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Juvenile orthopedic diseases (Proceedings)


Juvenile orthopedic diseases are a common cause of lameness and discomfort in young animals. A patient's signalment, history and complete physical examination are necessary to localize the disease, establish differential diagnoses and develop a diagnostic plan.

Juvenile orthopedic diseases are a common cause of lameness and discomfort in young animals. A patient's signalment, history and complete physical examination are necessary to localize the disease, establish differential diagnoses and develop a diagnostic plan. A thorough understanding of the etiology, pathophysiology and progression of possible differentials is important when recommending the appropriate medical and surgical intervention and predict a realistic outcome for prognosis.

Osgood-Schlatter disease in people is a benign, self-limiting avulsion or epiphysitis of cartilaginous or bony fragments from the insertion of the patellar tendon on the tibia. It is predominately seen in actively growing athletically active adolescents. The avulsion is thought to be secondary to acute or chronic excessive tensile trauma on the insertion of the patellar tendon or a form of osteochondrosis. Historically, people with Osgood-Schlatter disease will describe discomfort that worsens with exercise. During the initial phase there is swelling of the adjacent soft tissues and discomfort, usually bilaterally. Radiographically in humans, there is swelling of the patellar tendon with ossified particles within the tendon. In dogs, however, there may be mild separation of the entire tubercle from the proximal tibial metaphysis. Physical examination yields discomfort on direct palpation of the insertion of the patellar ligament and pain and resistance on full stifle flexion. Soft tissue damage seems to be the primary reason for pain and associated clinical signs. Depending on the severity of displacement and associated pain, treatment may be either conservative (rest) until skeletal maturity or may require surgical intervention.

Hypertrophic osteodystrophy (HOD) is a self limiting idiopathic disease affecting rapidly growing large to giant breed dogs between 2 and 8 months of age. German shepherds, Weimeraners, Great Danes and Chesapeake Bay Retrievers breeds have a higher incidence of this disease. The cause of hypertrophic osteodystrophy still remains unknown, however reported potential causes include: infection (canine distemper virus and E. coli), hypovitaminosis C, nutritional oversupplementation, vascular abnormalities and genetics. The importance of nutrition relative to the development of cannot be underestimated. Lesions similar to HOD have been experimentally induced in puppies fed a free choice calorically dense diet high in protein and calcium. Abnormalities occur in the metaphyseal bone immediately adjacent to the physis where the vasculature turns 180 degrees. Histologically, there is necrosis of these capillary loops with multiple focal areas of absorption, which may be accompanied by neutrophilic infiltration. This produced a necrotic band, which appears on radiographs as a radiolucent line termed a pseudophysis (double physeal line), pathognomonic for hypertrophic osteodystrophy. In some cases, there may also be irregular widening of the physis and periosteal new bone formation. Clinical signs include acute onset of lethargy, reluctance to walk, mild to severe lameness and generalized pain. There is typically an acute onset of discomfort and soft tissue swelling over the distal aspect of the front limbs and less commonly hindlimbs. The lesions are usually bilateral and symmetric. Systemic signs include anorexia, weight loss, fever and depression. Death can occur from sustained fever and systemic signs or by euthanasia from persistent discomfort. Treatment of HOD consists of supportive care to maintain hydration, prevent further injury from long term recumbancy and to alleviate discomfort. Nonsteroidal medications and occasionally steroids are used to control pain in most patients. Slowing the growth rate by switching to a less calorically dense diet may also be beneficial. Nutritional supplementation is not advocated and there is some evidence that supplementation with Vitamin C or D may increase the risk of dystrophic calcification. In cases of a persistent fever, blood cultures and broad spectrum antibiotics may be indicated. HOD is usually self limiting and carries a good prognosis in uncomplicated cases. In more severely and systemically affected patients, the prognosis is guarded due to systemic metabolic disease or secondary bateremia and sepsis. Specific vaccination protocols have been recommended in some breeds (Weimeraners) using separate vaccines or killed vaccines to avoid the possibility of vaccine induced HOD.

