ARTICLE IN PRESS
Current Orthopaedics (2003) 17, 369--377
c 2003 Published by Elsevier Ltd.
doi:10.1016/S0268 - 0890(03)00102- 6
THE KNEE
The anterior cruciate ligamentF1
S. Karmani1 and T. Ember2
1
Flat1, Level 1 Garden Place, Hamilton, New Zealand
2
Royal National Orthopaedic Hospital, Brockley Hill, Stanmore, Middlesex HA7 4LP, UK
INTRODUCTION
The transverse ligament of the Atlas is the most impor-
tant ligament in the body; without it death will soon fol-
low.The ulnar collateral ligament of the thumb is a most
useful ligament; without it the hand and thus the whole
upper limb is compromised. The anterior cruciate liga-
ment (ACL) however, remains the subject of more dis-
cussion, opinion and controversy than either.
American epidemiological data reports 250 000 ACL
injuries a year,1 with an incidence of between 0.3-- 0.34
ACL injuries per 1000 population.2 Ski injuries account
for approximately 100 000 ACL injuries a year.3 It is esti-
mated that the annual financial cost for treatment of
these injuries is $2 billion.4 Further it is estimated that
17 500 ACL reconstructions will be performed annually
in the USA in the next10 years, with the costs estimated
to rise to $3 billion annually over this time.5
ANATOMY
The anterior cruciate ligament (ACL) is the primary
restraint to anterior tibial translation.6 The average
length is 31--38 mm and width 11mm.7 It passes from the
posterior aspect of the medial surface of the lateral fe-
moral condyle to a fossa in front of and lateral to the
anterior tibial spine. The femoral attachment forms the
shape of a segment of circle with the long axis tilted
slightly forward from the vertical such that the posterior
convexity is parallel to the posterior articular margin of
the lateral femoral condyle.8
The ligament passes anteriorly, medially and distally
across the joint from the femur to the tibia. It turns on
itself to form a slight outward (lateral) spiral, passing be-
neath the transverse meniscal ligament at its tibial end. A
few fascicles may blend with the anterior attachment of
the lateral meniscus. The tibial attachment is wider and
stronger than the femoral attachment.8
The femoral and tibial attachments are not a single
cord but rather a collection of fascicles that fan out over
Correspondence to: SK. E-mail: karmani1@hotmail.com
a broad flattened area. These fascicles are divided into
two groups, the anteromedial band (AMB) and postero-
lateral band (PLB).8,9 The AMB consists of fascicles
originating from the proximal aspect of the femoral
attachment and inserting into the anteromedial aspect
of the tibial attachment.The PLB inserts into the poster-
olateral aspect of the tibial attachment. When the
knee is extended the AMB is lax and when flexed the
AMB tightens and the PLB becomes slack as the femoral
attachment of the ACL assumes a more horizontal
position.10
Some authors have divided the ACL into anterome-
dial, intermediate and posterolateral bundles.11 The
isometric point (the point about which the femoral
origin may be rotated with ligament length remaining
constant) has been studied by sequential band transec-
tion and is found to lie anterior and superior to the
femoral origin of the intermediate fibre bundle, towards
the roof of the intercondylar notch.12
The cruciate ligaments are covered by a fold of
synovial membrane and are therefore intra-articular
and extrasynovial. The synovial covering is supplied by
vessels from the middle geniculate artery with minor
contributions from the lateral inferior geniculate artery.
The nerve supply is from the tibial nerve that penetrates
the joint capsule posteriorly to run along the synovial
covering. Fibres are also observed in the substance of
the ligament, which are thought to have proprioceptive
and sensory functions. Small numbers of mechanorecep-
tors have been reported (two types of slowly adapting
Ruffini type and rapidly acting Pacinian corpuscles). The
ACL is the only structure that specifically antagonises
anterior tibial translation generated by quadriceps con-
traction. Its mechanoreceptors form the afferent limb
of a reflex influencing quadriceps function.6
Menschik 197413 introduced the concept of the ubers-
chlagenes gelenkviereckor four bar linkage.This is based
on the assumption that the distance between origin and
insertion of both cruciate ligaments is constant in all
positions of the joint, which implies that the entire ACL
and PCL are in a state of constant tension. Fuss 19898
showed that the state of ligament tension depends on the
 ARTICLE IN PRESS
370
distance between the origin and insertion of the
ligament fibres. He demonstrated that different fibres
in the ACL experienced different tensions from flexion
to extension and that the whole ligament was not in
a constant state of tension, as in the four bar linkage
model.Only certain parts of the ACL were in a constant
state of tension, these were called the guiding bundles.
