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Arch Orthop Trauma Surg (2007) 127:485–491
DOI 10.1007/s00402-007-0367-y
123
B A S I C S C I E N C E
Interruption of the blood supply of femoral head: an experimental
study on the pathogenesis of Legg-Calve-Perthes Disease
A. Mumtaz Alpaslan · M. Cemalettin Aksoy ·
Muharrem Yazici
Received: 27 September 2006 / Published online: 28 June 2007
©
Springer-Verlag 2007
Abstract
Introduction
The etiology of LCPD still is not clear.
Thrombosis has been accused in the pathogenesis of LCPD
but it is not proven untill now. The aim of this study is to
evaluate the results of single episode of obstruction of
blood supply to the femoral heads of dogs.
Material and method
Blood supply femoral heads of 45
dogs was interrupted with embolisation with gel foam. The
radiologic appearances, macroscopic and microscopic spec-
imes of the hips were evaluated and compared with the
human specimens of 15 LCPD patients obtained at the time
of femoral osteotomies.
Results
After one infarct, we demonstrated changes in
femoral heads of puppies showing close resemblance to the
Wndings of LCPD in human.
Conclusion
Obstruction of the femoral head caused by
single arti
Wcial emboli caused changes in the femoral head
similiar to LCPD. The cause of the obstruction is obscure,
intravascular and/or extravascular pathologies need speci
Wc
attention, further studies focusing especially on the coagu-
lation system are needed.
Keywords
LCPD · Coagulation · Experimental study
Introduction
Legg–Calve–Perthes disease (LCPD) is a unique self-lim-
ited microvascular occlusive disease leading to the repeated
interruptions of the blood supply to the proximal femur
[
,
]. The immediate etiology of ischemia however,
has not yet been discovered. Two basic mechanisms block the
arterial system of proximal femoral epiphysis, one tampon-
ade produced by an aseptic in
Xammatory exudates as in
transient synovitis or more rarely by hemorrhage into the
joint causing an increase in extravascular pressure, two ces-
sation of circulation in the femoral head because of intra-
vascular clots [
,
,
,
,
,
,
Hemodynamic alterations, endothelial injury, thrombotic
tendency due to hypercoagulability and/or hipo
Wbrinolysis
have all been proposed as the possible pathogenetic factors
in the etiology of the LCPD [
,
,
,
,
We recently demonstrated a increase in Tissue factor path-
way inhibitor (TFPI), global
Wbrinolytic capacity (GFC)
and thrombomodulin (TM) levels in LCPD compared to
normal population [
,
]. These two studies indirectly re
X-
ect the presence of thrombosis and/or embolisation, which
in turn activating the
Wbrinolytic system.
Immunological and in
Xammatory processes together
with disturbed endothelial functions may take place in the
microvascular compromise and decreased blood
Xow of
LCPD. Histopathological and electron microscopic exam-
inations revealed perivascular collections of plasma cells
and lymphocytes in the synovial tissue of the LCPD
[
,
]. Signi
Wcant synovitis as the consequence of, or
preceding, the loss of blood supply and epiphyseal necrosis
is also an important feature in the LCPD [
]. In
Xamma-
tion, itself, is a potent prothrombotic stimulus. In
Xamma-
tory mechanisms up regulate procoagulant factors, down
regulate natural anticoagulants and inhibit
Wbrinolytic
A. M. Alpaslan · M. C. Aksoy (&) · M. Yazici
Faculty of Medicine,
Department of Orthopaedics and Traumatology,
Hacettepe University, Zemin kat,
Ankara 06100, Turkey
e-mail: caksoy@hacettepe.edu.tr
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