What is Canine Hip Dysplasia?
By Gina Bisco and Carolyn Christman
Canine Hip Dysplasia (CHD) is one of the most widely and passionately discussed of all dog health issues. Owners want to learn more about CHD CHD in order to make good decisions for their dogs. Unfortunately, the information available to dog owners seems to disagree on a few key points about CHD. Even some of the basic definitions or descriptions appear to be in conflict: for example, some descriptions emphasize the shape of bones, while others emphasize the role of laxity. This type of disparity is confusing for everyone.
Broader descriptions of CHD include important elements that researchers agree on and this puts things into perspective, yet these more inclusive descriptions found in scientific papers are dense with technical terms and hard to decipher. In The Dog Owner’s Home Veterinary Handbook, Dr. Delbert Carlson, DVM and Dr. James Giffen, MD give a broad but understandable description of CHD.
“Dysplastic dogs are born with normal-appearing hips that subsequently undergo progressive structural changes. The problem lies in the structure of the hip joint. The head of the femur (thigh bone) should fit solidly in the acetabulum (or the cup). In hip dysplasia, loose ligaments allow the head to begin to work free. A shallow acetabulum also predisposes to joint laxity. Finally, the mass or tone of the muscles around the joint socket is an important factor. Tight ligaments, a broad pelvis with a well-cupped acetabulum and a good ratio of muscle mass to size of bone predispose to good hips . . . Environmental factors, including weight and nutrition of the puppy and rearing practices, figure into the final outcome . . . Because of joint laxity, there is abnormal wear and tear on the articulating surfaces of the joint. In time this leads to arthritic changes in the dysplastic hip.”1
This description includes many elements that are widely agreed upon by scientists and veterinarians. Both abnormal bone development and joint laxity are significant factors in hip dysplasia. In addition, scientists agree that CHD is not present at birth but is both developmental and inherited, and CHD is universally linked to degenerative joint disease (DJD). In fact, researchers and vets all seem to agree that the biggest problem with hip dysplasia is that it leads to painful, crippling DJD. In the worst cases, a puppy with deformed hip joints undergoes advanced degeneration before its first birthday. In other cases, where there is no obvious deformity, DJD is usually attributed to laxity. While several other inherited problems, infectious diseases and traumatic injury can cause debilitating arthritis, CHD is widely considered the most common cause of DJD in young dogs.
Degenerative Joint Disease
Degenerative joint disease, also known as osteoarthritis or osteoarthrosis, is a progressive, non-inflammatory degeneration of the joint cartilage that is secondary to some type of damage: acute trauma, milder but chronic repeated stress, or even wear due to age-related cartilage changes. This is in contrast to inflammatory arthritis, which results from infection such as brucellosis and Lyme disease, or immune-mediated disease such as rheumatoid arthritis and lupus. In the U.C. Davis Book of Dogs (another helpful reference for dog owners), Dr. Robert Leighton says that osteoarthritis is more common than inflammatory arthritis in dogs. “Degenerative arthritis . . . is usually considered the result of the normal aging process, but it can also be caused more acutely by traumatic injury to bone, cartilage or ligaments. . . . Osteoarthritis is not really a disease itself, but rather the secondary result of damage (either short-term or long-term) to joint structures.”2
How do normal joints work?
It is easier to explain the problems in damaged joints by starting with an explanation of how normal joints work. A clear, basic explanation of joint biomechanics is presented by Dr. Frederick A. Matsen III, MD on the University of Washington Orthopaedics and Sports Medicine website3. He writes that in the normal articular joint, “muscles, tendons, ligaments, cartilage, and bone all do their share to ensure smooth function… In this role, the supporting elements both unite the abutting bones and position the joints in the optimal relationship for low-friction load-bearing. Two important characteristics of normal joint function are stability and lubrication.”
Lubrication prevents friction – and therefore wear – of cartilage surfaces in the stable joint. Normal cartilage is very durable, has extremely low friction, and is somewhat elastic, providing a shock absorber for the joints. The cartilage is supplied with oxygen and nutrients from the lubricating fluid called synovial fluid that is produced by the interior lining of the joint capsule, the synovial membrane. The synovial fluid keeps the cartilage supplied with nutrients, provides necessary lubrication, and it also plays a critical role in joint stability.