For the ACL these fibres were in the anterior part of
the ligament. Additional fibres come into tension as
the position of the knee changes; the fibres in tension in
addition to the guiding bundles in a given knee position
are called the safety bundles. If a strain is applied to
the knee, further fibres can be recruited in any particu-
lar position to resist this; these are called the limiting
bundles.
The ACL acts as a ligament complex, different fibres
coming into play in different knee positions.The divisions
into anteromedial and posterolateral bundles is an
oversimplification.8
A ligament fulfils its function in a state of tension, in
which the vast majority of its fibres are taut; this can be
considered its functional position. For the ACL this is in
extreme flexion, when practically all the ACL fibres are
parallel. In extreme flexion the ACL fibres are in least
tension, this being its resting position. The converse is
true for the PCL.8
The insertion of the ACL to bone is via a fibrocartila-
ginous enthesis. This can be divided into four zones.
Zone 1 represents the end of the ACL, zone 2 the liga-
ment collagen fibres intermesh with a fibrocartilage
region, zone 3, there is progressive mineralisation of
the fibrocartilage, which eventually merges with bone
in zone 4. This specialised attachment reduces stress
concentration at the junction; the uncalcified region
allows a gradual dissipation of stress; the calcified
fibrocartilage region ensures that the insertion point is
not narrowed under tension creating a stress riser.14
FUNCTION
The primary function of the ACL is to prevent anterior
translation of the tibia and hyperextension of the knee. It
acts as a guide rope during the screw home mechanism
of knee extension. As a secondary stabiliser it restrains
varus and valgus stresses on the knee.6 The ACL is sub-
jected to significant forces during daily function, with
a force of 445 N when descending a ramp,15 823 N when
descending a 19% decline and 0.7% bodyweight during
level walking.16
BIOMECHANICS
Ligaments take up tensile loads applied to joints.They are
viscoelastic structures allowing flexibility and strength.
Ligaments can be parallel fibre or random fibre
CURRENT ORTHOPAEDICS
constructs, based on the organisation of the collagen
fibre bundles within the ligament.The ACL has a parallel
fibre arrangement. Viscoelasticity is a type of deforma-
tion exhibiting the mechanical characteristics of viscous
flow and elastic deformation. Associated with viscoelas-
tic behaviour are the related phenomena of stress relaxa-
tion (the decrease in the force required to hold a
material at a constant length with time) and creep (the
increase in strain in a material when a constant stress is
applied over time). The ACL like most other biological
materials is also anisotropic (its biomechanical proper-
ties vary according to the orientation in which these
properties are tested). The viscoelastic and anisotropic
behaviour is due to the complex fibre arrangement of
the ligament and the relationship of the collagen fibres
to their investing proteinaceous ground substance.17
Ex-vivo biomechanical studies
Studies of the tensile behaviour of ligaments are difficult,
as ligaments are small structures and their effective
manipulation in tensiometers can damage the ligament
ends compromising the behaviour studied. Also the
choice of specimen grips used, determines the degree of
specimen slippage during testing. This affects the accu-
racy of strain values recorded. Finally the ACL is a com-
plex geometrical structure and accurate calculation of
the cross-sectional area is difficult, but vital for stress
calculation. These difficulties in study have been over-
come by investigators in various ways. Noyes et al.18 used
bone--ACL--bone blocks. The load--elongation behaviour
of this complex is represented in Fig.1. The graph can be
divided into a number of distinct regions.
Primary toe region
The stiffness of the complex is low in this region and
represents the straightening of the crimp in the resting
collagen fibres and alignment of the fibres in the direction
of the applied load. As loading continues the stiffness
increases. The strain of the ligament--bone complex at
the end of the toe region is 1.5-- 4%. Noyes suggests that
the elongation is caused by interfibrillar sliding and shear
of the interfibrillar ground substance.
