The Dysplastic Hip Joint
Hip Dysplasia is a terrible genetic disease because of the various degrees of arthritis (also called degenerative joint disease, arthrosis, osteoarthrosis) it can eventually produce, leading to pain and debilitation.
The very first step in the development of arthritis is articular cartilage (the type of cartilage lining the joint) damage due to the inherited bad biomechanics of an abnormally developed hip joint. Traumatic articular fracture through the joint surface is another way cartilage is damaged. With cartilage damage, lots of degradative enzymes are released into the joint. These enzymes degrade and decrease the synthesis of important constituent molecules that form hyaline cartilage called proteoglycans. This causes the cartilage to lose its thickness and elasticity, which are important in absorbing mechanical loads placed across the joint during movement. Eventually, more debris and enzymes spill into the joint fluid and destroy molecules called glycosaminoglycan and hyaluronate which are important precursors that form the cartilage proteoglycans. The joint’s lubrication and ability to block inflammatory cells are lost and the debris-tainted joint fluid loses its ability to properly nourish the cartilage through impairment of nutrient-waste exchange across the joint cartilage cells. The damage then spreads to the synovial membrane lining the joint capsule and more degradative enzymes and inflammatory cells stream into the joint. Full thickness loss of cartilage allows the synovial fluid to contact nerve endings in the subchondral bone, resulting in pain. In an attempt to stabilize the joint to decrease the pain, the animal’s body produces new bone at the edges of the joint surface, joint capsule, ligament and muscle attachments (bone spurs). The joint capsule also eventually thickens and the joint’s range of motion decreases.
No one can predict when or even if a dysplastic dog will start showing clinical signs of lameness due to pain. There are multiple environmental factors such as caloric intake, level of exercise, and weather that can affect the severity of clinical signs and phenotypic expression (radiographic changes). There is no rhyme or reason to the severity of radiographic changes correlated with the clinical findings. There are a number of dysplastic dogs with severe arthritis that run,
Some of the environmental aspects that can affect the observable expression of hip dysplasia are the following
by T. J. Dunn, Jr. DVM
http://www.thepetcenter.com/xra/hd.html
“Nutrition – There are reports that in puppies a restricted calorie intake could restricted the growth rate, and in turn will lessen the potential for the dog to develop hip dysplasia. (I wouldn’t suggest doing this to any pup… it makes as much sense as stealing money from your own checking account!) The problem is that some restricted diets restrict the fat and protein content and increase the carbohydrate content of the food. Bad! The real goal should be to keep growing pups from becoming OVERWEIGHT. Restricting fat and protein in a growing pup can be a disaster. A high quality, meat-based diet is absolutely necessary for growing pups, just don’t feed so much of it that the pup becomes overweight”.
Hip dysplasia is not a “genetic malformation of the hip socket”, as commonly thought, but rather a weakness in the ligaments that support the hip joint. This allows the ball of this ball-in-socket joint to bang away at the joint surface, preventing the socket from forming properly. In other words, the instability created by weak supportive ligaments keeps the body from being able to manufacture a deep, smooth hip socket for the ball to fit snuggly into, resulting in the flattening of the acetabulum (hip socket) and a squaring of the femoral head (the ball).
READ, http://dogtorj.com/appetizers/newest-appetizers/hip-dysplasia/
Physical Activity – In a young, growing dog with a genotype (genetic makeup) for CHD who will eventually develop some trouble because of it, will develop more arthritis and have more eventual difficulty if it is highly active physically. Climbing stairs, jumping into and out of pick-up trucks, running with other normal dogs can all subject the growing hip structures to unwarranted stress and trauma and increase future discomfort for the dog. The effects of this excessive activity is worsened in an overweight pup. (In a normal, growing dog, all these activities will not cause hip dysplasia.
Bedding – There is no scientific proof, but lots of observational conclusions, that pups reared especially during the nursing period on slippery surfaces such as newspapers will be prone to hip difficulties. That is not to say that smooth concrete, wood or newspaper surfaces cause dysplasia, just that they can make a bad situation worse. Better surfaces for newborn pups would be blankets or towels… something they can get a better grip on”.
Baker Institute for Animal Health Research
“The time of appearance and the rate of progression of hip dysplasia are influenced by the growth rate of individual dogs. Studies at the Baker Institute and elsewhere have shown that slowing growth during the early months of life can lessen the severity of hip dysplasia and even prevent it. One study followed two groups of susceptible pups from the time they were eight weeks old until their death. One group of pups was fed nearly 25 percent less food than the second, which were permitted to eat all they wanted of the same diet. Over the course of the 14 year study, data was collected regarding general longevity and the development of hip dysplasia. Not only did the dogs eating a restricted diet live significantly longer than their well-fed counterparts, they developed hip dysplasia at a much lower rate than did the second group. Further, for those dogs on a restricted diet who did develop hip dysplasia, the risk of developing osteoarthritis decreased by 57 percent. This study of course involved a diet restriction that is difficult to enforce for many pet owners. It would be desirable to use a less restrictive dietary regime that would confer many of the same benefits this more severe diet did”.
Daniel C. Richardson
DVM Diplomate, American College of Veterinary Surgeons
“The large and giant breeds are the most susceptible to skeletal disease. Genetics, environment, and nutrition play key roles. Nutritionally, rate of growth, feed consumption, specific nutrients, and feeding methods influence our ability to optimize skeletal development and minimize skeletal disease. Maximizing the growth rate in young, growing puppies does not correlate to maximal adult size; however, it does increase the risk of skeletal disease. The growth phase of 3 to 8 months and possibly the phase prior to weaning are integral to ultimate skeletal integrity. The giant breeds may be limited in their ability to cope with excesses of minerals such as calcium, and the results are abnormal bone remodeling and skeletal disorders. This apparent increased sensitivity makes these breeds somewhat of a monitor of dietary influences”.