Legg-Calve Perthes disease/Slipped capital femoral epiphysiolysis (SCFE)/ Metaphyseal osteopathy:

Legg-Calve Perthes disease or avascular necrosis of the femoral head, is a developmental condition that occurs in primarily toy and miniature dogs. Most patients are 4 to 11months of age and both genders are equally represented. There does appear to be a hereditary component of the disease. It is reported that 12-15% of cases have bilateral disease. Several causes have been suspected leading to the development of Legg-Calve Perthes. Based on histological evaluation it does seem as though there is a temporary or transient vascular compromise rather than a permanent vascular insult as was initially suspected because there is evidence of reparative fibrosis and osteoblastic activity after the initial ischemic phase of the disease. Published reports indicate that lameness resolved in less than 25% of dogs treated conservatively. Slipped capital formal epiphysiolysis (SCFE) affects young cats that have undergone prepubertal gonadectomy and rarely occurs in dogs. Animals present with a hindlimb lameness of varying degrees of severity and duration. Serial radiographs are usually diagnostic and physeal dysplasia can be demonstrated in multiple physes concurrently, particularly the capital physis, distal femoral and distal radial physes. Histologic changes in the growth plates include loss of normal columnar architecture of chondrocytes, chondrocyte clustering, granulation tissue present within the growth plate, clefts of necrosis and overall wider growth plates (up to twice normal). Young, obese males are over-represented. Conservative therapy or surgical (femoral head and neck ostectomy) may be indicated depending on the severity of clinical signs. Metaphyseal osteopathy is condition is seen mainly in young male neutered cats, age 2 years or less. Affected cats present with a unilateral or bilateral hind limb lameness often with an insidious onset. Cats with metaphyseal osteopathy develop necrosis in the proximal metaphysis, which can subsequently result in a secondary pathologic fracture of the femoral neck. Unlike SCFE, radiographs show characteristic chronic degenerative changes in the femoral neck region including area of radiolucency, bone resorption, 'apple coring' or narrowing of the femoral neck, and femoral neck fracture. "Apple-coring" is a hypervascular response associated with attempts to repair the fracture. Biopsies of the affected femoral neck are consistent with evidence of fracture healing. In some cases the fracture has healed but a malunion is present. The other femoral head may fracture at a later date. Several etiologies have been proposed including; traumatic fracture with secondary bone resorption, avascular necrosis, osteomyelitis, feline herpes virus and changes secondary to SCFE. One review of 26 adult cats presenting with spontaneous femoral capital physeal fractures suggested that they were most likely to be heavier, neutered males with delayed physeal closure (McNicholas et al 2002). Treatment is femoral head and neck excision or total hip replacement.

Multiple cartilaginous exostoses –

Exostoses are analogous to miniature growth plates found in random regions of metaphyseal bone. The exostoses are present at birth and continue to grow as endochondral ossification occurs in affected animals. As they continue to grow, they form bony proliferations with a "mushroom" appearance and they stop growing when endochondral ossification ceases. Radiographs are highly suspicious but histopathology is needed to confirm the diagnosis. Clinical signs depend on the location of the multiple cartilaginous exostoses or can be an incidental finding. Compression of the spinal cord is fairly common resulting in paresis or ataxia and lameness can often be seen as the exostoses exert direct pressure on peripheral nerves, vessels and muscles or from interference with tendons or ligaments. Treatment if indicated is oriented toward correcting the secondary compression or irritation exerted from the exostoses. In humans, a small portion, approximately 20%, will transform into malignant neoplasia several years after the initial diagnosis though this rarely occurs in dogs. Any indication of neoplastic metaplasia indicated surgical excision. In cats, multiple cartilaginous exostoses have been associated with FeLV infection and predominately occurs in Siamese. Exostoses in cats are often aggressive and carries a poor prognosis though dogs usually have a good prognosis.

Incomplete ossification of the humeral condyle (IOHC). The humeral condyle is composed of two centers of ossification that typically fuse in 70 14days. In complete ossification or abnormal mineralization has been theorized to be 1. A form of osteochondrosis, 2. Cartilage weakening from abnormal forces from trauma or incongruity, or 3. Hypovascularity of the humeral condyle. Diagnosis is based on signalment, history, radiographic appearance, nature of the fracture surface and possible bilateral disease. This condition occurs mainly in spaniels, for which an autosomal recessive mode of inheritance has been suggested. However, several other breeds have been affected including Labrador retrievers, Rottweilers, Yorkshire terriers, Miniature Pinschers, and Dalmatians. The median age of diagnosis is typically between 3 and 8 years. Historically, these animals present with a lameness resulting from a stress fracture of the epicondyle with minimal trauma reported. Radiographically there is a fracture of the lateral (30%), medial (15%) or medial and lateral portions of the condyle (55%) ("T" or "Y" fractures). There is typically sclerosis present along the condylar fragments and periosteal new bone along the epicondyles. Radiographic positioning can be difficult to diagnose IOHC without concurrent fracture due to superimposition of the ulna over the site in question. Performing a 10-15 degree oblique cranio-caudal radiographic view is useful in visualizing the center of the condyle or CT scan of the area. Unless a fracture occurs, only a mild lameness may be noted therefore the overall incidence, risk and bilateral nature of this disease are unknown. It is important when assessing front limb lamenesses and performing radiographs to monitor for the potential of IOHC as the cause of lameness.

