Background: The developing capital femoral epiphysis
consists of a secondary center of ossification surrounded by epiphyseal
cartilage. Between the epiphyseal cartilage and the secondary center
of ossification is a growth plate, which contributes to the circumferential
increase in size of the secondary center of ossification during
development. The main objective of this study was to describe the
histopathologic changes that occur in the growth plate surrounding the
secondary center of ossification during the early and reparative
phases following the induction of ischemic necrosis of the capital
femoral epiphysis in immature pigs.
Methods: Ischemic necrosis of the capital femoral
epiphysis was induced in eighteen piglets by placing a nonabsorbable
suture ligature around the femoral neck following a capsulotomy
and transection of the ligamentum teres. The animals were killed
three days to eight weeks following the induction of ischemia, and
visual, radiographic, and histologic assessments were performed.
Results: Two to four weeks after the induction of
ischemic necrosis, the growth plate surrounding the secondary center
of ossification became necrotic. The observed histopathologic changes
included chondrocyte death, loss of safranin-O staining of the matrix
of the necrotic growth-plate cartilage, an absence of vascular invasion
of terminal hypertrophic chondrocytes, and a decrease in the amount of
primary spongiosa, indicating cessation of endochondral ossification.
In the reparative phase, at four to eight weeks postoperatively,
chondrocyte clusters and intense safranin-O staining were observed
in the epiphyseal cartilage around the necrotic growth-plate cartilage.
In the peripheral region of the femoral head, necrotic growth-plate cartilage
surrounding the secondary center of ossification was resorbed by
a fibrovascular tissue from the marrow space. By six weeks, new
accessory centers of ossification with restored endochondral ossification
were observed in the peripheral epiphyseal cartilage. New ossification
centers contributed to the fragmented radiographic appearance of
the secondary center of ossification. The physis appeared essentially
normal in most animals, although five of the eighteen piglets showed
mild or moderate histopathologic changes.
Conclusions: In this model, ischemic necrosis of
the capital femoral epiphysis resulted in necrosis of the growth plate
surrounding the secondary center of ossification. Small new ectopic
centers of ossification appeared in the epiphyseal cartilage, explaining
in part the fragmented radiographic appearance of the secondary
center of ossification.
Clinical Relevance: This immature swine model may
facilitate systematic study of the sequence of cellular and structural events
that follow ischemic injury to the capital femoral epiphysis. Better
understanding of the injury and repair processes that follow ischemia may
lead to novel treatment strategies to stimulate the repair of the
infarcted capital femoral epiphysis and to restore normal growth
of the secondary center of ossification.