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Approach to cartilage injury in the anterior cruciate
ligament-deficient knee
Andrew S. Levy, MD, Steven W. Meier, MD*
The Center for Advanced Sports Medicine, Knee & Shoulder, Overlook Hospital, 33 Overlook Road/MAC #409,
Summit, NJ 07902, USA
Injuries to the anterior cruciate ligament (ACL)
commonly occur during deceleration pivoting move-
ments. These motions also produce high shear forces
across the cartilaginous surfaces of the knee. When
the ACL tears, there is even further shear stress across
the knee joint and often blunt trauma to the osteo-
chondral surfaces. Consequently, damage to the artic-
ular cartilage has been reported to occur with a
frequency of 15–40% in acute ACL tears [1,2]. In
chronic ACL-deficient knees, the frequency of carti-
lage lesions has been reported to be 79% overall, with
yearly increases from 40% at 1 year to 60% at 5 years
and > 80% at 10 years [3]. The treatment of damaged
articular cartilage remains one of the greatest chal-
lenges facing the orthopedic surgeon today.
Though, classically, ACL reconstruction has been
performed to restore function and prevent instability,
one may now view it as part of the fulmative attempt
to preserve the meniscus and protect the articular
cartilage. It has yet to be shown that ACL recon-
struction can slow the progression of existing chon-
dral lesions or prevent the incidence of new ones, but
a comprehensive approach to repairing cartilagenous
structures at the time of ACL reconstruction hope-
fully will prolong optimal knee function [4,5]. In
order to delineate treatment options regarding artic-
ular cartilage injuries, it is necessary to understand
the biomechanics and biology of healthy and injured
articular cartilage.
Articular cartilage: function
Successful human athletic performance requires
the optimal function of our articulations. Proper joint
function requires not only adequate strength and
stability, but a smooth, gliding articular surface to
allow an effortless range of motion. Dysfunction of
this natural bearing surface results in pain, swelling,
and limitation of function [6]. It has also been known
that injury to this structure may result in progressive
degeneration into osteoarthritis [7].
Articular cartilage: structure
The junction of calcified and noncalcified tissues
has increasingly become implicated as the site of the
essential lesion in articular cartilage injury. The
limited ability of articular cartilage to repair itself
has come under increased scientific scrutiny. Carti-
lage science has blossomed over the past 10 years,
resulting in a dramatic advancement of our under-
standing of the mechanics and anatomy of cartilage
injury. We now have a better understanding of
articular cartilage as a composite tissue with specific
mechanical and physiologic properties.
Articular cartilage consists of a highly specialized
extracellular matrix surrounding a sparse population
of chondrocytes. Chondrocytes are derived from
mesenchymal cells, and it has been demonstrated that
perivascular mesenchymal cells in cell culture can be
recruited to form chondrocytes or osteocytes under
the influence of certain morphogenetic factors [8].
The chondrocytes are responsible for the production
and maintenance of the extracellular matrix. Cartilage
0030-5898/03/$ – see front matter D 2003, Elsevier Science (USA). All rights reserved.
PII: S0030 -5898 (02 )00065 -2
* Corresponding author.
E-mail address: [email protected] (S.W. Meier).
Orthop Clin N Am 34 (2003) 149–167
is aneural and avascular, leaving chondrocyte viabili-
ty dependent on diffusion of metabolites from the syn-
ovial fluid.
The extracellular matrix in articular cartilage is
responsible for its smooth gliding properties. The
extracellular matrix consists primarily of type 2
collagen, proteoglycans, and water. Type 2 collagen,
which makes up 90–95% of the collagen present in
articular cartilage, is largely responsible for the ability
of cartilage to resist shear stress [9,10].
The proteoglycans present in cartilage consist of
glycosoaminoglycans, including chondroitin sulfate
and keratin sulfate side chains bound to a protein core
to form the aggrecan macromolecule. The protein
core is bound noncovalently to hyaluronate via link
protein to form large aggregates of aggrecan-hyaluro-
nate complexes. Glycosaminoglycans in cartilage con-
tain both carboxy-terminal and sulfated ends, which
are ionized in solution. These ionized groups result
in aggrecan molecules being highly hydrophilic and
account for the swelling pressure of cartilage. As a
pressurized proteoglycan gel with collagen fiber
reenforcement, cartilage is highly resistant to com-
pressive loads.
Articular cartilage is organized into four distinct
layers: superficial, middle, deep, and the calcified
cartilage [11,12]. In the superficial layer, cells and
collagen are arranged in a plane parallel to the joint
surface and proteoglycans are at their lowest concen-
tration. This surface is especially well suited to
facilitate the gliding motion of joints and the large
shear forces acting at the articular surface. The
middle layer has more rounded cells and an oblique
orientation to the collagen fibers. In the deepest layer,
the cell population is at its largest concentration, as is
the proteoglycan concentration. The collagen fibers
in the deepest layer are oriented perpendicular to the
joint surface. Deepest and adjacent to bone is the
calcified cartilage. The calcified cartilage is separated
from the noncalcified deep cartilage layer by an
eosinophilic staining wavy line referred to as the
tidemark. This junction of calcified from noncalcified
tissue has been shown in recent cadaver, animal, and
mathematical models to be a likely source for the
initial injury in cartilage injuries caused by shear
stress [13].
Water molecules are delivered on the surface of
the articular cartilage when a load is applied. The
water is ‘‘squeezed’’ through pores present in the ar-
ticular cartilage. These water molecules add to the
already present synovial-fluid surface film. The fluid-
phase portion of cartilage thus adds to the low friction
surface layer between the two articular surfaces.
Cartilage demonstrates time-dependent deformation
under a constant load: the viscoelastic property of
creep. It is most likely the result of the water
molecules being slowly squeezed out of the proteo-
glycan gel. Water molecules experience drag, how-
ever, as they are squeezed through the porous
collagen fiber network toward the articular surface,
thereby resulting in cartilage’s excellent ability to re-
sist compression. Under normal conditions, cartilage
functions smoothly for decades.
Mechanism of injury
The majority of ACL tears occur through non-
impact rotational deceleration mechanisms.. At the
time of ACL failure, it has been shown that the tibia
can sublux anteriorly and impact the lateral femoral
condyle. Thus, initial ACL disruption also results in
high shear forces across the tibiofemoral articulation.
Additionally, the subsequent instability following
ACL disruption can allow for increased loads to be
transmitted to articular surfaces.
Analytic studies by Mow et al have demonstrated
that articular cartilage behaves as a biphasic material.
Consequently, shear and blunt forces are manifested
at the junction of the uncalcified and calcified carti-
lage [13]. Utilizing this mathematical model, the
authors were unable to derive a situation whereby
shearing forces would produce surface failure (abra-
sion) without first causing damage at the tidemark.
This has been demonstrated in a cadaver model in
which loads with variable speed and force were
applied to femoral condyles [14,15]. The low-speed,
low-energy injuries resulted in injuries below the
articular surface; at the junction of the calcified and
noncalcified tissues. A zone of shear forces radiates
from the impact site, producing injury to the junction
of calcified and noncalcified tissues.
Animal studies have supported this concept.
