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Hip Dysplasia

Tim Hutchinson BVSc CertSAS MRCVS - 22/03/2016

Hip Dysplasia



Of all the developmental orthopaedic disorders, hip dysplasia is probably the most widely known. However, misconceptions and poor advice persist, particularly from breeders so that vulnerable joints are damaged early in life, initiating the degenerative cycle of osteoarthritis.



Regardless of the ultimate severity of the condition, a dog with hip dysplasia is born with normal hips; the subsequent development of the dysplastic joints depends on a mixture of genotypic and phenotypic effects. The developing joint relies upon the coordinated growth of five bones (ilium, ischium, pubis, acetabular and femoral head), joint capsule, surrounding musculature and intra-articular structures (articular cartilage, synovial fluid and the teres ligament) and the phenotypic influences to which they are subjected (principally nutrition and exercise).

For the normal development of the coxofemoral joint there should be minimal joint laxity. This ensures that the femoral head and acetabulum are maintained in close contact throughout all normal movements. With this inherent congruency comes an even load-distribution from the femoral head to the acetabulum and the joint develops correspondingly in a normal fashion. Young growing bones are a very plastic tissue and their shape will develop according to the forces applied through them: a congruent joint with normally distributed load will continue to develop normally.

Conversely, in the development of a dysplastic joint there is increased joint laxity, resulting in subluxation of the joint, which becomes particularly pronounced during exercise. The result is that the surfaces of the joint available for weight-bearing are reduced in area and are often inappropriate (such as the acetabular rim). This has two main effects: firstly, there is focal damage to the acetabular rim and femoral head; secondly, because of the reduced load applied directly through the acetabulum the joint fails to develop its intended shape, leading to incongruency.

Joint Laxity... is key to the development of the disorder, however, this in itself is multifactorial. Laxity arises as the result of an increased volume of synovial fluid; increased elasticity of the fibrous supporting structures (joint capsule and teres ligament); and decreased support from the surrounding musculature. Different genes are responsible for the development of these different tissues, which complicates the heritability of the condition.

It is possible to assess the laxity of the coxo-femoral joint subjectively (see “diagnosis”) and to measure it objectively. Important research by Gail Smith1,2 has shown that the degree of joint laxity (or the degree to which the femoral head can be distracted from the acetabulum) can be measured as the distractive index, with a value of 0 representing no distraction of the femoral head from the acetabulum (no laxity) and a value of 1.0 representing maximum distraction (complete subluxation). Smith extended this idea to show that a distractive index of 0.3 was the cut-off point for the development of dysplasia and went on to suggest that some breeds (e.g. greyhounds) had populations with distractive indices almost exclusively <0.3 and therefore did not develop the disorder; whereas other breeds (e.g. German Shepherd dogs) had indices >0.3 and were therefore almost exclusively at risk of developing dysplastic hips.

Exercise is both useful and damaging for the developing joint and as a general rule it is the type rather than the quantity of exercise that is the problem: controlled exercise ensures that the joint moves in a defined range and encourages load transfer through the femoral head to the acetabulum and therefore favours the development of a congruent joint. Uncontrolled exercise, such as ball chasing and jumping, allows the femoral head to move out of the acetabulum (to the limit of the joint laxity) and impact on the acetabular rim. This impact trauma causes the development of micro-fractures along the rim, resulting in pain and remodelling of the bone. Inflammatory changes cause synovial effusion, which further compounds the laxity. Articular cartilage on the focused load-bearing part of the femoral head and acetabulum is damaged and the vicious cycle of osteoarthritic degeneration is established.

Nutrition also plays a role. It is rare, today, to find a commercially prepared food for dogs that is not well balanced nutritionally (though many owners, often under a breeder’s ill-informed advice, will still supplement a diet with raw meat and in doing so distort the calcium to phosphorous ratio), so rather than dietary imbalance the main current nutritional problem is over-feeding3 leading to rapid growth and weight-gain. Impact damage through uncontrolled exercise on a lax joint is exacerbated by increased bodyweight (therefore increased impact force) and rapid growth in height may lead to increased leverage on these vulnerable joints.

