Elbow dysplasia in the dog describes the abnormal development of the elbow and includes a number of different abnormalities which affect different sites in the joint.
The most common primary lesions are:
- Osteochondritis dissecans (OCD)
- Ununited Anconeal Process (UAP)
- Fragmented or Ununited Coronoid Process (FCP)
Primary lesions occur during the development of the puppy and usually occur in both elbows to the same degree.
The primary lesions may stabilise when the dog reaches maturity, but further secondary lesions, most importantly osteoarthritis, lead to irreversible changes and are a potential problem for the rest of the dog's life.
Elbow dysplasia is a multifactorial disease, but the most important cause is genetics. Other factors such as growth rate, diet and level of exercise may influence the severity of the disease slightly in an individual dog, but they cannot prevent the disease or reduce the potential of the dog to pass the disease on to offspring. Studies show that elbow dysplasia has a high heritability confirming that a high proportion of the cause of the disease is genetic.
In general, medium and large-breed dogs are more vulnerable to the disease, especially breeds such as German Shepherd Dogs, St Bernards and Labradors.
This is failure of endochondral ossification, which is usually more common in the shoulder joint.
The condition tends to be bilateral and targets the medial condyle of the humerus. There is a subchondral bone cyst, a core of necrotic cartilage surrounded by a sclerotic layer.
Ununited Anconeal Process
This describes the failure of the anconeal proces to unite with the ulna. It has a separate ossification centre which normally unites at 4-6 months of life.
The condition is bilateral in 30% of cases. The nonunion can be non-displaced or displaced, and this will determine different methods of treatment.
Fragmented Coronoid Process
There is improper development of the cartilaginous precursor of the medial coronoid process, which then fragments during growth of the animal.
This is often seen in combination with the other two conditions.
The clinical signs are of a variable lameness, which is usually weight-bearing and worsens after long periods of rest or exercise.
There may be swelling of the elbow joint.
Secondary changes of degenerative joint disease may be felt as a bony thickening of the joint.
History and clinical signs are usually suggestive of the condition.
Manipulation may also help the diagnosis. For example, UAP cases usually show crepitation and pain on extension of the elbow joint.
Different radiographic views allows detection of the abnormalities. The views include: extended lateral view, flexed lateral view and cranio-caudal view.
For elbow OCD: the cartilage is not seen on radiography, but subchondral bone changes may indicate cartilage damage. Serial films may have to be taken several weeks apart to diagnose the condition. Changes may include subchondral bone lucency in the medial condyle (on the cranio-caudal view), subchondral sclerosis and calcification of the flap, osteophyte formation.
For UAP: the flexed lateral view is the diagnostic view as it pulls the anconeal process out of the humerus. The condition is diagnosed if the anconeal process is ununited after 6 months of age. There may be degenerative joint disease on the joint margins.
For FCP: the cartilage cannot be seen radiographically, but there may be signs of degenerative joint disease such as bone proliferation on the cranial aspect of the olecranon process and sclerosis where the joint capsule attaches.
Conservative treatment is not recommended due to secondary degenerative joint disease.
Surgery should be performed via an arthrotomy to enable debridement and curettage of the defect. This will allow fibrocartilage to fill the defect.
The prognosis is good for soundness with early surgery, but poor if secondary changes are present.
If the animal is still young and the union is thought to be simply delayed, the dog should be confined and re-radiographed monthly to check for union.
If the nonunion is displaced, the most common treatment is surgical removal of the fragment. Excellent results are seen and lameness is reduced, even though crepitus and decreased range of motion may still be seen.
If the nonunion is non-displaced, compression of the fragment may be possible with a lag screw. This is technically difficult and removal of the fragment may be preferable. However good results seem to have been observed in most cases. Recovery is long and the screw may have to be removed at a later date.
The third possible treatment is proximal diaphyseal ulnar osteotomy: to restore congruency of the elbow and relieve the abnormal load of the anconeal process. This is most successful in young dogs.
Prognosis is excellent if surgery is successful but most dogs will show lameness at about 7 years of age.
Concommitant FCP or OCD dramatically alter the prognosis.
Conservative treatment is not recommended.
The osteochondral fragment should be removed via an arthrotomy from the medial side.
Prognosis is guarded and poor if the condition is diagnosed after 1 year of age.
Control of the condition involves radiographic screening of potential breeding animals and grading of elbows. Low-risk animals can then be selected for breeding, thus reducing the heritability of the condition and significantly reducing the number of elbow dysplasia cases.
|Elbow Dysplasia Learning Resources|
Test your knowledge using flashcard type questions
|Small Animal Orthopaedics Q&A 18|
Pasquini, C. (1999) Tschauner's Guide to Small Animal Clinics Sudz Publishing
Pead, M (2008) Elbow dysplasia in dogs - a new scheme explained BVA Publications
Slatter, D. (2002) Textbook of Small Animal Surgery Elsevier Health Sciences
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