Where low-energy blows produce selective injury to
the deep structures [14–16], they leave the articular
surface intact. This data implies that the junction
between calcified and noncalcified tissues may rep-
resent the ‘‘weak link’’ in articular cartilage’s ability
to resist shear forces. Transarticular loading of canine
metacarpal-phalangeal joints has resulted in cracks
appearing in the calcified cartilage [17] that went on
to osteoarthritis, thereby strengthening the argument
that injury to the deeper layers may ultimately lead to
articular degeneration. Recently, this phenomenon
has been demonstrated in athletes [18] and in patients
with a history of mechanical symptoms [6,19,20].
Many of these patients demonstrate arthroscopic
evidence of lesions that appeared to have a signifi-
A.S. Levy, S.W. Meier / Orthop Clin N Am 34 (2003) 149–167150
cantly larger deep component than the immediately
evident surface lesion. On probing, the uncalcified
tissue appeared to have ‘‘peeled’’ off from the cal-
cified layers.
The correlation between an acute shear-force
injury, such as during disruption of the ACL cartilage
lesions, is not definite. There is increasing evidence,
however, of the poor prognosis of predominant shear-
force injuries [16,18]. Indeed, a reconstructed liga-
ment may restore stability to the knee, but the
prognosis of the articular surface may depend on
factors other than stability [1]. Though an unstable
knee is functionally limiting, it can also lead to
subsequent meniscal injury. Meniscal pathology
resulting in meniscectomy is known to correlate with
joint degeneration, but initially stable or stable recon-
structed knees with intact menisci have also pro-
gressed to joint degeneration [1]. The origin of this
pathology may be the initial, silent insult to the
articular cartilage at the time of ACL disruption.
Additionally, athletes involved in pivoting sports
have developed cartilage lesions without ligament
or meniscal pathology [18]. The high shear forces
at the level of the tidemark in aggressive pivoting
athletes may be sufficient in some situations to induce
injury to the cartilage.
Progression of occult articular cartilage injuries is
an area of active scientific investigation in which
much is yet to be learned. One possible explanation
focuses on the potential space created between the
calcified and noncalcified cartilage at the time of
injury. As the joint is loaded, water molecules may
be delivered to this potential space as the cartilage
undergoes viscoelastic creep [13]. Thus pressurized,
the potential space may expand at the level of the
tidemark with each loading of the joint. Eventually,
the enlarged potential space may communicate with
the joint surface, and a surface lesion will become
evident. When probed, this small lesion will appear to
have delaminated from the calcified tissue, revealing
a much more extensive deep lesion.
Another theory postulates that the biologic
response to injury may result in a construct more
poorly suited to tolerate physiologic loads. A well-
designed animal study found that impulse loading of
rabbit knees resulted in subchondral plate fractures
that healed into a mechanically stiffer construct (via
tidemark advancement) than the normal joint [21].
These joints went on to joint degeneration with time.
Though abrasive and third-body wear does not
appear to cause chondral lesions, it will certainly
result in progression of articular injury and degen-
eration, and, eventually osteoarthritis. Acute injury,
progression of injury, multiple small insults, absent
menisci, alignment, and anatomy are among the
multitude of variables that may eventually result in
osteoarthritis. An articular lesion that progresses or
does not heal could, however, certainly result in a
roughened articular surface that could abrade the
surface with which it articulates.
Thus, disruption of the ACL can either be asso-
ciated with acute chondral injury or can result in
repetitive abnormal joint forces that subsequently
produce additional chondral injury. There may be
damage at the tidemark, furthermore, that may not
be evident at initial clinical evaluation. This may lead
to cartilage deterioration despite stabilization. It is
important, however, to realize that isolated chondral
lesions are often reported in patients who engage in
deceleration maneuvers, and some chondral lesions
found at ACL reconstruction may have been pre-
existing and asymptomatic.
Healing
Injury to the cartilage at either the surface or the
deep layers would not be significant if cartilage had a
strong ability to heal. Unfortunately, cartilage has a
limited ability for self-repair [19,22–31]. Numerous
studies have demonstrated that acutely injured chon-
drocytes respond with the production of collagen and
proteoglycans. This increased matrix production,
however, is insufficient to fill the injured region and
does not result in hyaline cartilage. Furthermore,
chondrocytes lack the ability to migrate into the
adjacent lesion and produce minimal mitotic activity
after adolescence [32].
The primary factor related to cartilage’s poor
healing response is the lack of blood supply to the
chondrocytes. This precludes the formation of fibrin
clot and inhibits the inflammatory cascade that most
tissues utilize in healing [32].
Bone bruises
The association of bone bruises with acute ACL
injury is well recognized. Bone bruises have been
demonstrated by magnetic resonance (MR) imaging in
more than 80% of knees after acute ACL rupture
[33–36]. These injuries typically occur in the lateral
compartment of the knee on the lateral femoral
condyle and posterolateral aspect of the tibia. These
impaction injuries necessarily also involve injury to
the overlying cartilage. Biopsy of the adjacent carti-
lage has demonstrated chondrocyte degeneration and
loss of proteoglycans [37]. The significance of bone
A.S. Levy, S.W. Meier / Orthop Clin N Am 34 (2003) 149–167 151
bruises and their relationship to chondral defects is not
well understood. An association seems to exist
between severe bone bruises and chondral injury.
Vellet et al described two types of bone bruises, based
on degree of bony involvement, as seen on MR
imaging. Reticular lesions, which occurred in 70%
of patients, are less severe and appear as hemorrhage
and edema in the medullary bone but do not involve
damage to subchondral bone. Geographic lesions,
occurring in 25% of patients, are more severe and
involve signal change contiguous with subchondral
bone. The authors found that the reticular lesions
tended to resolve after 6–12 months, whereas 62%
of the geographic lesions led to ‘‘osteochondral seque-
lae’’ [17]. Spindler et al found that when MR imaging
demonstrated impaction injury to the subchondral
bone with signal change in the overlying cartilage
layer, there was an increased incidence of arthroscopi-
cally apparent cartilage injury with bone bruises on
the lateral femoral condyle [35]. Careful evaluation
with arthroscopic probing of this region is thus war-
ranted at the time of arthroscopy. An association
between bone bruises induced in rabbits and late
degenerative change has been demonstrated. Al-
though this has not yet been shown in humans, it
should be taken into account in return-to-activity
decisions following ACL reconstruction.
Diagnosis
The presence of a chondral lesion may or may not
be known prior to performing an ACL reconstruction.
Physical examination in an unstable knee is not
reliable in detecting chondral lesions. MR imaging
has been shown to have a sensitivity as low as 21%
for detecting chondral lesions [18]. Joint effusion [38]
and the use of intra-articular gadolinium [39] have
been shown to increase the rate of detection, but MR
imaging, nevertheless, remains an unreliable diag-
nostic tool in identifying these lesions. Though
new MR imaging techniques (3D-SPGR) have
reported increased resolution of cartilage, sensitivity
for detecting chondral lesions remains poor (62%,
dependent on lesion location and grade), and their
availability to most clinicians limited. In the future,
imaging techniques that actually detect biochemical
and biomechanical changes and matrix degeneration
may increase sensitivity [40,41]. Because the current
gold standard for identifying chondral lesions is the
arthroscopic viewing and careful probing of articular
surfaces, many of these lesions that coexist with ACL
injury are often first diagnosed at the time of the
definitive ligament reconstructive procedure. This
fact can be used to illustrate the importance of the
surgeon’s need to be prepared to address a possible
chondral lesion each and every time an ACL recon-
struction is performed.