This can be thought of as the joint’s ability to prevent damaging movement. Joint stability results from complex interaction of many parts, so it depends on all of these parts developing normally in the growing pup.
Normal joint development
Puppies’ hip joints are not fully developed when they are born. Muscles, tendons and ligaments must all grow and lengthen to keep pace with the rapidly increasing size of the pup. In addition, the parts that will become the bony parts of the hip joint, the acetabulum and femoral head, are mostly cartilage at birth, and it takes several months for them to develop into bone. This process is called ossification.
Dr. Joe P. Morgan, author of Hereditary Bone and Joint Diseases in the Dog, states “Once ossification has begun, it proceeds in a specific and orderly pattern for that breed until the length of the long bones is determined, between 10 and 12 months of age in most large dogs. . . . During the time of skeletal growth, especially during the first six months of life, the dog is athletically active. At this time, the ends of the bones include the most important articular surfaces that remain in a cartilaginous form . . . The rapid increase in size and weight of the dog occurs when the ends of the bone are still cartilaginous and thus are more potentially vulnerable to injury.”4
How does CHD develop?
The earliest radiographically-detectable abnormality found associated with later confirmed hip dysplasia is delayed ossification of the femoral head.5 Laxity has also been reported as one of the first radiographic signs of CHD, as young as a few weeks of age, but research indicates that this is not a reliable sign of disease at such a young age. It is very difficult to read radiographs of puppies before 4 months old, because the appearance of both the space between bones and the shape of bones is affected by the incomplete state of ossification. There may already be changes to the cartilage or other soft tissues, the muscle, tendons and ligaments, but these don’t show up on radiographs. In fact, most researchers today state that the initial changes and initial cause of CHD is unknown.6 Technical advances in the future are sure to reveal more about how CHD starts and the earliest changes, but for now, most information about development of CHD relies upon radiographic signs.
Dysplasia changes already showing at 15 months
As the process of ossification proceeds, shape abnormalities of the acetabulum and femoral head start to become apparent on radiographs. Puppies with hip dysplasia that is detectable before they are a year old usually have developed shallow acetabulla and possibly flattening of the femoral head. According to Dr. Morgan, in such cases “this abnormal development occurs at an early age when the joint components are cartilaginous and thus soft and malleable resulting in deformation of the acetabulum (“shallow” acetabulum) . . .”7
Researchers seem to agree that instability of the femoral head is the likely cause of development of shallow acetabulum. The theory is that if the femoral head moves very much away from being centered in the acetabulum, any weight bearing puts an extra strain on its edge, which is still cartilage, and pushes the soft edge out of shape – and this abnormal shape then turns into bone. Different environmental conditions such as early rapid growth and weight gain may increase the deformity. “By affecting the ends of the growing bones (epiphyses), abnormal development directly influences the ultimate shape and contour of the articular surfaces . . . Failure to develop a perfectly formed articular surface that fits exactly or is congruent with the opposing articular surface leads to the development of osteoarthrosis that progresses as the dog ages.”8
If this was the only way that CHD developed, things would be a lot clearer and less confusing for dog owners, because the deformed acetabulum is visible on radiograph quite young and is rapidly followed by degenerative changes. However, there are several other scenarios that can delay diagnosis. For example, some puppies have no radiographic signs of CHD at age 1 year but are found to have CHD by the time they are 2 or 3 years old. This includes dogs that have normally developed and ossified hip bones but develop DJD at a young age due to excess laxity.
Why does CHD cause DJD?
Most people are aware that CHD and DJD are linked, but it is useful to clarify the connection. Like other known causes of DJD, CHD’s action leads to damaged cartilage. According to Dr. George Nuki, in an article for the Arthritis Research Council, DJD “results from an imbalance between mechanical strain and catabolic chemical processes acting on the joint and the capacity of the articular tissues to resist and repair the damage.”9 In short, DJD results from abnormal stress on normal cartilage or normal stress on abnormal cartilage.10 When the cartilage can’t repair itself adequately, the process of joint degeneration is started.