The greater the degree of joint laxity the less force is required to distract the joint and cause damage – hence when selecting dogs for breeding purposes it is important to assess the laxity of the joints.


The detection of hip pain in a young dog is relatively straight-forward for the clinician and susceptible breeds are well recognised. Breeds most at risk of developing hip dysplasia are listed on the BVA/KC website Clinically, dysplastic dogs present as two distinct subgroups: young dogs with signs associated with the development of the condition and older dogs with osteoarthritis secondary to the developmental disorder.

Juvenile dogs

Puppies are usually presented between 4 and 12 months of age with a history of lameness of one or both back legs and pain. Owners frequently report a bunny-hopping gait – the puppy uses both back legs together and thrusts with its back rather than swinging the painful hips individually. Signs may be insidious in onset or present as an acute lameness and typically the dog is stiff after rest. On examination there is discomfort on hip manipulation – particularly extension. There may be palpable (and even audible) “clunks” with a very lax joint when it reduces following subluxation. In extreme cases this can be detected by resting the hands over the joints and rocking the dog from side to side.

Adult dogs

The history is typical of degenerative joint disease: stiffness after rest, decreased exercise tolerance, difficulty climbing steps, behavioural changes etc. There is hip stiffness and discomfort on examination as well as decreased range of motion and possibly crepitus.

It is essential to perform a full clinical examination and to exclude other orthopaedic causes for the lameness, especially stifle disease (cruciate disease or patellae luxation) and lumbosacral disease.


The breed, presenting clinical signs and full examination give a reasonable degree of certainty to a presumptive diagnosis. However, definitive diagnosis relies on examination of the joints with a relaxed (heavily sedated or anaesthetised) patient and radiography. The main purpose of this examination is to demonstrate subluxation of the coxofemoral joints and to try to quantify (subjectively) this degree of laxity.


With the dog in lateral recumbency, the stifle is flexed to allow the distal femur to be grasped in one hand. The other hand rests over the pelvis with the thumb over the greater trochanter of the femur. The stifle is adducted and the femur pushed proximally (the hand on the pelvis preventing movement of the dog). These actions allow subluxation of the femoral head so that it rides up onto the dorsal acetabular rim. Maintaining the proximal thrust on the femur, the limb is abducted until the femoral head slips back over the dorsal acetabular rim and reduces into the acetabulum. This sudden reduction is accompanied by a palpable, and often audible “thud” – this is referred to as the “Ortolani Sign”. This laxity and Ortolani Sign can also be demonstrated bilaterally with the dog in dorsal recumbency and the femurs forced perpendicularly towards the table. However, the benefit of assessing each joint individually is that the degree of laxity when the femoral head abducts from the acetabulum can be felt with the overlying thumb. With experience this measurement – whilst still subjective – can be quite accurate.

It is possible to measure the angle at which the hip reduces from its subluxated position and also the angle at which it subluxates when the limb is rotated from an abducted position. These two angles may be useful in planning reconstructive procedures such as triple pelvic osteotomy.

The Ortolani sign

Fig 1 The left hand supports the pelvis, with the thumb on the greater trochanter; the stifle is flexed and the distal femur grasped firmly in the right hand

Fig 1. The left hand supports the pelvis, with the thumb on the greater trochanter; the stifle is flexed and the distal femur grasped firmly in the right hand.

Fig 2. The stifle is adducted and the femur pushed proximally to subluxate the femoral head

Fig 2. The stifle is adducted and the femur pushed proximally to subluxate the femoral head

Fig 3. The stifle is abducted to allow the femoral head to reduce

Fig 3. The stifle is abducted to allow the femoral head to reduce


The standard radiographic positioning required for ventro-dorsal hip radiographs is familiar to all vets. Additional views, such as a skyline view to assess the dorsal acetabular rim, may be useful for pre-operative planning.

When assessing any hip radiographs though, it is important to be systematic and evaluate all parts of the joint, from the perspectives of joint morphology and degenerative changes:

Morphology... essentially involves the degree of subluxation, congruency and the Norberg Angle.