Following successful ACL reconstruction, occult
chondral injuries that were not apparent at the time of
reconstruction may produce persistent symptomatol-
ogy. Patients with articular cartilage lesions may
present with a myriad of confusing signs and symp-
toms, but the most common complaint is knee pain.
The pain is generally intermittent and may or may not
have been related to an additional injury. The pain
may be reproducible with certain activities or within a
specific arc of motion [18]. Mechanical symptoms of
popping, locking, and catching may occur if a frag-
ment has broken loose or a flap of delaminated
cartilage is present. Physical examination should
proceed with thorough inspection of the knee and
alignment, palpation of structures, range of motion
testing, and evaluation of joint stability. Special
attention should be paid to the joint line and femoral
condyles because tenderness may be present if a
lesion extends far enough anteriorly to permit palpa-
tion. Clinically evident joint effusion is present in
only about 30% of patients, though swelling is a
common complaint. Joint crepitation may be present
but in only 25% of patients [18]. Lesions in the
patella-femoral joint are more difficult to identify.
The patella-femoral grind and quadriceps resistance
tests are sometimes helpful. These lesions can easily
be mistaken, however, for anterior knee pain syn-
drome, patellar instability, chronic chondromalacia,
or early patella-femoral osteoarthritis [6]. Although
history and physical examination can reveal some
cartilage lesions, they are sometimes difficult to
identify. The key to making the diagnosis is to
maintain a high index of suspicion.
Numerous classifications have been published
describing the appearance of chondral lesions [6,20,
42–46]. It is critical, however, to note that most of
these classifications involve not only visualizing the
articular surface but also noting the consistency of the
cartilage when arthroscopically probed. Essentially,
most classification schemes describe lesions, either
open or closed. Closed lesions are simply the softening
of the cartilage on probing, with or without surface
changes. Open lesions are classified according to size
and depth of involvement. Full-thickness lesions
involve true exposed subchondral bone, whereas par-
tial-thickness lesions may involve only the layers
superficial to the calcified cartilage. Larger and deeper
lesions obviously have a worse prognosis.
Arthroscopy is invaluable in the evaluation of
articular cartilage lesions in that it allows direct
A.S. Levy, S.W. Meier / Orthop Clin N Am 34 (2003) 149–167152
visualization and classification of the lesion. Coin-
cident meniscal or ligament pathology can be ad-
dressed, and, if amenable, the chondral lesion can be
treated at the same operative sitting. If a more
extensive lesion is found, accurate assessment of the
pathology can be attained, thus permitting the patient
and physician to pursue an objective evaluation of the
various more-complicated treatment options.
Treatment
Nonoperative treatment
Nonoperative treatment of chondral lesions asso-
ciated with ACL injuries is relevant only in the knee
with post-ACL reconstruction status. In most cases, a
course of nonoperative treatment should be instituted
for at least 12 weeks in suspected chondral lesions
before surgical intervention is contemplated. Closed
chain-muscle strengthening combined with cryother-
apy and oral anti-inflamatories are the mainstay of
this treatment. Supportive braces (ie, elastic or neo-
prene) often assist in controlling effusions and are felt
to be beneficial by many individuals with chondral
lesions. Open chain strengthening may be used in
some cases when the work can be performed outside
the painful arc of motion. Intra-articular cortisone
injections are contraindicated in athletes because of
the direct deleterious effect on the articular chondro-
cytes and the potential for additional knee injury.
Hylauronate injections may be helpful, though no
data exist on their use in focal chondral lesions. No
data exist concerning the success of nonoperative
treatments in patients with chondral lesions.
Surgical treatment
The ultimate goal in the surgical treatment of
articular cartilage lesions is the reproduction of viable
hyaline cartilage bound to a restored subchondral bone
plate and the surrounding hyaline cartilage. The
achievement of this goal implies that arthritic deteri-
oration is prevented and reversed with resumption of
full asymptomatic function. At present, these goals
remain elusive and successful treatment has been
directed toward reduction of pain and swelling and
improved function. Additional difficulties exist in
comparing animal studies of articular cartilage. The
animal models used often have articular cartilage
properties that are extremely different from those in
human cartilage, and the lesions created rarely
resemble the human condition. The outcomes of these
studies have been based, furthermore, on the surgeon’s
ability to fill the cartilage defect with hyaline-like
cartilage. No evidence exists to suggest that tissue that
is more hyaline-like will diminish pain, improve
function, and prevent deterioration of the joint.
The operative treatment of chondral injuries of the
articular surface can be divided into four basic
principles. In advanced articular cartilage destruction,
(ie, varus collapse in ACL-deficient knee), the alter-
ing of joint forces may be utilized to decrease pain
and improve function. In isolated chondral lesions,
treatment includes stabilization of loose or worn
articular cartilage, plus either stimulation of a repair
process derived from the subchondral bone or regen-
eration of an articular surface (via transplantation of a
cell line or precursor tissue into the defect). In many
cases, a treatment option will include a combination
of different techniques.
The anatomic location of the lesion must be taken
into account when treating chondral lesions. This is
most true of the patellofemoral joint where most
lesions are the result of lateral patellofemoral com-
pressive forces such as tilt and subluxation. In these
cases, all surgical cartilage treatment options are
likely to fail if the underlying mechanical problem
is not addressed. Different areas within the joint,
furthermore, are not easily accessible for many treat-
ment options. Once the surgeon is aware that a
chondral lesion exists, he or she must select the most
appropriate technique for treating it.
Cartilage stabilization and debridement
The pain associated with chondral lesions is
attributed to the free nerve endings found in the
subchondral bone and the effects of cartilage debris-
mitigated effusions [13,46]. Consequently, the
removal of debris from the joint is performed to
diminish its irritative effects on the synovium. This
may be achieved either through lavage or direct
particulate removal. The exact mechanisms whereby
isolated chondral lesions irritate free nerve endings in
subchondral bone are unknown. This may be attrib-
uted, however, to unstable chondral flaps producing
mechanical irritation of the subchondral plate. Stabi-
lization of the walls of the chondral lesion is thus
performed. Unfortunately, the term ‘‘stable’’ has not
been well defined, and one must be careful to avoid
completely ‘‘peeling the orange’’ and removing
excessive amounts of cartilage. Several authors
[18,20] have demonstrated that the visible chondral
lesion averages approximately one third of the site of
the final lesion once debridement is concluded. Addi-
tional data exist to suggest that tapering chondral
edges is less mechanically advantageous than main-
A.S. Levy, S.W. Meier / Orthop Clin N Am 34 (2003) 149–167 153
taining vertical chondral lesion walls [43]. In the
isolated chondral lesion, stabilization and debride-
ment are the initial preparatory phase in treatment.
Traditionally, debridement has been performed me-
chanically with the use of rotary power shavers or
other hand instruments. Mechanical debridement with
rotary shavers is relatively easy and does not require
unusual or expensive equipment. It may lead to exces-
sive removal of normal cartilage, however, or leave
an unstable margin that can continue to propagate.
We have found that liberal debridement with bent
curettes and osteotomes can eliminate unstable edges
effectively in focal defects without jeopardizing the
surrounding surface.