Secondary linear region
This second region demonstrates more linear behaviour,
here the collagen fibres have organised into parallel fibre
arrays, having lost their crimping. The progressive in-
crease in load results in the recruitment of more fibres
to resist load. This region is used to calculate ligament
stiffness experimentally.
End of secondary region
Small dips in the curve appear that represent failure
of individual fibre bundles. The end-point of this linear
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THE ANTERIOR CRUCIATE LIGAMENT--I
400
300
Load (N)
Secondary Linear Region
200
100 Primary toe region
0
0 2
Elongation (mm)
Figure 1 Structural properties of a bone--ligament--bone complex (load--elongation curve).
region corresponds to the yield point for the ligament--
bone complex.
Failure
This represents progressive fibre bundle failure, which
occurs in an unpredictable manner. The ACL fails by
serial tearing at10 --15% elongation.18 The ultimate tensile
strength has been reported from 1725 to 2195 N.18
The figures reported, represent the results of different
testing mechanisms and data from patients of varying
ages.
In-situ biomechanical studies
Various researchers have attempted to study the
behaviour of the ACL within the knee, as the knee is
subjected to externally applied loads.
Markolf et al.19,20 developed a method of directly mea-
suring the resultant force in the ACL. The technique
involved fresh frozen cadaveric specimens in which the
base of the ligaments tibial attachment was mechanically
isolated using a core cutter and then fixing a specially
designed load-transducer to the bone plug that con-
tained the ligaments tibial insertion.The resultant forces
could be directly measured.
Their findings were:
1. Passive extension of the knee generated forces in the
ligament only during the last 101 of extension.
2. Internal tibial torque generated more force in the liga-
ment than external torque; these forces were highest
in extension.
3. Varus forces generated more force in the ligament
than valgus.
4. At 51 hyperextension the forces ranged from 50 to
240 N.
371
Ultimate Load
Yield Point
Energy Absorbed
Ultimate Elongation
Failure
4 6 8 10
The authors therefore suggest that passive flexion--
extension exercises in the range 101 to full extension are
safe, as they found no forces in the ACL in this range.
The effect of strain rates
Noyes et al.18 showed that the ACL--bone ligament com-
plex failed at higher load and greater elongation, absorb-
ing significantly more energy when under tensile loading
conditions at a faster rate of deformation (rather than
slow rate). They also showed that the major failure me-
chanism changed from a predominance of tibial avulsion
fractures at slow rates to ligament substance ruptures at
fast rates.
Other researchers measured the modulus of the ACL
under different tensile strain rates, showing a 30% in-
crease in modulus as the strain rate was increased from
0.003 to 113 mm/s.21
The effect of age
In a study of tensile properties of human ACL in paired
cadaveric knees of different ages it was found that the
linear stiffness, ultimate load and energy absorbed at
failure all decreased significantly with increasing age. An
increase of collagen fibril concentration in the human
ACL, from 68 fibrils/mm2 in the young to 140 fibril/mm2
in the old is reported. This may be the result of an
increase in small collagen fibrils, which confer little
improvement in mechanical properties.22
The effect of immobilisation
Noyes et al. demonstrated a 39% decrease in maximum
load to failure and 32% decrease in energy stored
to failure in ACL--bone ligament complexes taken
from primates, immobilised in a body cast for 8 weeks.
 ARTICLE IN PRESS
372
Recovery of the mechanical properties took upto 12
months once a mobilisation rehabilitation programme
was instituted. It is believed that immobilisation has the
effect of increasing the content of immature collagen in
ligaments, with weaker and fewer crosslinks. Osteoclas-
tic activity in subperiosteal bone at the tibial insertion
promotes failure by bony avulsion.23
The effect of steroids exogenous and endogenous
In a primate study Noyes et al. showed that application
of the human dose equivalent of long-acting corticoster-
oids to the knees of uninjured monkeys, produced a 9%
decrease in maximum load to failure and 8% decrease
in energy absorption at failure, in knee ligaments. The
effect was maximal at 15 weeks.24
Liu et al. demonstrated the presence of oestrogen
receptors in the human ACL. He showed a 40% reduc-
tion in collagen production at physiological levels of oes-
trogen. This he proposed as a mechanism for the
predisposition of the female athlete to ACL injury.25
THE ACL INJURY
There are four commonly described mechanisms of ACL
injury:
1. Internal rotation of the tibia on the femurF80% of
ACL ruptures.
