Legg-Calv-Perthes Disease

Roberto E. Novo, DVM, DACVS

This disease was characterized in 1910 as a condition affecting the hip joint in children. In children,
the disease was characterized radiographically by flattening of the femoral head (coxa plana). The etiology of
this condition was eventually determined to be secondary to ischemic necrosis of the superior femoral
epiphysis. Over the years, this condition has also been referred as aseptic necrosis, epiphyseal aseptic necrosis,
ischemic necrosis, osteochondritis deformans juvenilis, coxa plana, Legg-Perthes or Calv-Perthes disease. The
disease condition that affects predominantly young, small breeds was first described in 1937. It was concluded
at that time that no difference existed between the human and canine condition, and hence the disease in dogs
has been known as Legg-Calv-Perthes Disease (LCPD).
In the canine, LCPD is an avascular necrosis of the femoral head, most frequently affecting toy breeds
and terriers. There is no sex predilection in the canine, with the disease generally being unilateral (15%
bilateral). The onset of clinical signs generally peaks at about 7 months of age (3-13 months).
Normal Blood Supply
The main blood supply to the femoral epiphysis comes from the lateral circumflex femoral artery,
medial circumflex femoral artery, and a branch of the cranial and caudal gluteal arteries. All of these vessels
develop into a retinaculum that penetrates through various aspects of the joint capsule, supplying blood to the
femoral head and neck. These retinacular vessels send branches into the femoral epiphysis, supplying about
70% of its blood supply. The remaining 30% of the epiphyseal blood supply comes from the ventral retinacular
arteries.
Pathology
Before radiographic signs are seen in the femoral head, synovitis and synovial effusion are present in
the affected hip joint. Hip joint laxity would be the only radiographic sign initially. Initially, there is a loss of
blood supply to the dorsal region of the femoral epiphysis, leaving a region of subchondral bone without blood
supply and therefore causing necrosis.
During the next phase of the disease, revascularization of the necrotic bone occurs, and the incoming
new arterioles and capillaries bring in sufficient blood supply to demineralize and thus weaken the subchondral
bone (which is NORMAL in bone healing). The bone eventually collapses into the defect due to stress or
leading pressure on it. At this point, characteristic radiographic changes of lucent areas and a flattened femoral
head become apparent. The base of the defect has granulation tissue and neovascularization. Osteoclasts
remove the necrotic bone while the new bone and cartilage are being laid down in an attempt to heal the defect.
The articular cartilage remains viable, as it receives its nutrition via the synovial fluid. However, when
the subchondral bone collapses, the overlying articular cartilage buckles in, creating a cracked and irregular
appearance. Eventually, the necrotic region is replaced by new bone or by densely organized collagenized
fibrous tissue. The congruity of the joint is lost due to the subchondral collapse, and degenerative osteoarthritis
involving both the femoral head and acetabulum progresses. The femoral neck also has a thickened appearance.
Etiology
Many theories have been given for the cause of the avascular event, including trauma, heredity,
endocrine disturbances, metabolic imbalances, fat embolism, and infection. The most likely cause for LCPD is
from trauma of some type. Chronic repetitive trauma affecting the dorsal retinacular blood supply seems the
most likely cause of the localized ischemia at the proximal femoral epiphysis. The traumatic insult may occur
in these small breeds due to excessive jumping on their rear legs, thus damaging the dorsal retinacular vessels.
Since the retinacular vessels to the femoral epiphysis course under the joint capsule and synovial membrane,
they would be susceptible to trauma when the dog jumps.
Radiology
The ventrodorsal view allows the diagnosis of LCPD. In the early stages, only a lucent area would be
present in the dorsal aspect of the femoral head, however this condition is rarely caught at such an early stage.
By the time the patient is present to the clinician, the most common radiographic finding is a slight, mild, or
severe flattening of the femoral head's dorsal aspect. Radiolucent areas also are present in the femoral head.
The femoral head is flattened and irregular in shape, and in some patients may appear fragmented. Some joint

laxity may be present. Over time, osteoarthritis becomes evident, with osteophyte formation around the femoral
head and acetabulum.
Treatment
Both nonsurgical and surgical treatments for LCPD are described, however most patients diagnosed
with LCPD are not candidates for nonsurgical treatment.
Nonsurgical. If a patient is to be treated nonsurgically, the diagnosis must be made before there is any
radiographic evidence of change to the femoral head and acetabular contour. During the treatment period, it is
essential that the affected joint be rested by cage confinement. During this period of confinement, the dog is
only allowed out of its cage for urination and defecation. The patient must be carried in and out of its cage and
kept on a short leash during elimination. The limb should NOT be placed in a non-weightbearing sling because
this would result in severe disuse atrophy and flexion contracture of the stifle. In addition, complete
immobilization of a joint for 6 weeks will initiate early degenerative changes in the articular cartilage. Monthly
radiographs are taken to follow progression of the disease. It generally takes up to 4-6 months before the
femoral head heals sufficiently to permit unrestricted weight bearing. If collapse of the femoral head occurs
during nonsurgical treatment, surgery is recommended.
Surgical. The surgical treatment consists of a femoral head and neck excision. The surgical procedure
is discussed elsewhere. Reported results clearly indicates this is the treatment of choice in canine patients with
LCPD. If left untreated, progressive osteoarthritis will occur, along with pain, lameness, and muscle atrophy.
If necessary, a femoral head and neck excision can be performed bilaterally. Advantages of the surgery are: 1)
high success rate, 2) unnecessary to confine patient to a small cage, 3) the young patient is free to move about
the home and become socialized, and 4) the patient will be weight bearing and having unrestricted activity more
quickly.

Legg-Calv-Perthes disease. (A) Bony destruction early in the disease causes both radiographic
lucency and actual loss of substance in the femoral neck. The epiphysis seems unaffected in this early
stage. (B) Fracture and collapse of the femoral neck. The epiphysis remains in the acetabulum, but
the deformed neck is displaced. (C) Early remodeling stage. Bone is again being deposited, but the
head and neck remain deformed. (D) Late, remodeled stage. The femoral head is flattened and
wrinkled, leading to instability and degenerative joint disease