Carpal laxity/ Carpal hyperflexion/ Carpal hyperextension. Puppy carpal laxity syndrome can either present as carpal hyperextension or carpal hyperflexion. Clinical signs of laxity present between 6 and 12 weeks of age and can affect one or more individuals in a litter. The etiology remains unknown, but may result from an imbalance in growth or tension between the flexor and extensor muscle groups or unequal rate of bone growth relative to the soft tissues. Nutritional abnormalities, excessive growth rates and exercise have also been proposed as causes, but have not been documented. On physical examination there is either unilateral or bilateral carpal laxity with excessive carpal hyperextension or hyperflexion without discomfort. No other physical examination or radiographic abnormalities are usually detected. The laxity is usually self-limiting in nature. Physical therapy and exercises promoting muscular strength and tendon stretching is usually promoted over splinting or bandaging. In severe cases of carpal hyperflexion, there is excessive tension on the humeral head of the flexor carpi ulnaris tendon, surgical transection of this tendon has previously been advocated, however appropriate exercise and range of motion has yielded similar or better results.

Pes Varus/ Pes valgus. Pes Varus is a deformity resulting from eccentric medial closure of the tibial physis resulting in varus angulation of the distal tibia and pes. The deformity is primarily varus with minimal loss of length. The condition is believed to have an underlying genetic component in Dachshunds (autosomal recessive) and be a form a tibial dysplasia rather than trauma as there is typically no trauma noted in the history and the condition is usually bilateral. Clinical signs vary from a mild lameness with reluctance to sustain prolonged activity to more severe cases with a tendency to sit after a few steps and inability to run or jump. During ambulation, in order to allow the plantar aspect of the paw to contact the ground, the stifle is abducted and extra-rotated conferring a typical bow-legged gait. Surgical correction to re-establish the mechanical axis of the limb has good to excellent results. Pes valgus is a similar deformity affecting the distal tibial growth plate resulting in valgus deformity of the pes with minimal loss of length. Shetland sheepdogs and Rottweilers are overrepresented and similar to pes varus in Dachshunds there is usually no history of trauma associated. Previously there was some speculation that the pes valgus deformity was similar in course to carpal valgus resulting from premature closure of the distal ulnar physis (fibular physis) and deformity from the tethering affect of the two bones, however this has been proven not to be the case in pes valgus.

Metatarsal rotation is a deformity seen most commonly in giant breed dogs with double dewclaws and polydactyly, such as Bernese Mountain dogs, Saint Bernards and Great Pyrenees. The deformity is primarily torsional originating in the central tarsal bone and resulting in external rotation of the pes. The condition is often bilateral and the hocks tend to "clap" together during ambulation. Mildly affected dogs (external rotation <45 degree) can often be managed conservatively, however, dogs with more severe deformities (>45 degrees external rotation) benefit from surgical correction.


Musculoskeletal disorders have been reported in up to 22% of dogs less then 1 year of age with up to 20% of these being nutrition related. Deficiencies in vitamin D or trace elements, excessive calcium or vitamin C, and high energy intake have been discussed as reasons for developmental growth abnormalities. For example, diets calorically dense and with calcium supplementation have been shown to slow chondrocyte maturation and increase the likelihood of retained cartilaginous cores and osteochodrosis (this is still true when the Ca:P is corrected). The recommended percentages, on a dry matter basis, of key nutrients in a diet for large-breed puppies to minimize the risk of orthopedic disease are as follows: protein, 29% to 34%; fat, 11% to 16%; mean energy, 3.4% to 4.1%; calcium, 0.8% to 1.4%; phosphorus, 0.7% to 1.2%; fiber, 2.4% to 5.6%.

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