Canine hip dysplasia is thought to be the most common orthopaedic condition diagnosed in the dog. It is most prevalent in large and giant breed dogs, with a complex polygenic mode of inheritance, and relatively low heritability. External factors, including caloric intake when growing, have a significant effect on phenotypic expression. Initial joint laxity progresses to osteoarthritis due to subluxation and abnormal wearing. Selective breeding programs to attempt to decrease prevalence have shown modest results so far.
Many studies have documented those genetics explains part of the variation among dogs in hip scores. This is usually 15-30% of the total variation. This means that environmental factors must account for the remainder of the variation; usually 70-85%.
When breeders are focusing on selection to improve hips, they are trying to chip away at genetics, which usually matters much less than environmental factors. When we health test our dogs (using BVA, PennHip and/or OFA), unfortunately we are only ‘acting’ on that 15-30%.
"Environment" as used here encompasses all factors that are "not genetic", which can be anything from type of exercise to food consumption.
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.
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 new-born 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.
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.
3) Environmental factors are also important
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 have resulted in only modest reductions in hip dysplasia in some breeds.
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.
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.
In dogs as well as many other vertebrates (including humans), the head of the femur in new-borns is held securely in place by a strong ligament variously called the "round ligament" or "teres ligament".
One end of this ligament is attached to the head of the femur and the other end to the inner wall of the acetabulum (the cup-like socket on the pelvis).
You can see the teres ligament in this illustration (labeled "LIGAM. TERES"). If this ligament is damaged or severed, the femur will not be held tightly in the socket, which will cause the joint to feel "loose".
If the femoral head is not positioned properly in the socket, the forces on the hip will be abnormal. Instead of being distributed across the inner surface of the socket, the forces on the joint will be concentrated in a smaller area on the weaker rim of the acetabulum. The result will be damage to the rim of the socket when a load is placed on the hip joint.
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 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 re-modeling 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. Puppies that weigh more at birth as well as those with higher growth rates (so they get heavier sooner) have a higher risk of degenerative changes in the hip joint (Vanden Berg-Foels et al 2006).
As this graph shows, puppies kept on a restricted diet (gray line) have a dramatically lower risk of dysplasia and it develops much later in life than in puppies kept on normal rations (black line) (Smith et al 2006).
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. We do advise new owner to get a veterinary examination immediately if there is any sign of lameness.
10) How can we 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.
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One way to tease out the effects of these environmental factors is to isolate one, manipulate it, and observe the effect on the trait of interest, in this case, the hip score.
There are hardly any studies of this sort on hip dysplasia dogs, but there is one on rats that is key to understanding the role of traction in the whelping box in the risk of developing hip dysplasia. I have explained to you the importance of a tiny ligament (teres ligament) in the hip socket that keeps the head of the femur snugly in the hip socket in new-born puppies.
box?]https://www.instituteofcaninebiology.org/blog/do-your-puppies-have-enough-traction-in-the-whelping-box). If you read the article on the link you can understand how that ligament is stressed when the puppy's legs are in the "extended and adducted" position (straight behind the puppy and pulled together). This position of the legs can result in hip dysplasia in human infants, as when the baby is swaddled up tightly like a burrito.
How can we prove that the same mechanism applies in animals besides humans?
You could do an experiment with animals that mimics the "burrito swaddle" by putting the legs in the extended/adducted position and looking at the effect on hip conformation. Here's a study that did exactly that. This experiment was on rats, but similar studies have been done with rabbits and other mammals. The experiment was simple. The legs of baby rats were taped together ("swaddled") and evaluated after 5 days and 10 days, and compared to a control group (no tape).
The prevalence of developmental dysplasia was highest in the pups that were swaddled for the entire 10 days (36 of 44 pups), and in most of these the hips were dislocated. Dysplasia (as subluxation) was less frequent (21 of 44) in the pups swaddled for only the first 5 days or the second 5 days.
Think about this. These rat pups differed only in whether their legs were taped together or not. So, it is the position of the legs - extended and adducted - that resulted in hip dysplasia. In the pups with legs taped for 10 days, the teres ligament was simply gone. In pups with legs taped for only 5 days, the teres ligament was present but damaged.
The first question you are asking is whether we know if this applies to dogs. A similar experiment has been done on puppies, but one leg was put in a cast to keep it in the extended position, and this also resulted in dysplasia in the hip on that side.
How is this relevant to dogs? Look at the many photos and videos of very young puppies nursing and crawling around in whelping boxes with poor traction. The back legs are extended and adducted, over and over, as the pup tries to push itself forward. Over the course of the three to four weeks before it starts to walk, a puppy could do this thousands of times, putting stress on the teres ligament every time.
From the experiment on rats and others that have been done on other new-born mammals, we should expect this leg movement that we usually call "crawling" will result in dysplastic hips. Notice that although all of the rat pups in a treatment group were treated the same way, not all of them developed hip dysplasia (e.g., 36 of 44 in the 10-day group). The reason for this would have to be revealed in additional studies, but it demonstrates that we should not expect clear, consistent differences among the animals in each group.
The purpose of Traction Mats (for example the active Non-Slip Vet Bedding we use in our Whelping Pens) is specifically preventing this leg position of extended and adducted. It does not provide general traction like a rough surface would, but instead provides a vertical surface the pup can push against instead of slipping over the surface of the floor. If you understand this, you will realize that we will never solve the hip dysplasia problem by trying to choose parents with better hips and removing the others from the breeding stock. This also means, however, that if the teres ligament is damaged early in a pup's life, other factors - both environmental, like exercise and overweight, and genetic, like large body size - can determine the weather dysplasia is modest or severe.
If we want to produce dogs with sound hips, we must protect the teres ligament from the damage that occurs when the puppy extends and adducts the back legs to try to move itself forward.
In fact, we cannot eliminate hip dysplasia in dogs without doing this, because the risk starts at the moment of birth, and the damage is done in the first few weeks after whelping. We know from the rat study that we can't expect every puppy, even in the same litter, to have excellent hips. But we should be able to reduce the incidence and severity of hip dysplasia by addressing the basic traction problem.
REFRENCES
Does Swaddling Influence Developmental Dysplasia of the Hip? (the rat study) http://bit.ly/Wang_rats
A Dynamic Canine Model of Experimental Hip Dysplasia (the dog study)