Thermal modification—coblation chondroplasty
In theory, thermal modification is an attractive
alternative to mechanical debridement because it
allows for more precise ablation of smaller amounts
of tissue. ‘‘Tissue welds’’ can be accomplished,
eliminating residual unstable free edges that may be
prone to propagation.
Lasers (light amplification by stimulated emission
of radiation) are used in orthopedics to produce an
intense beam for cutting, coagulating, and ablating of
tissue. This occurs because of the absorption of laser
energy and its subsequent conversion to heat based
on the water content of a given tissue. In the late
1980s, surgeons began applying the thermodestruc-
tive effects of the laser to damaged articular cartilage.
The use with articular cartilage lesions achieved
prominence in 1989 when some investigators claimed
that the holmium laser could be used to stimulate
hyaline cartilage formation. [46].
Further research has questioned these findings and
also suggested that the penetration of laser energy is
deeper than once thought, and that there is a delayed
zone of cartilage destruction that occurs after the
initial laser use. This area is more extensive than
the initial zone of visible damage [47]. Immediately
after 0.5 J/Pulse laser treatment of full- (5 pulses) and
partial-thickness (1–2 pulses) defects in sheep, a
zone of damage was noted extending up to 500
microns below the ablation crater. At 2- to 4-weeks
postlaser surgery, hyperchromatic nuclei were seen
up to 800 to 900 microns distal to the ablation crater,
and loss of osteocytes was noted in the subchondral
bone. There was no healing of partial-thickness
lesions, but some fibrocartilaginous healing was
noted in the full-thickness defects. Ten weeks post-
laser treatment, no repair tissue was left in the full-
thickness lesions and no repair response had occurred
in the partial thickness lesions. Granulation tissue was
present in the damaged subchondral bone, but not in
the chondral ablation crater. This increased damage
with time is attributed to a photo-acoustic effect.
Further concerns regarding the use of lasers on
articular cartilage arise because of the growing num-
bers of reports of laser-induced avascular necrosis of
the femoral condyles. At present, there is little evi-
dence to suggest that laser use will produce hyaline
repair, and its use is not advised in the treatment of
focal chondral defects.
Radiofrequency
The use of radiofrequency (RF) has proliferated
recently in orthopedics for various applications in
tissue modification such as capsular and ligamentous
shrinkage and debridement of meniscal and chondral
lesions. RF works by generating ultrasonic waves that
produce heat as they pass through the target tissue.
This heat results in the denaturing and shrinkage of
collagen fibers. Both monopolar RF (MPRF) and
bipolar RF (BPRF) devices are commercially avail-
able. RF has been used to debride meniscus tears and
chondral defects by ablating the tissue flaps and
rough edges associated with these lesions. An attract-
ive feature is the ease of accessing hard-to-reach areas
with the compact RF probe where mechanical
debridement may be difficult. Another feature that
makes RF popular is its ability to virtually ‘‘melt’’ or
‘‘weld’’ fragmented tissue to a stable margin. This is
theoretically attractive when dealing with certain
chondral lesions to avoid the excessive ‘‘peeling the
orange,’’ as mentioned, that can be associated with
mechanical debridement (Fig. 1).
The concern about this technique is that it could
cause residual thermal damage to the surrounding
Fig. 1. Thermal coblation of patella chondromalacia with
radiofrequency.
A.S. Levy, S.W. Meier / Orthop Clin N Am 34 (2003) 149–167154
cartilage and subchondral bone and possibly lead to
progression of cartilage degeneration or perhaps even
osteonecrosis. Lu reported on the effects of MPRF on
partial-thickness cartilage lesions in sheep and found
that, though the appearance of the treated surfaces was
more smooth when compared with mechanical
debridement, scanning electron microscopy revealed
significantly more chondrocyte death in the RF group.
Studies show that RF induces changes resulting in
decreased chondrocyte viability, and progressive loss
of proteoglycan over time [48,49]. Theoretically,
BPRF should cause less collateral damage than MPRF
because the current flows from electrode to electrode
at the probe tip in contrast with monopolar current
which travels from probe tip, through the patient, and
to the grounding pad. Current studies do not substan-
tiate this, though. Kaplan performed a study, support-
ing the use of BPRF, with fresh human cartilage from
total-knee arthroplasty specimens using hematoxylin
and eosin staining and found that the chondrocytes
remained in their lacuna when analyzed 6 hours post-
trauma [50]. Lu et al, however, did a similar study
with confocal laser microscopy and vital cell staining
because they felt that light microscopy did not evalu-
ate chondrocyte viability effectively. This study
revealed chondrocyte death to a depth of 1.5 mm to
2.5 mm. Depending on the degree of articular thinning
in the particular specimen, this sometimes involved
penetration all the way down to subchondral bone
[51]. Recent forthcoming work by Markel also shows
BPRF creating significant chondrocyte death, even to
a greater extent than MPRF.
Depth of penetration has been shown to be depen-
dent on temperature, duration, and tissue quality.
The collagen denaturation and shrinkage desired
for annealing chondral surfaces begins to occur at
65�Celsius, whereas chondrocyte death occurs at only45�. Exposure times of 5 seconds with MPRF have
been shown to create cellular destruction comparable
to mechanical debridement, but at least 15 seconds of
treatment may be required to smooth the surface
adequately, doubling the depth of cellular death [52].
Moller et al has shown that the more extensive the
chondromalacia, the greater the vulnerability of the
cartilage to thermodestructive effects [53]. This sug-
gests that the undesirable effects of RF may be more
pronounced in the very lesions it is used for most. Stein
et al have shown that, after 1 year, electocautery
chondroplasty actually produces inferior clinical
results in grade 3 and 4 chondromalacia when com-
pared with mechanical debridement [54].
We feel that radiofrequency coblation has a limited
role in cartilage debridement. It may be appropriate
for patellar chondromalacia where partial-thickness
fibrillation can be extensive and full-thickness chon-
drocyte death may be avoided because patellar carti-
lage is particularly thick. Great caution should be
exercised, though, when considering the use of these
devices on condylar lesions where cartilage typically
is thinner.
Marrow-stimulating techniques
Several different marrow-stimulating techniques
(MST) have been described, and they involve the
stimulation of a fibrocartilage repair response by
accessing vascular channels through mechanical pen-
etration of the subchondral bone [33–60]. The lesion
first fills with blood, creating a hematoma and result-
ing in the production of a fibrin clot [24,25]. This
allows migration of mesenchymal precursor cells.
Early on, hyaline-like cartilage with a high proportion
of type 2 collagen may be found in the repair matrix
[61]. Over time, however, type 1 collagen becomes
more prevalent, resulting in a fibrocartilage fill of the
lesion [26]. No evidence exists to suggest that the
fibrocartilage binds to the surrounding normal hya-
line cartilage. It is theorized that the fibrocartilage’s
beneficial effect is caused by its ability to seal over
the lesion, thus diminishing mechanical stress on the
subchondral bone. This same sealant effect may also
reduce joint effusions by diminishing cartilage debris
from floating free into the joint [24].
Techniques of cartilage repair include abrasion,
drilling, and ‘‘microfracture’’. These techniques vary
mainly in their method of achieving subchondral
penetration. All of these techniques first employ
chondral stabilization and debridement as part of
the procedure. A significant advantage of these tech-
niques is that they can all be performed arthroscop-
ically on an outpatient basis with minimal morbidity
to the patient.