2. Valgus/external rotationFcommon skiing injury.
3. HyperextensionFtackle from front with foot
planted.
4. Flexion with posterior tractionFdashboard injury.
Healing responses
Injuries to ligaments lead to the formation of a local
haematoma with excitation of an inflammatory response
that initiates healing by fibrosis. Healing of the ACL
depends on an intact synovial lining.26 When this synovial
sheath is torn blood dissipates within the joint and
a localised healing response is not possible. Synovium
has also been shown to initiate a healing response,
through the migration of synovial fibroblasts to the
injury site; for complete ruptures however no such
healing response is possible.26,27
ACL fibroblasts demonstrate greater matrix and col-
lagen production than medial collateral ligament (MCL)
fibroblasts;28 however, their proliferative and migratory
behaviour is inferior especially under the influence of
inflammatory mediators. This may explain why the MCL
has a greater potential for healing than the ACL.29
Partial tears
The ACL fails by progressive fibre bundle failure, which
under physiological failure loading usually results in com-
CURRENT ORTHOPAEDICS
plete tears. In milder injuries partial tears are possible;
these partial injuries have a limited potential for healing
as mentioned earlier. Fuss demonstrated the principle of
safety, guiding and limiting bundles. If the safety bundles
are injured in the partial injury this represents a cata-
strophic functional failure; damage to other fibre bundle
groups will result in instability predisposing to ultimate
failure.
CLINICAL ASSESSMENT
The correct diagnosis of ACL rupture is made by the ori-
ginal treating physician in only 6.8% of cases.30
History
About 40% of ACL injuries are associated with a pop at
the time of injury.The subject is unable to continue activ-
ity and swelling of the knee occurs within 2 h.31 It is an
error to assume that significant knee injury is unlikely in
the absence of swelling; associated capsular tears will
allow escape of the heamarthrosis into the leg compart-
ments. Pain is often not a significant feature.
Examination
Often it is difficult to examine a painful distended knee;
in such a case aspiration of the haemarthrosis and injec-
tion of local anaesthetic under sterile conditions is a
useful manoeuvre.
Specific tests of ACL integrity:
1. Lachman test. Introduced by Torg,32 it is performed
with the knee in 201 of flexion to nullify the effects of
hamstring spasm and doorstop effect of the posterior
horn of the medial meniscus on the medial femoral
condyle. The amount of anterior excursion of the tibia
under the femur is graded 1--3 (see later) and the quality
of the end-point (absent/spongy) noted. False negatives
may occur if one is unable to overcome hamstring spasm
or if there is a displaced bucket handle tear of the medial
meniscus. False positives may occur if one is actually
reducing a posteriorly displaced tibia secondary to a
PCL rupture. If there is an increased excursion but nor-
mal end-point then there is a partial ACL disruption, a
PCL injury or an injury to the posterolateral corner of
the knee.
2. Anterior drawer test. The patient is placed in a supine
position with the hip flexed to 451 and knees to 901. It is
important to apply the anterior drawer with the foot in
neutral to specifically test the ACL. With the foot on
internal and external rotation the posterolateral and
posteromedial complexes are tested also respectively.
The tibia is then pulled anteriorly. This test has been
shown to be less sensitive than the Lachman test in the
acute setting.30
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THE ANTERIOR CRUCIATE LIGAMENT--I
3. Pivot shift test. First introduced by Mackintosh,33
this is pathognomonic of a non-functioning ACL. The
test relies on an intact medial ligamentous complex
and intact iliotibial tract. It is performed with the knee
held in extension and internal rotation (this causes
the tibia to be subluxed anteriorly in the ACL deficient
knee). A valgus force is applied while the knee is
flexed. As the knee approaches 10 --201 of flexion the
tibia suddenly reduces with a clunk as the medial
ligament complex and iliotibial tract reduce the knee.
