higher than need caloric
intake during the rapid growth phase may result in earlier and more severe
dysplastic changes when the genetic potential for dysplasia is present. A lower than
normal caloric intake may temporarily hide the evidence of dysplasia in the
same dog, but will not change the genotype.



                 Heritablity indexes are purported to:
                 measure, on a scale of 0% to 100%, how
                 much of the phenotypic variation in a
                 studied population is of genetic origin.
                 The index is expected to vary depending
                 on the studied population.



3. Heritability estimates are statistically determined to estimate breeding values
   or to determine the best approach to use in a breeding program.

  Heritability indexes are purported to measure, on a scale of 0% to 100%, how
much of the phenotypic variation in a studied population is of genetic origin. The
index is expected to vary depending on the genetic background of the studied
population. The reported index for German Shepherd Dogs in several different
populations ranges from 20% to 60%. The most recent and comprehensive
report places the index between 40% and 50% in a large population. An index of
80% has been reported in a population of Samoyeds.


  Genetic selection for or against any trait is expected to yield poor results if
the heritability index is low (10%). When the index is moderate (20% to 40%),
selection based on individual phenotypes is expected to yield slow yet substan-
tial results, but more rapid results can be obtained if phenotypes of the relatives
are also considered. The most rapid results are obtained when the index is high
(40% to 100%), as the individual phenotype becomes a good predictor of the
genotype. Results of selective breeding practices indicate that the dysplastic trait
should be considered in the moderate to high category.


    Unfortunately, many breeders and veterinarians minterpret the meaning
and use of heritability estimates. For example: a calculated value of 50% means
that 50% of the variation in phenotypes in the studied population is controlled by
the genes. This does not mean that 50% of dysplastic dogs are of a genetic cause. Nor
does it mean that 50% of the changes in an individual dog are caused by the genes
and the remaming 50% by the environment.


4. Mass selection - breeding selection based on individual phenotype -appears
to be the method used by most breeders, as available  information on relatives
is somewhat limited. This approach will reduce the frequency of dysplasia in
the progeny. Progress will be substantial but slow.


5. Information on larger numbers of dogs makes it more feasible for the breeder
to apply greater selection pressure against the dysplastic trait by using other
long-standing genetic principles. The following paraphrased breeding criteria
have been demonstrated to more rapidly and effectively reduce the frequen-


                 A dog with excellent hips but with more
                 than 25% of its brothers and sisters being
                 dysplastic is a poorer breeding prospect
                 than a dog with fair hips and less than
                 25% of its brothers and sisters being dys-
                 plastic.


                   

cy of dysplasia: (a) breed only normal dogs to normal dogs, (b) the normal
dogs should come from normal parents and grandparents, (c) the normal
dogs should have over 75% normal siblings, (d) choose a sire that has a record
of producing normal progeny that excceeds the breed average, and (e) choose
replacement bitches that have better hip joint conformation than their
parents and the breed average.


   In other words, information on phenotypes of individual dogs has its limits.
For example, a dog with excellent hips but with more than 25% of its brothers
and sisters being dysplastic is a poorer breeding prospect than a dog with fair
hips and less than 25% of its brothers and sisters being dysplastic.


Clinical Findings of Dysplasia:


   Many dysplastic dogs demonstrate some observable sign between 3 and 15
months of age. In some, the signs may not be observed until between 15 and 36
months of age, while in a smaller number of dogs the signs are not observable
until old age. The signs vary from decreased exercise tolerance to severe
crippling. They include: a reluctance or inability to go up or down stairs,
difficulty in rising from a sitting or prone position, bunny-hopping gait when
running, stiffness early in the morning that improves as the dog warms up,
change in disposition due to pain, lameness after exercise, wobbly gait, a
clicking sound when walking, and many others. Many dogs will shift their
center of gravity forward in an effort to relieve weight and pressure on the hips.
These dogs generally present a front end that appears well-developed relative to
the rear end.


   In dysplastic dogs, the hip joint is a weakened structure that is more subject
to being injured by normal activity such as jumping off a couch, or rough
housing with a playmate. Frequently, this results in an acute lameness that in
the mind of the owner was caused by the injury, whereas the underlying
dysplasia actually made the joint more susceptible to injury. Obviously, the
normal hip can be injured, but the radiographic examination can usually
distinguish between a hip problem due to dysplasia and one due to other
causes.


    CHD can not be diagnosed by observing how the dog moves, acts, lies down,
etc. The clinical signs may be caused by other problems; therefore, a complete
orthopedic and radiographic exammation is requhed before arriving at the
conclusion that the signs are cawed by CHD.



Diagnosis of Hip Dysplasia


  Historically the diagnosis of hip dysplasia is determined by radiographic
examination of the hips. The dog placed on its back with the pelvis
symmetrical, both femurs extended and parallel, and with, the stifles (knees)
rotated internally placing the patellas (knee caps) on the midline. The radio-
graph should include the last 2 lumbar vertebra and the stifle joint. It is
essential, particularly in marginal cases, that the proper position and radiograph
ic technique be obtained.       


  The radiographic criteria of subluxation, shallow acetabula, remodeling,
and/or secondary degenerative joint disease are well documented However,
interpretation and application of these criteria differs between breeds, age, and
veterinarians. Figure 1 provides the nomenclature of the hip structures that are
evaluated by the veterinary radiologist. (SORRY MY ASCII PICTURES AREN'T GREAT)
The radiologist is concered with deviations in these structures from the
breed normal. Congruity and confluence of the hip joint are considered along
with evaluation of the following aspects of the hip:


   1) Subluxation
   2) Cranial acetabular margin
   3) Dorsal acetabular margin
   4) Craniolateral acetabular margin
   5) Acetabular notch
   6) Caudal acetabular margin
   7) Size, shape, and architecture of the femoral headlneck
   8) Presence of exostosis or osteophytes
   9) Subchondral bone ebumation


  Some radiologists will also make various measurements of the marginal hip,
such as Norberg angle, to assist in arriving at a diagnosis. Good hips and the
obviously dysplastic ones do not require measurements.


   Radiography has its problems as the diagnostic method of choice. Some of
these are:
1) Joint laxity, looseness of the joint, is a dynamic state that may not be
determined by routine radiography. The joint may appear radiographical-
ly normal on a radiograph but in actuality be loose.


  Laxity is generally considered to be one of the earliest pathologic findings in
CHD. Therefore, demonstration of laxity in the young dog 3-6 months of age,
may constitute a diagnosis of dysphsia or possibly a predictor of dysphsia.
Palpation of the hips to feel the looseness is not generally accepted as a single
diagnostic feature of CHD. Use of a fulcrum or wedge (placing an object
between the thighs and bringing the stifles together to force the head of the
femur out of the acetabulum) has been advocated to radiographically demon-
strate the degree of possible radiographic subluxation.


  
              FIGURE 1 (NOT)     
                                |
                                |\  Dats a hip isn't it obvious
                               /|
                              / |

   Some measurement criterion is usually employed, i.e. Norberg, millimeters
of displacement, distraction index, etc, to demonstrate the amount of displace-
ment of the femoral head when compared to a fixed anatomic structure or to a
standard radiograph taken without the fulcrum or wedge. The difference in the
measurements indicates the range of possible motion, joint laxity.


  The principles of the technique were described in 1972. The technique
since been refined at the University of Pennsylvania and Michigan State
University. Different devices, measurements, and positions have been developed
Use of the fulcrum technique has demonstrated that some laxity is expected



       End of page 9.... 19 pages to go including the much talked of tables.
   I'll send them soon.



  Good Reading


   Dennis Guldan
   BIRD DOG NEWS