To the Editor:
Thank you for your insightful comments regarding the contributing
factors to femoral neck fracture in resurfacing arthroplasty. We
acknowledge that disruption of the blood supply to the femoral head would
be one possible means of initiating a process of osteonecrosis which may,
in turn, contribute to neck fracture, particularly following trauma and,
in fact, we believe that in one of our reported cases this occurred. The
low incidence of avascular necrosis in failed resurfaced femoral heads
inserted through the posterior approach (3 out of 25 in our series to
date), as judged by histological examination of retrievals, does not
appear to support devascularization as an inevitable consequence of that
approach. Those 3 cases had atypically much deeper penetration of cement
into the trabecular bone, but we cannot be sure if this, or vessel damage,
caused the avascular necrosis. Similarly, we previously reported only 3 of
25 failed resurfacings from an earlier generation resurfacing had any
evidence of necrotic bone (2 with a pre-operative diagnosis of AVN and 1
with a previous resurfacing that was revised) (1) and none appeared to be
the cause of loosening Rarely, avascular necrosis leading to femoral neck
fracture has been observed after resurfacing with the anterior approach. (2,3)
Freeman (4) reported that an intraosseous blood supply is predominant
in arthritic femoral heads, which makes the contribution of the
retinacular vessels less important. The anatomic area where the
retinacular vessels enter the femoral head described in anatomy books or
the paper you quote by Gautier et al (5) is generally altered and obscured
by the osteophytic process. I routinely remove the posterior-superior
osteophytes (not those present anteriorly) and the soft tissue at the
head/neck junction in order to make certain that all available bone is
optimally prepared for acrylic cementation. I have often observed tiny
holes devoid of any vessels presumably the entry points of those former
vessels. Probably the best evidence for head viability is that the bone
surfaces bleed, often quite vigorously after bone preparation for
resurfacing. It is my belief that osteoarthritic process is accompanied by
diaphyseal neovasculature which, even though some may be destroyed by
reaming, appears to be ample to keep the head viable.
It was, and remains, a common misconception that femoral failure and
resorption of bone after cup arthroplasty and resurfacing with metal-
polyethylene bearings was due to surgically induced osteonecrosis. From
our histologic observations, the resorption process has always been
accompanied by vascularity.
If a surgeon performs resurfacing on a hip with minimal evidence of
osteoarthritis then the surgeon should be aware of those retinacular
vessels and avoid notching the neck where there may be subchondral
vessels.
Harlan C Amstutz, MD,
Joint Replacement Institute,
Orthopaedic Hospital, Los Angeles
1. Campbell P, Mirra J, Amstutz HC. Viability of femoral heads
treated with resurfacing arthroplasty. J. Arthroplasty.2000;15:120-122.
2. Howie DW, Cornish BL, Vernon-Roberts B. The viability of the femoral
head after resurfacing hip arthroplasty in humans. Clin. Orthop.1993;171-
184.
3. Bell RS, Schatzker J, Fornasier VL, Goodman SB. A study of implant
failure in the Wagner resurfacing arthroplasty. J. Bone and Joint
Surg.1985;67A:1165-1175.
4. Freeman MA. Some anatomical and mechanical considerations relevant to
the surface replacement of the femoral head. Clin. Orthop.1978;19-24.
5. Gautier E, Ganz K, Krugel N, Gill T, Ganz R. Anatomy of the medial
femoral circumflex artery and its surgical implications. J. Bone and Joint
Surg.2000;82:679-683.
Letters to the Editor: ![[Read Letter to the Editor]](/icons/misc/sectionDOWN.gif){kind=icon}