Patients with lax knees can demonstrate a pivot glide;
therefore it is important to compare with the contralat-
eral knee.
4. Losee test. A modification of the pivot shift with the
knee held in 451 of flexion, the foot held in external rota-
tion and hip in slight abduction. In this position the tibia
is reduced. A valgus force is exerted while the knee is
extended. As the knee reaches10 --201 the tibia suddenly
subluxes anteriroly. This manoeuvre is said to relax the
iliotibial band and therefore accentuates the sense of
pivot shift.34
Investigations
Plain radiographs
Standard views include anteroposterior, lateral, tunnel
(notch) and skyline (Merchant) views. These may reveal
a joint effusion, osseous fragments which can be ACL
attachment avulsions (seen on the lateral as corticated
bony fragments superior and anterior to the tibial spine),
or a Segund fragment (an avulsion of the mid-third of the
lateral capsule from the tibial plateau seen on the AP).
Degenerative changes suggesting previous ligament
injury are an effect of chronic ACL deficiency.
Arthrography
Shown to be 76 --94% accurate in demonstrating the sta-
tus of the ACL.35 Single contrast studies can visualise the
cruciates and articular cartilage. The main limitation to
this procedure is that it visualises the investing synovial
surface rather than the actual ligament and therefore
any abnormality of the synovium will interfere with its
accuracy (e.g. synovitis, clot, persisting vertical septum
and previous ligament repair). The test is also invasive
and often hindered by the presence of a large effusion. It
has thus been largely replaced by MRI.
Magnetic resonance imaging
The ACL is best evaluated on sagittal images with the
knee in 10 --151 of external rotation and full extension;
this aligns the ACL in the sagittal plane parallel with the
direction of the MRI cuts. It appears as a dark band of low
signal intensity on T1-weighted images, arising from the
373
medial aspect of the lateral femoral condyle and
inserting on the tibia.
In acute tears the ACL is discontinuous or serpentine
with a concave anterior margin. Angulation of the PCL
indicates complete ACL disruption as lack of anterior
restraint allows the tibia to sublux forward causing
the PCL to buckle.
Minck et al.36 found MRI to be 95% accurate in detect-
ing ACL tears confirmed by arthroscopy; this increased
to 97% if T2 images were added. He also showed that in
6% of normal knees the ACL is not seen at all. Fischer
et al.37 in a multi-centre trial comparing MRI with
arthroscopy findings demonstrated that MRI was 93%
accurate with evidence of over-sensitivity.
A variety of sequences are available to the radiologist,
T2 water sensitive sequences highlight contusions, oede-
ma and haemorrhage seen in association with ACL tears.
Inversion recovery orT2 sequences with fat suppression
are sensitive for marrow oedema and fractures; fast spin
echo or conventional sequences image the ACL. Thin
slices 3-- 4 mm are obtained in all three planes to avoid
volume averaging. Looking for secondary signs of ACL
injury such as buckled PCL and posterolateral bone
bruises can aid the diagnosis of ACL rupture. Gentili
et al.38 showed that the specificity of indirect signs for
ACL tears was between 91 and 100% but the sensitivity
was 19--90%.
Polly et al.39 devised a selective MRI protocol for
knees, namely 4 mmT1 sagittal slices with the foot in 201
external rotation. This procedure took 15 min compared
to the 1h for full T1 and T2 sequences. It visualised the
ACL in 76% of cases with 100% sensitivity, 96.9% specifi-
city and 97.3% accuracy.
Arthrometry
Liu et al.40 studied 38 patients with arthroscopically
proven complete ACL tears. All had MRI preoperatively
and KT-1000 arthrometry (scored positive for greater
than 3 mm differences). MRI was 97% sensitive for detec-
tion of ACL injuries but fell to 82% for complete rup-
tures. KT-1000 was 97% sensitive for 3 mm differences
and 100% for 2 mm. It was concluded that the decision
to reconstruct the ACL can be reliably made on arthro-
metry and clinical examination with associated meniscal
pathology detected and managed at arthroscopically
assisted ACL reconstruction.