Cartilage lesion abrasion is differentiated from
abrasion arthroplasty in that, in chondral lesion
abrasion, only the base of an isolated chondral lesion
is abraded to penetrate the subchondral bone and
stimulate punctate bleeding. Abrasion arthroplasty
has been described in arthritic patients as a diffuse
deep abrasion of entire joint surfaces to produce a
massive bleeding bone surface. By contrast, abrasion
of a chondral lesion usually employs a shaver rather
than a burr to minimize deep penetration of the
subchondral bone. Short-term data (1–2 years) has
demonstrated that this technique is effective in
athletes in diminishing symptomatology and permit-
ting a return to competitive sports at approximately
10 to 12 weeks [18]. Most athletes did note persist-
A.S. Levy, S.W. Meier / Orthop Clin N Am 34 (2003) 149–167 155
ence of dull aching pain after strenuous activity. The
overall relief of symptoms in this athletic population
was comparable to the preliminary data published
on the results of cartilage cell transplant in non-
athletes [62].
Another common way of penetrating the subchon-
dral bone at the base of a chondral lesion is through
drilling. Theoretically, this technique preserves part
of the calcified cartilage layer while creating vascular
channels to allow bleeding from the subchondral
bone. There are two basic concerns with this tech-
nique. The first is that the speed of the drill may
generate excessive heat and produce localized osteo-
necrosis. The second is that the vascular channels
themselves result in columns of fibrocartilage that
adversely effect later treatment options [63]. In a
single report of this technique via open arthrotomy,
patients returned to full activity at 6 months with 69%
rated as good, 3% fair, and 28% poor [43].
Another alternative technique for cartilage repair
involves the use of specially designed ‘‘awls’’ to make
perforations in the subchondral bone (Fig. 2). Light
arthroscopic shaving to remove debris follows. The
theoretical advantage of this microfracture technique is
that access to undifferentiated mesenchymal cells is
provided without the drawbacks of drilling. Though no
clinical studies of this technique have been published,
the inventors have presented early animal data on the
technique. In horses, microfracture technique gener-
ated 50% more type 2 collagen than controls and
demonstrated 60% to 90% fill of full-thickness lesions.
The inventors have also compared this technique with
deep abrasion in horses. Six weeks after treatment, the
microfracture group lesions were noted to have a more
hybrid cartilage fill that was felt to be more hyaline-
like than that of the deep abrasion group [64].
Favorable short-term results of MST have been
reported. Steadman has reported reduction in pain,
Fig. 2. (A) Chondral lesion. (B) Chondral lesion after debridement and establishment of a stable border. (C) Chondral lesion after
microfracture. (D) Fibrocartilage ingrowth one year later.
A.S. Levy, S.W. Meier / Orthop Clin N Am 34 (2003) 149–167156
swelling, and improved function with an average
follow-up of 6 years [65]. Longer-term results may
not be as satisfactory, however. Fibrocartilage lacks
proteoglycan concentration and is thought to be less
durable than themore desireable hyaline cartilage [61].
There are no long-term comparative studies on MST
but clinical results probably deteriorate over time
because of the poor wear characteristics of fibrocarti-
lage. Limited studies on abrasion arthroplasty dem-
onstrate some temporary symptomatic relief but these
beneficial effects do not last beyond 2 to 4 years
[66,67]. Examination of failed repairs has revealed
soft, fibrillated tissue with central degeneration [68].
MST remains the standard by which other tech-
niques are measured. Advantages of this method
include its ease of use, low cost, low morbidity,
ability to be performed arthroscopically as an out-
patient procedure, and no contraindications with the
technique based on lesion size or location. Smaller
and relatively acute lesions in the femoral condyle
and trochlear areas tend to respond best [69]. Dis-
advantages to this technique are the prolonged post-
operative period of restricted weight bearing and low
durability of repair tissue. Biomechanically, fibrocar-
tilage is markedly inferior to normal hyaline cartilage
in response to shear and compressive stress [70].
Combined with the stress riser between the fibro
and hyaline cartilage, this makes survivability ques-
tionable over long periods of time. The predictability
of a successful outcome of fibrocartilage producing
treatments may be quite variable in different patients.
Autogenous osteochondral grafting
The rationale behind autogenous osteochondral
grafting (AOG) is the vast array of analytical, cada-
ver, animal, and (recently) human data demonstrating
that the common essential lesion in the development
of chondral lesions occurs at or near the tidemark
where the subchondral plate (subchondral bone and
calcified cartilage) interfaces with the uncalcified
cartilage. By replacing the entire osteochondral unit,
one could theoretically address and remove the actual
site of damage that has led to the visible lesion.
The first known report of transplanting articular
cartilage bone fragments was by Judet in 1908 for the
treatment of osteochondritis descicans [71]. In 1959,
Campbell et al reported using fresh osteochondral
autografts with little or no destruction occurring over
the first year [72]. In 1961, Pap and Krompecher
reported the transplantation of articular cartilage frag-
ments and their associated < 5 mm of subchondral
bone in 51 dogs. They noted survival of the articular
cartilage of up to 2 years provided normal physio-
logic loads were applied [73]. In 1962, Entin per-
formed autogenous osteochondral transplantation
from the foot to the hand and found that the cartilage
was not replaced [74].
In 1963, Campbell again reported on the use of
osteochondral grafting on 42 dog knees. In this study,
grafts were limited to 1 cm wide � 2 cm long, with
subchondral bone depth limited to < 5 mm [75]. They
noted that the osseous portion healed by 14 days via
creeping substitution, and that the articular cartilage
appeared grossly and histiologically normal at 2 years
postgrafting. They did note, however, that the articular
cartilage of the grafts did not bind to the surrounding
cartilage. They also speculated that increasing the
depth of the subchondral bone might lead to increased
necrosis of deep bone.
The healing of osteochondral autografts has been
further studied by McDermott et al [12]. It appears
that the surface osteocytes in the subchondral bone
survive, whereas those deeper than 3 mm are replaced
within the first 4 weeks.
Limited biomechanical studies have also been
performed to evaluate the effects of graft size on
function. It has been shown that a 15% increase in
diameter results in a 50% increase in torsional
strength of the grafts [76]. The potential unknown
effects of radius mismatch must temper this, however.
In 1994, Hangody reported on a technique termed
‘‘mosaicplasty’’ [77]. Mosaicplasty utilizes multiple
plugs of autogenous osteochondral graft to fill chon-
dral lesions. This procedure was performed on
122 humans. There were 57 medial femoral condyle
lesions, 48 lateral femoral condyle lesions, and
17 patella lesions with > 1 year follow-up. The
lesions ranged from 1 to 8 cm2 and grafts varying
from 2.7 to 4.5 mm diameter were obtained from the
lateral and medial edge of the condyles to fill the
defect via an open arthrotomy. At 1 year follow-up,
there were no cases of loosening or backing out of
the grafts and the average Hospital for Special
Surgery (HSS) score was 88.4 (range: 61–100).
Second-look arthroscopy was performed in many
cases and showed good congruency.
A prospective multicenter study was initiated to
follow up 200 patients for 5 years. Lesions treated
averaged 143 mm2 (range, 80–25 mm2). A total of
81% were performed arthroscopically, with 19%
requiring miniopen technique. So far, patients reported
improvement with the technique, and no deterioration
of results has been noted at 2-year follow-up [78].