The prevailing view seems to be that in the case of CHD, the resulting DJD is mechanically induced; that is, the cartilage is normal but becomes damaged from abnormal stress.11 The shape of the bones of the normal hip allows loading forces to be distributed evenly. In the puppies with CHD that have abnormally shaped hip bones (acetabulla and femoral head), some areas of the cartilage are probably subjected to much greater loading forces and at those points the cartilage may become damaged. As Dr. Morgan explained, “Failure to develop a perfectly formed articular surface that fits exactly or is congruent with the opposing articular surface leads to the development of osteoarthrosis . . .”12
Other dysplastic dogs have normally-shaped hip bones when ossification is complete, but still develop DJD at a young age. In this case, excessive laxity is considered the probable cause of abnormal loading forces and thus DJD. Excessive laxity is often thought of as simply “lax ligaments,” but this is too simple. Instead of attributing excess laxity to the failure of just one part, the ligaments, it is better to think of excessive laxity as a failure of the entire joint to remain stable, which could involve more than one part. By the time joint instability is detected, several abnormal aspects may be found in the joint, but researchers have not yet pinpointed what is the initial cause of the instability.13
Muscle Diagram
Researchers are beginning to distinguish passive laxity from functional laxity.14 Passive laxity is evaluated while the dog is anesthetized and therefore the muscles and nerves are not engaged and contributing to joint stability. There has always been a question as to the significance of passive laxity for joint function. Some researchers in the past felt that any amount of passive laxity was abnormal.15 Others believe that passive laxity is only significant if it turns into functional laxity. Functional laxity is the kind of joint instability that happens when the dog is awake and moving. It has long been known that some dogs that seem to have unstable hips when they are anesthetized do not develop DJD, and some theorize that these dogs may have passive laxity but their hips actually function normally during use. Dr. Smith says that passive laxity is necessary for functional laxity to develop but that passive laxity not in itself sufficient to cause functional laxity.16
Regardless of the cause, joint instability or excessive functional laxity is the main factor believed to dispose the otherwise normally shaped joint to developing DJD. Functional laxity would allow the parts to move in abnormal ways. This heightens the loading stress on some areas of cartilage, resulting in damage which at some point overcomes the repair rate. What everyone would really like to know is how to reliably diagnose functional laxity. Unfortunately, Dr. Smith and other researchers agree that there is currently no way to reliably detect functional laxity in the canine hip.17
How does DJD progress and relate to symptoms in the dysplastic dog’s hips?
DJD is diagnosed on radiographs, and descriptions of DJD progression are typically based on radiographic change, so that is the frame of reference for owners and vets. However, Dr. Morgan explains that quite a bit has happened in the dogs hips by the time that the typical bony changes are evident on radiographs. “In the early stages, osteoarthrosis is particularly characterized by articular cartilage breakdown with an increase in production of synovial fluid that results in joint capsule distention. In addition, an increased production of lysosomal hydrolases causes exacerbation of the cartilage damage . . . These changes are accompanied by thickening of the joint capsule and interarticular ligaments.”18
These soft tissue changes are not visible on radiographs, but they are followed by bony changes that are visible at points where muscle tendons, ligaments, and joint capsule attach to bones. Bone spurs also grow at the cartilage margins. In time, these new bony growths change the shapes of the hip bones in a process called remodeling, a progressive aspect of DJD.
In some advanced cases, the acetabulum fills with new bone and becomes shallower and shallower. In reading about CHD, there is often reference to shallow acetabulla but sometimes it is not clearly specified as to whether the reference is to shallowness from the original, developmental deforming process during ossification or to shallowness due to remodeling. Awareness of the potential ambiguity will help avoid misunderstanding. For the individual dog described as having “shallow acetabulla”, the importance of the distinction is that in the former case, it may not have DJD yet, but in the latter case, it already has severe DJD.