Fig 4. Good hips


Subluxation – the femoral head should be viewed as a complete circle and its centre point determined (the use of actetate overlays can be of assistance here). The line of the dorsal acetabular rim should also be located. In a normal joint the centre of the femoral head should lie medial to the dorsal acetabular rim – this ensures good dorsal coverage to the femoral head in normal load-bearing. With mild subluxation the centre point lies close to or even over the acetabular rim – and consequently the area of the joint available for load-bearing is reduced. With more severe luxation the centre of the femoral head is outside the dorsal acetabular rim and in extreme cases (complete luxation) the medial aspect of the femoral head itself has moved beyond the rim.

2. Congruency – the contours of the cranial acetabulum and the cranial aspect of the femoral head should be noted. In a normal, congruent joint these two curves are parallel. As subluxation increases so does the incongruency.

3. Norberg Angle – two lines are marked on the radiograph: one extends from the centre of the femoral head cranially in a sagittal plane; the other is drawn from the centre of the femoral head to the lateral limit of the cranial acetabular rim. The angle between these lines is the Norberg Angle. In a normal joint this angle will be positive and greater than 15 degrees (the line to the cranial acetabular rim diverges laterally from the body of the dog). As subluxation and maldevelopment of the acetabulum increase the angle will reduce and even become negative.

Degenerative changes

Consistent with any osteoarthritic joint there will be the presence (in varying degrees) of new bone formation, sclerosis and remodelling. One of the earliest indicators is the presence of the “Morgan’s Line”. This is a radiodense line extending from the base of the femoral neck to the trochanteric fossa and is the result of new bone formation along the insertion of the joint capsule. All parts of the joint should be examined for pathologic changes: cranial, caudal and dorsal acetabulum, acetabular fossa, femoral head and neck.

N.B. When assessing the severity of the condition it is important to treat the dog, not its radiographs! Radiographic changes confirm the diagnosis of hip dysplasia, but the clinical severity can vary widely between dogs with apparently similar films.

Mild changes 

Moderate changes    Severe changes  TREATMENT

Juvenile dogs

Treatment of young dogs has two aims: controlling pain and trying to promote optimum joint formation. With this in mind treatment should begin before the onset of clinical signs, through the education of owners of susceptible breeds! The vicious circle of joint laxity ––> abnormal load bearing ––> abnormal development ––> incongruency ––> laxity begins at a young age and the key time for joint damage is between 8 and 20 weeks of age. Time should be spent with owners at the primary vaccination course discussing issues such as weight gain and the type of exercise appropriate for the pup. Frustratingly, breeders still sell many pups with the advice “don’t exercise until over six months old”, with the result that the exuberant young dog bounces round the garden, whereas its energy would be better diverted towards plentiful controlled lead walking.

Once clinical signs of the problem are evident and diagnosis has been made, treatment will focus on conservative or surgical options:

Conservative treatment

It is well documented4 that hip morphology can be improved in a clinically affected young dog by controlling its exercise so that direct load transmission from the femoral head through the acetabulum can improve the shape of the joint as it continues to develop. Conservative treatment will therefore centre on the use of moderate amounts of controlled (short lead) exercise coupled with analgesia through the use of an appropriate non-steroidal anti-inflammatory drug (NSAID). Hydrotherapy may be very useful at this stage to promote muscle development over the hind-quarters (and therefore increasing the support for the lax joints) without the concussive injury associated with walking and running. This should continue until the dog is skeletally mature (12 – 18 months depending on the breed).

This simple non-invasive treatment regime is the treatment of choice for mild cases and whilst surgical options can improve the results, conservative treatment can still be appropriate and yield good results if surgery is contraindicated or financially constrained. However, it does require significant discipline on behalf of the owner and possibly a life-style change, so time spent educating the client is vitally important.

Surgical options

These are aimed at either improving the morphology of the joints by creating joints with increased load-bearing acetabular contact (triple pelvic osteotomy, juvenile pubic symphysiodesis, augmentation of the dorsal acetabular rim etc.), or the use of artificial implants to create a false joint (total hip arthroplasty). Indications for these surgeries are well documented and beyond the scope of this article.

Adult dog

At this stage of the disease process treatment is aimed at controlling the signs associated with osteoarthritis. The “holy trinity” of arthritis control is:

1. Pain relief – through the judicial long-term use of an appropriate NSAID.

2. Exercise control – controlled (lead) exercise encourages movement of the joints through their normal range of motion and limits extremes of flexion and extension and shearing forces.

