Only text, without photos
Hip dysplasia is a hot topic in
dogs, if it's possible to stay "hot" for 50 years. Researchers have
been working hard for decades looking for solutions, and breeders have been
doing their best to reduce the risk of producing affected puppies. But still
the problem remains.
There are some simple things we could do to reduce the incidence of hip
dysplasia now if we understand a few basic things. Here are the 10 most
important things you need to know.
1) All puppies are born with perfectly normal hips
Hip dysplasia is not a congenital defect; it is not present at birth. Multiple
studies have demonstrated that all normal puppies are born with
"perfect" hips; that is, they are "normal" for a newborn with
no signs of dysplasia. The structures of the hip joint are cartilage at birth
and only become bone as the puppy grows. If a puppy is going to develop hip
dysplasia, the process begins shortly after birth.
2) The genes that cause hip dysplasia
remain a mystery
Hip dysplasia tends to be more common in some breeds than others and in some
lines than others, which indicates that there is a genetic component to the
disorder. However, scientists have been looking for genes that are responsible
for the development of hip dysplasia in dogs for decades without success.
Genes that are associated
with hip dysplasia have been identified in some breeds, but they are
breed-specific; that is, the assortment of genes is different in every breed.
(For example, see studies on the German Shepherd dog (Marschall & Distl
2007, Fells & Distl 2014, and Fels et al 2014), Bernese Mountain Dog
(Pfahler & Distl 2012), and Labrador Retriever (Phavaphutanon et al 2008).
Genes that could cause hip dysplasia have not been found in any
breed.
It's unlikely that researchers are going to discover an easy genetic solution
to the problem of hip dysplasia. It is a complex trait that is influenced by
both genes and environment, and there is no simple solution just over the
horizon. We should be able to improve genetic progress by using selection
strategies that are as efficient and effective as possible such as estimated
breeding values, EBVs. One great advantage of using EBVs is that the genes
responsible for a trait don't need to be known; you need only a pedigree
database and information about affected animals.
3) Environmental
factors are also important
Although there is a genetic influence on hip dysplasia, the heritability of the
trait is rather low. Many studies have shown that genetic variation accounts
for only a modest fraction of the variation in hip scores, usually 15-40%.
This means that some fraction of the variation in the quality of the hips is
the result of non-genetic, or "environmental" influences. This is one
reason why decades of strong selection has resulted in only modest reductions
in hip dysplasia in some breeds. At the current rate of progress and selecting
only by phenotype, it could take decades to achieve a meaningful reduction in
the incidence of hip dysplasia (Lewis et al 2013).
Understanding the specific environmental factors that play a role in the
development of hip dysplasia should allow us to reduce the number of animals
affected by hip dysplasia even if the genetic basis is not yet understood. This
would reduce significant pain and suffering as well as the expense and
heartache endured by owners of an afflicted dog. There is no reason why we
should not be taking active steps to do this now.
The top three environmental factors that have been
found to play a significant role in the develop of dysplastic hips are: a)
joint laxity, b) weight, and c) exercise (see below).
4) Joint laxity is
the primary cause of hip dysplasia
Puppies are born with perfect hips, and if the hips do not develop laxity the
dog does not develop hip dysplasia (Riser 1985). Joint laxity occurs when the
head of the femur does not fit snugly into the acetabulum. This could be the
result of traumatic injury, overloading of the joint by weight, lack of muscle
strength, or adductor forces (e.g., bringing the legs together). Joint laxity
is the primary factor that predisposes a dog to the development of hip
dysplasia.
5) Controlling joint stability is key
The teres ligament
should hold the head of the femur securely in the socket of the growing puppy
while the muscles that will support the hip develop and grow stronger.
But in some puppies, the ligament shows evidence of damage before they
are even a month old (Riser 1985).
"The teres ligaments of the hip joints were edematous [swollen], a few
ligament fibers were torn, and capillary hemorrhage dotted the surface of the
ligaments at the point of the tears. These changes were considered the first
findings fed
that might be linked to hip
dysplasia."
The abnormal forces on the femur and acetabulum that are caused by joint
laxity result in the trauma that causes hip dysplasia and osteoarthritis of the
hip.
