by C.A. Sharp
First published in Double Helix Network News, Winter 2001, Rev. April 2014
Elbow dysplasia (ED) may be the most unrecognized common health issue in Australian Shepherds. Affected dogs may only show lameness occasionally, something easy to dismiss as a minor injury in an active breed. A few affected dogs may not show signs at all. But testing results from Europe, where elbow exams are as standard as those for hips, makes it clear that this disease is much more frequent in Aussies than most breeders in North America are aware. In addition, having elbow dysplasia is a risk factor for also having hip dysplasia; the more serious the condition the higher the risk. The wise owner should consider it whenever he encounters an unexplained case of front-end lameness in one of his dogs. Breeders should make elbow screening part of their standard health screening practices.
ED is not a single disease, but rather a set of related defects that are grouped under the term “elbow dysplasia.” If your dog is diagnosed with ED, it may have any of the following:
- Fragmented medial Coronoid Process (FCP) – a prominence of the ulna at the elbow becomes separated from the bone below it. This is the most common ED defect. Roughly 60% of dogs with FCP will also have OCD (see below).
- Ununited Anconceal Process (UAP) – a prominence at the upper (elbow) end of the ulna is completely or partially detached from the rest of the bone. This occurs because the bone growth center between the process and the rest of the bone fails to join the pieces together. This normally happens around 4-5 months of age. In some cases UAP may be due to injury.
- Osteochondritis Desicans (OCD, also called osteochondrosis) – an area of cartilage fails to mature and becomes separated from the underlying tissue. It may be partially attached, like a flap, or become free-floating in the joint. (OCD can also occur in other joints than the elbow.)
Some dogs diagnosed with incomplete ossification of the humeral chondile are deemed to have elbow dysplasia. The condition arises in the cartilagenous growth plate at the elbow end of the humerus, the bone above the elbow joint when the growth plate fails to harden as it matures. This particular problem seems to be restricted to Spaniel breeds and is probably not be a concern for Aussie breeders.
The inheritance of elbow dysplasia is complex and no specific genes have yet been indicated. Unaffected parents can have affected offspring and if affected animals are bred together the offspring may not be affected. It is also possible that some or all of these conditions may be inherited independently though the frequency of the FCP/OCD connection indicates some relationship between them at least in a significant number of cases. OCD is also felt to be the same disease no matter what joint it occurs in, therefore breeders should keep shoulder OCD cases in mind in relation to ED until science gives us better genetic information than is available at present.
The defects are most common in large, heavy-boned or fast-growing breeds, so it is possible that the disease may be to some degree secondary to body morph (which is itself inherited) but not all large, heavy-boned or fast-growing dogs get ED. All of the ED defects are developmental in nature, arising from something going wrong during the growth of the bones that join at the elbow. Environmental factors play a part in shaping the growing puppy, but skeletal development is governed by the action of genes. Given that ED is more common in some breeds than others and in some families of dogs within a breed, an inherited cause should be assumed.
OCD, FCP and UAP all cause stiffness, stilted gait or lameness, usually while the dog is under a year of age and sometimes as young as 4 months. The affected joint will be swollen and painful. There may be atrophy of nearby muscles. The disease is often bilateral; occasionally one elbow may show signs before the other.
Untreated, the joint will degenerate, resulting in diminished range of motion and chronic pain. For the sake of the dog, early surgical treatment accompanied by weight reduction and restriction of activity is recommended. Some type of medication may be necessary. It should be noted that while husbandry practices may impact the severity of ED, it cannot be prevented or cured by diet, restriction of exercise and the like. Affected dogs remain affected and will pass ED genes on to their offspring if bred.
Diagnosis of ED is usually confirmed by x-ray of the affected joint. In very young dogs, the bone changes may not yet be visible in an x-ray so it is recommended that the procedure be repeated in 4-6 weeks to see if there is evidence of change to support an ED diagnosis. If x-rays still fail to reveal a cause for lameness, magnetic resonance imaging (MRI) or arthroscopy may be necessary.
Not all ED affected dogs will have clinical disease, so screening of apparently normal Aussies in ED families is very important. Screening of these dogs is vital to prevent the disease from becoming more widespread in the breed.
In North America the Orthopedic Foundation for Animals (OFA_ evaluates a lateral flexed view of each elbow. In this side-on view the elbow is flexed as much as possible. The x-rays are reviewed by board-certified veterinary radiologists and the elbows will be graded normal or dysplastic. They do not distinguish between the type of defect present (FCP, UAP or OCD.) If dysplastic, they are further graded I, II or III based on the amount of joint damage with III being worst. If the animal is 2 years or older, they will issue a numbered certificate which will also be reported to the appropriate breed club. OFA’s registry is “semi-open.” It will release information about affected dogs with the owner’s express permission to do so, however since it charges the same fee on all submissions, most people with affected dogs do not choose to spend the extra money and the results never reach OFA’s database.
European elbow evaluations are based on the findings of the International Elbow Working Group (IEWG), a group of veterinary radiologists and surgeons, geneticists and dog breeders who have developed a screening protocol to facilitate international exchange of data. It has proven effective for control of ED. They originally accepted the same single view as OFA, but beginning in 2001 they required two views, Lateral flexed and craniocaudal. The latter is taken with the joint extended and viewed from the top. IEWG does not feel a single view is adequate for diagnosis in all cases. European scoring systems are numerical, ranging from 0 to 5, with 0 being ED-free and scores of 1 – 5 indicating the severaity of the condition with 5 being worst. Dogs must be at least one year of age at time of screening.
ED is a disregarded risk in Aussies. It is crippling to the affected dog with correction requiring expensive surgery. Because of this, regular screening of breeding stock should become the norm. (It is a requirement for certification with the Canine Health Information Center – CHIC.) Affected dogs should not be bred. First-step relatives (parents, full and half siblings) should be bred only to mates screened clear of ED who do not have family history of HD. With more diligent screening practices we can limit the impact of this disease on the breed.