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M. VALOROSO, G. LA BARBERA, G. DEMEY, D. DEJOUR
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ACL rupture leads to antero-posterior and
rotatory instability. The last one, described by
patients as “knee giving away”, is clinically
demonstrated by the pivot-shift (PS) test.
However, it is difficult to find a gold standard
method for its quantification. The devices used to
quantify this test are usually complex and bulky.
Recently, the accelerometer KIRA
TM
shows
promising and reliable results. The limit of this
system is that a learning curve to performproperly
the PS is required. The objective evaluation of PS
allows the surgeon to confirm the clinical
diagnosis in case ofACL rupture and to verify the
ACL status after the reconstruction [12].
GENDER AND HYPER-
LAXITY
ACL injury occurs with a 4- to 6-fold greater
incidence in female athletes compared to male
athletes playing the same landing and cutting
sports. The mechanism responsible for the
gender disparity in ACL injury risk is
multifactorial and it is related both to extrinsic
(neuromuscular and sport activities) and
intrinsic factors (anatomical and hormonal
differences between genders) [13].
During the menstrual cycle phase, several
authors observe that estrogen reduces the rate
of fibroblast proliferation and type I procollagen
synthesis, while progesterone has an opposite
effect [14]. ACL biomechanical properties may
be influenced by fluctuations in estrogen and
progesterone concentrations, increasing the
risk of ACL rupture during the pre-ovulatory
phase [4].
In literature, the Beighton score is frequently
used to quantify the whole body joint laxity. In
a military cadet prospective cohort study, it is
reported that an increased generalized joint
laxity is a significant predictor of ACL ruptures
in both males and females. More specifically,
cadets with a Beighton score >5 are 2,8 times
more likely to sustain an ACL rupture [10].
Moreover, increased knee hyperextension
(genu recurvatum) of 10° and hamstring
flexibility are significantly associated with risk
of ACL lesion [4].
GENETIC RISK FACTORS
Familial predisposition and specific genetic
variants are described as other possible risk
factors for ACL lesion. Retrospective studies
report a familial predisposition to ACL tears.
Patients with bilateral ACL ruptures show a
highly significant incidence of ACL injury in
the family members compared to control
healthy subjects (35% versus 4% respectively).
Moreover, patients with an ACL lesion are
more likely to have a relative with an ACL
rupture compared with individuals without any
history of ACL tear. The risk is slightly
increased when only first-degree relatives are
considered. The familial predisposition of ACL
injury may probably due to the role of specific
genetic variants within genes (COL1A1,
COL5A1, and COL12A1) encoding for the
extracellular matrix and predisposing to ACL
fragility [4].
TREATMENT
During ACL reconstruction, the surgeon has to
consider all the modifiable intrinsic risk factors
such as narrow notch, increased PTS, postero-
medial meniscal lesion and a significant
rotatory instability. Several authors suggest
that the notchplasty is a possible solution for
graft impingement and it is particularly advised
in case of revision surgery. The menisci have to
be preserved during the surgery not only to
prevent the chondral degeneration but also to
improve the anterior and rotational stability.
We suppose that the posterior horn of the
medial meniscus acts like a “wedge” reducing
the anterior tibial translation.
The anterolateral plasty should be used as an
associated procedure both in primary and
revision ACL surgery for patients that
demonstrate an excessive anterolateral rotatory
laxity (fig. 4). In a recent systematic review,