The use of osteochondral autografts has also been
described in conjunction with ACL reconstruction. In
29 cases, 1- to 1.5-cm defects of the femoral condyles
A.S. Levy, S.W. Meier / Orthop Clin N Am 34 (2003) 149–167 157
were filled with osteochondral plugs (5 mm wide �10–15 mm long) harvested from the intercondylar
notch. At 2 to 3 years post-transplantation, the articular
cartilage on the transplants appears (via MR imaging
and probing) to have survived. The surrounding area is
filled with fibrocartilage. Clinically, this has correlated
with 19 excellent outcomes in 22 cases [79].
The resurgence in enthusiasm for osteochondral
grafting is associated with the increased development
of techniques that permit more predictable arthro-
scopic harvesting and delivery of the plugs. This,
however, applies only to limited areas of the femoral
condyles. The use of this technique on the patella,
trochlea, and posterior femoral condyles requires open
arthrotomy. Additionally, the treatment of defects
greater than 12 mm in diameter also require open
arthrotomy to ensure perpendicular graft placement.
Advantages of this technique include preservation
of hyaline cartilage, relative low cost, and the ability
to be performed arthroscopically as an outpatient
procedure in a single stage. Postoperative limitations
are less restrictive than the other techniques, requiring
only a few weeks of protected weight bearing. The
results appear to be at least comparable with MST in
the short term.
There are several disadvantages to this technique.
First of all, it is technically demanding and requires
advanced skill to be performed correctly. Obtaining
perpendicular graft harvesting and placement is crit-
ical, along with reproducing an accurate radius of
curvature. Very large lesions exceed the amount of
available graft tissue. Generally, defects < 2.5 cm in
area are most appropriate for this technique to not
surpass the capacity of graft sources. There are limi-
tations based on lesion location, and this method is not
recommended for patellar or tibial lesions. Far poste-
rior femoral defects are difficult to access with current
instrumentation. The harvesting of autologous graft
tissue necessitates a certain degree of graft site mor-
bidity, although very little is known about this. There
seems to be negligible graft site morbidity in the short
term, but no long-term studies have been done to re-
veal potential long-term adverse effects. Simonian et al
measured contact pressures throughout the knee and
determined that there are no true nonweight-bearing
areas of the knee, although the supero-lateral aspect of
the lateral femoral condyle above the sulcus terminalis
and the supero-medial area of the intercondylar notch
showed significantly less contact pressure [80]. Other
issues with this technique include cartilage thickness
mismatch, graft impaction forces, fibocartilaginous fill
around the plugs, and potential remaining stress riser
production between the two nonbinding cartilage sur-
faces. Multiple small plugs allow better radius curva-
ture matching versus a single large plug, but each graft
will be weaker in torsional strength, and more suscep-
tible to delamination during impaction. Grafts > 8 mm
in diameter raise concerns with harvest morbidity and
radius mismatch. Our preferred plug size is 6 mm.
Overall, autologous osteochondral grafting pro-
vides a very reliable means of reestablishing viable
hyaline cartilage to a lesion site (Figs. 3, 4).
Allograft osteochondral grafting
The use of osteochondral allografts for tumor
treatment dates back to the 1950s. In 1959, Campbell
et al reported using fresh osteochondral autografts
with little or no destruction occurring over the first
year [72]. When fresh and frozen allografts were
used, however, they became fibrillated and degener-
ated within a few months.
The important issues with osteochondral allograft-
ing include chondrocyte viability, graft incorporation
and remodeling, host immune reaction, and potential
for disease transmission. Historically, osteochondral
allografts were implanted ’’fresh’’ within 1 to 2 days of
harvesting. This presents certain logistical difficulties
as the patient and surgeon have to be ‘‘on call’’ if a
donor should become available. This also does not
allow sufficient time to process and screen specimens
adequately for disease transmission risk. As time
elapses after harvest, chondrocyte survivability dimin-
ishes progressively. It is not known what critical
percentage of viable chondrocytes is necessary for
optimal long-term durability of implanted cartilage,
but it is intuitive that lack of active chondrocytes will
lead to eventual cartilage degradation. Preservation
methods such as fresh freezing, freeze-drying, and
cryopreservation have been studied to prolong the
shelf life of specimens, but all have inferior results
when comparedwith fresh grafts [81,82]. Chondrocyte
survival has been improving, however, with newer
two-stage cryopreservation techniques. Cryoprotec-
tant use has subsequently produced 85% to 95%
chondrocyte survival rates with maintenance of chon-
drocyte phenotype [83].
Typically, osteochondral tissue has been consid-
ered ‘‘immunologically privileged’’ because many
believe that it does not generate a host-immune
response. Certainly, chondrocyte antigens have been
shown to be shielded from the humoral circulation by
cartilage matrix, allowing them to avoid recognition
by the host-immune system [84]. Though overt tissue
rejection does not occur as it would in soft tissue
organ transplantation, such as the heart or liver, which
requires immunosuppressive therapy, more subtle
A.S. Levy, S.W. Meier / Orthop Clin N Am 34 (2003) 149–167158
tissue incompatibility processes may still be occur-
ring. There is evidence to suggest that the bone
marrow elements are capable of generating a cell-
mediated host response that may impair graft incorpo-
ration and remodeling [85].
A major factor associated with the poor results of
osteochondral allografts appears to be related to the
normal remodeling of the cancellous bone. The
deterioration of the articular cartilage in allografts
appears to occur as a result of subchondral collapse
produced by bone turnover in the metaphysis [12,86].
Thus, the fate of the transplanted articular cartilage in
allografts is related to the fate of the subchondral
bone. It appears that for an allograft cartilage trans-
plant to be successful, the allograft must heal to the
surrounding bone incompletely so that extensive
Fig. 3. (A) Schematic of graft/inserter placement. (B) Schematic of final impaction of graft. (C) Schematic of final graft
placement. (From Levy AS. Osteochondral autograft for the treatment of focal cartilage lesions. In: Cole BJ, editor. Operative
techniques in orthopaedics, vol. 11, no. 2. Philadelphia: WB Saunders; 2001. p. 110–111.
A.S. Levy, S.W. Meier / Orthop Clin N Am 34 (2003) 149–167 159
revascularization and resorption does not result in
cartilage collapse.
To date, no studies exist that address the use of
modern osteochondral grafting techniques for allo-
graft. Theoretically, if successful, this would improve
graft thickness and radius of curvature mismatch
concerns in autograft techniques.
We feel that,with all the limitations currently
facing osteochondral allografting, it should not be
considered an initial treatment of choice. It is a major
Fig. 4. (A) Osteochondral grafting, chondral lesion. (B) Osteochondral grafting, roaming recipient site. (C) Placing graft in
recipient site. (D) Three osteochondral grafts in place. (E) Second look, 1-year later.
A.S. Levy, S.W. Meier / Orthop Clin N Am 34 (2003) 149–167160
reconstructive procedure that precludes all other repair
techniques. If the graft fails, the fall-back procedure
becomes prosthetic arthroplasty. In keeping with our
philosophy of not ‘‘burning bridges’’ whenever pos-
sible, we would consider osteochondral grafting a
salvage procedure and not for initial treatment.
Autologous chondrocyte reimplantation
Cartilage regeneration implies the transplantation
of functional cells or precursor cells into the defect.