"There is no evidence that a primary defect of bone exists but
rather the disease is a failure of the muscles and other soft tissues to
hold the hip joint in full congruity. This is further supported by the fact
that bony dysplasia can be increased, decreased, or prevented by
controlling the degree of joint instability and incongruity. No other
malformations are associated with the disease. A causal relationship between
muscles and soft tissue defects or pathologic changes other than lack of
muscle mass or strength has not been established... Hip dysplasia is a
concentration of factors from a pool of genetic weaknesses and
environmental stresses that fall into a programmed pattern of progressive
remodeling and degenerative joint disease." (Riser 1985)
6)Body weight is a MAJOR environmental factor
If there is laxity in the hip joint, the amount of damage done to the femur and
acetabulum will depend on the magnitude of the forces in the hip joint. The
heavier the dog, the greater the forces will be and also therefore the higher
the risk of hip dysplasia and osteoarthritis.
At four years old, less than 10% of dogs kept on a
restricted diet (25% less than the control diet) were dysplastic, while at the
same time more than 30% of the dogs in the control group were dysplastic. As an
added advantage, dogs on restricted diets live longer, too (Kealy et al
2002)!
Unfortunately, many dogs (including show dogs!) are overweight (McGreevy
et al 2005, Corbee 2013), and obesity could well be the single most significant
environmental factor affecting the development of hip dysplasia and
osteoarthritis. But body weight is a factor that we can control.
Although progress
from genetic selection will take many generations, the incidence of hip
dysplasia in dogs could be immediately and dramatically reduced simply
by practicing better weight management.
7) Exercise is good
and bad
Exercise strengthens the muscles of the legs and pelvis, and this will increase
the stability of the hip joint. But all exercise is not created equal.
Puppies raised on slippery surfaces or with access to stairs when they are less
than 3 months old have a higher risk of hip dysplasia,while those who are
allowed off-lead exercise on soft, uneven ground (such as in a park) have a
lower risk (Krontveit et al 2012). Dogs born in summer have a lower risk of
hip dysplasia, presumably because they have more opportunity for exercise
outdoors (Ktontveit et al 2012). On the other hand, dogs from 12-24 months
old that regularly chase a ball or stick thrown by the owner have an higher
risk of developing dysplastic hips (Sallander et al 2006).
The most critical period for proper growth and development of the hip in dogs
is from birth to 8 weeks old, so the type of exercise the puppies are exposed
to is most important during this time.
8) Nutrition is
important
While puppies are growing rapidly, it is critically important to get their
nutrition right.
Growing puppies need to eat enough to support growth but they should not be
fat, because any extra weight can increase the risk of developing hip dysplasia
(Hedhammar et al 1975, Kasstrom 1975). An additional problem is that puppies
getting too much food could also consume too much of specific nutrients.
Puppies provided a quality commercial puppy food that is fed in the proper
amount will have a nutritionally balanced diet and should not
receive any supplements. Dietary supplements, especially of calcium, are not
only unnecessary but could cause serious problems. There is no evidence that
supplemental protein or vitamins will reduce the risk of hip dysplasia (Kealy
et al 1991, Nap et al 1991, Richardson & Zentek 1998).
9) Early
intervention is critical
Most treatments for hip dysplasia are easier and more successful in younger
dogs. If early symptoms are overlooked and screening is done only after 24
months or more, the window of time with the best prognosis in response to
treatment will have passed (Morgan et al 2000). Signs of lameness usually first
appear when the puppy is 4 to 6 months old, but after a month or two the dog
will often seem better. This is because damage to the acetabular rim such as
microfractures will have healed and the dog is no longer in pain, but
development of dysplasia and osteoarthritis will continue. From there, the dog
might not display clinical signs again for years while the pathological damage
progresses.
Laxity in the joint can be determined as early as 4 months old (either by
palpation or PennHIP). If detected early, intervention to mitigate additional
damage can include weight loss, modifying exercise and activities, or surgery -
but it must be done early before skeletal growth is complete.
Breeders should educate new puppy owners about the factors that can increase
the risk of developing hip dysplasia and also advise them to get a veterinary
examination immediately if there is any sign of lameness.
10) We can dramatically reduce hip dysplasia now
Genetic selection should continue to produce modest progress in the reduction
of hip dysplasia. But a significant and immediate reduction in the number of
afflicted animals could be achieved by better control of non-genetic,
environmental factors. Weight management, appropriate exercise, proper
nutrition, and early intervention at the first sign of lameness are simple
steps we can take that will dramatically reduce the pain and suffering caused
by hip dysplasia. The research will surely continue, but we already have the
information we need to tackle this problem.