Examination under anaesthetic and arthroscopy
Dehaven41 compared the results of arthroscopy and
clinical evaluation. He found false-negative results in 72
and 84% of patients assessed by anterior drawer and
pivot shift tests respectively; this value was 16% for the
Lachman test. Examination under anaesthetic improved
evaluation by the pivot shift test to16% false negative and
 ARTICLE IN PRESS
374
100% accuracy for the Lachman test. The accuracy of
arthroscopy is quoted as being 64 --94%.
CLASSIFICATIONOF LIGAMENT
INJURIES
Several terms have been used to describe the injury of a
ligament. The two most commonly used are sprain and
instability.
Sprain
A sprain is an injury to a joint ligament that stretches or
tears ligament fibres but does not completely disrupt the
ligament structure. The following nomenclature has
been proposed:42
* First-degree sprainFTear of minimal number of fibres
(micro tears or less than 1/3 ligament substance).
There is localised tenderness but no instability or
laxity.
* Second-degree sprainFTear involving 1/3--2/3 of the
ligament substance with localised tenderness but no
instability.
* Third degree sprainFTear of greater than 2/3 of liga-
ment substance with demonstrable laxity. This group
is further divided into:
1. Grade I Less than 0.5 cm of joint surface opening.
2. Grade II Less than 0.5--1cm joint surface opening.
3. Grade III Greater than1cm joint opening.
Instability
The most widely used classification system with respect
to the knee is that developed by Hughston et al.42-- 44 This
system attempts to describe the instability by the direc-
tion of the tibial displacement and when possible by
structural defects. It classifies instability as straight
(non-rotatory) or rotatory (simple or combined).
Straight instability can be medial, lateral, anterior and
posterior. Instability is assessed by stressing the knee
and graded into:
* 0FNormal laxity.
* 1+ FTranslation of tibia less than 0.5 cm.
* 2+FTranslation of tibia 0.5--1cm.
* 3+FTranslation of tibia 1F1.5 cm.
Rotatory instability can be anteromedial, anterolateral,
posterolateral, posteromedial or a combination of these.
Anteromedial rotatory instability (AMRI)
The medial tibial plateau rotates or subluxes anteriorly
in relation to the femur. It is tested with the knee flexed
CURRENT ORTHOPAEDICS
901 and then rotating the foot outward with a forward
pull on the proximal tibia as with the standard drawer
test. Instability implies disruption of the medial capsular
ligament, MCL, posterior oblique ligament and ACL.
Anteromedial rotatory instability has received more
attention in the literature than any other instability. Sev-
eral authors stress the importance of the medial menis-
cus as a stabilising force in AMRI and advocate its repair
whenever possible.
Anterolateral rotatory instability
There is excessive internal rotation of the tibia on the
femur with the knee flexed to 901. It is due to disruption
of the lateral capsular ligament, arcuate complex and
ACL.
Posterolateral rotatory instability
The lateral tibial plateau rotates posteriorly in relation
to the femur with lateral joint opening. There is
disruption of the popliteus tendon, arcuate complex,
lateral ligament and possibly the PCL.
Posteromedial rotatory instability
The medial tibial plateau rotates posteriorly with
respect to the femur with medial joint opening. There
is disruption of the MCL, medial capsular ligament,
posterior oblique ligament, ACL and medial portion of
the posterior capsule.
THE NATURAL HISTORYOF THE
UNTREATED ACL RUPTURE
The natural history of the ruptured ACL has been stu-
died by numerous authors, but the results vary widely
between different reports. This is attributed to studies
of different age groups, pathological entities (isolated
vs combined injuries) and the use of different scoring
criteria.
Several authors45,46 have described the course of un-
treated ACL injuries as one of progressive deterioration
of knee function, with the development of rotatory in-
stability, meniscal tears and post-traumatic osteoarthri-
tis, due to stretching of the secondary restraints of the
knee (menisci, collateral ligaments, PCL and articular
cartilage).
