Developmental orthopedic diseases (Proceedings)

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Panosteitis is an acquired self-limiting condition of undetermined cause that affects the diaphyseal and metaphyseal regions of the long bones of young, large breed dogs.

Panosteitis is an acquired self-limiting condition of undetermined cause that affects the diaphyseal and metaphyseal regions of the long bones of young, large breed dogs.  German Shepherd, Dobermans, Goldens, Saint Bernards, Bassetts and Labs are overrepresented.  Dogs are typically 5-18 months of age at presentation.  Males are more frequently affected than females.  While the etiology is unknown, histopathology reveals an increased osteoblastic and fibroblastic activity replacing the medullary cavity with connective tissue. 

There are no inflammatory cells or necrosis, but instead a haphazard intramembranous ossification.  Clinical signs may include lethargy, anorexia and a shifting leg lameness which can be acute or chronic, but is often intermittent.  Pain can be elicited on palpation of the diaphysis of affected long bones.  The humerus, femur and proximal radius/ulnar are the most common sites. 

The pain can be cyclic and recurrent.  Radiographically you can visualize an increased density within the medullary cavity blurring the trabecular pattern, often near the nutrient foramen.  However, lameness is not always associated with radiographic lesions and early in the disease, radiographic signs may not be apparent.  This self-limiting disease often resolves in 1-2 weeks but can recur up to 18 months of age.  Conservative therapy may include NSAIDs, exercise restriction, weight reduction and dietary correction to avoid oversupplementation.  The prognosis is excellent with some dogs experiencing a shifting lameness until maturity.  Rarely, clinical signs persist after maturity. 

Osteochondrosis (OC) is a disturbance in the process of endochondral ossification in a focal area of developing articular surface.  Cartilage fails to undergo calcification and replacement by bone and therefore becomes degenerative.  Cartilage retention results in thickening of the articular epiphyseal cartilage and degrades because cartilage cannot handle high shearing forces.  The etiology may involve genetics, rapid growth, calcium supplementation, hormonal influences, ischemia and trauma as potential factors.  OC is seen in large breed, fast growing dogs from 4 to 7 months of age.  It is most commonly seen in the shoulder, stifle, elbow and tarsus.  The thickened articular-epiphyseal cartilage has poor diffusion of nutrients from the synovial fluid.  This leads to necrosis at the deep portion of the thickened cartilage.  The consequence is an abnormal arrangement of cells, metabolism and function of these chondrocytes. 

When a separation occurs between the noncalcified and calcified layers at this weakened site a cartilage flap is formed and called osteochondritis dessicans (OCD).  The flap may reattach or have a vertical fracture of the articular cartilage.  The vertical fracture has minimal motion during weight bearing but causes synovitis, irritation and lameness leading to osteoarthritis (OA).  When synovial fluid enters the vertical fracture it prevents it from healing.  The cartilage flap can also detach and become a joint mouse, which causes irritation.  The free floating flap can resorb or may enlarge due to nutrition from synovial fluid.  Clinical signs usually begin with an intermittent lameness that is worse after exercise.  Joint effusion and pain may also be present.  Muscle atrophy and OA will develop over time.  Radiographic findings will show a filling “defect” or “flattening” of the subchondral bone, which is the thickened area of cartilage that is not radiopaque. 

A joint mouse may also be visible if the flap is mineralized.  You may see radiographic signs of OA.  A positive contract arthrogram may aid in identifying a cartilaginous flap or joint mouse.  Ultrasound, MRI and CT have also been shown to be very sensitive and specific for OCD.  Conservative therapy can be utilized if there is no clinical pain or joint mouse present and in dogs less than 7 months of age with a small lesion.  Rest and a restricted diet are implemented for 6 weeks.  NSAIDs and chondroprotectants, with physical rehabilitation should also be used.  This may allow the cartilage defect to heal.  Surgical treatment is indicated for the presence of a non-healing flap, lameness of more than 6 weeks, a dog older than 8 months or a visible joint mouse on radiographs. 

The surgical objectives are to excise the cartilage flap and unadhered cartilage and well as encourage healing of the defect.  Healing of the defect occurs by production of fibrocartilage which requires bleeding from subchondral vessels to allow invasion of mesenchymal stem cells.  After surgery, the animal must be on restricted exercise for 4 to 6 weeks to allow the scar cartilage to form.  Shoulder OCD has a good to excellent prognosis with other joints being guarded due to OA.

