To the Editor:
The study "Ibandronate for Prevention of Femoral Head Deformity after
Ischemic Necrosis of the Capital Femoral Epiphysis in Immature Pigs"
(2005; 87:550-7) by Kim et al, is based on their concept that it is the
strength & shape of the bone of the ischemic capital femoral epiphysis
which defines the future of the immature hip and that, in particular,
these factors will determine the onset of premature osteoarthritis. This
thesis and chronology is, I believe, only partially correct.
The femoral capital epiphysis is an osteochondral structure and it is
the cartilage embracing the bone that ultimately defines the overall shape
of the femoral head at all ages. It is the joint cartilage shape &
biomechanical characteristics that mainly determine the development of
arthritic degeneration. That is, of course, not to claim that the
characteristics of the underlying osseous structure have no significance
at all.
In Legg-Calve-Perthes disease (LCPD), which the authors specifically
cite as an example of femoral capital ischemic necrosis, the femoral head
cartilage becomes absolutely thickened & deformed, the superior region
of the enlarged head being flattened parallel with the underlying osseous
epiphysis very early in the disease process (1).The repair process in the
osseous epiphysis may make the bone weaker and the deformity of the head
greater but treatment aimed at strengthening the necrotic bony capital
epiphysis, as described in the current work, cannot have "prevented
femoral head deformity" because it is already deformed usually in the
early stages of the disease process. The analysis of the experimental head
deformity in this study was confined to examining the bony epiphysis and
ignored the cartilaginous component of the head, thereby nullifying the
possibility of reporting on the results of drug therapy on the complete
osteochondral femoral head.
Furthermore, the necrotic bone of the immature femoral capital
epiphysis in LCPD inevitably reconstitutes its viability and structure.
Based on this understanding, the consensus approach to treat LCPD has been
to improve the mechanical environment of the osteochondral head in
relation to the acetabulum by surgical or orthotic means and thereby
decrease the inevitable, extremely early, articular deformity in children
at risk for later osteoarthritis; there should not be any need for
biphosphonate therapy to achieve this.
When considering the clinical relevance of this study, enthusiastic
clinicians should heed the authors' caveat that more animal studies will
be necessary before subjecting any children with LCPD, or other causes of
ischemic necrosis of the femoral capital epiphysis, to a potentially toxic
drug which may well alter the children's bone growth.
David H. Gershuni M.D., F.R.C.S.
61 Yigal Allon,
Zichron Ya'akov 30900,
Israel.
gershuni@actcom.net.il
Reference
1. Gershuni DH, Axer A, Hendel D. Arthrographic findings in Legg-
Calve-Perthes disease and transient synovitis of the hip. J. Bone Joint
Surg Am. 1978;60:457-64.
Letters to the Editor: ![[Read Letter to the Editor]](/icons/misc/sectionDOWN.gif){kind=icon}