Regenerative techniques include autogenous peri-
chondral transplant, autogenous periosteal transplant,
and autogenous chondrocyte transplant.
Rib perichondrium has been utilized in an attempt
to fill osteochondral lesions in young patients. Its use
has not been documented in isolated chondral lesions.
Early success in osteochondral lesions did not persist
because of the high propensity for perichondrium to
calcify. Its use is not recommended in chondral lesions.
Periosteum is plentiful throughout the body,
although its thickness diminishes with age. Several
studies have demonstrated that the cambium layer of
periosteum can differentiate into chondrocytes and
form hyaline cartilage [7]. When sutured to the base
of a lesion, a hyaline-like repair tissue was formed
with similar histiologic characteristics (87% type 2
collagen) and biomechanical characteristics as normal
hyaline cartilage. The use of continuous passive
motion (CPM) has been found to be advantageous
in increasing the success rate of periosteal transplanta-
tion in animals [87]. Preliminary data has demonstra-
ted the efficacy of this technique in reducing pain in
lesions of the patella and the femoral condyle [88].
Controversy exists as to whether the periosteum is
best placed with the cambium layer facing into the
joint [87–89] or into the lesion [20,21].
The advantages of periosteal transplant are that the
supply is virtually unlimited and that minimal instru-
mentation and commercial supplies (cell culturing) are
required. Unfortunately, the promising early results of
periosteal transplant to the femur appear to diminish
with time [90]. Patient morbidity is fairly high, as this
requires a formal arthrotomy and prolonged CPM.
Additional concerns exist as to the fact that the
cellularity of the periosteal harvest appears to be
closely related to the experience of the harvester [90].
In order to augment the periosteal transplantation,
in 1989, Grande et al reported placing cultured auto-
genous chondrocytes under periosteum sutured
directly to the surrounding hyaline cartilage. In rabbit
defects, this was found to produce greater filling of the
defects than in controls (periosteum alone sutured to
cartilage). Histologically. this repair tissue was felt to
be significantly more hyaline-like than the controls. In
1995, Brittberg et al reported on the results of this
technique in 23 human subjects [62]. They reported
eight good (occasional pain and swelling), six excel-
lent, and two fair, with poor results on femoral lesions
1 year post-transplant. Patellar lesion treatment did not
perform as well—yielding two good results, three fair,
and two poor. Arthroscopic second looks revealed that
there was soft repair tissue in the defects without
incorporation into the surrounding hyaline cartilage.
This conflicted with the data from previous studies that
showed early degeneration at 12 weeks post-transplant
[91]. These improved results were attributed to
changes in postoperative regimen.
Recently, long-term follow-up has been reported
by Peterson et al with a group of 61 patients who
have been treated with autologous chondrocyte
implantation (ACI) for femoral and patellar lesions
[76]. These researchers found that 82% of patients
had a good/excellent result after 2 years, and 84% had
a good/excellent result after 5 to 11 years. They
concluded that most failures occurred within the first
two years of surgery, and that if patients had good
function at 2 years, they would most likely continue
to do so. This suggests that successful ACI results in
durable regenerated tissue. In 8 of 12 patients, biopsy
of regenerated tissue revealed hyaline-like matrix
composed primarily of type 2 collagen, well anchored
to the subchondral bone. The remaining biopsies
were predominantly fibrous in nature.
Recent data from the Cartilage Repair Registry
reveals that 81.8% of patients who had ACI for
femoral lesions were significantly improved after
6 years [92]. Medial femoral condyle lesions were
most numerous, and 70% of these patients experi-
enced improvement. Lateral femoral condyle and
trochlear lesions tended to do better but presented
relatively infrequently. The function of improved pa-
tients was typically assessed as ‘‘good’’ because there
were no ‘‘excellent’’ ratings. The majority of these
patients, however, were rated as poor prior to im-
plantation, and ACI was often used as a salvage treat-
ment in very severe cases. Most frequently, reported
adverse events include hypertrophic repair tissue and
intra-articular adhesions.
Enthusiasm for this technique in the United States
has been hampered by theoretic and economic con-
cerns. This staged procedure is invasive and requires a
formal arthrotomy. It is also expensive and requires
prolonged postoperative limitations. Expectations in
this patient group tend to be more modest and directed
toward returning patients to activities of daily living as
opposed to sports. This may be because this technique
A.S. Levy, S.W. Meier / Orthop Clin N Am 34 (2003) 149–167 161
is often employed in patients with severe conditions
involving very extensive disease and history of pre-
vious failed surgery. Recent follow-up provides prom-
ise for this technique, however, in properly selected
patients. Use of this technique in younger ACL-injury
patients with large lesions in knees that are otherwise
relatively intact may produce more good-to-excellent
results and make returning to sports a realistic
expectation (Fig. 5).
Cartilage stimulation via growth factors
An exciting area of cartilage repair and regenera-
tion involves the use of growth factors. These poly-
peptides attach to chondrocyte cell surface receptors
(integrins) and influence matrix production, prolifera-
tion, and migration and replication [7]. The two most
promising factors at present are insulin-like growth
factor I and transforming growth factor beta. These
have been shown to enhance matrix synthesis in
animal studies. Unfortunately, these growth factors
are not specific for chondrocytes and can affect an
entire joint adversely. Further research is needed into
delivery, regulation, and modulation of these factors
before they are utilized in human joints.
Authors’ preferred treatment
Symptomatic lesions require treatment. The pres-
ence of a symptomatic chondral lesion may or may
Fig. 5. (A) Delamination of chondral lesion. (B) Autologous chondrocyte reimplantation. (C,D) One-year follow-up—hyaline
cartilage ingrowth.
A.S. Levy, S.W. Meier / Orthop Clin N Am 34 (2003) 149–167162
not be known prior to ACL reconstructive surgery.
When physical findings of pain, joint line tender-
ness, and catching or locking are present, it is
seldom clear whether meniscal or chondral patho-
logy or both are responsible. As previously stated,
MR imaging is of limited benefit as chondral lesions
are identified by MR imaging in only a minority of
cases. MR imaging is fairly sensitive in detecting
meniscal tears, but the mere presence of a meniscus
tear on a preoperative scan does not preclude a
coexistent chondral lesion that may be causing either
a portion or all of the symptoms. Certainly, a normal
appearing MR image in the presence of mechanical
symptoms is even less helpful. A symptomatic
lesion can be considered one whose existence is
apparent on arthroscopic viewing in a patient with
the appropriate preoperative signs and symptoms.
Treatment options in this context include MST,
AOG, or ACI.
Alternatively, chondral lesions may be found in
patients with no preoperative mechanical symptoms.
We believe that asymptomatic lesions discovered
incidentally at the time of arthroscopy for ACL
reconstruction should be treated with at least a
marrow-stimulating technique. There is very little
disadvantage to this approach in that it does not
‘‘burn any bridges.’’ Minimal additional morbidity is
incurred, and any of the more extensive chondral
resurfacing techniques can still be performed at a
later date if the need arises with no adverse effect.
ACL injury patients are typically very active and
place high demands on their knees. Even though
researchers have not been able to prove that cartilage
repair or regeneration has any effect on the devel-
opment of degenerative change in the knee, it makes
sense that some attempt should be made to address
the deficient articular surface in this setting, particu-
larly if the additional procedure adds very little in
the way of morbidity. If lesions are on the central
and anterior third of the femoral condyles, the
surgeon may be justified in performing an osteo-
chondral graft. The harvesting of up to three plugs
from the lateral notch can be performed as part of
the notchplasty.