Unfortunately (or sometimes fortunately), radiographic changes are not well correlated with symptoms in the dog. Some dogs may have very bad looking hips with advanced bony remodeling but little or no evidence of pain or disability. Other dogs may have apparently slight bony changes but distinct symptoms and pain. According to Dr. Morgan and Dr. Smith, in adolescent pups there is often a period of severe pain possibly in part due to synovial effusion and distention of the joint capsule and synovium, but after a time the pain lessens and may disappear as some compensating changes help stabilize the joint, including thickening of the joint capsule. Dr. Smith does not recommend preemptive surgery based on presence of excess laxity. In fact he reports that conservative management of CHD is usually successful. He suggests that if a vet recommends surgery for a young dog, the wary dog owner should always seek a second opinion.19
What’s next?
In this introductory overview we briefly described healthy joint stability biomechanics and puppy joint development. This provides the needed frame of reference for explanations of what goes wrong in dogs with CHD and how that leads to DJD. The initiating cause and very first changes of CHD are not yet known, but researchers agree that CHD is inherited, involves abnormal bone development and joint instability, and leads to mechanically induced DJD. In the next article we will look at how CHD is evaluated and how the evaluation methods compare.
References
1 Carlson DG and Giffen JM (1992). The Dog Owners Home Veterinary Handbook. New York, Howell Book House.(See pages 276-277).
2 Leighton R (1995). Chapter 26: The skeleton and disorders; in UC Davis Book of Dogs,edited by Mordecai Siegal. New York, HarperCollins Publishers, Inc. (See page 264).
3 Matsen III, F (2002). University of Washington Orthopaedics and Sports Medicine website, http://www.orthop.washington.edu/arthritis/general/joints/01 and www…03; last updated Jan18 2002, accessed November 2004.
4 Morgan JP, et al (2000). Hereditary Bone and Joint Diseases in the Dog. Hannover, Germany; Schlütersche GmbH & Co. (See pages 3-4.)
5 Todhunter RJ, et al (1999). An outcrossed canine pedigree for linkage analysis of hip dysplasia. The Journal of Heredity; 90: 85-92.
6 This point is summarized in Cardinet III G and Lust G (1997) The international symposium on hip dysplasia and osteoarthritis in dogs. Journal of the American Veterinary Medical Association; 210: 1417- 1418. Also stated in the articles by Smith GK et al (1990) , and Todhunter RJ, et al (1999), listed above and Madsen JS (1997) listed below.
7 Morgan JP (2000), as above. (See page 109.)
8 Morgan JP (2000), as above. (See page 11)
9 Nuki, G (2002). Osteoarthritis: risk factors and pathogenisis. Arthritis Research Council website, Rheumatic Disease Topical Reviews, Sept 2002, No 9 (http://www.arc.org.uk/about_arth/med_reports/series4/tr/6609/6609.htm). Accessed November 2004.
10 Rooks, RL and Jankowski C (1997). Canine Orthopedics. New York: Howell Book House. (See page 121.)
also see Amersham Medcyclopedia (http://www.amershamhealth.com/medcyclopaedia/medical/volume%20iii%201/osteoarthritis.asp)
11 Todhunter RJ, et al (1999), as above. (See page 84.)
12 Morgan JP (2000), as above. (See page 11)
13 Madsen JS (1997). The joint capsule and joint laxity in dogs with hip dysplasia. Journal of the American Veterinary Medical Association, 210: 1463-1465.
14 Farese JP, et al (1998). Dorsolateral subluxation of hip joints in dogs measured in a weight-bearing position with radiograpahy and computed tomography. Veterinary Surgery; 27: 393-405. (See page 394.)
15 Henry JD and Park RD (1972). Wedge technique for demonstration of coxofemoral joint laxity in the canine. Canine Hip Dysplasia: Proceedings of the Canine Hip Dysplasia Symposium and Workshop held in St. Louis, Missouri October 19-20, 1972: 117-126. (See pages 119-120.)
16 Smith GK, et al (1993). Coxofemoral joint laxity from distraction radiography and its contemporaneous and prospective correlation with laxity, subjective score, and evidence of degenerative joint disease from conventional hip-extended radiography in dogs. American Journal of Veterinary Research; 54: 1021-1042. (See page 1039.)
17 Smith GK (1993) as above; and Farese JP (1998) as above (see page 394.)
18 Morgan JP (2000) as above (see page 115).
19 Smith GK (2003). Treatment options and decision-making for canine hip dysplasia. BSAVA Congress 2003 Scientific Proceedings: 465-467