Many studies have reported satisfactory results with
non-operative treatments, with a large proportion of
patients returning to strenuous sports. These studies
stress the importance of an intensive rehabilitation
programme for strengthening thigh musculature and
emphasised the role of the hamstring in controlling the
ACL deficient knee.47,48 Roos et al.49 failed to show
a higher proportion of contact sports participation
 ARTICLE IN PRESS
THE ANTERIOR CRUCIATE LIGAMENT--I
at 7 years after surgical reconstruction as compared
with conservative treatment.
Knee function in the ACL deficient knee
Hawkins et al.50 published a retrospective follow-up of
non-operatively treated isolated ACL ruptures; this
showed 87.5% to have fair to poor results at 4 years.
Only 14% had returned to unlimited athletic activity,
30% required late reconstruction for disabling instability.
He therefore advocated the role of early surgery to pre-
vent such degeneration.
Mcdaniel51 reported a10 -year follow-up of 55 patients
with surgically verified ruptures of the ACL. 72% had
returned to strenuous sporting activity and 47% felt no
restrictions because of their knee.
Castleyn52 reported 2--12 year follow-up of 228 con-
secutive patients (excluding professional and high level
athletes) with arthroscopically proven ACL rupture.
Only 5.4% required secondary ACL surgery and 3.5%
secondary meniscal surgery.The International knee doc-
umentation assessment score showed 23% of the group
as grade A and 50% as grade B.
The meniscus in the ACL deficient knee
There is an increase in tears of the medial meniscus in
the chronically ACL deficient knee53,54 probably because
the medial meniscus is less mobile.This meniscal damage
may lead to subsequent arthritis.46,51 The medial menis-
cus is important in limiting anterior tibial translation
in response to anterior tibial loads in the ACL deficient
knee; the lateral meniscus is less important in this
instance. Allen55 postulated that the posterior horn of
the medial meniscus in the ACL deficient knee acts as
a buttress, by wedging against the posterior aspect of
the medial femoral condyle and restraining anterior tibial
translation. Of interest is that an isolated medial or
lateral menisectomy does not result in an increase in
anterior tibial translation.
Woods et al.53 arthroscoped 122 patients with func-
tional instability, on average 3-years post ACL rupture,
they demonstrated 88% had meniscal tears. Indellicato
et al.54 demonstrated that 68% of patients had meniscal
tears acutely post ACL rupture while 91% of those with
chronic instability developed tears.
The earliest findings of meniscal damage are longitudi-
nal fissures in the outer zone, usually on the undersur-
face of the posterior horn of the lateral meniscus.This is
probably due to the increased roll back of the femoral
condyles (especially lateral) at the beginning of flexion in
the ACL deficient knee.
The results of meniscal repair in the ACL recon-
structed knee are good56,57 and in the ACL deficient
knee encouraging,57,58 it is better to repair and create a
stable degenerate meniscus than to perform a partial
375
menisectomy. Casscells59 showed that degenerative me-
nisci did not cause degeneration of joint surfaces and
even in a chronically ACL deficient knee the degenerate
meniscus still distributes some load.
The evidence supports ACL reconstruction in
patients with established meniscal tears in the poste-
rior horns with strongly positive Lachmann or Pivot
shifts in order to protect the meniscus from progressive
damage.60,61
Osteoarthritis in the ACL deficient knee
The unstable ACL deficient knee will undergo progres-
sive degeneration.60,61 This is essentially secondary to
meniscal attrition, which increases point loading due to
loss of hoop stresses in the damaged meniscus.60,61
Degenerative changes are also described in the
ACL deficient knee without meniscal damage; this is
attributed to increased translation of the tibio-femoral
joint. Chondral damage at the time of ACL injury is
reported as high as 40% in chronic ACL injured
knees, with medial and patellar damage being greater
than lateral.54
REFERENCES
Key references are in bold type.
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program proven to prevent knee injury (videotape). Cinncinati
Sports Medicine Research and Education Foundation, Cinncinati,
1989.
2. Nielson A B, Yde J. Epidemiology of acute knee injuries.
A prospective hospital investigation. J Trauma 1991; 31:
1644--1648.
3. Feagin J A, Lambert K L, Cunningham RR et al. Consideration of
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