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.