Elbow dysplasia

Canine elbow dysplasia is a syndrome characterized by development of secondary degenerative arthritis following several distinct primary diseases of the elbow. Asynchronous (unequal) growth between the radius and ulna during growth of the dog is the likely linking etiology between the individual diseases leading to elbow dysplasia. Normal elbow joint congruency is based on uniform growth of the humeral, radial, and ulnar joint components, and unequal growth of any of these bones leads to elbow incongruency and later degenerative joint disease (osteoarthritis). The individual diseases are Ununited Anconeal Process (UAP), Fragmented Coronoid Process (FCP) and Osteochondrosis (OC) of the distal medial humeral condyle. Cases of elbow dysplasia with severe secondary osteoarthritis but without the specific surgically-approached diseases listed above should be treated as arthritic patients.

Ununited Anconeal Process (UAP)
The anconeal process is a separate center of ossification of the developing ulna that unites with the rest of the bone at 20-24 weeks of age in the dog. Failure of the anconeal process to unite at the normal period of 20-24 weeks of age results in elbow instability and development of secondary degenerative joint disease. Ununited anconeal process is a congenital disease of dogs that has been related to osteochondrosis or to unequal growth of the radius and ulna. The disease may have a heritable component in German shepherd dogs.

Clinical Signs:
Forelimb lameness is evident in large dogs beginning at 5 months of age. Pain may be elicited on extension of the elbow joint and palpation of the proximal ulna. Joint effusion may be present in affected elbows. Chronic cases may exhibit classic signs of degenerative joint disease.

Diagnosis:
The diagnosis is based on clinical signs and lateral elbow radiographs (straight or flexed) that demonstrate the absence of union of the anconeal process and ulna in dogs > 6 months of age. Radiographs of the contralateral elbow are obtained for comparison and to rule-out bilateral disease. Signs of secondary degenerative joint disease (effusion, osteophytosis) may also be evident on lateral radiographs.

Treatment:
Surgical removal of the ununited anconeal process following a lateral arthrotomy is most frequently performed and results in return to normal function in >90% of affected dogs. An alternative surgical approach is lag screw fixation of the anconeal process to the ulna, but this procedure is controversial and provides no proven benefit beyond removal of the UAP. Recent reports indicate that midshaft ulnar osteotomy may provide effective relief of asynchronous growth and result in union of the anconeal process and ulna in young dogs, but careful selection of patients for this procedure is necessary.

Fragmented Medial Coronoid Process (FCP)
The coronoid process is the cranial and medial articular process of the ulna distal to the trochlear notch. Asynchronus growth of the radius and ulna may result in abnormal biomechanical stresses on the process and result in separation of the process from the ulna during development. Fragmented coronoid process is a congenital disease of large-breed dogs that may have a heritable component. Cases of traumatically-induced FCP have been reported, primarily in racing greyhounds and other working breeds. In the Midwest, Rottweiler's and Labrador Retrievers are the most common breeds with FCP.

Clinical Signs:
Forelimb lameness in large breed dogs with onset usually between 4 and 12 months of age, although a number of dogs may not show lameness until advancing osteoarthritis causes pain at 3-4 or more years of age. Pain may be elicited during flexion of the elbow or on palpation of the medial elbow joint compartment. There may be palpable elbow effusion.

Diagnosis:
Flexed lateral radiographs demonstrate periosteal proliferation on the dorsal anconeal process and (occasionally), the separate coronoid fragment may be observed. Cranial-caudal radiographs show the fragment in the medial joint compartment often associated with an osteochondral defect of the distal medial humeral condyle. The opposite elbow should be radiographed since the disease is often bilateral. Older dogs may exhibit radiographic signs of degenerative joint disease. Computed tomography (CT) may be useful in practices that have access to the equipment to demonstrate the fragmented process.

Treatment:
Removal of the coronoid process is undertaken through a medial surgical approach to the elbow. Bilateral lesions may be treated by separate procedures performed 6 weeks apart in each elbow or simultaneously. In older animals, some controversy exists about the benefits of removal of the fragmented process, but removal is probably still indicated. Postoperatively, soft padded bandaging and leash-walking are instituted for 10-14 days. Lameness may recur due to progressive secondary degenerative joint disease.

Osteochondrosis
Osteochondrosis (OC) is a defect in articular cartilage development in large breed dogs. Osteochondrosis is heritable in horses, pigs, man, and other species, and may be heritable in dogs.

Osteochondrosis is a defect in endochondral ossification that results in abnormal subchondral bone development and may result in the formation of a cartilage flap in the joint. Abnormal cartilage congruency, cartilage flap, or joint debris cause inflammation of the joint lining (synovium) and subsequent degeneration of the joint due to release of inflammatory mediators.

Clinical signs:
Unilateral or bilateral lameness may be seen. Joint effusion is variable and variably palpated.

Diagnosis:
Lateral, medial or craniocaudal radiographs of the affected joint demonstrate a flattened or concave subchondral area. Radiographic signs (bone spurs, subchondral bone sclerosis, joint mice) of secondary degenerative joint disease may be present. Contrast arthrography may be performed to delineate subtle dissecting lesions or cartilage flaps. The opposite joint should be radiographed since the disease is often bilateral. Cartilage flaps often do not form in the elbow.

Treatment:
OC should be treated by opening the joint, removal of the cartilage flap if present, and deepening of the OC lesion to stimulate fibrocartilage growth. In patients with bilateral radiographic lesions, only joints with clinical signs of OC (effusion or lameness) are curetted. Postoperatively, the animal should be allowed controlled exercise for 2-4 weeks, followed by return to normal function. Prognosis is dependent on the amount of degenerative joint disease present.