Postoperatively, the ACL protocol needs to be
modified. Early active range of motion, exercise
bicycle, and isometric quadriceps exercises are ini-
tiated while the limb is kept nonweight-bearing for
3 weeks. From 3 to 6 weeks, partial weight bearing
is initiated. After 6 weeks, the patient is advanced to
full weight bearing, and strengthening exercises are
instituted. Sports-specific rehab is initiated at 10 to
12 weeks with full return to activities based on a func-
tional assessment.
MST for a chondral lesion should not be termed a
treatment failure until symptoms continue for at least
6 months postop. If pain and/or swelling persist and
function is diminished, consideration can be given to
a salvage procedure. In salvage situations, it is
important to allow the subchondral plate to recover
from the initial surgery. Once a patient has failed a
less-aggressive treatment option, our preference is to
perform an ACI technique for lesions of the femoral
condyle and trochlea. It is important to begin prepar-
ing the patient for this procedure and its implications
prior to harvesting the chondrocytes for culture. If
this is unachievable for socioeconomic reasons, con-
sideration is given toward osteochondral grafting via
a formal open arthrotomy.
ACL-dependent scenarios
ACL surgery with known chondral lesion
The presence of a chondral lesion after acute ACL
injury may be known to the surgeon if it is visible on
MR imaging. In this scenario, the physician has plenty
of time to plan addressing the chondral lesion at the
time of ACL reconstructive surgery and to counsel the
patient appropriately. The surgeon may choose from
MST, AOG, or ACI depending on the size and
location of lesion. If AOG is used, a natural choice
for the graft source site would be the intercondylar
notch because a notchplasty may be performed any-
way—lessening the concern of graft site morbidity. If
the lesion is extensive and ACI is determined as the
most appropriate choice, the procedure will have to be
staged, with the chondrocyte biopsy performed ini-
tially. ACL reconstruction could also be performed at
the time of the initial procedure or 4 to 6 weeks later at
the time of chondrocyte reimplantaton.
ACL surgery with incidental chondral lesion
It is not unusual to find an unexpected chondral
lesion at the time of ACL reconstruction. Patient
preparation and pre-perative discussion is paramount
for success in all cases. Because of the frequent
overlap in symptoms with meniscal pathology, we
inform all arthroscopy patients that there is a like-
lihood that an articular cartilage procedure may be
required at surgery. One must explain the potential
divergence in surgical technique and the postopera-
tive treatment regimen should a cartilage lesion be
identified. Because symptomatology is unknown, the
surgeon should strive to select treatment options that
minimize potential morbidity.
A.S. Levy, S.W. Meier / Orthop Clin N Am 34 (2003) 149–167 163
Chronic ACL with symptomatic chondral lesion
Based on natural history data it is obvious that
ACL deficient knees are prone to developing chon-
dral injury. The incidence of lesion formation
increases as time passes from the initial ligamentous
disruption. A chronically ACL-deficient knee with a
symptomatic chondral lesion requires treatment. As
mentioned before, proper preoperative patient coun-
seling is absolutely essential. If arthoscopy is being
planned on a knee with mechanical symptoms, the
surgeon may not know if the symptoms are caused by
a meniscus tear or a chondral lesion. The expectation
may be that the procedure will be a simple knee
arthroscopy with partial menisectomy, but the patient
needs to be aware that it may be more involved if a
chondral lesion is found and AOG or ACI is selected
for treatment. Because cruciate insufficiency may
jeopardize a healing cartilage graft, cruciate integrity
should be restored to protect a new graft from shear
forces and episodes of instability with either concom-
itant or staged surgery [93,94]. As a general rule,
whenever a chondral lesion in an ACL-deficient knee
is grafted, the ACL should be reconstructed.
An additional and novel graft source for AOG,
unique to chronically ACL-deficient knees, has been
described by Bobic et al as the ‘‘chondro-osteophyte’’
often found on the lateral aspect of the medial
femoral notch [3].
Reconstructed ACL with new lesion
Apatient with a previously reconstructed ACLmay
present with a new symptomatic chondral lesion. This
may be a result of new injury or possibly late sequelae
from the initial injury. The natural history of bone
bruises and their possible role in late chondral lesions
is unclear. In any case, this requires treatment. First of
all, it is critical to assess and ensure integrity of the
ACL graft prior to treating a cartilage lesion because
cruciate integrity must be restored to protect a new
graft from shear forces and episodes of instability.
Assessing the functional status of a reconstructed
ACL can be a challenge, though. Clinical history is
helpful in raising suspicion of a disrupted graft if
there has been an acute reinjury. Physical examina-
tion is helpful, but a knee with a functioning ACL
graft can still exhibit increased anterior translation on
the Lachman test and a positive pivot shift test. MR
image scanning can be helpful but does not provide
functional information about a reconstructed liga-
ment. Instrumented testing of knee laxity, on the
other hand, such as the KT-1000 can reveal functional
information and play a role. Normally, testing is
performed on both knees and the side-to-side differ-
ence in manual maximum anterior translation of the
tibia is compared with the knee at 30� of flexion.
ACL disruption is likely when there is greater than a
3-mm difference. This has been described for acute
tears. Using this technique for evaluating ACL recon-
struction grafts may not be as reliable because a
certain amount of increased laxity is commonly noted
when compared with the normal knee despite a well-
functioning graft. If post-reconstruction baseline val-
ues are available, however, a significant increase in
same-side values may suggest graft rupture. Finally,
direct probing of the ACL graft during a diagnostic
arthroscopy can also provide helpful information.
If AOG is performed, it is important to be aware
that the intercondylar notch may not be available as a
graft source if a notchplasty was performed during
the initial procedure. This is an important considera-
tion because availability of graft material will deter-
mine the maximum-size lesion that can be treated
with this technique. For ACI, an initial arthroscopic
cartilage biopsy would precede concurrent ACL
reconstruction/ACI by 4 to 6 weeks. Rehabilitation
would proceed as it would for an isolated ACI
procedure as outlined above.
Summary
The treatment of articular cartilage lesions remains
one of the great challenges facing orthopedic surgeons
today. The technique of chondrocyte transplantation
has opened the door for the application of biologic
solutions to difficult problems. These techniques will
prove the keystone of further advances into biologic
joint repair and replacement. Enthusiasm, however,
must be tempered by the numerous gaps in cartilage
science and the overwhelming need for further long-
term data to demonstrate the efficacy of these tech-
niques in thwarting the presumed eventual progression
of these lesions toward osteoarthritis. The status of the
articular cartilage is of paramount importance in ACL
decision-making. Every effort must be made to protect
the existing hyaline articular cartilage during ACL
reconstruction. Though current cartilage repair tech-
niques are in their infancy, they remain stepping-
stones to future developments. It is hoped that we will
one day be able to regenerate normal hyaline cartilage
without great morbidity. At present, the ACL surgeon
must accept techniques that diminish symptoms and
do not burn bridges to future advances. The orthopedic
surgeon must increase his knowledge of the basic
science of articular cartilage in order to best choose
from the various cartilage treatments that evolve.
A.S. Levy, S.W. Meier / Orthop Clin N Am 34 (2003) 149–167164
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