By Margaret Muns DVM
“The degree to which CHD is manifested in a particular dog depends on the degree of the animal’s genetic predisposition, and the influence of a variety of environmental stresses. The greatest incidence of CHD occurs in the most rapidly growing breeds of dogs. Therefore, mix-breed dogs are much less susceptible than highly bred dogs.
In most cases, the rapid growth rate of the disease is directly related to young dogs that are fed a high-calorie diet, and therefore develop excess body weight at a rapid rate. These diets only serve to enhance the bio mechanical imbalance present in genetically susceptible dogs. Limiting the rate of a dog’s growth results in less joint looseness and fewer signs of hip dysplasia.
Another major factor in the development of skeletal disease in young growing dogs is too much calcium intake. Excessive blood calcium levels disrupt the normal maturation of both bone and cartilage. Other clinical diseases related to calcium imbalances include osteochondrosis dissecans (OCD), retained cartilaginous cores, radius curvus syndrome, and stunted growth. Dogs that are affected with these syndromes lack the biochemical ability to protect themselves from chronic calcium excess”.
Locating the genes for hip dysplasia in dogs (Psssst! Look in the kibble bag)
by Carol Beuchat PhD
There is probably no other non-lethal health problem except perhaps allergies that afflicts so many breeds of dogs as hip dysplasia. It cripples dogs with pain, sometimes in the prime of their lives, and there is very little modern veterinary care can do about it. It seems clear that it has some genetic component (it is thought to be polygenic) but there are clearly environmental (i.e., non-genetic) influences as well. There has been some modest success in reducing its incidence in some breeds by screening programs, but for the most part it remains an intractable problem and the focus of many research programs.
Consequently, I was quite surprised to run across a paper (1) published in 2006 about a study that was able to substantially reduce in incidence and severity of hip dysplasia in Labradors – not by locating particular genes or implementing strategically-designed breeding programs – but by reducing food consumption. (Download a copy here – pdf) Conducted by Nestle Purina in collaboration with a slate of veterinarians and academics, the study used 48 Labrador Retriever puppies from 7 litters. In each litter, puppies were paired and one assigned to the control group and one to the treatment group. The control group was provided food ad libitum (unrestricted) starting at 8 weeks, and each puppy in the treatment group was fed 25% less than the amount consumed by its pair in the control group. Their weight was monitored and hips x-rayed at regular intervals throughout the lifetimes of the dogs.
Dogs that were fed less had dramatically lower incidence of hip dysplasia. How dramatic? Have a look at these graphs (modified from Smith etal’s paper).
Dogs allowed to eat as much as they wanted showed evidence of hip dysplasia at younger ages than dogs fed less, and the difference between the groups got worse as they got older. By 6 years of age, 50% of dogs in the unlimited food group had evidence of osteoarthritis, compared with only 10% of dogs in the restricted food group. More than 50% of the dogs in the restricted food group still had radiographically normal hips at 12 years old; in the other group, 90% were arthritic. Dogs fed 25% less food than their pair in the control group weighed about 25% less throughout their lives. Heavier dogs had worse hips.
I was astonished to see these results. By any scientific, medical, or veterinary standard, the effect of diet restriction on incidence of osteoarthritis in Labradors would be considered profound. If somebody was to submit a grant proposal to test a treatment that promised to reduce the incidence of hip dysplasia in dogs – not by 10%, or even 25%, but 50% – I should hope it would receive very serious consideration for funding. And what about the Canine Health Foundation and also the Orthopedic Foundation for Animals (OFA), which owes its founding to concern about the high incidence and crippling effects of hip dysplasia in dogs? A browse of the information on their websites about the disease makes no mention of this study or the potential benefits of lifelong food limitation. I showed this paper to a few breeders.
Most were surprised to see these data. Some breeders, especially of large breeds, said they managed food intake of their puppies so they didn’t grow to fast, but they were worried about growth rate and not adult body weight.
“Less Food” you are killing me…
Such a simple (and cost-effective!) way to substantially reduce the suffering of dogs, reduce veterinary bills for treatment, x-rays, and pain relief, and increase the amount of time the family dog can continue to lead an active life. Millions of dollars are spent every year looking for sources and cures of disease in dogs so that we can offer them better lives. Maybe we should direct some of this funding to an informational public service campaign to get this simple information to breeders and pet owners, and perhaps also some clear recommendations on dog food bags, maybe even brochures in veterinary offices.
I mentioned up top that there was also most certainly some genetic component to development of hip dysplasia, and that’s certainly worth talking about because there might be some surprises there as well. Getting back to genetics, I’ll be addressing those in another post.
In the meantime, I’m taking a pound or two off my dog.
(1) Smith, GK, ER Paster, MY Powers, DF Lawler, DN Biery, FS Shofer, PJ McKellvie & RD Kealy. 2006. Lifelong diet restriction and radiographic evidence of osteoarthritis of the hip joint in dogs.
Important please read on…
Look at how far the bones have to grow before they become a proper bony joint! This is why you should never let puppies jump, walk up/down stairs, over exercise or over train. Doing too much impact activity at a young age will cause serious issues later in life, or even at a young age as hip dysplasia and other orthopaedic conditions are rising in puppies!