 

Elbow dysplasia is an inclusive term used to describe all developmental conditions resulting in elbow arthrosis.  The growth discrepancy within the antebrachial growth plates, genetics, conformation and oversupplementation are all proposed etiologies for elbow dysplasia.  Elbow incongruency can occur with the trochlear notch, radial head and humeral condyle.  An elliptical trochlear notch will change the contact points of the elbow joint.  Ununited anconeal process is when the anconeal process fails to unite with the proximal ulna before 20 weeks of age.  It is common in large dogs including the German Shepherds, Bassett hounds and Saint Bernard's.  While the etiology is undetermined it may be OCD-related, trauma or genetics. Lameness, stiffness, pain and creptius are commonly seen and usually bilateral. Radiographically a cleavage line can be seen along with sclerosis and OA of the elbow.  Conservative therapy is described but rarely efficacious.  In young dogs there are variable techniques to attach the fragment, but these are technically challenging.  In dogs over 6 months of age excision of the ununited fragment is recommended. 

The prognosis is generally fair due to the inevitable OA and early surgical intervention may help limit OA.  Fragmented medial coronoid process (FCP) is the third component of elbow dysplasia.  It may be a result of excessive loading of the coronoid process during abnormal development or joint incongruency, direct trauma or OCD-complex.  Lameness usually begins at 4 to 9 months of age and occurs in large breed dogs as well, with males being over represented.  Elbow pain and lameness are similar with signs of OCD, and the two may occur together.  Elbows may also be abducted when standing or have joint effusion localized to the medial aspect of the elbow joint.  The best radiographic view is a 25 degree craniocaudal-lateromedial oblique view flexed 30 degrees.  However, CT scans are much more sensitive for diagnosing FCP.  Often signs on plain films are non-specific and include periarticular osteophytes, sclerosis and rarely soft tissue swelling. 

Conservative therapy with restricted exercise and weight control can be tried or surgical therapy with excision of the fragment via arthrotomy or arthroscopy can be used to remove the coronoid and evaluate for “kissing lesions” on the humerus.  FCP carries a fair to guarded prognosis with inevitable OA.  The choice between medical and surgical management for FCP remains controversial but surgery is generally recommended in dogs under a year. 

Hypertrophic osteodystrophy is an idiopathic disease that affects rapidly growing large breed dogs and involves the long bone metaphysis. Dogs generally present between 2 to 8 months of age with males being overrepresented.  German Shepherds, Irish Setter, Weimeraners, Great Danes and Chesies are more commonly affected.  Clinical signs may include lameness with a reluctance to walk and warm painful swelling of the metaphysis of the distal radius/ulna, and tibia bilaterally.  Patients can be anorexic, run a high fever, and exhibit depression or lethargy.  Radiographs show a radiolucent region in the metaphysis with neighboring sclerosis called the “double physeal line”. 

There may also be irregular widening of the physis and extraperiosteal cuffing.  The etiology remains unknown but theories have been proposed for vitamin-C deficiency, oversupplementation of vitamins and minerals, E. coli, canine distemper, genetics, vascular abnormalities, and vaccine induced.  Treatment is aimed at supportive care to maintain hydration, nutrition support, NSAIDs for pain and to correct any dietary imbalances.  The prognosis is good with most patients recovering in 7 to 10 days with this self-limiting disease.  Possible sequela may include growth disturbances of affected limbs, systemic illness, or death.

Legg-Calve-Perthes Disease (LCPD) is avascular necrosis of the femoral head.  It has also been called ischemic necrosis, or coxa plana.  LCPD typically occurs in small and miniature breeds between 4 to 11 months of age with no apparent sex predilection.  Etiology may be traumatic, vascular, autosomal recessive, infectious or hormonal.  But an ischemic event occurs that results in the death of the affected bone.  Bone necrosis occurs and subsequent remolding of the femoral epiphysis occurs. 

Hip pain and lameness with crepitus are the most common clinical signs.  Muscle atrophy can be seen, especially in bilateral cases which compromise 15-18% of LCPD cases.  Radiographically you can see a flattening or irregular surface of the femoral head with a moth eaten appearance.  Occasionally femoral neck fractures can also be seen.  Conservative therapy may be tried unless a fracture is present indicating an FHO.  Overall prognosis is good to excellent. 

Capital Physeal Dysplasia is an uncommon disorder of the proximal femoral metaphysis seen in overweight male neutered cats as well as Shelties.  It classically appears as an atraumatic Salter Harris Type I or II.  It is often called a slipped epiphysis. While the pathophysiology is unknown the disease appears to be a combination of delayed physeal closure, decreased gonadal hormones, dysplastic chondrocytes and obesity.  Typically cats are young, presenting from 5 months to 2 years.  OA is already present at the time of diagnosis.  The treatment of choice is FHO.

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