3. Weight loss – force-plate studies have shown that the peak vertical force through joints can be up to five times the dog’s bodyweight, so tackling obesity is a major tool to reduce impact injury to the joints.

Careful discussion with the client will be required because the above measures may necessitate lifestyle changes and significant input on their behalf. It is also important to manage a client’s expectations: a client who views success as being able to return to the terraces to watch his favourite football team will be far more satisfied than one who expects to return to the pitch itself!

Once these golden rules of arthritis control are in place, adjunctive therapies such as hydrotherapy, physiotherapy, massage and, possibly, nutritional support may prove useful. However, it is vital that the “holy trinity” is embraced first and that other measures are seen as adjuncts.

If the above measures provide a good quality of life for the dog, then they can be continued for the rest of its life, with regular veterinary checks to offer support and tweak the management as required. If response is poor then surgical options may be considered. Essentially at this stage surgery is merely salvage in nature and involves either total hip arthroplasty or femoral head and neck excision. The choice may be financially dependent.


A scheme for assessing hips of breeding dogs was first introduced to the UK in 1965, with a simple “pass” or “fail” result. This was replaced in 1984 by the scheme still in use today. Each hip is assessed on a standard ventro-dorsal radiograph and scored, in nine categories, out of a total of 53 per hip. Of these nine categories two (subluxation and Norberg Angle) are concerned with the underlying morphology and the other seven relate to remodelling changes associated with secondary osteoarthritis. Despite its virtues and good intent, the scheme is inherently flawed for several reasons:

1. Only a small part of the score derives from those criteria that are directly associated with the underlying laxity.

2. The degree of laxity is inferred rather than measured directly.

3. Radiographic changes associated with osteoarthritis increase with the age of the animal, so the same dog could produce two different scores if radiographed at different times in its life. It is conceivable that a dog could be radiographed at one year old and be considered “good for breeding”, but radiographed again five years later and rejected!

4. There is the potential for false negative results: a dog with significant laxity, but reared in a very controlled manner, could have radiographically “good” hips.

For these reasons it is vital that the vet taking the radiograph should examine the joints thoroughly and discuss the results of the examination together with the score of the radiograph with a client considering using the dog for breeding. A low score “below the breed mean average” does not mean that the dog has normal hips!

Gail Smith and co-workers at the University of Pennsylvania, have devised an alternative scoring scheme that is based on the degree of laxity present in the joints. Two radiographs are taken. The first is a standard V-D view. The second view is taken with the joints “distracted” – a fulcrum is placed between the thighs and the stifles compressed together so that the femoral heads are abducted from the acetabulae to the extent allowed by the degree of laxity. The distance that the femoral head has moved (proportional to the size of the femoral head) is called the distractive index and correlates very closely with the likelihood of displaying clinical signs of hip dysplasia.

Unfortunately, in order to obtain films for this “PennHIP” scheme there must be manual holding of the animal during radiography and this is not permissible under current UK H&S legislation, although several UK orthopaedic surgeons are currently trying to develop a distracting device that will obtain consistent results and satisfy the Health and Safety Executive.Effects of age


This article was provided by Merial, makers of Previcox:


1. Smith GK, Biery DN and Gregor TP. New concepts of coxofemoral joint stability and the development of a clinical stress-radiographic method for quantitating hip joint laxity in the dog. J Am Vet Med Assoc, 1990; 196: 59-70.

2. Smith GK, Gregor TP, Rhodes WH and Biery DN. 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. J Am Vet Med Assoc, 1993; 54: 1021-1042.

3. Smith GK, Biery DN, Kealy RD and Lawler DF. Clinical significance of osteoarthritis and hip dysplasia findings in the restricted feeding trial. The Purina Pet Institute Symposium: Advancing life through diet restriction. St Louis MO. September 20-21, 2002 p27-28.

4. Barr ARS, Denny HR and Gibbs C. Clinical hip dysplasia in growing dogs: the long-term results of conservative management. JSAP, 1987; 28: 243-252.

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